emergency neuroradiology

EMERGENCY NEURORADIOLOGY

T. SCARABINO • U. SALVOLINI • J.R. JINKINS(Editors)

ii edizione

With 294 Figures in 793 Parts and 10 Tables

EMERGENCYNEURORADIOLOGY

EDITORS

Tommaso ScarabinoDepartment of Neuroradiology, Scientific Institute “Casa Sollievo della Sofferenza”, San Giovanni Rotondo (FG), ITALY

Department of Radiology, ASL BA/1, Hospital of Andria (BA), ITALY

Ugo SalvoliniNeuroradiology and Department of Radiology, University of Ancona, ITALY

J. Randy JinkinsDepartment of Radiology, Downstate Medical Center, State University of New York, Brooklyn, NY, USA

This edition of Emergency Neuroradiology by Scarabino – Salvolini – Jinkins is publishedby arrangement with Casa Editrice Idelson-Gnocchi srl, Naples, Italy

ISBN-10 3-540-29626-3 Springer Berlin Heidelberg New YorkISBN-13 978-3-540-29626-3 Springer Berlin Heidelberg New York

Library of Congress Control Number: 2005934099

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© Springer Berlin Heidelberg 2006

Printed in Germany

The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and

regulations and therefore free for general use.

Product liability: The publishers cannot guarantee the accuracy of any information about the application of operative techniques and medications contained in this book. In every individual case the user must check such

information by consulting the relevant literature.

Editor: Dr. Ute HeilmannDesk Editor: Meike Stoeck

Production Editor: Joachim W. SchmidtCover Design: eStudio Calamar, Spain

Typesetting: FotoSatz Pfeifer GmbH, 82166 Gräfelfing, GermanyPrinted on acid-free paper – 24/3151 – 5 4 3 2 1 0

CONTRIBUTORS

R. Agati, M. Armillotta, S. Balzano, A. Bertolino, M.G. Bonetti, M. Cammisa, A. Carella, A. Carriero, A. Casillo, M. Caulo, A. Ceddia, G. Cerone, S. Cirillo, P. Ciritella, C. Colosimo, V. D’Angelo, P. D’Aprile, R. De Amicis, G.M. Di Lella, F. Florio, A. Fresina, M. Gallucci, T. Garribba, S. Ghirlanda, G.M. Gianna-tempo, M. Impagliatelli, A. Lorusso, S. Lorusso, P. Maggi, A. Maggialetti, N. Maggialetti, M. Maiorano, M. Mariano, C. Masciocchi, F. Menichelli, M. Nardella, F. Nemore, M. Pacilli, T. Parracino, U. Pasquini,

L. Pazienza, C. Piana, F. Perfetto, S. Perugini, G. Polonara, T. Popolizio, M. Rollo, B. Rossi, R. Rossi, M. Schiavariello, C. Settecasi, A. Simeone, L. Simonetti, A. Splendiani, A. Stranieri, V. Strizzi, A. Tarantino,

T. Tartaglione, G. Valle, N. Zamponi, N. Zarrelli

FOREWORD

Encouraged by the success of the Italian editions, the Authors have decided to publish an Englishversion taking into account the latest technical and methodological advances and the consequentnew acquisitions in clinical practice. The contribution of Professor R. Jinkins has been essential tocarry out both these tasks.

The resulting work is an up-to-date technical tool that preserves its original aim of contributingto the training of those radiologists who work in emergency departments.

We hope that this revised and extended English version will have the same success as the previ-ous Italian editions, thereby confirming the validity of our initiative.

The work of all the friends and colleagues who have contributed to the making of this book isgratefully acknowledged.

Tommaso ScarabinoUgo Salvolini

CONTENTS

I. CEREBROVASCULAR EMERGENCIES1.1 Clinical and diagnostic summary

Neuroradiological protocol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Haemorrhagic stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4Ischaemic stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

1.2 CT in ischaemiaIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7Particular forms of infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21Differential diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

1.3 CT in intraparenchymal haemorrhageIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27The role of CT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34Particular forms of IPH . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47

1.4 CT use in subarachnoid haemorrhageIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58Postsurgical follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60

1.5 MRI in ischaemiaIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64Possible uses of clinical MR in the diagnosis of emergency ischaemia

after the hyperacute phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70

1.6 Functional MRI in ischaemiaIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73Diffusion MRI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73Perfusion MRI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75MR spectroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80

Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

1.7 MRI in haemorrhageIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92

1.8 UltrasoundIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94Clinical applications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100

1.9 MR angiographyIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102MR angiography of the supraaortic vessels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103Intracranial vessels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105Clinical applications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116

1.10 Conventional angiographyIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117Clinical indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118Applications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128

II. HEAD INJURIES

2.1 Clinical and diagnostic summaryNeuroradiological protocols . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135

2.2 CT in head injuriesIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161

2.3 MRI in head injuriesIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163Drawbacks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177

2.4 CT in facial traumaIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179

X CONTENTS

Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190

III. INTRACRANIAL HYPERTENSION3.1 Pathophysiology and imaging

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195The pathophysiology of intracranial hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196Pathophysiological classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201ICH related to abnormal CSF physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203Hydrocephalus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203ICH related to vascular causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210Aetiological causes of intracranial hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211

3.2 Neoplastic craniocerebral emergenciesIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213Imaging examination technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214Posttherapeutic neoplastic emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226

3.3 Angiography in brain tumoursIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229Meningiomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230Gliomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233Other cerebral neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234Metastases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237

IV. EMERGENCY NEURORESUSCITATION4.1 Toxic encephalopathy

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241Alcoholic encephalopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241Methanol intoxication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 246Ethylene-glycol intoxication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 246Intoxication from narcotic inhalation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 246Intoxication from medicines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247Carbon monoxide (CO) intoxication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251

4.2 The neuroradiological approach to patients in comaIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253Modes of intracranial analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253Technical considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258Acute primary focal cerebral lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 259Widespread insult/brain swelling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 264

4.3 Nuclear medicine in neurological emergenciesIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265

CONTENTS XI

Measuring CBF . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266Clinical usage of HM-PAO SPECT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272

4.4 Diagnosing brain deathIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 282

4.5 Postsurgical craniospinal emergenciesIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283Cranial emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 284Hypophysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 288Spinal emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 288References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 292

V. SPINAL EMERGENCIES

5.1 Clinical and diagnostic summaryNeuroradiological protocols . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 298

5.2 CT in spinal trauma emergenciesIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 299Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319

5.3 MRI in emergency spinal trauma casesIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321Semeiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 323References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 334

5.4 Emergency imaging of the spine in the non-trauma patientIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337Imaging techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 338Extradural pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 338Other types . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 367

VI. NEUROPAEDIATRIC EMERGENCIES

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 371Cerebrovascular disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 371Head injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380CNS infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 387Intracranial hypertension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 400

SUBJECT INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403

XII CONTENTS

I

CEREBROVASCULAR EMERGENCIES

3

Stroke, a clinical diagnosis of acute, sudden-onset neurological deficit, is one of the maincauses of death and permanent disability in theindustrialized world. Pathologically the processmay be an ischaemic or a haemorrhagic event,or both. About 85% of cerebrovascular acci-dents result from ischaemia, predominantlysecondary to carotid thromboembolism.

The stroke patient may clinically presentwith typical symptoms of focal neurologicaldeficit, a combination of deficit with coma, ameningeal irritation syndrome in the form ofheadache, vomiting and neck stiffness, or lessfrequently with the gradual appearance of anextrapyramidal or pseudo-bulbar syndrome of-ten associated with progressive mental deterio-ration.

The clinical picture in stroke patients can beclassified according to how long the neurologi-cal deficit lasts, or alternatively whether or notthe deficit is permanent. Four different suchclinical categories can be distinguished. Thetransient ischaemic attack (TIA) is representedby a sudden, focal non-convulsive onset of aneurological deficit that usually subsides in afew minutes and always resolves within 24hours; the reversible ischaemic neurologicaldeficit (RIND) lasts at most for a period of 48hours followed by a return to complete nor-mality within 3 weeks; progressive ictus is a tem-

porally worsening clinical condition during thefirst 24 to 48 hours following acute onset asso-ciated with persistent functional deficit; com-plete ictus is a clinically stable condition, withthe deficit being present from the outset,though some improvement may be observed inthe long term.

NEURORADIOLOGICAL PROTOCOL

The role of the neuroradiologist in strokecases is to provide the clinician with the maxi-mum morphological and functional informa-tion concerning the condition of the cerebralparenchyma as is possible, as well as the condi-tion of the intra- and extracranial brachio-cephalic blood vessels. One should particularlyassess whether or not there is a direct causal re-lationship between the craniocervical vascularpattern and the stroke, whether the lesion is is-chaemic or haemorrhagic, if there are signs ofother vasculopathic changes, and if the aetio-logic factors responsible for the stroke are in-tra- or extracranial.

The recent development of specific fibri-nolytic treatments that can potentially reverseischaemic injury in the early stages has changedthe role of imaging in this area (5). It is nolonger sufficient to simply distinguish is-

1.1

CLINICAL AND DIAGNOSTIC SUMMARYT. Scarabino, G.M. Giannatempo, A. Maggialetti

chaemic alteration from primary haemorrhage.It is now necessary to identify cerebral is-chaemia within the first few hours when treat-ment can be most effective. It is also importantto quickly distinguish normal cerebral tissuefrom that which is “at risk”, and that parenchy-ma which is irreversibly damaged. Thus, themedical imaging investigation is now a funda-mental part of planning effective emergencytreatment potentially capable of preventing ir-reversible cerebral damage and long-term pa-tient disability. The neuroradiologist musttherefore find the optimal means of supplyingthe required information through both invasiveand non-invasive investigative methods.

Angiography has to date been the most com-monly used of the available tools to analyse thebrachiocephalic vascular system directly. Lessinvasive methods include computed tomogra-phy (CT), ultrasound and magnetic resonanceimaging (MRI), both conventional (basic mor-phological imaging and angiography) and func-tional (spectroscopy, diffusion and perfusion).Single photon emission computed tomography(SPECT) and positron emission tomography(PET) are able to show local changes in bloodflow and metabolism, respectively, both mark-ers for cerebral damage. However, these lattermethods are not commonly available, and re-quire the injection of radioactive tracers.

In emergency situations, the cerebral investi-gation of choice is CT due to its non-invasive-ness, the fact that it is widely available, its easeand speed of use and its relatively low cost (7).CT distinguishes between haemorrhagic and is-chaemic stroke at an early stage, a factor thatmay be of vital importance in prognosis andtreatment. If the CT is negative or incongruousin some way with the clinical picture, MRImakes possible a more detailed brain investiga-tion to be carried out non-invasively.

HAEMORRHAGIC STROKE

CT has always been considered useful inanalysing cerebral haemorrhage, whether sub-arachnoid or intraparenchymal in location. In-tracranial haemorrhage is apparent on CT im-

mediately after the bleeding episode due to itshigh density relative to brain tissue. However,haemorrhage has a more complex appearanceand explanation on MRI. An acute cerebralhaemorrhage is primarily oxyhaemoglobin, asubstance with no paramagnetic properties thatbehaves much like an aqueous solution, almostindistinguishable from an area of parenchymalischaemia. In subacute haemorrhage, theparenchymal blood that was originally oxy-haemoglobin first turns into deoxyhaemoglo-bin, and then into intracellular and next intoextracellular metahaemoglobin. These sub-stances are paramagnetic and/or magneticallysusceptible and therefore are able to influencerelaxation times and change the MR signal in asomewhat predictable manner.

Recently released high field strength, highspeed MR equipment and imaging sequencesare particularly sensitive to magnetic suscepti-bility differences (e.g., echo planar imaging:EPI) has demonstrated that it is possible toclearly reveal even small areas of cerebral haem-orrhage on MRI (15). Because of this ability ofMRI to distinguish between non-haemorrhagicischaemia and haematoma, MRI may replaceCT at some time in the future where this is prac-ticable. However, the fact that high fieldstrength, high speed gradient performance MRIis presently less widely available and more cost-ly than CT determines that CT will still be thefirst diagnostic imaging examination carried outin such situations for the foreseeable future. Onthe other hand, emergency angiography shouldbe reserved for cases of subarachnoid haemor-rhage in order to search for causative pathologyof stroke (i.e., haemorrhage) such as aneurysmsor vascular malformations (3).

ISCHAEMIC STROKE

CT has been shown to be unable to documentthe presence of non-haemorrhagic ischaemic al-teration in the first few hours following the clini-cal onset of stroke. Over a period of hours andwith proper experience, it is in practice possibleto identify the subtle initial signs of ischaemic tis-sue damage as relatively lower attenuation brain

4 I. CEREBROVASCULAR EMERGENCIES

tissue resulting from cytotoxic oedema, and ma-jor cerebral arterial hyperdensity (e.g., middlecerebral artery stem, basilar artery) due to vascu-lar embolus/thrombosis (12, 14, 16).

Although conventional T2-weighted MRI(e.g., spin echo, fast spin echo) is particularlysensitive to changes in the water content of tis-sue and therefore to oedema, it is still frequent-ly negative in cases of hyperacute stroke (i.e.,first 1-6 hours). This is due to the fact that only3% of the water in the cellular cytoplasm con-sists of free water, which is the principal type ofwater molecule capable of altering MRI signalintensity in instances of cytotoxic oedema.

MR diffusion weighted imaging (DWI),however, can visualize hyperacute cerebral is-chaemia with some degree of certainty. Never-theless, DWI does not indicate whether the in-volved tissue is irreversibly damaged or is stillvital, and therefore amenable to benefitingfrom interventional recanalization treatment (9,10, 11). For this purpose MR perfusion imagingcan be used to evaluate the presence or absenceof discrepancy between the diffusion and per-fusion of affected tissue. If such discrepanciesexist, for example in a case of a circumscribedarea having abnormal diffusion but showinggreater relative perfusion, then it is apparentthat the “shadow” tissue area or ischaemicpenumbra may benefit from recanalization;conversely, where there is no such ischaemicpenumbra, it is unlikely that fibrinolytic thera-py will be successful (2, 4). MR spectroscopymay provide yet further information on the vi-able status of ischaemic brain tissue, even if atthe present time this is limited to some extentby the long examination times involved (13).

In a similar manner to what has been shownwith functional MRI, recent studies haveshown that it may also be possible to obtainfunctional data with CT (8). Therefore, it maybe that emerging technologies will have an im-pact on the diagnosis and treatment of patientswith cerebral stroke.

In order to identify suitable candidates forthrombolytic therapy, it is necessary to knowclearly whether there has actually been a vascu-lar occlusion. If this is indeed the case, an MR(or CT) angiographic study acquired during the

acute clinical stage is imperative (1). With MRangiography it is possible to evaluate the arteri-al anatomy of the major vessels at the base ofthe brain. Good anatomical imaging shows ei-ther the normal vessels composing the circle ofWillis, or their absence in the ischaemic cere-bral area. This may at times be the key to the di-agnosis of major vascular occlusion, in whichcase it is useful to extend the MR angiographicexamination to the vessels in the neck and eventhe aortic arch, the latter requiring intravascu-lar gadolinium injection and timed imaging ofthe aortic arch and cervical region. These tech-niques can also be useful as a treatment-moni-toring tool, serially imaging the vascularstenoses and occlusions non-invasively in pa-tients on specific therapy. However, there aresome limitations associated with the MR angio-graphic technique, such as less temporal andspatial resolution as compared to digital an-giography. It is partly for this reason that con-ventional invasive angiography remains the in-vestigative method of choice when the imagingdiagnosis of vasculitis, vascular dissection orembolism is in doubt, and also for purposes ofunequivocal vascular examination in suspectedcases of cerebral cortical venous and cranial ve-nous sinus thrombosis (3, 6).

Some authors have advocated the use of CTangiography, in part because of its ability toshow associated dystrophic atherosclerotic cal-cification of arterial walls in addition to the vas-cular luminal characteristics. However, the needto introduce contrast media as a part of the CTangiographic technique, involving in most caseshigh dosages of 100 to 200 cc, is a relative con-traindication in cases of suspected ischaemiawith blood-brain barrier disruption. In suchcases the possible further adverse effects of ex-travasated contrast material upon the underly-ing cerebral parenchyma must be considered, asthe tissue is already ischaemically injured. Forthis reason MR angiography is preferred be-cause of the small quantities of intravasculargadolinium contrast agent required and the es-sentially harmless nature of the paramagneticcontrast medium used. MR angiography has theadditional advantage of showing not so muchthe flow itself, but instead the “cast” of the ar-

1.1 CLINICAL AND DIAGNOSTIC SUMMARY 5

terial lumen, with the imaging findings beingvery similar to those of digital angiography.

CONCLUSIONS

In conclusion, the neuroradiologist today hasmany means available to him for the investiga-tion of the lesions associated with clinical strokeand their underlying pathophysiology. Ideally,all of the neuroradiological investigations out-lined in this discussion should be carried out inwithin the first few hours of onset of the stroke.In such cases the imaging protocol must in-clude: 1) a CT examination and, when possible,2) a basic MRI to confirm the clinical diagnosisand to exclude other acute onset non-ischaemicpathological process potentially responsible forthe neurological deficit; 3) MR diffusion weight-ed imaging to evaluate the extent of the is-chaemic injury; 4) MR perfusion imaging toshow the extent of the remaining vital tissue;and 5) MR angiography to establish the pres-ence or absence of a vascular luminal defectwith certainty so that fibrinolytic therapy can beinitiated when appropriate. In this way it is pos-sible within 45-60 minutes to have a morpho-logical and pathophysiological assessment of theischaemic injury, an assessment that may also beuseful for prognostic purposes.

However, for this to be possible, much de-pends on environmental factors such as equip-ment availability, compliance with the constrain-ing time elements requiring that the patient beready for imaging analysis within a very fewminutes or hours after the onset of the strokesyndrome, adequate patient cooperation andspecific physician skills, competence and experi-ence. In any case, an accurately performed andinterpreted CT examination is required, and inthe case of a negative CT, a baseline MR exami-nation and MR angiogram.

REFERENCES

1. Atlas SW: MR angiography in neurologic disease. Radiolo-gy 193:1-16, 1994.

2. Barber PA, Darby DG, Desmond PM et al: Prediction ofstroke outcome with echoplanar perfusion and diffusionweighted MRI. Neurology 51:418-426, 1998.

3. Brant-Zawadzki M, Gould R: Digital subtraction cerebralangiography. AJR 140:347-353, 1983.

4. De Boer JA, Folkers PJM: MR perfusion and diffusion im-aging in ischaemic brain disease. Medica Mundi 41:20,1997.

5. Hacke W, Kaste M, Fieschi C et al: Intravenous thrombol-ysis with recombinant tissue plasminogen activator foracute hemisferic stroke. The European Cooperative AcuteStroke Study (ECASS). JAMA 274:1017-1025, 1995.

6. Hankey GJ, Warlow CP, Molyneux AJ: Complications ofcerebral angiography for patients with mild carotid terri-tory ischaemia being considered for carotid endarterecto-my. J Neurol Neurosurg Psychiatry 53:542-548, 1990.

7. John C, Elsner E, Muller A et al: Computed tomographicdiagnosis of acute cerebral ischemia. Radiologe 37(11):853-858, 1997.

8. Koening M, Klotz E, Luka B et al: Perfusion CT of thebrain: diagnostic approach for early detection of ischemicstroke. Radiology 209(1):85-93, 1998.

9. Li TQ, Chen ZG, Hindmarsh T: Diffusion-weighted MRimaging of acute cerebral ischemia. Acta Radiologica39:460-473, 1998.

10. Lovblad KO, Laubach HJ, Baird AE et al: Clinical experi-ence with diffusion-weighted MR in patients with acutestroke. AJNR 19:1061-1066, 1998.

11. Lutsep HL, Albers GW, DeCrespigny A et al: Clinical util-ity of diffusion-weighted magnetic resonance imaging inthe assessment of ischemic stroke. Ann Neurol 41:574-580, 1997.

12. Marks MP, Homgren EB, Fox A et al: Evaluation of earlycomputed tomography findings in acute ischemic stroke30(2):389-392, 1999.

13. Mattews VP, Barker PB, Blackband SJ et al: Cerebralmetabolities in patients with acute and subacute strokes: aserial MR and proton MR spectroscopy study. AJR165:633-638, 1995.

14. Pressman BD, Tourse EJ, Thompson JR et al: An early CTsign of ischemic infarction: increased density in a cerebralartery. AJR 149:583-586, 1987.

15. Schellinger PD, Jansen O, Frebach JB et al: A standard-ized MRI stroke protocol: comparison with CT in hypera-cute intracerebral hemorrhage. Stroke 30(4):765-768,1999.

16. Von Kummer R, Allen KL, Holle R et al: Acute stroke: use-fulness of early CT findings before thrombolytic therapy.Radiology 205:327-333, 1997.


7

INTRODUCTION

Cerebral ischaemia is the pathological condi-tion that affects the cerebral parenchyma whenblood flow drops to levels that are insufficient topermit normal function, metabolism and structu-ral integrity. The ischaemic state can be incomple-te or complete, according to whether blood sup-ply is insufficient or totally interrupted, respecti-vely; and whether the problem is global or regio-nal, depending on the parenchymal territory in-volved. By far the most frequent cause of cerebralischaemia is arteriosclerosis of the arteries thatsupply blood to the brain, when an embolus or athrombus occludes such a vessel. Other causes in-clude emboligenic cardiopathies, sudden globaldrops in cerebral perfusion pressure, non-athero-matous arteritis (e.g., inflammatory, traumaticcauses, etc.), haematological disorders such aspolyglobulia or drepanocytosis and oestroproge-stinic treatment. At the current time, CT repre-sents the most suitable method for diagnosic ima-ging of cerebral ischaemic conditions, especiallyin cases of a complete neurological injury/deficit.It is, however, less suitable for diagnosing tran-sient ischaemic attacks (TIA) and reversibleischaemic neurological deficits (RIND), which aretemporary and subside rapidly, and in which caseit is more important to assess the status of the lar-

ger intra- and extracranial vessels (for which pur-pose echo-Doppler and MR angiography investi-gations may be more appropriate).

SEMEIOTICS

The resulting CT picture obtained dependson a number of factors including the type, com-pleteness and location of the vascular occlu-sion, the time required for the ischaemic pro-cess to become established and the presence orabsence of anastomotic pathways. Unlike com-plete neurological deficits, in transitory formsof ischaemia a negative CT can be expected,and in only 14% of all cases does the site de-tected coincide with that region suggested bythe patient’s syndrome. In certain cases, howe-ver, it can reveal signs linked to the underlyingvasculopathy such as the dilation, tortuosityand parietal calcification of vessel walls in thevessels comprising the circle of Willis. Althou-gh somewhat rare, in certain cases, TIA’s can beaccompanied by vascular malformation, a smallhaematoma or a neoplastic process. On theother hand, infarctions can be completelyasymptomatic, especially when small and whenlocated in mute parenchymal areas. The impor-tance of an ischaemic lesion, as diagnosed byCT, in causing neurological signs and symp-

1.2

CT IN ISCHAEMIA

T. Scarabino, N. Zarrelli, M.G. Bonetti, F. Florio, N. Maggialetti, A. Lorusso, A. Maggialetti, A. Carriero

toms depends on both its age and site and cantherefore only be held responsible for symp-toms in progress that are in keeping; if this isnot the case it must merely be considered as anincidental finding, expression of the samestroke-causing cerebrovascular pathology (18).Regardless of clinical criteria, there are a num-ber of semeiotic CT findings to be consideredin order to identify the nature of a given ischae-mic lesion, namely: 1) site and morphology, 2)evolution of lesion density, 3) presence of masseffect, and, 4) enhancement following endova-scular injection of contrast agents (i.e., patternof contrast enhancement, CE) (Fig. 1.1).

Site and morphology

The site of the lesion has considerable impor-tance in diagnosis as it reflects a vascular bloodsupply territory (Fig. 1.2). One or more large ar-terial vessel territories can be partially or totallyaffected (depending in part on the efficiency ofany collateral circulation present) (Figs. 1.3, 1.4,1.5, 1.6, 1.7); alternatively a reduction of cardiacoutput can affect the border zones between thevarious vascular territories or between the deepand superficial districts of the same territory (theso-called “watershed” areas), or the end point ofa vascular territory (the so-called “last mea-

Fig. 1.1 - Evolution over time of certain aspects of CT semeiotics: density, CE and mass effect of the ischaemic lesion.


HYPODENSITY

FOGGING EFFECT

MASS EFFECT

C.E.

TIME (days)7 14 21 28

1.2 CT IN ISCHAEMIA 9

Fig. 1.2 - Vascular territories (ACA: anterior cerebral artery; PCA: posterior cerebral artery; ACHA: anterior choroid artery; PICA:posterior inferior cerebellar artery; AICA: anterior inferior cerebellar artery; MCA: middle cerebral artery; SCA: superior cerebellarartery; BA: basilar artery).

dows”). Typical watershed infarcts are situated atthe frontal-parietal border (between the anteriorcerebral artery territory and that of the middlecerebral artery), at the gyrus angularis (betweenthe territories of the anterior, middle and poste-rior cerebral arteries), between the putamen andthe insula (on the border of the deep and super-

ficial branches of the middle cerebral artery)(Fig. 1.8). “Last meadow” infarcts affect Heub-ner’s artery (Fig. 1.9), lenticulostriate arteries orperforating arteries (31).

The most frequently affected vascular terri-tory is that of the middle cerebral artery, fol-lowed by that of the posterior cerebral artery, the


Fig. 1.3 - Infarct of the middle cerebral artery territory;a-b) partial infarct with involvement of the superficial left district only;c-d) complete infarct on the left with mass effect on the adjacent lateral ventricle, which appears compressed; on the right, other small-er ischaemic hypodensities can be seen.

a

b

c

d

anterior cerebral artery and the basilar artery(Fig. 1.10). Infarcts less commonly occur in cer-tain territories such as the brainstem (Fig. 1.11)and the thalamus (Fig. 1.12). It is also possible toobserve pathologically multiple small infarcts(0.5 - 1 cm), which are somewhat problematic todetect on imaging studies, especially when situa-ted in the posterior fossa (due to the bony arte-

facts at the base of the skull) (Fig. 1.11). As men-tioned previously, the morphology of the ischae-mic area is also important. The occlusion of theinternal carotid artery produces an infarct th-roughout the ipsilateral hemisphere (Fig. 1.7)and may or may not spare the thalamus. Theselarger lesions may demonstrate severe mass ef-fect and the prognosis in such cases can in


Fig. 1.4 - Partial infarct of the left anterior cerebral artery ter-ritory.

Fig. 1.5 - Infarct in the territories of a) the right posterior andb) bilateral cerebral arteries.

a

b

a

b

part be dependent upon the presence of collate-rals of the circle of Willis and leptomeninges.

Infarcts affecting the branches of the middlecerebral artery are wedge-shaped, with theirbase at the convexity and tip at the 3rd ventricle,whereas a curved trapezoid shape is typical of adistal occlusion at the beginning of the lenticu-

lostriate branches (Fig. 1.3 c-d). The occlusionof the posterior cerebral artery, which appearsas a rectangular shape, affects the medial terri-tory of the lateral ventricle junction and the-refore the occipital, temporal posteromedialand posteroparietal areas and, in some cases,the thalamus (Fig. 1.5). Infarcts of the anteriorcerebral artery affect the frontal parasagittaland parietal areas (Fig. 1.4); they are triangularin shape at the base of the frontal lobe but li-near in the remainder of the parasagittal fronto-parietal region. In addition to their site, water-shed infarcts are characterized by their shapeand usually have a linear appearance.

Despite the fact that they affect both whiteand grey matter, ischaemic alterations are moreclearly visible in the former with axial CT sec-tions. If they are of medium dimensions, theyappear irregular, round or elliptical rather thantriangular. Those lesions that affect the centralgrey matter nuclei tend to reflect the shape ofthese structures; those of the grey matter cortexare somewhat triangular with their base at theconvexity if only one branch is occluded, andtrapezoid-shaped when more than one branchis occluded.


Fig. 1.6 - Infarct of the right anterior and middle cerebral ar-tery territory, with clear mass effect on the shifted midlinestructures contralaterally.

Fig. 1.7 - Vast infarct of the right anterior, middle and posteri-or cerebral artery territories.

a

b

Evolution with time

Four distinct temporal phases can be identi-fied, including: 1) hyperacute, 2) acute, 3) suba-cute, and 4) chronic (3, 8, 10, 15, 17, 27). Thehyperacute phase occurs within 6 hours fromonset. From a neuropathological point of view,

the main alteration is best described as cyto-toxic oedema represented by the shift of waterin neurons. Because this is a relatively modestchange, the CT in this stage is usually negative.In this phase, the clinical and CT findings maynot agree. In this early stage, despite the factthat the patient may present with complete he-miplegia and unconsciousness, the CT scan of-ten remains normal (Fig. 1.13a). However, withthe passage of time, the CT becomes positive.


Fig. 1.9 - Ischaemic lesion at the head of the left caudate nu-cleus; there is also a lacunar infarct of the contralateral externalcapsule.

Fig. 1.8 - “Watershed” infarcts. a) between the right anterior and middle cerebral artery terri-tories;b) between the right middle and posterior cerebral artery terri-tories;c) between the left deep and superficial middle cerebral arteryterritories.

a c

b

Obviously, the clinical deficit caused by theischaemia takes place before oedema is appa-rent on CT. However, negative CT scans acqui-red in the early stages of ischaemia are valuablein ruling out other types of pathology, and espe-cially associated abnormalities including hae-morrhage. It is therefore essential that when cli-nical suspicion points to hyperacute acuteischaemia and the initial CT is negative, a sub-sequent scan should be performed during the

upcoming hours to evaluate for evolution of theabnormality (5). On occasion, a CT scan obtai-ned in the hyperacute phase can give direct si-gns (e.g., vessel hyperdensity, subtle parenchy-mal hypodensity) or indirect signals (e.g., sulcaleffacement, gyral swelling, ventricular compres-sion, fading of the white matter/grey matter in-terface) of hyperacute ischaemia. Such findingshave a negative prognostic value and are direc-tly associated with the degree of neurological di-sability (23). Vessel hyperdensity in major cere-bral arteries or one of their branches (the midd-le cerebral artery is the most commonly affec-ted) can be observed within the first minutesfollowing the onset of neurological signs andsymptoms and takes place before the appearan-ce of CT findings of the parenchymal infarct inthe corresponding territory (Fig. 1.14). This in-crease in intravascular density, which is visibleon CT without the use of contrast agents, ap-pears to be caused by the formation of an endo-luminal clot, either by arterial thrombosis orembolism (19, 30). For this reason, when clini-cal signs point to cerebral infarction, a CT scanthrough the cerebral arteries traversing the ba-sal subarachnoid cisterns must be performedimmediately (14), acquired with multiple thinslices (e.g., 1.5 - 4 mm). In 40-60% of cases, se-lective angiography reveals a thromboembolicocclusion, a finding that disappears subsequen-tly as the endoluminal clot lyses (2). Subtle pa-


Fig. 1.10 - Infarct in the vertebrobasilar territory. Large, non-homogeneous hypodense area involving the brain-stem, the anterior and external faces of the brain hemispheresas well as the medial and posterior faces of the temporal lobes.The hyperdensity is associated as with thrombosis of the basi-lar stem (b) and the ectasia of the supratentorial ventricles (c).

a c

b

renchymal hypodensities can sometimes be ob-served in these early stages, as even the slightestincrease in water content alters the CT attenua-tion coefficients, and therefore the relative tis-sue contrast (in particular, a 1% increase inbrain water content yields an attenuation of 2.5Hounsfield units).

– The acute phase of ischaemia occurs withinthe first 24 hours of the event, but typically be-gins within 6 hours after the stroke onset. Froma neuropathological point of view, vasogenic oe-dema is present as supported by the filling ofthe extracellular spaces of the brain due to ablood-brain barrier breakdown. Because of su-


Fig. 1.11 - Infarcts in the posterior fossa and in particular in thepons (a), midbrain (b) and left cerebral hemisphere (a-b).

Fig. 1.12 - Thalamic infarcts: on the left (a) and bilaterally (b).

a

b

a

b

ch tissue alterations, the ischaemic area appearson CT as a poorly marginated, hypodense le-sion. Retrospective analyses of CT investiga-tions have shown that the involvement of morethan 50% of the middle cerebral artery territoryis associated to an 85% mortality rate (28). Mo-reover, data provided by the European Co-ope-rative for Acute Stroke Study shows that the re-

sponse to thrombolytic treatment can vary grea-tly depending in part upon the volume of theischaemic oedematous area as shown on the ini-tial CT (9). In fact, it has been observed that rt-PA (recombinant tissue plasminogen activator)treatment increases the risk of death in caseswhere the hypodense area(s) exceed 1/3 of theperfused territory of the occluded artery. In su-


Fig. 1.13 - Typical evolution of an infarct in the right middle cerebral artery territory.a) acute phaseb) early subacute phase (2 days from clinical onset)c) late subacute phase (2 weeks later)d) chronic phase (1 year later).

ch cases, therefore, patients do not benefit fromfibrinolytic treatment because they are more su-sceptible to brain haemorrhages if such treat-ment is undertaken, as opposed to if they aretreated conservatively.

– The subacute phase of ischaemia com-mences 24 hours after the event and continuesuntil six weeks from the onset. From a neuro-pathological point of view, beginning in thestart of the second week there is an increase in

the vasogenic oedema as shown in CT by anarea with increasingly low attenuation coeffi-cients, better defined margins and mass effect(internal cerebral herniations are possible,especially in cases of massive ischaemia) (Fig.1.13b); the ischaemic area appears most clearlytwo to three days after clinical onset of stroke.From the second week after the event, the oe-dema and mass effect gradually subside andthe area of hypodensity becomes less clear(Fig. 1.13c); in some cases it disappears alto-gether and the ischaemic area becomes diffi-cult or impossible to distinguish from the nor-mal brain surrounding it. This is the so-called“fogging effect”, which is supported neuro-pathologically by an increase in cellularity dueto the invasion of microphages and the prolife-ration of capillaries (i.e., neoangiogenesis)(24). In massive infarctions, this process isusually partial and particularly affects the greymatter of the cortical mantle, where the cellu-lar reaction is more marked than in the whitematter. This must therefore be taken into ac-count when evaluating the dimensions of an in-farction, as scans performed one to two weeksafter the stroke could result in the underesti-mation of its size or even failure of recognition.In this phase, CT can provide important infor-mation in terms of prognosis, such as when in-traparenchymal haemorrhage (i.e., haematomaor haemorrhagic infarction) and extraparen-


Fig. 1.14 - a) Thrombosis of the left middle cerebral artery (ar-row head). b-c) CT check shortly after onset: ischaemic lesionin the corresponding vascular territory.

chymal bleeding (i.e., intraventricular or suba-rachnoid) accompany the otherwise bland in-farct. A recent study on this matter conductedby the Multicenter Acute Stroke Trial (Italy)demonstrated that in this phase, haemorrhagictransformation is frequent, and that patientswho develop intraparenchymal haemorrhage,extraparenchymal bleeding or even continuedcerebral oedema have an unfavourable outco-me (83%, 100% and 80%, respectively) (16).

The onset of the chronic stage of ischaemiacoincides with the start of the sixth weekfrom the onset of the clinical stroke and ischaracterized by repair processes. Parenchy-mal hypodensity with well-defined marginsappears with attenuation values in the CSFrange (Fig. 1.13d). In the larger ischaemic fo-ci, the necrotic areas evolve towards poren-cephalic cavitation with CSF density on CT.This is accompanied by the dilation of theipsilateral ventricle and adjacent subarach-noid cisterns and, in some cases, by an ipsila-teral displacement of midline structures.However, it is also possible that complete re-covery takes place.

Mass effect

During the initial phases of ischaemic in-farction, oedema and mass effect affect boththe white and the grey matter; these altera-tions are present in the ischaemic area alone(Figs. 1.3 c-d, 1.6, 1.7) and they never persistbeyond the third week after the event (Fig.1.13c). Prolonged presence after week threesuggests a different type of pathology such asneoplasia; in such cases an angiographic eva-luation is required to distinguish between dif-ferent pathological types unless prior CTscans showed haemorrhage (in fact, some neo-plasms do hemorrhage, so that further cautionmust be exercised in such instances). If hae-morrhage is present, the combination of thevolume of the haemorrhage with the volumeof the ischaemia may produce sufficient masseffect to worsen the prognosis. For example,in the case of large cerebellar infarctions, com-

pression of the lower brainstem may occur, re-sulting in occlusion of the fourth ventricle ou-tlets and consequent acute triventricular hy-drocephalus; in this case, suboccipital surgicaldecompression can be a “lifesaving” procedu-re (Fig. 1.10).


Fig. 1.15 - Ischaemic lesion of the lenticular nucleus (15 daysfrom clinical onset) with nodular and homogeneous CE. a) direct examination: small hypodense lacunar area in left thal-amic location;b) examination after contrast medium administration: markedCE in the right putamen.

a

b

Contrast enhancement (CE)

Enhancement on CT following the intrave-nous injection of contrast agents may vary duringthe different stages of ischaemia. There are threetypes of enhancement: intravascular, meningealand intraparenchymal. Intravascular enhance-ment is the first to occur, due in part to the re-

duction in flow caused by stenosis or frank oc-clusion of the visualized vessel, an effect that isworsened by the cytotoxic oedema. Abnormalvascular enhancement can in fact be documen-ted within two hours of the onset of signs andsymptoms. This type of enhancement is presentmainly in a superficial cortical location, whereasit is poorly visualized in the deep grey matter andwhite matter. Intravascular enhancement provi-des valuable information on prognosis, as it is in-versely proportional to the clinical seriousness ofthe lesion. In the cases of both total occlusion(with retrograde collateral flow) and partial oc-


Fig. 1.16 - Widespread infarct lesion in the left middle cerebralartery territory, with non-homogeneous CE: a) direct examina-tion; b) examination after contrast medium administration.

Fig. 1.17 - Right parietal-occipital infarct with gyral enhance-ment: a) direct examination; b) examination after contrastmedium administration.

a

b

a

b

clusion (with direct antegrade flow), the area ofthe enhancing vessel’s watershed is perfused, andtherefore there is a possibility of recovery. Due tomeningeal inflammation accompanying pial con-gestion, abnormal leptomeningeal enhancementis somewhat delayed when there is simultaneousparenchymal hypodensity on CT.

Both abnormal intravascular and meningealenhancement are more clearly observed on

enhanced MRI scans, having greater contrastresolution as compared to CT. Moreover, therelative degree of enhancement using parama-gnetic contrast media with MRI is more con-spicuous than that observed using a water-solu-ble iodine contrast agent with CT.

Parenchymal enhancement is usually evenmore delayed in appearing (in some cases, tem-porary hyperacute contrast enhancement maybe seen on MRI). In particular, in the first 5-6days after onset of the clinical stroke, the con-trast medium does not alter or only slightly al-ters the attenuation values in the area of the in-


Fig. 1.18 - Fogging effect of an ischaemic lesion in the leftfrontal region (12 days from clinical onset); a) the direct exam-ination is negative; b) CE of the lesion.

Fig. 1.19 - Ischaemic lesion of the right capsulothalamic area ondirect examination (a); lesion visibility is reduced after contrastmedium administration (b).

aa

b

b

farction, and therefore, the presence of denseenhancement in this phase suggests an alterna-tive pathological entity such as neoplasia.However, after the first week, some degree ofparenchymal enhancement can be observed inthe vast majority of cases of infarction. It is par-ticularly evident two to three weeks after the ic-tus and can last up to a month or more. Afterthis time the parenchymal enhancement gra-dually subsides.

Parenchymal enhancement primarily af-fects the grey matter of both the superficialcortical mantle and the deep basal nuclei, butthe pattern of enhancement may have diffe-rent appearances. For example, a nodular andhomogeneous form may be seen in deep nuclei(Fig. 1.15); alternatively, a non-homogeneouspattern may be observed, especially in thewhite matter along the border between the su-perficial and deep vascular territories (Fig.1.16); and a gyral pattern of enhancement istypical of the form encountered within the su-perficial cerebral cortex (Fig. 1.17). Whileenhancement patterns such as these are typicalof cerebral infarction, they can occasionally beconfused with enhancement accompanying ar-teriovenous malformations, cases of active me-ningitis, instances of recent subarachnoid hae-morrhage, meningeal carcinomatosis andlymphoma.

Pathological parenchymal enhancement inthe chronic phase can be attributed to the va-scular proliferation of neocapillaries havingabnormally permeable endothelium. This me-chanism of enhancement is observed in the se-cond and third weeks after the stroke, whenthis vascular proliferative process is at its mo-st active.

In the typical case, CE is transitory and ge-nerally follows the same pattern as the foggingeffect, and therefore may not be observed ifonly a single CT is performed, or if that studyis obtained in a phase during which it is usual-ly absent (4, 29). Scans performed at shortertime intervals will enable the visualization ofCE during the evolution of the infarction asdescribed above. This protocol of enhancedimaging can be particularly useful during thesecond stage, especially if the fogging effect is

present, as it tends to improve recognition ofthe infarction (Fig. 1.18). However, in the ini-tial phase, the typical increase in attenuationvalues accompanying the administration ofcontrast media occurring within a hypodenseischaemic area can render it invisible (i.e., iso-dense enhancement as compared to the sur-rounding normal parenchyma); this mandatesthe performance of a pre-enhancement imagein all cases so as not to miss the infarction al-together (Fig. 1.19). However, contrast mediashould only be administered in certain cases(e.g., unusual clinical presentation, atypicalimaging presentation forcing a broader diffe-rential diagnosis), because the extravasation ofhyperosmolar substances into the extracellularspace, especially in the early stages, can hy-pothetically increase the cellular and vascularinsult over and above that caused by theischaemia, thereby slowing the repair proces-ses and possibly even contributing to the finalirreversible degree of injury (11). In caseswhere contrast agent use is mandatory uponclinical grounds, the use of a non-ionic con-trast agent with less potential for harmful ef-fects is preferable.

PARTICULAR FORMS OF INFARCTION

Lacunar infarction

Common in patients with high blood pres-sure, lacunar infarction usually occurs insmall penetrating branches of the middle andposterior cerebral arteries, the anterior cho-roidal and the basilar arteries. This may bedue to lipohyalinosis, fibrinoid necrosis, mi-croatheromatous plaques or even cardiac em-bolism (6). These lacunar infarcts give rise toa large number of typical clinical disorders.Their recognition is proportionate to their si-ze, and visualization largely depends uponthe imaging technique used. Lacunar lesionsof just a few millimetres in diameter can ea-sily go unnoticed, whereas larger ones (from0.5 to 1.5 cm) are more easily recognized,especially when thin imaging slices are used(Fig. 1.20).


Haemorrhagic arterial infarcts

Ischaemic infarcts usually become hae-morrhagic when blood returns to the capillarybed after a period of absence, by means of col-lateral circulation or due to the lysis and frag-mentation of the original embolus. CT scanswill usually show a mixture of hypodense and

hyperdense areas in the parenchymal water-shed of the involved vessel (Fig. 1.21a) (26); incertain cases, massive confluent haemorrhagescan give rise to a homogeneously hyperdenselesion that can be impossible to distinguish


Fig. 1.21 - Infarct of the right hemisphere with hyperdensehaemorrhagic component (a); in b) massive and non-homoge-neous impregnation of the ischaemic-haemorrhagic region.

a

b

Fig. 1.20 - Multiple infarcts in the right basal ganglia region.

a

b

from a non-ischaemic haemorrhage unless itsshape reflects the territorial distribution of a ce-rebral artery. CE can either be barely visible ormassive in such cases (Fig. 1.21b).

In haemorrhage of arterial origin, the blee-ding primarily takes place in the grey matter(cortical and deep grey matter) and is almostalways present, on condition that the ischaemialasted long enough to damage the capillary wal-ls and the systemic blood pressure remained hi-gher than 60 mm of Hg. Although in wide-spread infarctions the infarcted grey matter canbecome entirely haemorrhagic, it may only beaffected peripherally.

Small, irregularly dispersed petechial hae-morrhages are a very frequent microscopic fin-ding in all infarcts; however, a diapedesis of redblood cells capable of causing a haemorrhagicinfarction is observed in 20% of cases. In actualfact, it is somewhat rare to view minor hae-morrhagic infarctions using CT for two rea-sons: 1) small petechial haemorrhages often gounnoticed due to their size, and 2) the petechialphenomenon lasts for such a short period thatit can be missed unless sequential scans areperformed at very short intervals.

Minor parenchymal hypodensity in the hy-peracute phase, accompanied by cytotoxic oe-dema and detected at an early stage by CTscans, is considered a useful element for foreca-sting the development of a haemorrhagic in-farction. This unfavourable event can befurther precipitated by anticoagulation (e.g., fi-brinolytic) treatment.

Venous haemorrhagic infarctions

Haemorrhagic infarctions can be caused bythromboses within the dural venous sinuses, acomplication that arises in association withmany pathological conditions (e.g., infections,head injuries, hypercoagulability, dehydrationin newborns and infants, leukaemia) (26). Theclinical presentation is often similar to that ofstrokes, although the picture can often be ac-companied by epileptic convulsions, lethargyand signs of increased intracranial pressure(20). CT makes it possible to identify both di-

rect and indirect signs of dural venous sinusocclusion. The former appear as small hyper-densities within the intravenous space (Fig.1.22a). Following bolus contrast medium infu-sion, dural venous sinus thromboses generallyappear as non-contrasted areas: the so-called


Fig. 1.22 - Hyperdensity of the upper sagittal sinus due tothrombosis (a) with adjacent ischaemic-haemorrhagic focus (b).

a

b

“empty delta sign”, a finding which can be so-metimes better documented by imaging withhigh window widths and levels. “Gyral enhan-cement” can also be observed, although it isuncommon (7, 20). Indirect signs, a conse-quence of venous obstruction, are representedby ischaemic-haemorrhagic parenchymal fociaffecting the subcortical white matter (Fig.1.22b). Venous events can sometimes be di-stinguished from arterial ones by the size ofthe haemorrhage(s) (e.g., single or multiple,unilateral or bilateral), the widespread topo-graphy that does not point to an arterial event,and by theire triangular shape with the baselying at the overlying cerebral cortex and theapex that points towards the ventricular sy-stem.

A definitive diagnosis of this condition is notalways easy because bone artefacts can simula-te an apparent venous filling defect at the skullbase and division or duplication of the venoussinus can also result in a smaller delta sign.

DIFFERENTIAL DIAGNOSIS

Infarctions should not be confused with:

– non-ischaemic primary haemorrhages Given the hyperdensity of the hemorrhagic

component, this problem cannot arise duringthe acute and subacute phases; and a peripheral“ring enhancement” pattern following intrave-nous contrast administration is typical, althoughit is neither constant nor specific, during the su-bacute phase. In the late stage, a well-defined,hypodense area is observed, and therefore diffe-rentiation of a simple haemorrhage from one ofischaemic origin is only possible on the basis ofwhether or not the lesion conforms to a vascularterritory.

– neoplasiaThe differential diagnosis is difficult in the

case of low degree, iso- or hypodense astrocy-tomas devoid of CE following contrast agentadministration (Fig. 1.23). In such cases, it isimportant to determine whether or not there isa failure to respect a vascular territory, the pat-

tern of evolution over time and the clinical fin-dings. With infarcts, the mass effect can be mo-dest and subsides within 3 weeks; a late appea-rance of ipsilateral ventricular enlargement andcortical atrophic alterations can also be fre-quently observed in cases of ischaemia. In thecase of neoplastic pathology, on the other hand,vasogenic oedema is confined to the white mat-ter only and gradually spreads over time. Mo-reover, in tumours that show some degree ofcontrast enhancement, non-homogeneous pe-ripheral enhancement or a “ring enhancement”can be observed, which is often not continuousbut is markedly irregular. At equal lesion volu-


Fig. 1.23 - Low-grade astrocytoma in a right frontal position(a), insensitive to contrast medium (b).

a

b

mes, the neurological deficit is much less inneoplasia as compared to ischaemia.

– arteriovenous malformationsOnly slightly hyperdense when imaged

without contrast agents, after CE arteriovenousmalformations (AVM’s) show a serpentine pat-tern of enhancement that can spread within avascular territory, affecting not only the super-ficial cortex, but also the deep grey and whitematter structures. Although smaller vascularmalformations do not cause visible shift of re-gional structures, the larger AVM’s can cause aconsiderable degree of mass effect.

– bacterial or viral encephalitisThe encephalitides appear in the form of hy-

podense areas that may also be associated withmass effect; they may or may not enhance in avery irregular pattern, and they do not respectvascular territories.

– cystic formations Leptomeningeal cysts are lesions having

CSF density and are often associated with masseffect with overlying cranial deformation andthinning of the internal table of the skull. Bycontrast, in complete ischaemic vascular le-sions, mass effect is not present, similary to thelarger porencephalic cysts or cerebral cavita-tions with or without communication with theventricular system, secondary to various non-specific destructive processes as observed inthe chronic stages (e.g., infectious, vascular ortraumatic).

CONCLUSIONS

The ease at which machines can be accessed,the rapidity and ease of scanning (even in co-matose patients), the relatively low cost, theinherent ability to frequently be able to differen-tiate between acute ischaemic and primary hae-morrhagic events (accurately assessing their si-ze, site, relationship to adjacent structures andpresence of mass effect and haemorrhage), allcontribute to making CT the imaging techni-que of choice in the diagnosis of stroke. Despi-

te its restrictions, CT is fundamental to fol-lowing the evolution and effects of treatment inacute stroke patients.

The advent of helical CT has not broughtabout any significant advantages or alterationsin stroke diagnosis, and the evaluation ofpathological and normal cerebral structures isin fact very similar (1). However, the spiral te-chnique is fundamental to angiographic andperfusion imaging.

Angio-CT of the basal cerebral structuresenables the clinician to view the circle of Willisand therefore determine whether or not thevessel pertaining to the ischaemic cerebral areais occluded. In addition, it gives more detailedinformation concerning the condition of the va-scular wall than is possible with MR angio-graphy.

Perfusion CT is a rapid acquisition functio-nal imaging technique that is capable ofshowing cerebral ischaemia at a very early stage(prior to the appearance of significant morpho-logical and density variations as observed instatic CT), of following sequential evolution,and above all, of providing important informa-tion concerning the best choice of treatment. Infact, by evaluating alterations in cerebral perfu-sion, and in particular cerebral blood flow(CBF) values, it is often possible to distinguishclearly between reversible and irreversibleischaemia areas (12, 13, 21, 25).

Thanks to this recent technological advance-ment, CT has become of yet greater value instroke diagnosis than MR. However, MRI doeshave certain advantages, such as direct multi-planar acquisition possibilities, an absence ofbone artefacts in the middle and posterior fos-sae, better contrast resolution and greater sen-sitivity in detecting abnormal variations in thewater content and water diffusion characteri-stics during the earliest stages of ischaemia (22).

REFERENCES

1. Bahner ML, Reith W, Zuna I et al: Spiral CT vs incremen-tal CT: is spiral CT superior in imaging of the brain ? EurRadiol 8(3):416-420, 1998.

2. Bozzao L, Angeloni V, Bastianello S et al: Early angio-graphic and CT findings in patients with haemorrhagic in-


farction in the distribution of the middle cerebral artery.AJNR 2:1115-1121, 1991.

3. Bozzao L, Bastianello S, Ternullo S: Imaging anatomo-fun-zionale dell’ischemia encefalica. In: Pistolesi GF, Beltra-mello A: “L’imaging endocranico”, Gnocchi Editore, Na-poli, 1997:211-304.

4. Caillè JM, Guibert F, Bidabè AM et al: Enhancement ofcerebral infarcts with CT. Comput Tomogr 4:73, 1980.

5. Constant P, Renou AM, Caillè JM et al: Cerebral ischemiawith CT. Comput Tomogr 1:235, 1977.

6. Fisher CM: Lacunar strokes and infarcts: a review. Neuro-logy 32:871, 1982.

7. Ford K, Sarwar M: Computed tomography of dural sinusthrombosis. AJR 2:539, 1981.

8. Gaskill-Shipley MF: Routine evaluation of acute stroke.Neuroimaging Clin N Am 9(3):411-422, 1999.

9. Hacke W, Kaste M, Fieschi C et al: Intravenous throm-bolysis with recombinant tissue plasminogen activator foracute hemisferic stroke. The European Cooperative AcuteStroke Study (ECASS). JAMA 274:1017-1025, 1995.

10. John C, Elsner E, Muller A et al: Computed tomographicdiagnosis of acute cerebral ischemia. Radiologe 37(11):853-858, 1997.

11. Kendall BE, Pullicini P: Intravascular contrast injection inischaemic lesions. II. Effect on prognosis. Neuroradiology19:241, 1980.

12. Klozt E, Konig M: Perfusion measurements of the brain:using dynamic CT for the quantitative assessment of cerebralischemia in acute stroke. Eur J Radiol 30(3),170-184, 1999.

13. Koenig M, Klotz E, Luka B et al: Perfusion CT of thebrain: diagnostic approach for early detection of ischemicstroke. Radiology 209(1):85-93, 1998.

14. Lutman M: Diagnosi precoce dell’infarto cerebrale: l’iper-densità dell’arteria cerebrale media come primo segno TCdi lesione ischemica. Radiol Med 77:171-173, 1989.

15. Marks MP, Homgren EB, Fox A et al: Evaluation of earlycomputed tomographic findings in acute ischemic stroke.Stroke 30(2):389-392, 1999.

16. Motto C, Ciccone A, Aritzu E et al: Haemorrhage after anacute ischemic stroke. MAST-I Collaborative Group.Stroke 30(4):761-764, 1999.

17. Moulin T, Tatu L, Vuillier F et al: Brain CT scan for acute

cerebral infarction: early signs of ischemia. Rev Neurol1555(9):649-655, 1999.

18. Perrone P, Landelise L, Scotti G et al: CT evaluation in pa-tients with transient ischemic attack. Correlation betweenclinical and angiographic findings. Eur Neurol 18:217, 1979.

19. Pressman BD, Tourje EJ, Thompson JR: An early CT signof ischemic infarction: increased density in a cerebral ar-tery. AJR 149:583-586, 1987.

20. Rao KCVG, Knipp HC, Wagner EJ: Computed tomo-graphic findings in cerebral sinus and venous thrombosis.Radiology 140:391, 1981.

21. Reichenbach JR, Rother J, Jonetz-Mentzel L et al: Acutestroke evaluated by time-to-peak mapping during initialand early follow-up perfusion CT studies. AJNR20(10):1842-1850, 1999.

22. Schellinger PD, Jansen O, Fiebach JB et al: A standardizedMRI stroke protocol: comparison with CT in hyperacuteintracerebral haemorrhage. Stroke 30(4):765-768, 1999.

23. Scott JN, Buchan AM, Sevich RJ: Correlation of neurolo-gic dysfunction with CT findings in early acute stroke. CanJ Neurol Sci 26(3):182-189, 1999.

24. Skriver ED, Esbach O: Transient disappearance of cere-bral infarct on CT scan, the so-called fogging effect. Neu-roradiology 22:61, 1981.

25. Ueda T, Yuh WT, Taoka T: Clinical application of perfu-sion and diffusion MR imaging in acute ischemic stroke. JMagn Reson Imaging 10(3):305-309, 1999.

26. Vonofakos D, Artmann H: CT findings in haemorragic ce-rebral infarct. Comput Radiol 7:75, 1983.

27. von Kummer R, Allen KL, Holle R et al: Acute stroke: use-fulness of early CT findings before thrombolytic therapy.Radiology 205:327-333, 1997.

28. von Kummer R, Meyding-Lamadè U, Forsting M et al:Sensitivity and prognostic value of early CT in occlusion ofthe middle cerebral artery trunk. AJN 15:9-18, 1994.

29. Wing SD, Normann D, Pollack JA et al: Contrast enhan-cement of cerebral infarcts in computed tomography. Ra-diology 121:89,1976.

30. Yock DH: CT demonstration of cerebral emboli. J Com-put Assist Tomogr 5:190-196, 1981.

31. Zulck KJ, Esbach O: The interhemisferic steal syndromes.Neuroradiology 4:179-185, 1972.


27

INTRODUCTION

The term intraparenchymal haemorrhage(IPH) refers to non-traumatic bleeding withinthe cerebral parenchyma. IPH accounts for15% of all cerebrovascular disease, and statis-tics on this common pathological condition de-termine that from 10-20 new cases per annumoccur for every 100,000 inhabitants in the pop-ulation. This variation can be accounted for bytwo factors, the first being a drop in the moresevere forms due to the recent progress made intreating hypertension, and the second being theimprovement in diagnostic accuracy as a resultof the advent of computed tomography (CT).CT now makes it possible to establish thehaemorrhagic nature of certain relatively “mi-nor” events that were previously supposedwholly ischaemic.

In 88% of cases, the haemorrage occurs with-in the cerebral hemispheres, in 8% in the cere-bellum and in 4% in the brainstem (Fig. 1.24).IPH’s located in the cerebral hemispheres canbe further subdivided into two subcategories:those in typical (75%) and those is atypical(13%) positions. The former are found in thebasal ganglia and are almost invariably associat-ed with high blood pressure. The latter, alsoknown as lobar or subcortical haemorrhages,can sometimes be attributed to hypertension,

1.3

CT IN INTRAPARENCHYMAL HAEMORRHAGEN. Zarrelli, F. Perfetto, T. Parracino, T. Garribba, P. Maggi, N. Maggialetti, T. Scarabino

Fig. 1.24 - Modified from (12).This diagram shows the different percentages of intra-parenchymal haemorrhage distribution: 88% affect the cere-bral hemispheres (75% the paranuclear structures and 13%the white matter); 8% the cerebellum and 4% the brainstem.Deep-seated haemorrhages are included inside the sector of thecircle (delimited by the corpus callosum above, the externalcapsule to the side and the brainstem below). Superficial intra-parenchymal haemorrhages develop outside this boundary. So-called “advanced” haemorrhages originate from the basal gan-glia and spread through the adjacent white matter, crossing thisperipheral border.

but are more commonly caused by aneurysmrupture, arteriovascular malformation ruptureor by other pathology characterized by abnor-mal vascularization (including neoplasia). Incases of IPH, CT scanning is important as itpermits the differentiation of primary haemor-rhages from ischaemic forms (Fig. 1.48), whichthe clinical data alone is often unable to estab-lish. In addition, the CT examination providesaccurate information regarding the site, ap-pearance, dimensions and evolution of thehaemorrhagic focus.

THE ROLE OF CT

The introduction of CT immediately re-vealed that IPH is far more common than pre-viously supposed on the basis of clinical dataalone. Prior to the advent of this technique, on-ly those clinical strokes in which the sudden on-set and severity of symptoms were accompa-nied by the presence of blood in the CSF (de-termined by lumbar spinal tap), and in whichan avascular mass was detected by selective an-giography (22) were considered haemorrhagic.

Today, both of these examinations are onlyrarely considered due to their invasiveness andrelative inaccuracy. In 50% of IPH’s document-ed using CT, the CSF is not found to containblood; angiography is only used very occasion-ally for haemorrhages in typical locations, butcan be useful in confirming clinical suspicion ofsuch underlying pathology as vascular malfor-mations, aneurysms, angiitis and neoplasia (24).

CT is useful for documenting both largerhaemorrhages, which may include ventricularrupture, as well as smaller ones with minor neu-rological symptoms. CT is so sensitive that it isable to document all acute, clinically sympto-matic haematomas correctly (21). The clinicaldiagnosis is somewhat inaccurate even whensophisticated score systems are used (11), thusunderscoring CT’s fundamental role in evaluat-ing neurological emergencies (2).

In the hyperacute phase that follows a clini-cal stroke, when the differentiation of primaryhaemorrhage from other pathological entities ismost important, MR is only rarely used, be-

cause of its relatively long scanning times.These extended examination times often makeit inappropriate for use in emergency situa-tions, as these patients are not always able to re-main immobile, and continuous clinical checksare required is such cases. Moreover, on the fewoccasions in which it is used, the MRI signal ofthe haemorrhagic focus is not usually sufficient


Fig. 1.25 - The presence of fluid levels is not rare (blood levelsstratify in the sloping part). In (a) a large putaminal haematomapresents with a deep, more recent and compact component andanother, superficial one characterized by a clear fluid-fluid lev-el (arrowhead). A level can also be observed in the irregular andwidespread multifocal intraparenchymal haemorrhage of a pa-tient treated with anticoagulants for a heart attack (b).

a

b

to distinguish it from other types of pathologythat may bleed (3).

However, MRI can prove to be very usefulin defining the anatomical-topographical na-ture of the IPH and, above all, in monitoringits evolution during the subacute and chronicphases (Fig. 1.26). Persistent documentation ofhaemoglobin derivatives makes it possible toestablish the haemorrhagic nature of a vascularaccident even some time after onset, a distinc-tion that is not always possible using CT. Insome cases, MRI can also contribute to identi-fying the pathology underlying the bleeding(Fig. 1.27), evaluate hemorrhages within theposterior fossa (where it is not hindered byartefacts such as those that occur with CT, Fig.1.26) and thanks to its greater relative contrastresolution, it is also possible to identify smallerfoci that are not visualized using CT.

Angiography is only used in cases of non-spontaneous haemorrhage, whose causes can-not be demonstrated by MR or CT (with/with-out contrast media) in the acute phase. It is al-so routinely performed in the evaluation of pa-tients under 45 years of age, especially when theIPH has a lobar location and the patient has nopast history of high blood pressure (24).

CAUSES

IPH can be attributed to a great number ofcauses, although by far the most common isthe so-called “spontaneous” form, which is al-most invariably associated with systemic highblood pressure. Haemorrhagic extravasationoccurs most commonly in the basal ganglia(usually between the insula and the lenticularnucleus); it also typically affects the claustrum,the lateral portion of the putamen, and the ex-ternal capsule and causes extensive injury ofthe surrounding cerebral parenchyma as thehaematoma dissects its way through the cere-bral tissue.

The haemorrhage occurs due to a rupture ofan artery (usually one of the lenticulostriate ar-teries, which are particularly sensitive tochanges in pressure), whose walls have beendamaged by the chronic effects of arterial hy-

1.3 CT IN INTRAPARENCHYMAL HAEMORRHAGE 29

Fig. 1.26 - Relations between CT and MR.A recent haematoma affects the left paramidline portion of thecerebellum (a). It is not subject to surgical removal (because itdoes not cause a «narrow» posterior fossa). It is checked oneweek later using MR (b), here represented in a coronal T1weighted spin-echo sequence. MR is superior during the sub-acute phase as it better documents haemoglobin breakdownproducts; in particular around the posterior fossa, due to theabsence of artefacts from the cranial theca that are inevitablewith CT; in each phase and position due to its superior (threedimensional) spatial localization (7).

a

b

pertension. The blood flows outwardly quite vi-olently, and due to its kinetic energy, it forms avortex at the outlet point. Under direct obser-vation, haemorrhagic foci are therefore massesof more or less clotted blood, with poorly de-fined margins (due to peripheral mingling withnecrotic strands of brain tissue). The adjacentparenchyma is infiltrated with frank blood, andis more or less destroyed. The clinical presenta-tion (most patients are in their 7th decade oflife) is characterized by an abrupt onset and arapid evolution of signs and symptoms. In 1/3of all cases, the neurological deficit reaches apeak at onset, and in the remaining 2/3 of pa-tients the clinical picture worsens graduallyover the course of minutes or hours in propor-tion to the dimensions of the arteries involvedand the speed at which bleeding occurs. In cer-tain rare cases, the clinical evolution can last anumber of days, thus mimicking the clinicalpicture typically manifested by neoplasias (19).

Prodromic symptoms such as headaches,paleness and nausea only occur somewhat rarely.In 2/3 of cases, the severe form of onset, or cere-bral apoplexy, strikes patients during full activityand only rarely occurs during rest. The systemicblood pressure is high in 75-80% of cases, andtherefore plays a prominent role in categorizingthe likely aetiology of the haemorrhage. Unlikeaneurysm ruptures (which may have multipleepisodes), in most cases only one haemorrhagicevent occurs, and active/progressive bleeding orlate recurrence in the same site is rare.

A gradual worsening of clinical symptoms istherefore more frequently caused by a perile-sional increase in oedema (with a consequentialmass effect) or by the intraventricular or sub-arachnoid spread of the bleed rather than an in-crease in haematoma volume. In certain circum-stances, CT images may not undergo any majorchange, therefore indicating metabolic factorsor medical complications (22). In massive formsof IPH (Fig. 1.33), the patient is comatose andusually has severe alterations of the vegetativefunctions (e.g., considerable breathing difficul-ties, cardiovascular alterations, incontinenceand hyperthermia). In this phase, neurologicallateralizing signs can prove difficult to evaluategiven the massive hypotonia.

When onset is more gradual, taking a num-ber of hours, even sluggish patients are awareof the occurrence of the neurological deficit. In


Fig. 1.27 - IPH caused by the rupture of a cavernous angioma.In this 22 year-old female, a localized haemorrhagic lesion af-fects the rear arm of the internal capsula (a). With its varioussequences (in b it is represented by a PD-weighted SE se-quence), MR demonstrates that it is consequential to the rup-ture of a cavernous angioma.

b

a

2/3 of cases, neurological or neurovegetative al-terations tend to worsen during the first 24-48hours, with a rapid evolution towards death,which is sometimes ultimately caused by acutepulmonary oedema.

In the so-called regressive forms, which ac-count for the remaining 1/3 of patients, theevolution is less aggressive, and following theinitial phase, which does not differ greatly fromthat described, within 7-10 days the patient’sconsciousness and neurovegetative state maystabilize or even improve.

In addition to high blood pressure, whichaccounts for some 80% of cases, there aremany other causes of IPH. The most commonare aneurysm ruptures and arteriovenous mal-formation (AVM) and cryptic angioma rup-tures, all of which usually occur in lobar posi-tions and are often accompanied by subarach-noid haemorrhage (Fig. 1.35).

2-10% of IPH’s are caused by an underlyingneoplasm, the most common metastatic formsbeing melanomas, kidney and lung tumours andchoriocarcinomas. Primitive forms of tumoursthat may lead to IPH include gliocarcinomas,

mesogliomas, angioblastic meningiomas and hy-pophyseal adenomas.

Haemorrhagic mechanisms within the tu-mour may be due to a number of factors, includ-ing: the rupture of pathological neovessels asso-ciated with the tumour, such as those observed ina gliocarcinoma; the rapid growth of the neopla-sia outstripping its blood supply, typical of neo-plastic metastases and the associated systemic


Fig. 1.28 - Large parenchymal bleed in a chronic alcoholic, withmore recent, irregular hyperdense foci, alternated with areas ofwidespread colliquation in the white matter. The concomitanceof cerebral atrophy and the somewhat limited «mass effect»caused by the lesion should also be noted.

Fig. 1.29 - Thalamic haematomas.In (a) thalamic haematoma with limited extent, resolved byconservative treatment alone (note the hypodense wedge-shaped lesion in contralateral parietal location, outcome of aprevious ischaemic accident). In (b) a coarser haematoma withmarked mass effect (deformation of the 3rd ventricle) and in-traventricular inundation with fatal outcome.

a

b

complications, such as coagulation disorders(22). In approximately one-half of these patients,the clinical onset takes the form of a haemor-rhagic ictus, whereas in others the symptoms aresubtler and the CT detection of peritumoralbleeding can be an unexpected finding (22).

IPH is also often caused by clotting disorders(e.g., complications of anticoagulation treat-ment, haemophilia, thrombocytopenic purpura,leukaemia and aplastic anaemia), where bleed-ing often occurs either spontaneously or sec-ondary to minor trauma. The CT picture can betypical or can very often reveal a fluid/blood in-terface combined with fluid stratification as aneffect of blood sedimentation below the overly-ing plasma (Fig. 1.25b).

IPH is also commonly observed in chronic al-coholics, being caused by a number of differentpathogenic factors, especially the frequent fallsto which such subjects are prone due to im-paired coordination; clotting disorders, mostcommonly that of reduced platelet function; andcerebral atrophy that exposes brain surface ves-sels and bridging vessels (i.e., from brain surfaceto parietal dura mater) to greater risk of trau-matic injury. Bleeding can be quite widespread,and usually originates in the subcortical white

matter. For this reason the haemorrhage canthereby be differentiated from more seriouspost-traumatic contusive haemorrhage, whichtend to be smaller and often multiple, and occu-py a more superficial position (Fig. 1.28). Due tothe accompanying atrophy, even when extreme-ly widespread, the haemorrhaging gives less sig-nificant mass effect than might be expected inother forms of haemorrhage with similar dimen-


Fig. 1.30 - A «globous-midline» IPH (2), with dimensions (2.5cm) larger than those usually observed for such formations,which completely obliterates the putamen (compare delin-eation with that of the healthy contralateral). The peripheralcrown-shaped hypodensity is also larger than normal.

Fig. 1.31 - Two examples of putaminal haematomas spread tothe external capsule, with the classic elongated shape in an an-terior-posterior direction. That on the right (a) is smaller andsurrounded by a clearer hypodense border. These forms ac-count for 11% of all putaminal IPH’s and usually have a goodprognosis.

a

b

sions. Following surgical evacuation of thehaematoma, the brain parenchyma often returnsto its previously occupied space (22).

IPH’s may also be caused by cerebral amy-loid angiopathy or CAA, most commonly en-countered in elderly patients (13), and in casesof sympathomimetic drug abuse, more com-monly observed in the young (9).

In addition, cases of IPH are not infrequent-ly observed secondary to arterial or venous in-

flammation (thrombosis/rupture of arteries andof cortical veins or the dural venous sinuses) andthe forms of vascular inflammatory change oc-curring in systemic or infectious illnesses.


Fig. 1.32 - Typical example of putaminal haematoma thatspreads to the internal capsule (a) and to the semioval centre(b). These forms account for 32% of all putaminal locations.

Fig. 1.33 - «Great cerebral haemorrhage».Recent occurrence of widespread bleed massively involving theleft thalamic and putaminal basal ganglia. Concomitance of: amarked mass effect (with conspicuous contralateral shift of themidline structures) and a blocking of the ventricular cavities(the homolateral ventricle is completely obliterated, the rightone only in the occipital horn). However, the amount of peri-focal oedema is, as usual, restricted to a peripheral border on-ly. The patient died a few hours later.

Fig. 1.34 - Recent, voluminous IHP involving the so-called tem-poral-parietal-occipital junction.

a

b

SEMEIOTICS

In comparison to the surrounding parenchy-ma, acute phase IPH appears on CT scans asclearly defined hyperdense, non-calcified le-sions having mass (volume). The hyperdensityis linked primarily (90%) to haemoglobin andonly partly (8%) to the concentration of iron(6). For this reason it is less hyperdense in pa-tients suffering from severe anaemia, where insome unusual cases it can be difficult to per-ceive (14). Clot formation and its subsequentretraction cause a considerable increase in thepacked cell volume and thus a further increasein density of up to 90-100 H.U. (6). IPH’s usu-ally present as round or oval in shape, but incertain haemorrhages, especially in the largerones, the haemorrhagic mass can be irregular(Figs. 1.25b, 1.32b, 1.39a, 1.42a, 1.48a, 1.49a).The profile of the haemorrhagic mass is usuallywell defined, however blurred margin, tree-shaped, jagged borders or map-shaped profilescan also be observed. These shapes are a resultmainly of the quantity of the extravasatedblood (i.e., the greater the quantity, the greaterthe dissecting effect upon the surrounding neu-ral parenchyma), although in IPH forms associ-ated with blood dyscrasias, irregular bordersare more common due to irregular clot forma-tion (6) (Fig. 1.25b).

The appearance of the internal aspect of thehaematoma can either be homogeneous or canbe characterized by hyper- and hypodensities ofvarying degree, size and configuration (Figs.1.28a, 1.48a). Horizontal fluid-fluid levels mayalso be seen (Figs. 1.25, 1.42). Occasionally,shortly after onset of the haemorrhagic event, aradiodense core surrounded by a less dense,thin circumferential border area can be ob-served. Over several days’ time, the peripheralhypodensity is seen to enlarge and vary in width(Figs. 1.26, 1.29a, 1.30, 1.31a, 1.32a, 1.33, 1.34,1.36, 1.41a, 1.42, 1.47, 1.49a). This peripheraloedematous layer yet later becomes visible asmore extensive digitations of oedema that pene-trate the white matter extending away from thehaemorrhagic focus (Figs. 1.32b, 1.44, 1.45).The origin of this peripheral oedema is partlydue to a serous exudation from the regional

blood vessels, and partly to the oedematous re-action of the surrounding neural tissue to theblood clot.

Larger hemispheric IPH’s (Figs. 1.25b, 1.33)generally cause mass effect with midline shift,and eventually a transfalx internal herniation ofthe cingulate gyrus and downward transtentor-


Fig. 1.35 and 1.36 - Lobar and white matter haematomas. Theleft frontal haematoma (Fig. 1.35) is secondary to the ruptureof an aneurysm of the anterior communicating artery and is ac-companied by subarachnoid bleeding, intraventricular inunda-tion and hydrocephalus. The right parietal haematoma (Fig.1.36) is of the «spontaneous» kind in a hypertensive patient.

ial internal herniation of the hippocampal un-cus. The latter event may ultimately result in aseries of secondary parenchymal softenings orhaemorrhages, especially within the midbrainand pons (1).

During the first five days from IPH onset,contrast enhancement on CT is never observed,unless the haemorrhage is due to a discrete un-derlying pathological entity (e.g., neoplasm)(Fig. 1.42).

Some IPH’s, especially those in deeper posi-tions (and not necessarily the largest ones),rupture into the cerebral ventricles (Figs.1.25b, 1.29b, 1.33, 1.47a, 1.49). Subarachnoidbleeding is not uncommonly encountered, butsuch cases usually suggest a ruptured vascularmalformation or cerebral aneurysm as the un-derlying cause (Fig. 1.35).

Evolution

In non-fatal, conservatively treated haemor-rhagic stroke cases, and especially in those inwhich the clinical picture progressively wors-ens, IPH evolution is often monitored sequen-

tially with CT. In other cases, the first scan isperformed some time after bleeding com-mences, for example perhaps because the pa-tient presented with a gradual progression ofsigns and symptoms and a less abrupt onset.For these and other reasons, it is therefore use-ful to know how the blood collection evolves aswell as its collateral effects upon the overlyingtissues in order to monitor the situation duringfollow-up, and be alerted to if and when furtherintervention may become necessary.

Diagram 1.40 shows the changes that the var-ious IPH parameters undergo over time asjudged by CT. Density tends to decrease, pass-ing from a hyper- to an iso- and finally to an areaof hypodensity (Fig. 1.41), as a result of a seriesof phenomena including the phagocytosis ofblood pigments, the persistence of necroticbrain tissue and a mingling the whole with xan-thochromic fluid (e.g., expressed serum). This


Fig. 1.37 - Voluminous IPH of the left hemisphere causes a de-formation and deviation of the 4th ventricle and a closed pos-terior fossa condition.

Fig. 1.38 - An eight year-old girl falls into a sudden coma. TheCT picture shows a coarse IPH of the vermis with a subarach-noid haemorrhagic shift, obviously a non-spontaneous form.All the conditions (age, site and concomitant SAH) point tosecondary forms. CT documents two further findings: thewidespread ischaemic hypodensity of the brainstem and hydro-cephalus (signalled by the ectasia of the temporal horns). Thereis no time to perform an angiographic check or other neurora-diological investigations. The vermis is one of the most com-mon sites for «cryptic» angiomas (18).

progressive reduction in density that com-mences during the first week, continues for sev-eral months, and can usually be associated witha parallel reduction in the overall size of the IPH(19). The subacute phase, which starts 3-5 daysafter the haemorrhagic event, is characterized byclot lysis; the blood clot focus is surrounded bya mainly mononuclear cellular infiltrate, whichcauses fibrinolytic resolution, erythrocytephagocytosis, enzymatic digestion of the molec-ular components and the accumulation ofhaemoglobin breakdown products. The CT pic-ture shows a gradual centripetally directed re-duction in density (i.e., loss of hyperdensityfrom the outermost layers of the blood clot, andprogressing temporally inward). The IPH as-sumes a characteristic rosette type appearance(Fig. 1.43a), having a central hyperdense portion(represented by the centre of the clot), an inter-mediate hypodense area (composed of cellulardebris, clot breakdown products and lowhaemoglobin concentration serum), and finallyan even more hypodense outer portion causedby the oedema (6). In larger haemorrhages, thismodel can be replaced by a global, progressivereduction in clot density (4). The appearance ofthe IPH may also be altered by mixing with CSFor, less frequently, by rebleeding. Towards thethird week, it tends to become isodense as com-pared to normal brain parenchyma, before sub-sequently becoming relatively hypodense. Twoto three months after the event, the centre of thehaemorrhagic focus has a density similar or nearto that of CSF, transforming itself into a poren-cephalic cystic cavity (i.e., communicating withthe cerbral ventricular system) or alternativelyan area of cystic encephalomalacia (i.e., notcommunicating with the ventricles). The dimen-sions of intraparenchymal haemorrhages at thislate stage are notably smaller than at onset, andan ex-vacuo dilation of the adjacent ventricular-cisternal system always occurs (Fig. 1.41c).

Smaller IPH’s may not leave macroscopic re-mains, passing from hyper- to isodensity with-out the subsequent evolution towards poren-cephaly (in such cases, the focus of thehaematoma is replaced by a glial-type reaction).In the chronic phase (after 3 months), the den-sity values can be variable, with isodensity in

the case of a complete restituto ad integrum, hy-podensity (the most frequent case) when theporencephalic/encephalomalacic cavity forms,and more infrequently, hyperdensity when cal-cium deposits occur. As a general rule, largerhaematomas require more time to transit thesephases than do smaller ones.

White matter oedema, which is visualized ashypodensity around the haemorrhage on CT,develops towards the end of the first week andsubsequently diminishes in degree, although incertain cases it can persist for some time (Figs.1.32 b, 1.41b, 1.44, 1.45). The mass effect, andin particular the compression of the cerebralventricular system, is usually directly propor-tionate to the amount of oedema entity; theoedema eventually disappears after 20-30 days(Figs. 1.25a, 1.32, 1.33, 1.41b, 1.42, 1.43, 1.44,1.45, 1.47a, 1.49a).

Evolution of the haemorrhage principallytakes place in two stages: a) during the initialfew days the size is related to the growth of thehaematoma, and b) in the subsequent 2-3weeks the overall mass effect is determined bythe increase in the perihaemorrhagic oedema(the clinical significance of late appearing oede-ma is as yet unclear) (23). The progressive re-duction of this mass effect is typically more rap-id in the smaller initial haemorrhages and thehaemorrhages associated to less perilesionaloedema (4-16).

Site

Pinpointing the location of the bleed, whichis usually easy with CT, is of fundamental im-portance as it largely determines: a) clinicalsymptomatology, which is closely linked to theneural structures affected by the bleed; b) aeti-ology and pathogenesis, because the sponta-neous forms linked to hypertension develop inthe basal ganglia (the typical site), whereasthose due to ruptured aneurysms, AVM’s orneoplasia are usually located in variable sites,(lobar, posterior fossa, etc.); c) prognosis, whichcorrelates with haemorrhage location and ex-tent; and d) treatment, which can differ fromone form to another, as some types may benefit


by surgery while others (although opinions mayvary) are usually treated conservatively. Anycerebral location can be involved, albeit withvarying frequency (Fig. 1.24).

The most typical hypertensive forms, whichaccount for some three-quarters of all IPH’s,can be subdivided into medial (thalamic) or lat-eral (putaminal) events. The former are less fre-quent (15-25%) and tend to be smaller due toboth the smaller dimensions of the thalamic nu-

clei as well as their containing fibres that form abarrier to blood diffusion (Fig. 1.29). However,because of their deeper-seated location, thesehaemorrhages are more likely to rupture intothe ventricular system (60% of all cases). In thelarger haemorrhages, the process may reach thewhite matter (above) and the midbrain (below).

Putaminal haemorrhages are considerablymore frequent than the thalamic and tend tohave greater extension outwardly and frontally.When they are confined to the putamen(17%), they present as a rounded mass with atypical diameter of 10-18 mm. They may man-ifest potentially reversible symptoms as theyprimarily cause compression of the fibres ofthe internal capsule. In one-third of all cases,these haemorrhages are observed in IV drugabusers (Fig. 1.30).

However, with the exception of these morelimited forms, putaminal haemorrhages tend toextend towards the surrounding neural struc-tures, with imaging studies that depend mainlyon their dimensions and expansion vectors.Lateral haematomas that extend to the externalcapsule (11%) commonly have an oval or com-ma-like shape (Fig. 1.31), a thickness that canvary between 1.5 and 2 cm, and a length of 3-5cm. They originate in the lateral part of theputamen and principally spread in an antero-posterior direction across the external capsule;they typically do not extend either to the hemi-spheric white matter or deep into the internalcapsule. Due to the relative lack of mass effectand absence of ventricular rupture, they com-monly have a favourable prognosis and canusually be removed surgically.

Forms of haemorrhage that spread moreeasily to the structures noted above are includ-ed in a third group (32% of the total) and arecharacterized by a rounded core (2-3 cm) withlinear bands that extend medially towards theinternal capsule and are therefore known ascapsulo-putaminal haematomas; these haemor-rhages also extend rostrally towards the cen-trum semiovale (Fig. 1.32).

These first three groups are only rarely fatal,although in a variable percentage of cases (1/3- 2/3) they do result in some residual neurolog-ical deficit.


Fig. 1.39 - A large haematoma with a fragmented appearancemassively occupies the brainstem (a) and spreads upwards to-wards the thalamic nuclei.

a

b

A fourth group (19%) of larger IPH’s (3-5cm) tend to expand concentrically from theputamen towards the corona radiata and thecortex of the cerebral hemispheres (frontal,temporal and parietal lobes), with either ajagged or a rounded appearance (Fig. 1.49).Unlike the forms of haemorrhage associatedwith middle cerebral artery aneurysm rup-tures, their spread towards the Sylvian fissureis not usually accompanied by subarachnoidbleeding.

A last group (19%), with the exception ofthe rare bilateral haemorrhages that account foronly approximately 2%, is composed of mas-sive mixed putaminal-thalamic forms that en-tail complex haemorrhagic involvement of allthe deep nuclear structures (22-24), (Fig. 1.33).

These latter IPH’s are large (up to 7 - 8 cm),involve considerable midline shift and, in mostcases, ventricular rupture. They have poorprognosis and often a rapidly fatal evolution inthree-quarters of cases. Principally this is due


Fig. 1.40 - Modified from (4).This chart shows the variations that the density of blood collections and other collateral parameters undergo during the phases sub-sequent to acute haemorrhagic accidents.

poroencephaliccavity

Time1 day 1 week 2 week 3 week 1 month 2 month

Haemorrhage

CE

Oedema

«Mass effect»

hyperdensity

hypodensity

to associated brainstem injury, be it direct or aconsequence of transtentorial herniation, eitherof which worsens the degree of coma, and if

unchecked eventually results in a severe neu-rovegetative state (1).

It is therefore possible to formulate a progres-sive grading of thalamic and putaminal haemor-rhages. Together with clinical grading (e.g., pa-tient awake; drowsy with or without neurologicaldeficit; sluggish with slight to severe neurologicaldeficit; semi-comatose with severe neurologicaldeficit or early signs of herniation; deep comawith decerebration), it enables an immediateprognostic assessment, which is useful in decid-ing upon subsequent possible courses of treat-ment (16). The debate between the supporters ofconservative medical treatment on the one hand,and surgery on the other is still open. Whereas itseems universally accepted that surgical evacua-tion is the preferable treatment for lobar haem-orrhages (especially when they are larger than 35-44 cm3 and therefore have a greater probabilityof causing brainstem compression and hernia-tion), the management of haemorrhages occur-ring in more common locations is still somewhatcontroversial.

It should also be pointed out that surgery isnot necessarily considered as an alternative tomedical treatment, but rather as a complementto it, especially when conservative managementproves inadequate alone (5, 8). For example,surgery may be employed when medical thera-py is unable to adequately control intracranial


Fig. 1.41 - Evolution of IPH over time.CT is commonly used in IPH follow-up. In (a) the haematomais documented a few hours from the stroke (note the deep po-sition, the jagged edges and the presence of small satellite foci).On a check carried out 14 days later (b), the haematoma pres-ents modest reductions in volume and density; it is however,surrounded by a vaster hypodense area (with a prevalence ofthe oedematous component developing in the white matter).Three months later (c), the haematic hyperdensity is replacedby an irregular porencephalic cavity with a star shape, whichproduces discreet ectasia of the homolateral ventricle.

ac

b

hypertension. However, generally speaking,haemorrhages in thalamic positions are notsubject to surgery, because surgery at this loca-tion is associated with higher mortality rates(80%); nevertheless, these patients often re-quire ventriculostomy, due to the frequency ofassociated hydrocephalus (9).


Fig. 1.42 - The use of contrast medium in atypically positionedacute haematomas. A voluminous lobar haematoma with a prima-rily occipital expansion (a) is constituted by a more hyperdensecomponent (*), an expression of recent bleeding, and by anothersubacute, more widespread, and partially levelled component.The site and the lack of association with hypertension suggested asecondary haemorrhage and therefore an examination was per-formed after intravenous administration of contrast medium (b).There was no documentation of pathologically significant impreg-nations adjacent to the haematomas, nor alterations in density.The spontaneous haemorrhagic picture, with clots in variousphases of evolution, was confirmed during surgery.

Fig. 1.43 - The use of contrast media in the subacute phase.Twenty-five days from the stroke, this haematoma presents with(a) a target-shaped form and a blurred central hyperdensity.The contrast medium (b) impregnates a thin and uniform pe-ripheral rim. This ring is clearly distinguishable, despite the factthat the patient had received long-term steroid treatment,therefore in this «late» phase it is essentially supported by thehypervascularization of granulation tissue.

a

a

b

*

b

With regard to putaminal haemorrhages,surgery and its timing depend upon the clinicalstatus of the patient at the time. Haemorrhageswith a statistically favourable expectation basedon past experience are usually treated conserv-atively; those with stationary or slowly worsen-ing clinical pictures are operated in an electivemanner; those IPH’s with early signs of internalbrain herniation are traditionally taken to emer-gency surgery; and the massive haemorrhagesin those patients having a dire general and neu-rological status (e.g., deep coma, decerebra-tion) are not usually treated surgically (17).

The second form of hemispheric IPH (15-25%) is localized wholly within the white mat-ter. These so-called lobar or subcortical intra-parenchymal haemorrhages are linked in one-third of all cases to high blood pressure and inthe remaining two-thirds of cases to other caus-es described previously.

The position of these lobar haemorrhagescan be parietal (30%), frontal (20%), occipital(15%) or mixed (35%). In fact, they often oc-cur at the temporo-parietal-occipital junction(Fig. 1.34). Their CT appearance and evolution

are very similar or identical to that previouslydiscussed for more “typical” positions of IPH.

Frontal haemorrhages (Fig. 1.35) are usuallyunilateral (lobar haemorrhages can be bilateralin forms secondary to aneurysm ruptures of theanterior communicating artery). They are round


Fig. 1.44 - The influence of steroids on the outer ring.17 days after the ictus, this IPH presents a reduction in its cen-tral density, an ample quantity of perifocal oedema and discreetmass effect. After CE it is demarcated by a ring, which becauseof cortisone treatment is incomplete and blurred (arrowhead).

Fig. 1.45 - Contrast medium use in the diagnosis of forms en-countered in the subacute phase only.For approximately two weeks the patient has been sufferingfrom worsening symptoms of intracranial hypertension, withprogressive hemiplegia of the left side. Clinical suspicion pointsto a neoplastic pathology. The lesion documented by CT (a) ishyperdense as with IPH, but with atypical site (and symptoma-tology); it is accompanied by abundant oedema of the whitematter and exerts a marked mass effect. The subsequent exam-ination after CE, with the demonstration of the «ring» en-hancement, would therefore strongly suggest a haemorrhagicnature (as confirmed by subsequent checks). It should be not-ed that, despite its circumvolute appearance, also in this phasethe ring is thin and regular; which arouses further doubts, be-cause the patient has not yet been treated with steroids.

a

b

or oval in rostral positions and wedge-shaped(with the apex directed at the ventricles and thebase towards the brain surface) if located in afrontal-basal position. Only 20% of lobarhaemorrhages rupture into the cerebral ventric-ular system. At least 50% are life-threatening(22). Those lobar haemorrhages with locationsin the temporal lobes are round; they can rup-ture into the temporal horns and develop earlyinternal transtentorial brain herniation. Whenthey develop within the Sylvian fissure, thus be-coming frontal-temporal, they are more likelycaused by ruptured aneurysms of the middlecerebral artery. Larger haemorrhages often ex-tend deep into the basal ganglia, although theydo not usually cross the internal capsule, an im-portant distinction with regard to subsequenttreatment.

Parietal lobar haemorhages (Fig. 1.36) havethe most favourable prognosis and often re-solve with little or no neurological sequelae,even without surgery.

10% of occipital lobar haemorrhages rup-ture into the occipital horns of the cerebral ven-

tricles. Nevertheless, these haemorrhages alsotypically resolve spontaneously in the vast ma-jority of cases, although they often leave somedegree of visual deficits.

Cerebellar IPH’s account for approximately8% of the total, which more or less correspondsto the proportion of the space occupied by thecerebellum as compared to the remainder of thebrain. Once again, in this position hypertensionis by far the most common cause. Hypertensivebleeds are followed, in second place, by vascu-lar malformations that account for 10-15% ofthe total; these haemorrhages are usually causedby the rupture of cryptic angiomas, which areeven more frequent at this location than in thecerebral hemispheres (Fig. 1.38).

Approximately 80% of cerebellar IPH’shave lobar origins (Fig. 1.37), initially affectingthe dentate nucleus; this is where vessel wall al-terations such as Charcot-Bouchard aneurysmsas observed in the lenticulostriate arteries in as-sociation with basal ganglia haemorrhages areseen pathologically. From here, the haemor-rhage can cross the midline, affecting the ver-mian area to enter the contralateral cerebellarhemisphere; it may also rupture into the 4th

ventricle. More infrequently, it can dissect intothe brainstem, which more commonly is simplyaffected by compression or displacement.

Less frequently, IPH’s may primarily affectthe cerebellar vermis, especially in the case ofaneurysm ruptures (Fig. 1.38).

In cases where consciousness is largely unaf-fected and CT presents an IPH devoid of masseffect with a diameter of less than 3 cm, com-plete recovery can be expected and surgery isgenerally not required (Fig. 1.26). However,emergency surgery is usually essential (and mustbe carried out urgently, in order to be lifesav-ing), in most of the other cases, especially whenthere are CT or clinical indications of brainstemand fourth ventricle compression (e.g., con-tralateral brainstem displacement, distortionand marked brainstem compression with associ-ated obstruction of the 4th ventricle, loss of thebasal subarachnoid cisterns, and obstructivesupratentorial hydrocephalus) (22) (Fig. 1.37).

With regard to the brainstem, three anatomi-cal and pathological distinctions can be made for


Fig. 1.46 - Haemorrhagic infarct.An extensive ischaemic infarct that massively affects the terri-tory of the left middle cerebral artery, four days from onsetpresents an unexpected worsening of clinical conditions. CT documents irregular circumvolute hyperdensities, whichcan refer to overlapping bleeding phenomena.

non-traumatic parenchymal haemorrhages: 1)those haemorrhages encapsulated within thebrainstem parenchyma, 2) large brainstem IPH’swith ventricular rupture (Fig. 1.39); 3) petechialbrainstem haemorrhages secondary to expandingsupratentorial mass effect complicated by inter-nal transtentorial cerebral herniation (22). The

small dimensions of the latter make them difficultto perceive on CT. Pontine haemorrhages havevariable appearances and longitudinal extentsdepending on the size of the vessels from whichthey originate and the point at which they occur.If bleeding is caused by the rupture of larger ar-terioles, the haemorrhage is more commonly me-dial, affecting the base of the pons and thetegmen and spreading to the fourth ventricle.Due to mass effect, in 80% of cases the peri-brainstem subarachnoid cisterns are obliterated.

However, in haemorrhages associated withsmaller vessels (having a more lateral andtegmental position), the bleeds are usuallysmaller and unilateral and do not rupture intothe fourth ventricle.

CT is invaluable in differentiating pontinehaemorrhages from those affecting the adjacentcerebellar peduncles and especially the fourthventricle; the latter are paramedial, pyramid-shaped (reproducing the form of the ventricle,which is usually dilated), and are often accom-panied by hydrocephalus and the presence ofblood in the basal subarachnoid cisterns (22).

IPH’s rarely occur in the midbrain; whenthey do they are not usually caused by hyper-tension but are instead often related toaneurysm ruptures. They rarely spread to thepons or the thalamus (above, Fig. 1.39).

In the majority of cases, CT permits a pre-cise spatial definition of bleeding and its exten-sions. In certain cases, more accurate informa-tion may be required, which is now easily ob-tainable with CT angiography using 3D recon-structions, especially with the use of computer-ized postprocessing analysis (10).

Contrast agent use

During the acute phase, paranuclear IPH’sdo not require enhanced examinations using IVcontrast medium administration. This tech-nique is used when the diagnosis is in doubt, ifthe aetiology of the haemorrhage is uncertain(Fig. 1.42), or in the following conditions:

a) patients under 40;b) absence of history of high blood pressure

documentation;


Fig. 1.47 - Although rarely, IPH’s can also present with bilater-al multiple localizations.In (a) an example of a deep form, in (b) lobar forms. Thehaematomas of (a) are both putamino-thalamic; that on the lefthas a non-homogeneous core and, due to its larger dimensions,prevails in the shift effect on the contralateral ventricular cham-bers. The IPH’s in (b) are due to the recent bleeding of breastcancer metastases.

a

b

c) progression of neurological deficit overmore than 4 hours;

d) history of transitory prodromes; e) an atypical CT appearance and dispro-

portionate degree of subarachnoid and/or sub-dural haemorrhage;

f) presence of possible combined pathology,such as proven neoplasia, bacterial endocarditisor arteritis (22).

Contrast agent use is therefore essential inall cases where an IPH potentially caused byother types of pathology is suspected. In fact, inthe case of bleeding tumours, contrast agentsusually only enhance the solid mass compo-nent, which can therefore be better distin-guished from the surrounding parenchyma (ifisodense) and the haemorrhage (if hyperdense).Enhancement can be nodular, diffuse or ring-shaped (thickened and irregular). The haemor-rhage is most frequently found at the interfacebetween the tumour and the surrounding oede-matous parenchyma; it can sometimes present

with a pseudo-cystic appearance or appear witha fluid-fluid level of differing densities (22).

During the subacute phase, in other wordswhen the IPH tends to be accompanied bygreater degrees of perilesional oedema and con-sequent greater mass effect, and starts to lose itscharacteristic hyperdensity, it can sometimesreveal an atypical CT picture, similar to thatseen in cases of neoplasia. On the other hand,these IPH’s usually have a lobar location, andtherefore at onset their symptomatology may bemild and progress slowly; for this reason theymay not be seen in hospital until the subacutephase. In such circumstances, the use of IVcontrast agents can aid in the determination ofthe diagnosis (Fig. 1.45). From the second tothe sixth week, IPH’s show a characteristic butminor ring of enhancement along the margin ofthe haemorrhagic portion. However, this find-ing is not constant and in fact does not appearin some 50% of cases (Figs. 1.43, 1.44). Thisring enhancement may also be present in theiso- and hypodensity phases of haemorrhageevolution, when the perilesional oedema andmass effect are completely resolved. The en-hancing ring is usually thin, approximately 3mm wide, and of uniform thickness (this ap-pearance of the rim enhancement is thereforedifferent from that which often surrounds neo-plastic masses, which is thicker and has unevendimensions).

In the absence of other definitive differen-tiating elements between the two conditions,the final diagnosis is possible on the basis ofsubsequent serial imaging studies, which, inthe case of IPH’s show a gradual decrease inthe contrast enhancing intensity of the rim, to-gether with a further reduction in the diame-ter and density of the central haemorrhagiccomponent.

There are at least two mechanisms that ex-plain this semeiological aspect of contrast en-hancement surrounding benign IPH’s: one pre-vails in the first stage (3-4 weeks from onset ofhaemorrhage), which depends on the brain-blood barrier breakdown of otherwise normalnative vessels and is reduced in degree by theuse of steroids (Figs. 1.43, 1.44); the other,which takes place during the later phases, is


Fig. 1.48 - CT in differential diagnosis between infarct andhaemorrhage.It is rare for ischaemic and haemorrhagic pathologies to pres-ent associated. This case serves to demonstrate the differencebetween the CT pictures for the two.On the right the sequelae of an extensive infarctual lesion (hy-podense), which affects the territory of the middle cerebral ar-tery and, immediately adjacent, a recent rounded formation(hyperdense) of haemorrhagic type, which expands in depth tothe basal grey nuclei.


Fig. 1.49 - CT is also valid in postsurgical follow-up.(a) documents a coarse putaminal IPH, spread to the cerebralcortex (note the concomitant haemorrhagic extravasation inthe ventricular cavities, with scattered clots in the frontalhorns and a minimal amount of fluid sloping in the occipitalhorns). Three days later (b), the haematoma was surgically re-moved. The CT picture is characterized by the presence of alarge hypodense area and a small gas bubble; more externallythere is a malacic appearance of the parietal lobe (however thepractically unaltered intraventricular haemorrhagic compo-nent persists). On check-up ten days later, there is a residual ir-regular deep hypodensity that subsequently, one month afterthe ictus, is surrounded by a granulation tissue with an intense,albeit thin, ring of contrast medium impregnation (d). The fol-lowing week this cavity is subject to drainage; and the tip ofthe deviation catheter is clearly visible. The periencephalic flu-id-filled spaces and the ventricular cavities contain air (whichalso occupies the non-sloping parts of the ventricles).

a d

e

b

c

linked to the hyperneovascularization of thegranulation tissue that surrounds the IPH andis not altered by steroid treatment (Fig. 1.45).

It is believed by some researchers that func-tional recovery is better in cases in which thecontrast-enhancing rim is present. Besides IPHand neoplasia (glioma, metastasis, lymphoma),other types of pathology with similar appear-ances include abscesses (in which the ring en-hancement is usually thicker and denser, al-though regular in its thikness, and is accompa-nied by nodular daughter components or ringenhancing satellite foci), and thrombosedaneurysms and angiomas (in which calcificationsor vascular components that can aid in the cor-rect diagnosis are often found).

PARTICULAR FORMS OF IPH

Haemorrhagic infarction

A haemorrhage may develop within an is-chaemic lesion when a lack of oxygen that caus-es the necrosis of the endothelial cells of thecapillaries occurs. In actual fact, infarctions al-most always contain a variable haemorrhagiccomponent as determined pathologically,sometimes in the form of small petechial haem-orrhages that are not visible on CT. It is there-fore the presence or absence of this CT visual-ized component that indicates or dispels suspi-cion of haemorrhagic infarction (12). This typeof event is most frequently observed as a resultof cardiogenic cerebral emboli or anticoagula-tion treatment. These haemorrhages are usuallyvisible on CT scans performed 4-5 days afterthe infarct (up to a maximum of 2 weeks) (22)and are often accompanied by a worsening inthe patient’s clinical condition. Haemorrhagicinfarctions occur in 20% of cases of ischaemiccerebral disease (small petechial haemorrhagesare present in at least 50% of autopsy findings).The haemorrhages are almost always confinedto the cerebral cortex and usually affect thedeeper gyri. On CT scans these infarcts appearas a hypodense area that reflects the circulationterritory (i.e., watershed) of the affected artery;however, due to the larger degree of accompa-

nying oedema, the low density area has greaterdimensions than the actual dimensions of theinfarct. These infarcts do not usually have sig-nificant mass effect and usually show small hy-perdense haemorrhagic components within theinfarcted region (Fig. 1.46). Small diapedeticforms are not usually visible with CT, in partdue to the limited spatial and contrast resolu-tion of the technique. The most widespreadcortical haemorrhages usually have a gyral dis-tribution with convolutional hyperdensity orare only visible in the apex of the infarct area.Intravenous contrast agent administration withCT in the subacute phase results in a classic gy-ral enhancement pattern.

Intraventricular haemorrhage

Intraventricular haemorrhages can be divid-ed into two categories: one, the more frequent,secondary to the spread of an IPH that dissectsthrough the ependymal lining of the ventricularsurface; and two, a primitive type of haemor-rhage due to the rupture of vessels of thechoroid plexus or the ventricle walls. The mostcommon causes of the latter are connected toregional vascular malformations, haeman-giomas of the choroid plexus or, more rarely,malignant neoplasia affecting the paraventricu-lar tissues.

CT is able to establish both the presence aswell as the aetiology of the intraventricularbleed with considerable accuracy, showing ahyperdense haemorrhage that forms a cast ofthe morphology of the ventricular chambers(Figs. 1.25b, 1.29b, 1.33, 1.35). A blood-fluid(i.e., blood-CSF) level can often be observed, inwhich hyperdense blood due to gravity layers inthe occipital horns in supine patients (Figs.1.33, 1.35). However, in some rare cases the in-traventricular blood occupies the temporalhorns alone. If the intraventricular haemor-rhage is a result of an ipsilateral hemisphericIPH, the ventricular blood may be present inthe adjacent lateral ventricle only.

These two conditions, that is IPH versusintraventricular haemorrhage (IVH), can usu-ally be differentiated relatively easily, al-


though, especially if the IPH is particularlysmall, they may be confused as a single-com-partment hyperdense haemorhage due to par-tial volume averaging effects. In fact, there isno absolute correlation between IPH dimen-sions and association of IVH; in some casessmall haematomas of the caudate nucleus orthe thalamus are accompanied by massive in-traventricular bleeding.

Certain studies have shown a direct relation-ship between the volume of intraventricularblood (e.g., presence of blood in the intraven-tricular space, number of ventricles containingblood, intraventricular extension of hyperden-sity from adjacent brain parenchyma) and theprognosis of these patients (20). Within a fewdays, blood hyperdensity is gradually dilutedby the CSF circulation and by the breakdownof haemoglobin products. Due to the effect ofCSF flow obstructions at various levels withinthe ventricular system, partial or total locula-tions of the ventricular chambers may formover time.

Multiple IPH’s

IPH recurrences at the same site are some-what rare, as are multifocal haemorrhages(Fig. 1.47). These types do not account formore than 3% of all intraparenchymal haem-orrhages. The causes of multiple haemor-rhages are often the same as those of singleones, although they usually occur in patientswith normal blood pressure, and tend tospecifically be seen in patients with clottingdefects, cerebral metastatic neoplastic disease(Fig. 1.47b), thrombosis of the dural venoussinuses, herpes simplex encephalitis or bacter-ial endocarditis with cerebral septic emboli.However, even after selective cerebral angiog-raphy, it is often difficult to trace the originalcause. In two-thirds of cases, the IPH’s havebilateral lobar positions, and in the remainingone-third they are lobar-nuclear (basal ganglianuclei), thalamic-cerebellar, paranuclear-bilat-eral, etc. (22).

In general this does not pose a diagnosticproblem in distinguishing multiple benign

IPH’s from other multiple spontaneously hy-perdense lesions (metastases, multiple menin-giomas, rare multifocal angiomas, etc.), all ofwhich significantly enhance on CT with IVcontrast agents.

CONCLUSIONS

CT enables the direct visualization of haem-orrhagic lesions and assists in the differentia-tion from other acute cerebrovascular events(Fig. 1.48). CT typically accurately illustratesthe site(s), extent and volume of the IPH(s). Inthe early phases CT is helpful in monitoringmorphological and densitometric characteris-tics as well as for revealing complications suchas intraventricular rupture or progressive hy-drocephalus.

CT is later useful in identifying spontaneousprogression and postsurgical recurrence, in thecase of surgical removal (Fig. 1.49). The easeand rapidity with which the examination is per-formed, its high sensitivity and specific naturemake CT the examination of choice for study-ing this type of pathology. Spiral CT, the latesttechnological innovation of this technique andone that has proved particularly useful in anumber of disease categories (including injuriesof polytraumatized patients), has more limitedapplications in the evaluation of clinical stroke.In reality, its use is not indispensable: tradition-al CT scans of the cranium are nearly as fastand equally accurate. In this part of the body,there are no problems posed by breathing mis-recording, correct contrast agent timing oreven motion artefacts caused by long examina-tion times. However, the spiral CT techniquemay play a role due to its application in multi-planar image reconstruction studies (15).

REFERENCES

1. Andrews BT, Chiles W, Olsen W et al: The effect of in-tracerebral hematoma location on the risk of brainstemcompression and clinical outcome. J Neurosurg 69:518-522, 1988.

2. Bagley LJ: Imaging of neurological emergencies: trauma,hemorrhage, and infections. Semin Roentgenol 34:144-159, 1999.


3. Blankenberg FG, Loh NN, Bracci P et al: Sonography, CT,and MR imaging: a prospective comparison of neonateswith suspected intracranial ischemia and hemorrhage.AJNR 21:213-218, 2000.

4. Boulin A: Les affections vasculaires. In: Vignaud J, BoulinA: Tomodensitométrie cranio-encéphalique. Ed VigotParis, 1987.

5. Broderick JP, Brott TG, Tomsick T et al: Ultra-early eval-uation of the intracerebral hemorrhage. J Neurosurg72:195-199, 1990.

6. Cirillo S, Simonetti L, Sirabella G et al: Patologia vasco-lare. In: Dal Pozzo G (ed): Compendio di TomografiaComputerizzata (pp. 127-147). USES Ed. Scientifiche Flo-rence, 1991.

7. Grossman CB: Magnetic resonance imaging and comput-ed tomography of the head and spine (pp. 145-183).Williams & Wilkins Baltimore, 1990.

8. Juvela S, Heiskanen O, Poranen A et al: The treatmentof spontaneous intracerebral hemorrhage. J Neurosurg70:755-758, 1989.

9. Kase C: Diagnosis and treatment of intracerebral hemor-rhage. Rev Neurol 29:1330-1337, 1999.

10. Loncaric S, Dhawan AP, Broderick J et al: 3-D imaging analy-sis of intra-cerebral brain hemorrhage from digitized CTfilms. Comput Method Programs Biomed 46:207-216, 1995.

11. Mader TJ, Mandel A: A new clinical scoring system failsto differentiate hemorrhagic from ischemic stroke whenused in the acute care setting. J Emerg Med 16:9-13,1998.

12. Masdeu JC, Fine M: Cerebrovascular disorders. In: Gon-zalez CF, Grossman CB, Masdeu JC (eds) Head andspine imaging (pp. 283-356). John Wiley & Sons NewYork, 1985.

13. Miller JH, Warlaw JM, Lammie GA: Intracerebral haemor-rhagic and cerebral amyloid angiopathy: CT features withpathological correlation. Clin Radiol 54:422-429, 1999.

14. Modic MT, Weinstein MA: Cerebrovascular disease of thebrain. In: Haaga JR, Alfidi RJ (eds) Computed tomogra-phy of the brain, head and neck (pp. 136-169). The C.V.Mosby Co. St. Louis, 1985.

15. Novelline RA, Rhea JT, Rao PM et al: Helical CT in emer-gency radiology. Radiology 213:321-339, 1999.

16. Ross DA, Olsen WL, Ross AM et al: Brain shift, level ofconsciouness and restoration of consciousness in patientswith acute intracranial hematoma. J Neurosurg 71:498-502, 1989.

17. Scarano E, De Falco R, Guarnieri L et al: Classificazione etrattamento delle emorragie cerebrali spontanee. RicercaNeurochirurgica 1-2:21-32, 1990.

18. Sellier N, Lalande G, Kalifa G: Pathologie vasculaire. In:Montagne JP, Couture A: Tomodensitométrie pédiatrique(pp. 70-90). Ed. Vigot Paris, 1987.

19. Takasugi S, Ueda S, Matsumoto K: Chronological changesin spontaneous intracranial hematoma - an experimentaland clinical study. Stroke 16:651, 1985.

20. Tuhrim S, Horowitz DR, Sacher M et al: Volume of ven-tricular blood is an important determinant of outcome insupratentorial intracerebral hemorrhage. Crit Care Med27:617-621, 1999.

21. Waga S, Miyazaki M, Okada M et al: Hypertensive putam-inal haemorrhage: analysis of 182 patients. Surg Neurol26:159-166, 1986.

22. Weisberg LA, Nice C: Cerebral computed tomography. Atext atlas (pp. 133-162) W.B. Saunders Co. Philadelphia,1989.

23. Zazulia AR, Diringer MN, Derdeyn CP et al: Progression ofmass effect after intracerebral hemorrhage. Stroke 30:1167-1173, 1999.

24. Zhu XL, Chan MS, Poon WS: Spontaneous intracranialhemorrhage: which patients need diagnostic cerebral an-giography? A prospective study of 206 cases and review ofthe literature. Stroke 28:1406-1409, 1997.


49

INTRODUCTION

Subarachnoid haemorrhages (SAH’s) are thefourth most frequent type of acute cerebrovas-cular event and account for approximately 8%of the total. In most cases (at least 75%), SAH’sare caused by the rupture of aneurysms of thecircle of Willis, with the aneurysm itself lyingwithin the subarachnoid space. SAH’s affectapproximately 11 of every 100,000 inhabitantsin the general population. The most critical pe-riod is during the first few days after the haem-orrhage: 25% of deaths occur on the first dayand 50% in the first five days. Remedying thissituation calls for rapid and specific diagnosis,which is not possible using clinical data alone.

In recent years SAH survival rates have in-creased, due in part to progress in intensive careand surgical techniques, but above all thanks tothe more precise diagnostic methods that arenow available (6). Computerized Tomography(CT) plays a fundamental role (19). From theoutset its non-invasive nature and sensitivityhave made it an examination technique capableof achieving early diagnosis. More specifically,its sensitivity is given as ranging between 93-100% if performed within the first 12 hours ofthe onset of symptoms (24, 26). In addition tothe observation of subarachnoid bleeding (withthe typical hyperdensity of the basal subarach-

noid cisterns and within the cortical sulci), CTis also able to document collateral phenomenaand complications such as intraparenchymal, in-traventricular and subdural haemorrhages, anymass effect upon the cerebrum, hydrocephalusand cerebral infarcts associated with vasospasm.In some cases, it is possible to establish themore or less precise origin of the haemorrhagefrom the distribution pattern of blood collec-tion, which is particularly useful in directingsubsequent selective angiographic examina-tions. In the case of multiple aneurysms, the pat-tern of the blood collection on CT is importantin indicating which of them has bled (4). CT al-lows approximative prognosis assessment (e.g.,widespread and massive forms of SAH have amore severe prognosis than smaller ones). Last-ly, CT is useful in selecting which patients are toundergo angiography and in determining whenit should be performed (28).

SEMEIOTICS

On CT, the more or less pathognomonic ap-pearance of SAH is revealed by the increase indensity of the cisternal subarachnoid spacesthat appear proportionately denser as a factorof the concentration of blood they contain.Lesser extravasations of blood or those that oc-

1.4

CT USE IN SUBARACHNOID HAEMORRHAGEN. Zarrelli, L. Pazienza, N. Maggialetti, M. Schiavariello, M. Mariano, A. Stranieri, T. Scarabino

cur in subjects with low haemoglobin countsmay be less hyperdense and therefore more dif-ficult to identify. On the contrary, larger SAH’s,which tend to clot in contact with the CSF,

form clearly visible and somewhat focal bloodcollections (6). On average, the density of freshextravasated blood has a value of approximate-ly 70-80 H.U. (normal CSF = ~10 H.U.).

Generally speaking, abnormal hyperdensitytypically involves the suprasellar and perimes-encephalic cisterns (or more broadly speaking,the CSF spaces of the basal subarachnoid cis-terns), the Sylvian fissures and the cortical sul-ci. Although infrequent, CT scans performedat the onset of symptoms can prove falsely neg-ative. However, this false negative tendencybecomes more frequent the longer the time pe-riod is between the initial bleed and the per-formance of the CT examination. In reality: 1)in the milder clinical forms that may only pres-ent clinically at a later stage, the subarachnoidblood will have undergone dilution and dis-persal within the native CSF, and therefore de-tection is understandably more problematic;and, 2) in awake patients with good neurologi-cal status, it is probable that bleeding is onlyminor.

MR using conventional acquisitions is notpreferable to CT in patients suspected of hav-ing an acute SAH; in fact, in this phase, con-ventional MR acquisitions may be negativedue in part to the slower conversion of oxy-haemoglobin into metahaemaglobin (resultingin relative hyperintensity) within the erythro-cytes in the subarachnoid space (the oxygentension in the subarachnoid space is relativelyhigh, thereby maintaining oxyhaemoglobin forlonger periods of time than might otherwise beexpected).

As mentioned previously, statistics on CTsensitivity in demonstrating SAH’s vary greatly(e.g., from 55 to 100% if we consider data pub-lished over the last 20 years). This great vari-ability can be attributed to at least two factors:the first being the time of the CT examinationperformance, because those performed within24 hours of the onset of symptoms result inpositive rates of 93% - 100% of cases, whereasfor those performed on the second day the fig-ures drop to 63-87%; and the second factor be-ing the particular medical centre where the pa-tient is hospitalized, as those with greater expe-rience also treat more serious cases in which


Fig. 1.50 - CT pictures of SAH’s subsequent to the rupture ofan aneurysm of the anterior cerebral artery, a few hours afterthe ictus.a and b: in both cases, the widespread haemorrhagic extravasa-tion demarcates the perimesencephalic and supra-sellar cis-terns, the initial part of the Sylvian fissures and the interhemi-spheric fissure with its hyperdensity. In b the blood collectionsare clearly less thick in the perimesencephalic location, but theyare accompanied by the blocking of the 3rd ventricle.Both cause a discreet early ectasia of the ventricular chambers.

widespread bleeding is more common and istherefore more easily detected using CT.

With the exception of these findings, thecurrent improvements in sensitivity are duelargely to the progress made in the technologywith regard to higher spatial and contrast reso-lution; from the 55% sensitivity of first genera-tion equipment, we have now reached numbersapproaching 100% sensitivity for modern dayCT appliances (26). It should also be noted thatthe reduction in the time elapsing between theevent and the moment in which the CT scan isperformed can be attributed to the greater dis-tribution of equipment throughout the world.Lastly, progress has been made in the interpre-tation of subtle changes, which are usuallycaused by more focal blood collections (Fig.1.51). In stable patients, CT is suitable for de-

termining not only the presence of extravasatedblood in the subarachnoid space (which con-firms the clinical suspicion of SAH), but alsothe dominant site of the haemorrhage, the di-mensions of the cerebral ventricular chamberson sequential scans, and the presence of earlycomplications, which may or may not be de-tected during clinical examinations.

In this acute phase, and depending on theexperience and expectations of the surgicalstaff, CT documentation of SAH may make itunnecessary to perform emergency angiogra-phy; this is especially true when early surgery isnot planned. However, in the case of a negativeCT scan and a clinical picture suggestive ofSAH, the definitive diagnosis relies on a diag-nostic lumbar puncture. This happens mostcommonly when CT is carried out late (i.e.,more than 12 hours from the ictus) (24, 26) oroccasionally very early, within the first fewhours (1). The former situation has alreadybeen sufficiently discussed, while the secondcircumstance is somewhat rare. Nevertheless,when the initial CT scan is negative, a diagnos-tic lumbar puncture is mandated in patientsthat present with meningeal symptoms (e.g.,spontaneous onset of stiff neck), when its mainfunction is to exclude other types of pathologythat might be responsible for the clinical signs,such as meningitis.

In patients with poor neurological status,CT should be the first diagnostic imaging in-vestigation performed, considering the possiblerisk of internal herniation of the cerebellar ton-sils posed by a diagnostic lumbar puncture.Subject to emergency angiography, many suchcases may require early surgery aimed at ad-dressing complications such as acute hydro-cephalus and intraparenchymal haematomas.Such surgery can remove the viscous clots fromthe basal subarachnoid cisterns and place clipson aneurysms before vasospasm develops (34).The ability of CT to detect such complicationsin the hyperacute phase, which often prove fa-tal, makes CT essential in order to definewhether surgery is required or whether, for ex-ample, conservative monitoring of the intracra-nial pressure is preferable.

At some point in the patient’s clinicalcourse, selective cerebral angiography is almostalways recommended in order to establish thenature of the responsible vascular lesion (e.g.,aneurysm, arteriovenous malformation) as wellas the dimensions, orientation and accessibilityof the intracranial vessels and the vascular ori-gin of the anomaly, which are sometimes al-tered by vasospasm.

1.4 CT USE IN SUBARACHNOID HAEMORRHAGE 51

Fig. 1.51 - Curcumscribed SAH signalled by focal blood ex-travasations in some of the cortical sulci (arrows).

Cisternal hyperdensity related to the SAHdeclines with time as a consequence of clot andred blood cell lysis, in part in proportion to theresorption of haemoglobin and plasma proteins(8). Generally speaking, blood is no longer doc-umented by CT within a week following the ic-tus, and if hyperdensity does persist beyond thisperiod, it is more likely that it is due to rebleed-ing. In the subacute phase, typically more thanthree days after the bleed, and especially inchronic cases, a rapid decline in CT sensitivity isusually mirrored by increasing MRI sensitivity.In certain studies, MR has proved to be 100%accurate in cases studied 3-45 days after thestroke (21); in particular this has been observedin those cases where FLAIR (fluid attenuationinversion recovery) sequences have been used,making it the technique of choice in the suba-cute phase of SAH.

CAUSES

As mentioned previously, most SAH’s arecaused by the rupture of aneurysms at the baseof the brain. This condition is rather frequent,as aneurysms are found in approximately 1-2%of all routine autopsies. Fortunately, it has alsobeen found that only a small number of all aneurysms subsequently rupture (1 in 17).Aneurysm ruptures are infrequent during child-hood and adolescence, and reach a peak be-tween 35 and 65 years of age. Aneurysms arethought to form as a consequence of congenitaldefects or weaknesses in arterial walls coupledwith subsequent degenerative changes associat-ed with aging. Aneurysms statistically prevail incertain families, and there is a considerablyhigher incidence of such aneurysms in hyper-tensive patients, those with polycystic kidneydisease or coarctation of the thoracic aorta. Ap-proximately 90-95% of aneurysms originate inthe anterior half of the circle of Willis. The fourmost common sites are the anterior communi-cating artery (30%), the origin of the posteriorcommunicating artery from the internal carotidartery (25%), the middle cerebral artery bifur-cation/trifurcation (20%), and the bifurcationof the supraclinoid internal carotid artery into

the middle and anterior cerebral arteries (10%).Other locations are rare; the basilar artery is in-volved only in 5% of cases. In 20% of cases,aneurysms are multiple, and their dimensionsare variable among each other. However, bleed-ing is more frequent in those aneurysms that areless than 1 cm in diameter, and is most commonin those with a diameter of 3-5 mm (Fig. 1.53b).This accounts for the rarity of their being iden-tified using CT, at least when “standard” tech-niques are employed. Large (i.e., diameter 1-2.5cm) and giant (i.e., diameter 2.5 cm or larger)aneurysms rarely present with SAH. Instead,they often present with neurological symptomsrelated to their mass effect (e.g., paralysis of the3rd cranial nerve due to an aneurysm of the pos-terior communicating artery in the parasellararea). Other types of aneurysms, including my-cotic and atherosclerotic aneurysms, in turn dis-tinguished by their morphology into fusiform,or diffuse globular, only rupture very rarely.

The CT findings of intracranial aneurysmsare closely linked to their site and vessel origin.As most aneurysms are small and localized in


Fig. 1.52 - So-called «sine materia» SAH picture, with exclusiveblood localization in the perimesencephalic area (in this casemainly towards the left side, arrows). The angiograph of the 4vessels is completely negative, both at the time of hospitaliza-tion and on a control performed one week later.The patient, who was awake and in good conditions at onset,recovered completely a few days later.

the base of the brain, identification in the pastwas hindered by the spatial resolution of theavailable CT equipment. In most cases, non-thrombosed saccular aneurysms with thin wallspresent as round or elongated masses, withmoderately high CT density, and are not calci-fied. After IV contrast administration, enhance-ment of their residual lumen is uniformly hy-perdense. Smaller aneurysms are more difficultto visualize, and this is usually only possiblewhen they are located within or next to the sub-arachnoid spaces. With the advent of spiral CTtechnology, so-called CT angiography has madedetection of these smaller aneurysms much eas-ier. This technique uses three-dimensional re-constructions of the vessels after IV administra-tion of a contrast agent bolus and can providevaluable information for surgical planning (22),sometimes even more so than conventional an-giography. In many cases, it is more effectivethan conventional angiographic techniques in il-lustrating the neck, shape and dimensions of theaneurysm as well as its position and relationshipwith surrounding structures (18).

MRI and MR angiography in particular are of-ten even more effective in detecting aneurysmsthan CT; nevertheless, a conventional selectiveangiographic investigation remains compulsory(Figs. 1.53b and 1.55b). Despite the fact thatuncontrolled use of the latter affects overallmedical costs in this condition, it is neverthelessconsidered essential, especially in surgical plan-ning (14).

We do not intend to prolong this discussionof aneurysms beyond its application in SAH,except to highlight the fact that in recent yearsa number of studies have been performed toanalyse the use of CT and especially MRI inscreening for potential occult, asymptomaticaneurysms, particularly when there is a familyhistory of aneurysms (5), and known, non-rup-tured aneurysms (33).

Aneurysm rupture usually presents in a dra-matic fashion and typically causes sudden, vio-lent headaches, cardio-circulatory collapse, rela-tive conservation of consciousness and a pauci-ty of lateralizing signs (34). The second most fre-quent cause of SAH after aneurysms (with theexception of traumatic forms, which will be

dealt with separately) is the rupture of arteri-ovenous malformations (AVM’s), of which some50% present with haemorrhage (both intra-parenchymal and subarachnoid); in a small per-centage of cases the patients have prodromicsigns such as epileptic disorders. They are mostfrequent during childhood and are often direct-


Fig. 1.53 - (a) large right frontal haematoma (*) and widespreadsubarachnoid bleeding mainly at the root of the Sylvian fissureare the most striking aspects of this small aneurysm which rup-tured in the stretch between A1 and A2 (b). This is accompa-nied by a small haematic layer in the fourth ventricle and theperimesencephalic cisterns.

a

b

*

ly documented by CT, although MRI and selec-tive angiography in particular are yet more sen-sitive. The latter documents AVM’s in accurateanatomical and haemodynamic detail.

Another condition that may be associatedwith SAH (approx. 12%) is non-specific spon-taneous intraparenchymal haemorrhages. Oth-er rarer causes of SAH are blood dyscrasias, in-traventricular neoplasia and metastases thatare cortically located (especially metastaticmelanoma) (8).

Interestingly, in a percentage of cases thatranges from 7 to 28% according to differentpublished studies, SAH’s occur without any de-finable cause. These cases have had completelynegative selective angiography, even when thestudy is repeated some time after the ictus.These cases are termed idiopathic or sine mate-ria, indicating the failure to identify the deter-mining cause rather than the actual absence ofa pathological cause. Such forms typically pres-ent with a specific haemorrhage distributionpattern within the perimesencephalic cisterns,and therefore they are often termed perimesen-cephalic SAH’s (11, 25). In fact, unlikeaneurysm ruptures, in which CT shows bloodin the basal subarachnoid cisterns that alsospreads to the Sylvian and interhemispheric cis-terns, these idiopathic cases (Fig. 1.52) general-ly show a focal blood deposit in the perimesen-cephalic cistern alone, without spreading tocontiguous subarachnoid spaces. These focalhaemorrhages are also clearly different fromthe blood of ruptured aneurysms in the poste-rior aspect of the circle of Willis, in which CTusually documents massive bleeding into thebasal subarachnoid cisterns, and occasionallyreveals retrograde haemorrhage into the fourthventricle. These forms are also sometimestermed “benign” because at onset their clinicalconditions are far less dramatic and their even-tual clinical outcome is more favourable, in partbecause these SAH’s are much less subject tocomplications. Although their blood distribu-tion is sufficiently typical, it is common practiceto follow CT with selective angiography tostudy all four vessels. In order to rule outaneurysm rupture altogether, selective angiog-raphy must be repeated some time later (9).

With the exception of these forms of SAH,selective angiography can be falsely negativedue to: 1) severe vascular spasm that preventsthe blood flow from reaching the aneurysm;and 2) the presence of thrombus within theaneurysm lumen that makes it angiographicallyinvisible (34).

Site

As we have already mentioned, CT does notreliably document the presence of aneurysms.Nevertheless, on the basis of the predominantlocalization of haemorrhagic hyperdensity inparticular cisternal areas, CT is often able todefine the probable origin of the bleed, and byinference the location of the aneurysm respon-sible for the haemorrhage. This is possible inup to 52% of cases; the highest accuracy rate isobtained for the rupture of aneurysms of theanterior cerebral and anterior communicatingarteries (sensitivity 79%, specificity 96%).

However, CT’s ability to accurately forecastthe localization of ruptured aneurysms of themiddle cerebral artery, the supraclinoid internalcarotid artery, and the posterior circulation ar-teries is far lower (29). Although the associationof an intraparenchymal haematoma contributesto determining the location of aneurysms, thisfactor does not account for more than one-quar-ter of all SAH’s.

Despite these limitations, we will attempt todefine the most common findings concerningthe various sites of aneurysm rupture.

1) In aneurysm ruptures of the anterior com-munication artery, hyperdensity prevails in thesuprasellar cisterns and the anterior aspect ofthe interhemispheric fissure, from where ittends to spread to the bifrontal regions. Thecallosal and cingulate gyri are often “outlined”by blood, which is also frequently present sur-rounding the brainstem and within the Sylvianfissures; in some cases this haemorrhage is in a somewhat asymmetrical distribution (Fig.1.54b). Unilateral dominance of the bloodtherefore does not exclude bleeding from theanterior communicating artery. In the largerhaemorrhages, these findings may be accompa-nied by satellite frontobasal or septal intracere-


bral haematomas. Haematomas localized in thecavum septi pellucidi are more or less diagnos-tic of such aneurysms; however, such findingsare not observed in more than 50% of cases (32).

Failure to demonstrate blood within the anteri-or interhemispheric fissure militates against therupture of an anterior communicating arteryaneurysm (34). It should also be pointed outthat it is important to pay attention to distin-guishing the normal falx cerebri from the ex-travasated blood. The posterior or retrocallosalfalx cerebri can in fact be visualised in 88% ofnormal patients, whereas the anterior extent ofthe falx is only visible in 38% of cases (35).Therefore, if interhemispheric hyperdensity(Figs. 1.50, 1.54, 1.56) does not spread laterallyto the paramedian sulci and does not show evo-lution in density, volume or extent on subse-quent CT examinations, it obviously representsa normal finding.

2) Aneurysms of the middle cerebral arterybifurcation/trifurcation (Fig. 1.55) invariablyproduce a unilateral bleed within the Sylvian fis-sure and often in the adjacent suprasellar cistern.Other possible findings in such cases includetemporal or insular lobe parasylvian intra-parenchymal haematomas and rupture into thetemporal horns of the lateral ventricles (usuallyonly present in cases of lobar haematoma).Whereas bleeding in the Sylvian cisterns is of-ten caused by an aneurysm of the middle cere-bral artery, temporal haematomas can also bedue to other causes, including bleeding fromAVM, neoplasm or more rarely hypertension(i.e., “spontaneous” form).

3) Aneurysms of the supraclinoid internalcarotid artery and the posterior cerebral arterymay present with a range of haemorrhagic lo-calizations including the suprasellar and in-terpeduncular cisterns, the medial temporallobe, the Sylvian fissure, the anterior interhemi-spheric fissure and the paranuclear area adja-cent to the head of the caudate nucleus.

4) Aneurysms at the tip of the basilar arterytend to bleed in the interpeduncular, perimes-encephalic and suprasellar cisterns, and spreadto the peripeduncular and prepontine cisernsand the parasylvian regions, with or withoutparenchymal brainstem haematoma formation.

5) Aneurysms of the intradural segment ofthe distal vertebral or posterior inferior cere-bellar artery present with bleeding that mainlyaffects the prepontine and pericerebellar cis-


Fig. 1.54 - Validity of CT in defining the site of the bleed.The presence of a haematoma of the septum pellucidum hollow(*) in its typical midline position between the frontal hornsconstitutes an accurate localizing element, as it is almost invari-ably associated with the rupture of an aneurysm of the anteriorcerebral artery. In (a) the following are present: widespreadbleed inside the Sylvian fissures, the cortical sulci and the ante-rior interhemisperic fissure and massive inundation of the ven-tricular chambers. In (b): a blood collection in the right Sylvianfissure, blocking of the 3rd ventricle and involvement of thesloping part of the lateral ventricles.

a

b

*

*

terns; in these cases, obstruction of the outletsof the 4th ventricle may occur.

6) Aneurysms arising from the pericallosalartery are somewhat rare, and when they

bleed tend to result in a pathognomonichaemorrhage within the anterior pericallosalcistern. They are also often associated withfrontal lobe and callosal intraparenchymalhaematomas.

7) In addition to the distribution of blood inthe subarachnoid spaces, a further importantand accurate topographic criterion is represent-ed by parenchymal haematomas adjacent to theSAH (24). We have already mentioned exam-ples of haematomas of the cavum septi pelluci-di (e.g., in anterior communicating arteryaneurysms), and temporal lobe and paranuclearbleeds (e.g., in middle and posterior cerebralartery aneurysms). So-called “comma-shaped”haematomas of the Sylvian fissure (Fig. 1.55a)are characteristic of middle cerebral arteryaneuryms and can usually be easily differentiat-ed from those of the external capsule in hyper-tensive patients presenting with spontaneousforms.

8) Finally, it has been observed that in thepresence of parenchymal haematomas, the per-centage of aneurysms directly visualized on CTafter bolus IV contrast administration is esti-mated to be between 30% and 76% (32).

Size of haemorrhage vs. prognosis

CT enables an overall assessment of thequantity of blood that has extravasated duringa SAH. This means that it is possible to utiliseCT to estimate patient prognosis at the onsetof the ictus (10). The general rule in such cas-es is: “the more blood, the worse prognosis”;scoring systems have been proposed for SAHevaluation using CT aimed at linking thesescores to the patient’s clinical evolution, in-cluding the occurrence of subsequent sequelaesuch as rebleeding, vasospasm and cerebral in-farction (13). Consideration is given to eitherthe widespread (Figs. 1.50, 1.54a) or focal (Fig.1.56a) appearance of the bleeding and the sizeof clots in the cisterns and fissures. These clotscan be divided into “thin” and “thick” cate-gories based on their greatest dimension (Fig.1.56). Generally speaking, a “thin”, focalhaemorrhage indicates a limited SAH, and is


Fig. 1.55 - (a) the irregular haemorrhagic collection inside theSylvian fissure (*) and above all, the presence of an adjacentcomma-shaped haematoma suggest the rupture of an aneurysmof the middle cerebral artery. The angiograph (b) confirmed thepresence of a «giant» aneurysm in this position.

a

b

typically accompanied by a milder onset ofsymptomatology, a more favourable outcomeand a reduced probability of complications.The widespread or locally “thick” forms of

haemorrhage are commonly seen in patients inmore grave clinical condition and with worseprognoses, in whom serious sequelae are likelyto occur. Despite the obvious inaccuracy ofthis approach, it does tend to be relativelyvalid in forecasting survival and the probabili-ty of the development of subsequent neurolog-ical symptoms (2).

Contrast agent use

In acute SAH, CT is usually performedwithout the IV administration of contrastagents, as this does not typically affect pa-tient management. In fact, within the first 72hours of the ictus it may mask the presenceof SAH due to the enhancement of the ves-sels and even the leptomeninges surround-ing the basal subarachmnoid cisterns, a re-sult of the ongoing chemical meningitis re-lated to the SAH. Gross extravasation of con-trast material into the subarachnoid spacethrough a ruptured aneurysm during a CTexamination is rare, but when observed is as-sociated with an extremely unfavourableprognosis (16). IV contrast agent use in CTsometimes makes it possible to visualize thelumens of smaller aneurysms, although is iteasy to confuse the findings with loops with-in native arteries.

Later, within one to two weeks of the ictus,it is possible to see a subtle widespread or focalenhancement of the basal cisterns and the re-gional surfaces of the cortical sulci (50-60% ofcases). As noted above, this is linked to a chem-ical meningitis in response to the SAH. This isassociated with increased vascularization and achange in vessel permeability of the lep-tomeninges, which favours the accumulation ofcontrast material in these regions (20). This isfurther associated with an increased incidenceof delayed hydrocephalus, which may be sec-ondary to the chemical arachnoiditis (27). Fi-nally, contrast agents can be helpful in a limitednumber of cases in the subacute stage in whichthe presence of enhancement of the lep-tomeninges and basal arachnoid cisterns re-veals a prior noxious event (i.e., SAH).


Fig. 1.56 - CT’s role in the prognostic definition of SAH. CTscans concerning two cases of aneurysm ruptures of the anteri-or communicating artery. In both the haematoma of the septumpellucidum hollow is typical. The different entity of the bleedis clearly shown by the thickness of hyperdensity in the anteri-or interhemispheric fissure and in the adjacent cortical sulci(very in a thin and thick in b), by the diffusion of the bleed(widespread in b), by the type of ventricular involvement (in arestricted to a clot in the frontal horn, massive in b). The pa-tient in case (a) was in discreet neurological conditions and wassubjected to surgery without subsequent complications. Patientb was in a coma when the examination was carried out and dieda few hours later.

a

b

COMPLICATIONS

Vasospasm, ischaemia, infarction

Cerebral ischaemia during the acute phaserepresents the most frequent cause of deathand disability in SAH’s (6, 12). The incidenceof vasospasm as determined from angiographystatistics and transcranial echo-Doppler exami-nations varies from 20 to 75%. In general, va-sospasm usually occurs approximately 3-6 daysafter the ictus and reaches a peak of severityaround day ten.

The pathogenesis of vasospasm and its se-quelae is not completely clear and a number ofcontributing factors have been considered.These factors are primarily attributed to thetoxic or irritational actions of substances with-in the clots or the subsequent blood break-down products.

Vasospasm is usually diagnosed using tran-scranial Doppler techniques to measure bloodflow velocity (2). There is usually a prognosticcorrelation between the SAH characteristics onthe CT study with the subsequent developmentof a significant vasospasm. If, for example, theamount of SAH blood is minimal as determinedby CT, vasospasm only occurs in 8-10% of cas-es. This correlation is more valid in younger pa-tients; it is well known that vasospasm is some-what age-dependent and occurs more frequent-ly and to a greater degree in the elderly.

The relationship of vasospasm to rebleedingis important (34). In fact, in the case of a singlehaemorrhage, cerebral infarction occurs in 22%of cases, while infarction occurs in 41% of casesof rebleeding (12). Vasospasm can be either fo-cal and in proximity to an aneurysm, or diffuse.

Clinically, significant vasospasm always causesa neurological deterioration due to the underly-ing cerebral ischaemia caused by the vascular nar-rowing, which tends to be progressive althoughgradual (a rapid worsening usually indicates re-bleeding) (17). CT is obviously not able to showvasospasm, but it does reveal the ischaemic con-sequences upon the cerebral parenchyma, themost serious of which is infarction.

Even though vasospasm is the most commoncause of infarcts following SAH, ischaemic al-

teration can also be secondary to compressionof vessels resulting from the mass effect of a re-gional intraparenchymal haematoma, or lessfrequently thrombic emboli originating fromvascular flow reduction (20).

In agreement with angiographic findings,delayed ischaemic lesions occur in 22-60% ofcases of aneurysms (12). The resolution of thevasospasm is usually accompanied by an im-provement in the clinical condition (15).

Hydrocephalus

Hydrocephalus may occur either in the im-mediate period following the SAH or alterna-tively from two weeks to six months later. Hy-drocephalus results from alterations in normalCSF reabsorption or from mechanical obstruc-tion, both of which are caused by subarachnoidspace and intraventricular blood. Many SAHpatients develop acute hydrocephalus withinthe first 48 hours of the initial bleed (one to twocases out of three).

There is a certain correlation between thequantity of blood in the ventricles and the sub-sequent development of hydrocephalus. Theinitial CT examination is therefore important inestablishing the extent of haemorrhage and thebaseline ventricular size for the purpose ofmonitoring the patient in whom clinical condi-tions are not critical and do not therefore re-quire immediate shunt placement.

Acute hydrocephalus can be transient, if nor-mal CSF dynamics are restored after reabsorp-tion of the SAH. However, so long as there isblood in the subarachnoid pathways, the forma-tion of adhesions is a risk (i.e., basal arachnoidi-tis) with the potential of resulting in permanenthydrocephalus of the communicating type (8).In many such patients a shunt may therefore berequired. Hydrocephalus and the associatedneurological deterioration can benefit by pro-longed treatment with tranexamic acid (31).

Rebleeding

The incidence of this complication reaches apeak 7 to 12 days after the initial SAH and oc-


curs in 20 - 25% of cases (34); rebleeding carrieswith it a mortality rate of approximately 50%. Itis accompanied by a worsening in neurologicalstatus. Rebleeding remains the most importantcause of a seriously worsening prognosis, even incases that have undergone early surgery (23).

The most important diagnostic criterion ofrebleeding is an obvious sequential increase indensity of the subarachnoid spaces on CT thatfollows an initial gradual reduction in the initialhaemorrhagic hyperdensity during the first fewdays after the ictus. It is also important to con-sider persistent hyperdensity apparent on a CTexamination performed more than seven daysafter the ictus as a probable expression of re-bleeding.

Intraparenchymal haematoma (IPH)

IPH occurring adjacent to a rupturedaneurysm is identified on CT in 15% (29) to27% (8) of cases of SAH. These figures areprobably slightly overestimated as they only in-clude the most seriously ill patients, in whomcomplications are most frequently encoun-tered. IPH’s are almost always accompanied bya rapidly progressive deterioration in clinicalstatus (34). The appearance of IPH in thesecases is much the same as with other forms ofclinical stroke, irrespective of the SAH.

Intraventricular haemorrhage (IVH)

IVH can be observed in association with anyruptured aneurysm, although the distributionof intraventricular blood seldom indicates theorigin of the haemorrhage. However, rupturedaneurysms of the AICA (anterior communicat-ing artery) can rupture into the 3rd ventricle andthe area of the intraventricular foramen ofMonro; and aneurysms of the PICA (posteriorinferior cerebellar artery), vertebral artery andbasilar trunk often cause reflux of blood intothe 3rd and the 4th ventricles, without reachingthe lateral ventricles.

Blood in the cerebral ventricles is almostalways accompanied by dilation, accounting

for the most frequent cause of hydrocephalusin patients with SAH. It has been observedthat the dimensions of the ventricular cham-bers correlate with clinical outcome more ac-curately than the dimensions of the bloodclots they contain. Generally speaking, themore dilated are the ventricles, the worse isthe clinical status and the greater is the needfor a ventricular shunt (some experts holdthat this can cause greater risk of aneurysmrebleeding) (34).

Subdural haematoma (SDH)

SDH’s in association with SAH are mostcommonly caused by ruptures of circle of Willisand middle cerebral artery bifurcation/trifurca-tion aneurysms. The CT characteristics of theseSDH’s are not dissimilar to traumatic forms.They are always accompanied by progressiveneurological deterioration and usually requiresurgical drainage.

A progressive worsening of neurologicalconditions in patients with SAH can be causedby a number of extracerebral causes, such as in-fections, pulmonary embolism, gastric haemor-rhage and myocardial infarcts. In such cases,CT is obviously negative with regard to SDH.

POSTSURGICAL FOLLOW-UP

After surgical aneurysm clipping, the CT ac-curacy for focal SAH or aneurysm recurrencediminishes due to the imaging artefacts createdby the metal clips (Fig. 1.57). Nevertheless, CTremains the imaging technique of choice in cas-es of worsening of post-surgical condition orwhen there is a delay in the normally expectedtimeframe of recovery. CT is particularly suit-able for the demonstration or sequential fol-low-up of infarcted areas caused by post-surgi-cal vasospasm. Vasospasm can also be indirect-ly presumed from CT in emergent forms wherefrank cerebral infarction is not evident, espe-cially if the other more frequent postsurgicalcomplications such as hydrocephalus and re-bleeding are excluded (34).


CONCLUSIONS

CT has had dramatic effects upon the pri-mary diagnosis and management of SAH pa-tients. The rapidity with which it is performedand its overall accuracy make it the imagingtechnique of choice in all patients with suspect-ed SAH. It is preferable that the CT examina-tion be performed at an early stage as it hasbeen shown that those having CT studies per-formed later ultimately have the more severeprognoses (7).

Immediately after the stroke, CT providesinformation on the extent and distribution of bleeding, as well as signs of possible earlycomplications such as hydrocephalus, intra-parenchymal haemorrhage, and presence of de-veloping ischaemic areas. The appearance ofsome of these complications, in particular in-tracerebral haematomas with mass effect andacute hydrocephalus, is of practical importanceas they usually require immediate neurosurgicaltreatment.

CT findings correlate well with patient sta-tus as the imaging observations are usually

more striking in those patients with disordersof consciousness or other severe neurologicalalterations. The role of CT in long-term recov-ery prognosis is not yet clear (3). However, itsability of early diagnosis undeniably improvesoverall clinical outcomes.

CT can also demonstrate SAH in patients inwhom SAH is not clinically suspected, and pos-itive findings can also exclude the need to per-form diagnostic lumbar punctures; the latterare usually only performed in patients whosesymptoms suggest SAH but in whom CT isnegative (24, 26). With regard to other medicalimaging techniques, we have already men-tioned that MRI has a limited role to play in theacute and hyperacute phases of SAH; MRI ismore suitable than CT in subacute phases, in-dicating that the two imaging techniques play acomplementary roles from a temporal point ofview. MRI also plays a role in aneurysm, andparticularly AVM, evaluation when combinedwith MR angiography.

CT has had a considerable effect on the useof selective cerebral angiography in the diagno-sis and follow-up of patients with SAH.Surgery can be postponed after the emergentphase, especially in gravely ill patients, untilclinical conditions have stabilized. In turn, CTcan direct both angiography and surgery to-wards the more likely area of aneurysm rupture(28). All of these reasons make CT not only themost suitable, but also the most rapidly accessi-ble imaging examination to be performed inpatients with acute clinical stroke.

REFERENCES

1. Andrioli G, Cavazzani P: Differential diagnosis of sub-arachnoid hemorrhage. Minerva Anestesiol 64:141-144,1998.

2. Boecher-Schwartz HG, Fries G, Mueller-Forell W et al:Cerebral blood flow velocities after subarachnoid haemor-rhage in relation to the amount of blood clots in the initialcomputed tomography. Acta Neurochir 140:573-578,1998.

3. Botia E, Vivancos J, Leon T et al: Predictive mortality fac-tors and the development of major complications in non-traumatic subarachnoid hemorrhage. Rev Neurol 24:193-198, 1996.

4. Brouwers PJ, Dippel DW, Vermeulen M et al: Amount ofblood on computed tomography as an independent pre-dictor after aneurysm rupture. Stroke 24:809-814, 1993.


Fig. 1.57 - Postsurgical CT may not always prove accurate dueto the overlapping of artefacts produced by the metal clips. Itis usually required to distinguish between the main surgicalcomplications (hydrocephalus, vasospasm, rebleeding). Inthis case there is widespread hypodensity adjacent to the cran-iotomy, presumably exclusively due to subsequent malacic se-quelae.

5. Brown BM, Soldevilla F: MR angiography and surgery forunruptured familiar intracranial aneurysms in personswith a family history of cerebral aneurysms. AJR 173:133-138, 1999.

6. Cesarini KG, Hardemark HG, Persson L: Improved sur-vival after aneurysmal subarachnoid hemorrhage: reviewof case management during a 12-year period. J Neurosurg90:664-672, 1999.

7. Chan BS, Dorsch NW: Delayed diagnosis in subarachnoidhaemorrhage. Med J Aust 154:509-511, 1991.

8. Cirillo S, Simonetti L, Sirabella G et al: Patologia vascolare.In: Dal Pozzo G: Compendio di Tomografia Computerizza-ta (pp. 127-147) USES Edizioni Scientifiche Florence, 1991.

9. Duong H, Melancon D, Tampieri D et al: The negative an-giogram in subarachnoid haemorrhage. Neuroradiology38:15-19, 1996.

10. Germanson TP, Lanzino G, Kongable GL et al.: Risk clas-sification after aneurysmal subarachnoid hemorrhage.Surg Neurol 49:155-163, 1998.

11. Gilbert JW, Lee C, Young B: Repeat cerebral panangiog-raphy in subarachnoid hemorrage of unknown etiology.Surg Neurol 33:19-21, 1990.

12. Gruber A, Dietrich W, Richling B: Recurrent aneurysmalsubarachnoid haemorrhage: bleeding pattern and inci-dence of posthaemorrhagic ischaemic infarction. Br J Neu-rosurg 11:121-126, 1997.

13. Hijdra A, van Gijn J, Nagelkerke NJ et al: Prediction ofdelayed cerebral ischaemia, rebleeding, and outcome afteraneurysmal subarachnoid haemorrage. Stroke 19:1250-1256, 1988.

14. Kallmes DF, Kallmes MH: Cost-effectiveness of angiogra-phy performed during surgery for ruptured intracranialaneurysms. AJNR 18:1453-1462, 1997.

15. Kassel NF, Sasaki T, Colohan AR et al: Cerebral vasospasmfollowing aneurysmal SAH. Stroke 15:562, 1985.

16. Kingsley DP: Extravasation of contrast-enhanced bloodinto the subarachnoid space during computed tomogra-phy. Neuroradiology 18:259-262, 1979.

17. Kistler JP, Crowell RM, Davis KR: The relation of cerebralvasospasm to the extent and location of subarachnoidblood visualized by CT scan: a prospective study. Neurol-ogy 33:424, 1983.

18. Lenhart M, Bretschneider T, Gmeinwieser J et al: CerebralCT angiography in the diagnosis of acute subarachnoidhemorrhage. Acta Radiol 38:791-796, 1997.

19. Leonardi M: Diagnosis and general assessment of acutesubarachnoid hemorrhage. Minerva Anestesiol 64:145-147, 1998.

20. Modic MT, Weinstein MA: Cerebrovascular disease of thebrain. In: Haaga JR, Alfidi RJ (eds): Computed tomogra-

phy of the brain, head and neck (pp. 136-169) The CVMosby Company St. Louis 1985.

21. Noguchi K, Ogawa T, Seto H et al: Subacute and chronic sub-arachnoid hemorrhage: diagnosis with fluid attenuated inver-sion recovery MR imaging. Radiology 203:257-262, 1997.

22. Ohkawa M, Tanabe M, Toyama Y et al: CT angiographywith helical CT in the assessment of acute stage of sub-arachnoid hemorrhage. Radiat Med 16:91-97, 1998.

23. Roos YB, Beenen LF, Goen RJ et al: Timing of surgery inpatients with aneurysmal subarachnoid haemorrhage: re-bleeding is still the major cause of poor outcome in neuro-surgical units that aim at early surgery. J Neurol NeurosurgPsychiatry 63:490-493, 1997.

24. Sames TA, Storrow AB, Finkelstein JA et al: Sensitivity ofnew-generation computed tomography in subarachnoidhemorrhage. Acad Emerg Med 3:16-20, 1996.

25. Schwartz TH, Solomon RA: Perimesencephalic nona-neurysmal subarachnoid hemorrhage: review of the litera-ture. Neurosurgery 39:433-440, 1996.

26. Sidman R, Connolly E, Lemke T: Subarachnoid hemor-rhage diagnosis: lumbar puncture is still needed when thecomputed tomography scan is normal. Acad Emerg Med3:827-831, 1996.

27. Sobal D: Cisternal enhancement after subarachnoid he-morrage. AJNR 2:549-552, 1981.

28. Terbrugge KG, Rao KC, Lee SH: Cerebral vascular anom-alies. In: Lee SH, Rao KC (eds): Cranial Computed To-mography and MRI (pp. 607-641) Mc Graw- Hill BookCompany New York, 1987.

29. van der Jagt M, Hasan D, Bijvoet HW et al: Validity of pre-diction of the site of ruptured intracranial aneurysms withCT. Neurology 52:34-39, 1999.

30. Vale FL, Bradley EL, Fisher WS: The relationship of sub-arachnoid hemorrhage and the need for postoperativeshunting. J Neurosurgery 86:462-466, 1997.

31. Vermeij FH, Hasan D, Vermeulen M et al: Predictive fac-tors for deterioration from hydrocephalus after subarach-noid hemorrhage. Neurology 44:1851-1855, 1994.

32. Yock DH, Larson DA: Computed Tomography of he-morrage from anterior communicating artery aneurysmswith angiographic correlation. Radiology 134:399-407,1980.

33. Yoshimoto Y, Wakai S: Cost-effectiveness analysis of screen-ing for asymptomatic, unrupted intracranial aneurysms. Amathematical model. Stroke 30:1621-1627, 1999.

34. Weisberg LA, Nice C: Cerebral Computed Tomography: Atext atlas (pp. 163-179). WB Saunders Philadelphia, 1989.

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INTRODUCTION

Magnetic Resonance Imaging (MRI) hasbrought about substantial changes in the diag-nostic algorithms formulated in almost all as-pects of Central Nervous System (CNS) pathol-ogy. This has occurred in part secondary toMRI’s greater sensitivity to changes in the watercontent of the tissue examined, and therefore, indemonstrating all categories of CNS pathology.

However, in the particular case of ischaemiccerebral vascular disease, MRI initially had amore limited impact, due mainly to the largepreceding experience gained in the treatmentof this type of pathology using CT, and there-fore the resulting clinical reliance on the CTsemeiology (3, 4). This situation has recentlyundergone profound changes, both with re-gard to the technical progress made in MRI aswell as to the newer treatments that are beingintroduced, in particular thrombolysis (2, 5, 7,12-15).

The diagnostic questions a clinician poseswith regard to the patient with ischaemic cere-brovascular disease are mainly concerned withthe site, extent and time of the ictus, the clini-cal severity of the ischaemic lesion, the poten-tial reversibility of the damage and the presenceor absence of reperfusion. Because it is now

universally recognized that early surgery canpotentially improve or even reverse otherwiseserious events such as cerebral ischemia, the ne-cessity to respond in the very first minutes andhours following the onset of the neurologicaldeficit has become all the more pressing (1, 6,8-11, 16).

The responses to such important considera-tions often surpass the capabilities of tradition-al neuroradiological imaging techniques to aidin this emergent situation; in the past, CT andMRI only very rarely provided direct diagnosticinformation during the first six hours from anischaemic cerebral event. This is predictablegiven that even from a pathoanatomical pointof view “… identification of an ischaemic lesionon human or animal brains cannot be detectedby macroscopic examinations less than 24-72hours from the event” (Davis, 1997).

It therefore follows that, in order to obtainuseful diagnostic neuroimaging information inthe hyperacute phase, other aspects of ischaemicdisease including morphological, macroscopic,submacroscopic, and pathophysiological param-eters must be explored.

The rational use of MRI in a way that en-hances its intrinsic potential, as well as takingadvantages of recent progress in acquisitiontechniques (e.g., perfusion, diffusion and spec-

1.5

MRI IN ISCHAEMIAL. Simonetti, S. Cirillo, R. Agati

63

troscopy) have begun to provide answers to theclinical questions posed during the hyperacutephase of cerebral ischaemia. The goal of thischapter is to explore the chronology of thepathophysiological events of acute/hyperacutecerebral ischaemia and consider how these al-terations can be investigated using the neweradvancements of MRI.

SEMEIOTICS

Arterial occlusion

Generally speaking, the principal cause ofcerebral ischaemia is vessel occlusion, in theform of an embolus or a thrombus. It there-fore follows that the simplest manner ofdemonstrating the cause of hyperacute cere-bral ischaemia non-invasively is MR angiogra-phy to examine the cerebral blood vessels insearch of the partially or completely occludedvessel. However, in practice this theoreticalobservation can be limited by a number of fac-tors:– the acquisition time required to perform an

MR angiographic examination is not com-patible with the clinical condition of manypatients in the hyperacute phase of cere-brovascular ischaemia, who are often agitat-ed or otherwise uncooperative;

– the poor anatomical definition of the 2nd and3rd order vascular branches of the cerebralarteries, especially in cases of complete ornear complete occlusion;

– the age-related alterations in vascular arbo-ration of the cerebral vasculature in elderlypatients results in generalized flow reduc-tion, which can erroneously point to pathol-ogy, especially in the presence of flow asym-metries between one hemisphere and theopposite side;

– the presence of clinically silent past vesselstenoses/occlusions.In short, MR angiography in the hyperacute

phase of cerebral ischaemia is a reliable diagnos-tic technique in young, cooperative patients, aconclusion that is somewhat out of line with thetypical profile of the patient presenting with

cerebral ischaemia. Although rare in youngerage groups, the advantage of MR angiography inthe young lies in the fact that it is this category ofpatient that potentially has the most to gain fromprompt, correct diagnosis of vascular events.

Reduction of cerebral perfusion

If prolonged beyond a somewhat unpre-dictable time period, the reduction in regionalcerebral perfusion secondary to arterial steno-sis/occlusion leads to the establishment of anischaemic or frankly infarcted area. This reduc-tion in flow can be studied using MR perfusion.

Generally speaking, there are two mainstrategies for studying cerebral blood flow: theuse of diffusible tracers and the use of strictlyintravascular tracers. The use of diffusible trac-ers represents the traditional strategy for study-ing cerebral perfusion, beginning with Kety’snitrous oxide method, through CT with xenon-133 inhalation, and to PET (positron emissiontomography) with H2

15O. Although deuterium,fluorine-19 and H2

17O can be used as diffusibletracers in studying brain flow and oxygen con-sumption with MRI, at present these isotopesare still confined to animal experimentation. Inparticular, although H2

17O would appear to bevery promising, these latter techniques are un-likely to be clinically feasible due to their highcost and to the limited availability of the vari-ous isotopes.

Perhaps the most clinically feasible possibil-ities might include the use of endogenous dif-fusible tracers such as “arterial” water, whosespins could be marked by the inversion of theMR radiofrequency pulses; if perfected, thistechnique would have the advantages of beinginexpensive, physiological and non-invasive.

The use of endogenous or exogenous vascu-lar tracers is currently the most widely em-ployed human brain perfusion study technique.In commonly used experimental models em-ploying this kind of tracer, blood flow is a func-tion of the volume of blood in a tissue and themean transit time of an ideal instantaneous bo-lus of the tracer substance passing through thetissue.


MR perfusion images can be obtained eitherusing a bolus of exogenous contrast agent orusing methods dependent on the phase con-trast of blood flow.

Currently the most common method usedemploys paramagnetic exogenous contrastagents, in particular gadolinium, which exploitstheir effects on relaxation times and magneticsusceptibility.

The reduction in T1 relaxation times gainedby the IV injection of a gadolinium agent overtime is obviously proportionate to the concen-tration of the contrast agent used, and thereforeprovides information on tissue perfusion. Forexample, MR sequences that use inversion pre-pulses (e.g., FLASH, TURBOFLASH) thatpermit the acquisition of T1-weighted imagesin less than one second, make it possible toshow the hyperaemic areas to be relatively hy-perintense as compared to normal brain, whileischaemic areas appear relatively hypointense.

With regard to techniques that exploit themagnetic susceptibility of gadolinium, it shouldbe remembered that magnetic susceptibility re-sults in part in the distortion of the appliedmagnetic field by the presence of a paramag-netic substance (e.g., gadolinium); this causesartefacts in the MR image, especially if acquiredusing the pulse sequences referred to above.Such techniques are therefore based on the ex-ploitation of this artefact obtained using longTE sequences, thus obtaining T2*-weightedimages. If a series of these pictures are acquiredduring the injection of a bolus of a paramag-netic contrast agent, it will be possible to eval-uate variations in the local blood volume overtime. The intravascular passage of a high con-centration of the contrast agent through thebrain distorts the local magnetic field, thuscausing a dephasing of spins in the brain tissueadjacent to the blood vessels and consequen-tially the artefactual loss of signal due to the ef-fects of magnetic susceptibility and a reductionin T2* relaxation time. This reduction can bemeasured, and using a complex formula, T2*variation can be correlated to blood volume.Having acquired a series of images that give themean transit time, we can also obtain a bloodvolume transit time ratio that corresponds to

the cerebral blood flow in traditional vasculartracer models.

The study of animal models and human pa-tients with hyperacute cerebral ischaemia usingthis technique has demonstrated its validity inillustrating regional hypoperfusion distal to aproximal cerebrovascular occlusion within afew minutes after the vascular blockage. Thistechnique also has the advantage that it can beperformed using clinical MRI units fitted to en-able the acquisition of serial T2*-weighted im-ages in the brief timeframes referred to above.From this point of view, it is most useful to haveaccess to an MR unit having the capability ofultra-fast echo planar imaging (EPI) acquisi-tions, which has the advantage of greater tem-poral definition (i.e., capability of a greaternumber of images acquired per unit of time)and therefore allows a more accurate discrimi-nation of the relative delay in passage of thecontrast media through the ischemic tissue aswell as a greater relative degree of sensitivity tomagnetic susceptibility artefacts.

Alteration of the Na+-K+ ion pump

An alteration of the Na+-K+ ion pump oc-curs within 30 minutes of the cerebrovascularocclusion secondary to the consumption andconsequent reduction of ATP, which is nolonger produced due to the anoxia that blocksthe aerobic glycolysis chain. Approximatelythree minutes after the vascular occlusion, theNa+-K+ ion pump dysfunction and the resultingelectrolytic alteration it causes, there is an un-controlled entry of water into the cell, andtherefore the establishment of cytotoxic oede-ma. This intracellular oedema affects variouscompartments and components of brain tissue(e.g., astrocytes, dendrites, endothelial cells,pericytes, oligodendrocytes); these alterationscan be studied using the MR diffusion tech-nique, that demonstrates the “macroscopic”molecular movement of the water. The under-lying principle of diffusion-sensitive MR pulsesequences is the addition of a pair of diffusionsensitising pulses to a sequence of otherwisestandard imaging pulses that dephases the

1.5 MR IN ISCHAEMIA 65

spins proceeding along the applied diffusiongradient. Due to the signal attenuation causedby the resulting loss of phase coherence, nor-mal diffusion causes a tissue signal loss on im-ages dependent on this parameter. Conversely,tissue areas in which diffusion is reduced (e.g.,ischaemia, cytotoxic oedema) appear relativelyhyperintense. In vivo diffusion can be quanti-fied using the apparent diffusion coefficient(ADC), which is a function of two parameters:the difference in signal between two differentlycalibrated diffusion images and a constantknown as the “diffusion weighted factor”; inthis manner, diffusion weighted images meas-ure variations in the ADC.

Hyperacute ischaemic lesions can appear asareas of reduced diffusion as early as three min-utes after occurrence of the embolus/throm-bus. It is assumed that the reduction of diffu-sion in the ischaemic area is connected to thecytotoxic oedema, resulting in part from the al-teration of the ion pump, as there is a move-ment of water from the vast extracellular com-partment to the more restricted intracellularcompartment. The extent of the area detectedat an early stage using diffusion weighted im-ages generally has an excellent correspondencewith the actual ischaemic lesion.

Clinically speaking, the largest drawback ofMR diffusion imaging techniques is that imagequality and sensitivity to variations in the ADCare considerably affected by even the slightestpatient movement during the examination,thus restricting its use in acute phase patientswho are unable to cooperate fully. ThereforeEPI and the possibility it offers of ultrafast ac-quisitions, is expected to improve the clinicalapplicability of diffusion weighted imaging.

Lactic acid accumulation

Within ten minutes of cerebrovascular oc-clusion, intracellular pH drops from approxi-matey 7.1 to 6.64 due to an increase in lac-tates secondary to the metabolic shift duringhypoxia towards anaerobic glycolysis. Thislactic acid increase can multiply fivefold with-in a very few minutes and contributes to tis-

sue necrosis due to the resulting increase incellular swelling and the alteration to theblood-brain barrier that it causes; therefore,in cases of ischaemia, hyperglycaemia must beavoided at all costs, as it will only cause an in-crease in the lactic acid concentration. Thismetabolic factor can be evaluated using MRspectroscopy; this MRI technique studies thebiochemical aspects of brain tissue, not as ab-solute concentrations of metabolites, butrather as relative concentrations given by thesize of the spectroscopic peak correspondingto various molecular species. Proton MRspectroscopy is currently the most widelyused technique; this method enables thestudy of relative concentrations of N-acetyl-aspartate, choline, creatinine and lactate (thelactate peak is almost absent in the normalspectrum). In hyperacute infarcts it is there-fore theoretically possible to identify the is-chaemic area by the appearance of a notice-able lactate peak in the MR spectrum, whichprecedes the subsequent drop in N-acetyl-as-partate, a neuron population reduction mark-er. The main limits to the clinical applicationof MR spectroscopy are the lengthy acquisi-tion times and the fact that in the area of in-terest selected the technique requires a voxelsize that is generally too large to avoid partialvolume effects (i.e., contamination of thesample by relatively normal tissue surround-ing the tissue of interest).

Cerebral microcirculation damage

Experiments have shown that within a fewminutes after occlusion of the middle cere-bral artery, a reduction in flow occurs withthe stacking up or stasis of red blood cells inthe cerebral microvessels (arterioles, capillar-ies, venules) and the microcirculation of thenucleus of the ischaemic lesion. This causes aswelling of endothelial cells and perivascularastrocytes and an adhesion between the sur-face receptors of PMN leucocytes and thecorresponding ligands of endothelial cellswhich brings about a further deterioration of themicrocirculation. The mechanical stenosis is



Fig. 1.58 - Acute phase ischaemia (30 hours) in the territory of the left middle cerebral artery in a 20 year-old patient without appar-ent risk factors. Axial T1- (a) a,d PD- (b) dependent scans. AP (c) and axial (d) projections TOF MRA reconstructions. In T1, signalhypointensity in the grey matter of the caudate and left lenticular nuclei, with mass effect on the frontal horn of the homolateral ven-tricle; signal alteration, as hyperintensity, is clearer in the PD-dependent images. The MRA examination shows a clear reduction incalibre of the left internal carotid artery, from the origin to the siphon, with visualization of the sole M1 tract of the middle cerebralartery, which appears filiform.

a

c

db

accompanied by a necrotizing effect upon theendothelial cells and the neurons due to theliberation of free radicals. The importance of

leukocyte adhesion is shown by the fact that,by administering monoclonal antibodies thatprevent leukocyte adhesion, a reduction inthe stenosis of the microcircle is obtained,while with administration of interleukin 2 (aleukocyte activator), the clinical status wors-ens due to an increase in nerve cell damage.

Microcirculation alteration and the conse-quent congestion and stasis of the local circula-tion and the pial vessels in hyperacute is-chaemia can be studied with MR by the acqui-sition of T1-dependent images after injection ofgadolinium contrast medium. Pathological en-hancement of small and medium sized vesselsthat “mark” the affected area, accompanied byadjacent pial congestion, have been observedwithin six hours of onset of the ischaemicevent. This enhancement is not in any way con-nected to the extravascular tissue enhancementlater observed secondary to blood-brain barrierinjury, and is exclusively confined to the vascu-lar compartment.

Oedema

Based on pathoanatomical findings and onmicro- and macroscopic clinical, rather than


Fig. 1.60 - Acute phase ischaemia (20 hours) in the anterior superficial territory of the left middle cerebral artery. Axial PD-depend-ent scans: increase in signal of the cortex with increase in volume of the gyri. The white matter is spared.

Fig. 1.59 - Acute phase ischaemia in the territory of the perforat-ing arteries. Axial PD-dependent scan. Note the loss of the bound-aries of the anatomical structures affected (lenticular nucleus, cau-date nucleus, claustrum, internal, external and extreme capsule.

experimental, features, the development of antypes of oedema over time can be broken downas follows:– 2 hours from vascular occlusion it is possible

to observe cytotoxic oedema that com-mences within a few minutes of the vascularocclusive event;

– 12 hours after the event, cytotoxic oedemacan be identified histologically on stainedmacrosections as a paleness of the affectedarea; it appears earlier and more obviously inthe caudate-putaminal complex than in thecortex;

– after 72-96 hours, the vasogenic oedema re-sults in mass effect;

– in the absence of complications, there is pro-gressive resolution of oedema and mass ef-fect from the 4th day.It is therefore the cytotoxic oedema that,

within 12 hours and occasionally as early as6 hours from the event, causes the appear-ance of altered signal areas due to T1- andT2-lengthening (i.e., hypointensity on T1-weighted images, hyperintensity on PD- andT2-weighted images), localized in the cau-

date-putamen complex (Figs. 1.58, 1.59) inischaemia affecting the perisylvian region. Inthe subsequent hours, it is still the cytotox-ic oedema that appears in much the samefashion in the overlying cortex (Figs. 1.60,1.61, 1.62).

If studied accurately, CT can also documentthis pathophysiological situation within the first12 hours of ictus, seen as disappearance of thenormal caudate and putamen hyperdensity astheir tissue margins blend into the surroundingwhite matter. This sign, which indicates vascu-lar occlusion in the territory, is somewhat diffi-cult to perceive (especially if it is not comparedwith the contralateral putamen), but it is im-portant and has a verified role in early diagno-sis as well as in predicting ad unfavourable out-come.

With these CT and MRI signs explained, wewill now move from theoretical and experi-mental neuroradiology to clinical neuroradiolo-gy, after concluding that the principal draw-back of medical imaging is the large individualvariability in appearance times of the findings(from 4 to 12 hours from onset of ictus), a fact


Fig. 1.61 - Acute phase (36 hours) left parietal ischaemia associated with contralateral ischaemia in stabilization phase. Coronal T1-(a) and T2-dependent (b) scans. The recent ischaemia appears as a hypodense cortical area in T1, with an increase in volume of thegyrus circumvolution. The finding is less clear in T2, where the difference in signal between acute focus and resolution phase is how-ever evident.

a b

that does not always make them suitable for thepractical diagnostic evaluation of the patientpresenting with clinical evidence of hyperacutecerebral ischaemia.

POSSIBLE USES OF CLINICAL MR IN THE DIAGNOSIS OF EMERGENCYISCHAEMIA AFTER THE HYPERACUTE PHASE

MRI’s greater sensitivity over that of otherimaging modalities is useful in identifyingparenchymal lesions caused by transient is-chaemic attacks (TIA’s), where MRI’s sensitivi-ty is greater than 70%, compared to approxi-mately 40% for CT.

The clinical course of cerebral infarctioncan include sudden alteration in the classicprogression. Clinical and pathological studiesshow that such shifts are principally due tothe haemorrhagic conversion of the primaryischaemic lesion in the time period betweenthe 2nd and 3rd week; this haemorrhagic inci-dence can be as high as 80% in infarctscaused by cerebrovascualr embolism. Formany years CT contradicted, at least with re-gard to frequency, the existence of this haem-orrhagic phenomenon. However, since the ad-vent of MRI, evidence of haemorrhagic con-version of cerebral infarction is more fre-quently observed (Fig. 1.63) in MR examina-tions performed between the 10th and 20th

days of the ischaemic ictus; this is especiallytrue in cases arising from embolism or thoseinfarcts located in the vascular territory of theposterior cerebral artery. Such areas were notpreviously visualized on CT images for a num-ber of reasons, including technical factors,such as partial volume averaging effects andlimitations concerning mean attenuation coef-ficients, and biological factors, such as the rel-atively rapid evolution of blood products inischaemic areas. Therefore, in cases of cere-bral ischaemia having sudden alterations ofclinical status that could be a result of haem-orrhagic conversion, the examination ofchoice is MR rather than CT.

REFERENCES

1. Adams RD, Victor M: Principles of Neurology. McGraw-Hill, Inc., New York: 1985, 508-572.

2. Awad L, Modic M et al: Focal parenchymal lesions in TIA:correlation of CT and MRI. Stroke 17:399-403, 1986.


Fig. 1.62 - Acute phase ischaemia in the left anterior cerebralartery territory. Axial PD-dependent scan: note the increase insignal with obliteration of the adjacent cortical sulci.

Fig. 1.63 - Hyperintense, haematic rim in T1, in an acute phaseischaemic lesion: note the spiral shape.

3. Bastianello S, Brughitta G, Pierallini A et al: Neuroradiolo-gical findings in acute cerebral ischemia. In: Ottorino Ros-si Award Conference. Zappoli F, Martelli A. (eds). Edizio-ni del Centauro, Udine, 131-140, 1992.

4. Bozzao L, Angeloni U et al: Early angiographic and CT fin-dings in patients with hemorragic infarction in the distribu-tion of the middle cerebral artery. AJNR, 12:1115-1121, 1991.

5. Brant-Zawadzki M, Pereira B et al: MRI of acute experi-mental ischemia in rats. AJNR 7:7-11, 1986.

6. Brierley JB: Cerebral hypoxia. In: Blackwood W, CorsellisJAN (eds). “Greenfield’s Neuropathology” Chicago: YearBook Medical Publishers 43-85, 1976.

7. Bryan RN, Whitlow WD, Levy LM: Cerebral infarctionand ischemic disease. In: Atlas SW (ed). “MRI of brain andspine”. New York: Raven Press 411-437, 1991.

8. Duchen LW: General pathology of neurons and neuroglia.In: “Greenfield’s neuropathology” Chicago: Year BookMedical Publishers 1-68, 1992.

9. Garcia JH, Anderson ML: Circulatory disorders and their ef-fects on the brain. In: Textbook of Neuropathology. Davis RL& Robertson DL. (eds). William&Wilkins, Baltimore, 1997.

10. Graham DI: Hypoxia and vascular disorders. In: “Green-field’s Neuropathology” Chicago:Year Book Medical Publi-shers 153-268, 1992.

11. Gullotta F: Vasculopatie cerebrali. In: Schiffer D ed. “Neu-ropatologia” Roma: Il pensiero scientifico, 1980:155-178.

12. Kendall B: Cerebral ischemia. Rivista di Neuroradiologia 3(suppl. 2):35-38, 1990.

13. Mathews WP, Witlow WD, Bryan RN: Cerebral Ischemiaand Infarction. In: MRI of brain and spine. (ed). Atlas SWLippincott-Raven, Philadelphia, 1997.

14. Savoiardo M, Sberna M, Grisoli M: RM e patologia vasco-lare del sistema nervoso centrale. Rivista di Neuroradiolo-gia 1 (suppl. 1):95-100, 1988.

15. Simonetti L, Cirillo S, Menditto M: Hemorrhagic infarcts ofarterial origin: physiopathological aspects and MR semeio-logy. In: Ottorino Rossi Award Conference. Zappoli F, Mar-telli A. (eds). Edizioni del Centauro, Udine 141-145, 1992.

16. Von Kummer R: Changing role of the neuroradiologist inthe investigation of acute ischemic stroke. In: Syllabus of 7th

Advanced Course of the ESNR. Byrne JW. (ed). Edizionidel Centauro, Udine 41-44, 1997.


73

INTRODUCTION

The performance and capabilities of magnet-ic resonance imaging (MRI) equipment have re-cently been greatly improved by innovations toboth the hardware (e.g., magnets, gradients andcoils) and software (e.g., image acquisition se-quences and data processing). These enhance-ments have made MRI more powerful and ver-satile than previously. This progress has trans-lated into beneficial reductions in the overall ex-amination times with regard to static imagingstudies that are essential for primary diagnosis,and also the practical implementation of func-tional imaging, offering the promise of an in-crease the diagnostic power of MRI in terms ofboth sensitivity and specificity. These functionalstudies are increasingly being used togetherwith conventional MR to obtain a more com-plete pathophysiological and prognostic pictureof the CNS pathology in question. In addition,these MR techniques provide information onthe movement of water molecules caused bythermal agitation (i.e., diffusion), microvascularhaemodynamics (i.e., perfusion) and cerebralmetabolism (i.e., spectroscopy).

In cases of cerebrovascular disease, thesetypes of examinations permit very early and ac-curate diagnosis, and are capble of indicating

the optimal treatment programme to be adopt-ed (9). In addition to detecting irreversiblydamaged tissue, they also point out areas at riskof infarction that could benefit from furthertreatment. In the particular case of hyperacutecerebral ischaemia, in which conventional T2-weighted MRI can be negative or ambiguous(1), diffusion weighted imaging is nearly alwayspositive, clearly revealing the areas of infarc-tion. Surrounding the ischaemic core, mostcerebral infarctions also include a peripheralzone that is ischaemic but uninfarcted, the so-called ischaemic penumbra, which could po-tentially progress to frank infarction; thispenumbra can be distinguished using perfusionMRI and/or spectroscopy.

The information obtained using such tech-niques can be expressed with qualitative data inthe form of variations in MR signal intensity, orwith quantitative data, thus making it possibleto interpret the results in a somewhat unbiasedmanner, irrespective of the reader.

DIFFUSION MRI

Diffusion MRI (DWI) examinations havefound a concrete application in clinical prac-tice. DWI studies the diffusion potential of

1.6

FUNCTIONAL MRI IN ISCHAEMIA

T. Scarabino, G.M. Giannatempo, T. Popolizio, M. Armillotta,

water, or rather the proclivity of water mole-cules to undergo random microscopic move-ment, driven in part by the thermal energygenerated by the body. According to the vari-ations in this physiological motion, the molec-ular motion of water in different tissues can becharacterized in just a few seconds by meansof DWI.

Technique

DWI uses spin echo sequences acquired ide-ally using the echoplanar technique, to whichdiffusion weighting is layered, thus making theresulting image sensitive to the movement ofwater. This characteristic is made possible bythe use of two powerful bipolar diffusion gra-dients applied symmetrically to the 180° ra-diofrequency pulse. The application of thesegradients causes the dephasing and subsequentrephasing of the protons in water, which variesaccording to the diffusion potential of the wa-ter molecules in different regions of the brain,which in turn translates into variations in MRIsignal intensity. The water molecules that dif-fuse freely during or after the application of the dephasing gradients are not completelybrought back into phase by the rephasing gra-dient, which does not happen for normal tis-sues. Following the 180° pulse, the protons thatdiffuse more slowly will be in a different phasethan those that diffuse more quickly and willtherefore have a different signal than the latter.Therefore, relatively high diffusion areas (suchas normal brain) will show comparably lowersignal than will slow diffusion areas (such as hy-peracute infarction), which are characterizedby a relatively higher signal. It is for this reasonthat DWI provides the key clinical informationrequired in stroke cases: what tissue is under-going hyperacute infarction.

Gradients of different strength can also beused to obtain a quantitative analysis of varia-tions in water diffusion potential. The parame-ter used to quantify the in vivo results of DWIis the apparent diffusion coefficient (ADC),which can also be expressed in the form of amap in which high diffusion areas are relative-

ly hyperintense and low diffusion areas are rel-atively hypointense. However, the fact thatADC maps require complex and timely post-processing and because they are less well spa-tially defined than is DWI, makes them non-essential in the emergent examination of clini-cal stroke cases.

Applications

DWI is principally used to assess hyperacuteischaemic cerebral lesions (11, 14). In this hy-peracute phase, there is a reduction in bloodsupply to the cerebral tissues, which makes theoxygen that is essential for cerebral metabolismunavailable; this in turn causes a reduction inadenosine triphosphate (ATP), damage to thesodium-potassium ion pump that in part main-tains cellular homeostasis, a flow of Na+, Ca++and Cl- ions from the extracellular to the intra-cellular space and a passive influx of water mol-ecules from the extracellular compartment tothe intracellular space (i.e., cytotoxic oedema).This restricts the diffusion capabilities of watermolecules in the intracellular space, revealingthe pathological tissue as an area of hyperinten-sity on DWI in comparison to normal brain(Fig. 1.64). Underlying these semeiotics, andwithin minutes after the onset of the clinicalstroke, there is a sudden drop in ADC valueswhich decrease over time by 30-60%; thesechanges occur at a time when conventionalMRI is still negative. These ADC values tend tonormalize within 5-10 days after onset of thestroke in part due to the appearance of vaso-genic oedema. During the hyperacute phase,the ischaemic focus is characterized by a core oftissue having markedly reduced ADC values,surrounded by a layer of brain in which this re-duction is less severe. Subsequent further re-duction in the ADC values within the peripher-al area would indicate irreversible impairmentof the tissue in the ischaemic penumbra with anenlargement of the final extent of the infarc-tion. The evaluation of the changes in ADC val-ues over time is therefore important with re-gard to forecasting the evolution and ultimatevolume of the infarct (11).


Quantitative and qualitative diffusion stud-ies are both highly sensitive as well as specificfor infarction. The earlier the examination isperformed and the longer the duration of thesyntomatology, the greater is this degree of sen-sitivity and specificity (within the first 6 hoursfollowing the acute event).

Negative diffusion studies do not necessarilyexclude the diagnosis of cerebral ischaemia(Fig. 1.65) (12). An alteration in DWI diffusion

signal is not universal to all patients with typi-cal strokes, and in certain cases patients withclinical symptoms compatible with TIA’s com-pletely recover (10); in other cases, the DWIexamination may be performed before the is-chaemia has developed into a frank infarct; andin others, the site of the ischaemic lesion (e.g.,in the posterior fossa) or the small dimensionsof the infarct focus may lead to non-visualiza-tion. In reality, however, the spatial definitionof DWI is usually sufficient to allow documen-tation of lesions only measuring a few millime-tres (Fig. 1.66).

DWI also makes it possible to determine theage of mixed duration ischaemic lesions, andtherefore declare which lesion(s) is responsiblefor the current signs and symptoms. When twoor more cerebral lesions present are hyperin-tense on conventional T2-weighted MRI, it ispossible to distinguish chronic lesions (i.e.,isointense on DWI) from recent ones (i.e., hy-perintense on DWI) (Figs. 1.67, 1.68).

The hyperintense pathological area on DWIcan remain stable in its dimensions and ulti-mately undergo necrosis; it can shrink or disap-pear completely, depending on the duration ofthe occlusion or on the response to treatment;or it can increase due to repeated episodes of is-chaemia (13).

In addition to serially monitoring an infarct’stemporal and spatial evolution, DWI proves al-so useful in monitoring the effects and responseof treatment. In cases where patient conditionsallow repeated examinations, tailored throm-bolytic and/or neuroprotective treatment pro-grammes can be individually devised for eachpatient. However, the beneficial effects of thiskind of management can be reduced by the oc-currence of haemorrhagic complications, whichtherefore calls for more critical patient analysisusing a combination of diffusion and perfusionimaging (2, 3).

PERFUSION MRI

Perfusion MR, a potentially valuable elementin the assessment of acute cerebral ischaemia,studies microvascular haemodynamics.

1.6 FUNCTIONAL MRI IN ISCHAEMIA 75

Fig. 1.64 - Hyperacute ischaemia in the supply territory of theleft middle cerebral artery. Diffusion weighted MR imagesshow (a) the pathological hyperintensity of the ischaemic area;CT (b) findings were negative.

a

b

Technique

There are a number of ways in which to per-form studies of brain perfusion (4). The mostcommonly used methods involve the intra-venous administration of gadolinium, a para-magnetic contrast medium, and the utilization


Fig. 1.65 - Acute ischaemia of the right middle cerebral arteryterritory. At clinical onset, the conventional (T2-weighted FSEsequence) (a) and diffusion (b) MR findings were negative. CT(c), performed 3 days later, showed a vast cortical-subcorticalhypodensity with associated mass effect.

Fig. 1.66 - Lacunar ischaemia (millimetric dimensions) of theright lower cerebellar peduncle.

a c

b

of ultrafast sequences (e.g., echoplanar se-quences), which are able to simultaneously ac-quire a number of sections having a temporal

resolution of approximately one second. As analternative to this MRI technique, certain inves-tigators employ selective radiofrequency (RF)pulses for labelling arterial spins (phase la-belling) (5).

Alternatives to MRI exist for analysis ofcerebral perfusion. One example is SPECT


Fig. 1.67 - Previous multiple lacunar infarcts in the periventric-ular, bi-hemispheric white matter. The lesions appear hyperin-tense in the EPI-FLAIR sequence (a), whilst the weighted dif-fusion images (b) are isointense.

a

b

Fig. 1.68 - Hyperacute ischaemia of the left middle cerebral ar-tery territory visible only in the weighted diffusion MR images(a) and not in CT (b) or EPI-FLAIR sequence (c) in which it ispossible to see a chronic paraventricular vascular sufferancesustained with hypodensity and hyperintesity, respectively.

a

b

(single photon emission computerized tomog-raphy); however, perfusion MR by comparisonis more sensitive and specific and has the addedadvantage of greater spatial definition. It can al-so be performed at the same time as conven-tional MR examinations, with consequential re-ductions in cost and time.

In the same manner as diffusion imaging,the results obtained with MR perfusion can beboth qualitative and quantitative. Qualitativeevaluation uses variations or asymmetries ofsignal intensity viewed using cine-loop display.In normal conditions of cerebral perfusion, thegadolinium passage through the cerebral capil-lary bed causes a drop in T2 signal intensity,not only in the vessels but also in the perfusedbrain itself. If, however, the perfusion of a spe-cific region of the brain is impaired, there willbe a delay or an attenuation of the loss of sig-nal intensity that varies in relation to the de-gree of reduction in the blood flow. In certaincases qualitative evaluations alone are insuffi-cient for an accurate study of perfusion, andfor this reason quantitative data, especially that

using signal/time curves, can be used. The de-gree of signal reduction in such curves is di-rectly proportional to the tissue concentrationof the contrast agent, which is in turn propor-tional to the regional cerebral blood flow(rCBF), as well as to the regional cerebralblood volume (rCBV). This makes it possible toobtain regional cerebral perfusion maps fromthe data gained from the perfusion MR. Fur-ther analysis of the concentration/time curveprovides information from which to calculateadditional parameters of perfusion such as themean transit time (MTT), the time required topass through the tissue and the peak time (PT),or the time required to reach peak perfusion.

Applications

Within the field of cerebrovascular disease,the most important applications of perfusionMR are related to cerebral ischaemia; however,its usefulness is not in the hyperacute phase aswith diffusion, but rather in the hours that fol-low. Principally, perfusion is valuable for the as-sessment of the ischaemic penumbra, or the is-chaemic area surrounding the core of the in-farction. The perfusion of this penumbra andneuronal vitality within this tissue depend onthe severity of the regional ischaemia and thecollateral circulation.

In the presence of hyperacute cerebral is-chaemia caused by the occlusion of a given ves-sel, the rCBV map will show a reduction in theMR signal intensity in the ischaemic area.Moreover, by using comparative region of in-terest (ROI) calculations in the contralateralhomologous areas of the cerebrum, it is possi-ble to observe the delay in or reduction of sig-nal loss, and therefore the differential in thepeak time. It is possible in this way to distin-guish the areas destined to infarction from theareas of the ischaemic penumbra. The penum-bra is the target of fibrinolytic treatment, with-in the area of hypoperfusion and therefore fore-casts the final infarct territory. In fact, by ex-amining the time/intensity curve, one can seethree different curves reflecting a decrease insignal intensity that is variable in relation to the


cFig. 1.68 - (Cont.).

cerebral perfusion of the ischaemic core (no de-crease in signal intensity due to an absence ofperfusion), of the area of ischaemic penumbra(reduction in signal intensity due to reducedperfusion), of the surrounding intact parenchy-ma (normal decrease in signal intensity causedby normal perfusion) (Fig. 1.69) (6).

The distribution of the perfusion deficittherefore permits the identification of poten-tially reversible ischaemic brain tissue, the se-lection of patients for various treatment proto-cols and the formulation of an early prognosticevaluation.

Diffusion/perfusion MR

The combined use of diffusion/perfusionMR can be more informative than the resultsobtained using a single examination alone, es-pecially with regard to predicting the evolutionof the cerebral infarction and clinical outcome.For these reasons, the two studies together maybe more helpful in determining importanttreatment decisions (3, 16). It is possible toidentify at least six different imaging patternsusing diffusion and perfusion MR in combina-tion (2):

1) Visualized ischaemic area is greater inperfusion than in diffusion. This is the mostcommon situation (approx. 55-77% of cases),especially when the imaging examination is per-formed within 6 hours from the onset of the is-chaemic event. In this case, the hyperacutephase shows the lesions of both the rCBV andthe ADC to be relatively minor, but still posi-tive, despite the negative CT and MR findings.However, in DWI the area of reduced ADC isgenerally smaller than the area demonstratedon the rCBV in the perfusion study, which in-cludes both the area of frank infarction as wellas the penumbra area. From a prognostic pointof view, the early lesions visualized on the per-fusion MR examination represent the maxi-mum potential dimension of infarction and in-dicate the worst probable clinical outcome inthe absence of further vascular occlusions ordisruption of collateral circulation. Generallyspeaking, in DWI the size of the infarction

tends to grow over time, but with regard to per-fusion MR, the volume of ischemic tissue tendsto shrink.

2) Visualized ischaemic area in perfusionMR is the same as the ischaemic region demon-strated in DWI.

3) Visualized ischaemic area in perfusion isless than in DWI. In this case reperfusion prob-ably occurs in the interim between the start ofirreversible tissue damage and the MR exami-nation. The interim appearance of collateralcirculation or the enlargment of the ischaemicarea beyond the initial perfusion deficit may al-so be considered as causes of this imaging pic-ture.

4) Presence of a DWI deficit without a per-fusion abnormality.

5) Presence of a perfusion deficit without aDWI abnormality (associated with a transientneurological deficit).

6) Absence of a visualized lesion in bothDWI and perfusion MR, despite a positive clin-ical picture.

The observation of an early deficit in perfu-sion MR that is greater than the volume of theabnormality seen in diffusion (patterns 1 and5) indicates the presence of tissue “at risk” inthe ischaemic penumbra, which can thereforepotentially be saved by forms of reperfusion


Fig. 1.69 - Perfusion study of an acute ischaemia. The intensi-ty/time graph shows 3 different curves indicating a drop in sig-nal intensity that varies with the entity of the cerebral perfusionof the ischaemic core (absence of drop in signal intensity due tothe absence of perfusion), of the ischaemic penumbra area (re-duction of the drop in signal intensity due to reduced perfu-sion), of the intact surrounding parenchyma (normal reductionin signal intensity due to normal perfusion).

treatment. When the perfusion deficits onMRI are absent or smaller than those in diffu-sion (patterns 2, 3, and 4), treatment involvingneuroprotective drugs is felt to be more suit-able.

MR SPECTROSCOPY

MR spectroscopy is a real time non-invasivestudy of some of the biochemical elements in-volved in cerebral metabolism.

Technique

The technique of spectroscopy is based onthe physical principle of the so-called “chemi-cal shift” that reflects the variation in frequen-cy of resonance of the nuclei of different mole-cules; this variation is influenced by the mag-netic field that is generated by the cloud ofelectrons that surrounds these nuclei, as well asby the electrons of nearby atoms. Therefore,the same atom can exhibit different degrees ofchemical shift depending on the environmentin which it finds itself, and on the basis of thisit is possible to identify the molecule containingthe atom in question.

We usually speak of proton spectroscopy, be-cause the nucleus typically chosen to study, andfor which to calibrate the MR unit, is the hy-drogen proton. This choice is in part made be-cause the hydrogen proton is particularly plen-tiful in organic structures.

Proton spectroscopy provides metabolic in-formation concerning molecules having a lowmolecular weight that are present in relativelyhigh concentrations (0.1-1 mM); these includeN-acetyl-aspartate (NAA), choline (Cho), crea-tine (Cr), phosphocreatine (PCr), myoinositol(mI), lactate (Lac), lipids (Lip), glutamine andglutamate (Glx). The concentration of thesemetabolites is detected in the form of spectra inwhich each peak in a given position (expressedin parts per million: ppm) represents a particu-lar metabolite.

Normally in adults, NAA has the highestpeak among the expected metabolites, where it

is localized to about 2 ppm. This metabolite isonly found in the central nervous system, andin particular is detected in neurons and, to alesser extent, in certain glial precursor cells.For this reason it is considered a neuronalmarker. Its presence is more or less equal in thewhite and grey matter, so that it is also consid-ered an axonal marker.

NAA concentration is depressed or non-detectable in certain types of brain pathology.Cho, with a peak of approximately 3.2 ppm,contains composites containing choline prin-cipally represented by membrane lipids; it istherefore considered a membrane marker. It isseen to increase in diseases characterized byan elevation in cellular turnover, an increase inthe number of cells or by membrane dam-age/degeneration. Cr and PCr can be ob-served with a single peak at 3.02 ppm. Thesemetabolites are derived from the high energyphosphate pool involved in metabolism. Beinga stable peak, it can be used as a control valueeven in the presence of pathology. MI, whichis a specific marker for glial cells, is localizedat 3.3-3.6 ppm.

When present, Lac has an unusual “dou-blet” peak at 1.32 ppm. When present, it indi-cates the production of energy in conditions ofinsufficient oxygen supply. An example ofwhen this situation can occur is when incom-plete vascular occlusion results in the activationof the enzymatic pathway that leads to anaero-bic glycolysis. It can also accumulate due to theinfiltration of microphages that contain lactate,or because the production of lactate is trappedby the ongoing pathological process and is notremoved from the tissue under study.

Lipids, which can be observed in necroticprocesses, produce peaks of 0.8, 1.2, 1.5 ppm.Glx is represented by peaks at 2.1, 2.5 and at3.6-3.8 ppm and includes the signal from theneurotransmitters glutamate and glutamine.

These metabolites can be studied using twolocalization techniques: 1) the single volumetechnique, with which it is possible to acquirespectra from specific regions of the brain, and2) the spectroscopic imaging technique, withwhich one can simultaneously obtain spectrafrom tissue volumes acquired from one or


more imaging sections in order to obtain thespatial distribution of the metabolites underexamination.

Applications

Spectroscopy can be used for the early de-tection and better characterization of ischaemiclesions, for monitoring the effects of treatment,and most importantly, for distinguishing the in-farct focus from the area of surrounding is-chaemic penumbra (6, 15). The area of cellularnecrosis is characterized by a depression ofNAA (50% within the first 6 hours), whereasthe ischaemic penumbra is characterized by thepresence of an increase in the peak of lacticacid in the absence of significant NAA alter-ations (Fig. 1.70).

A serious NAA depression and a marked in-crease in lactate in the acute phase have provedto be prognostic indexes of more marked is-chemic lesion (7, 8).

CONCLUSIONS

The various functional MR examinationtechniques (diffusion, perfusion, spectroscopy)are essential to the meaningful, productivetherapeutic management of acute stroke pa-tients.

The goal of fibrinolytic treatment is to safe-guard the ischaemic tissue that has suffered re-versible damage so that it can be properlyreperfused, together with the prevention ofreperfusion of irreversibly damaged, non-vitaltissue. This requires diagnostic techniques ca-pable of distinguishing vital ischaemic tissuefrom that which is frankly infarcted, wherethere is a risk of damage from reperfusion re-sulting in haemorrhagic complications.

Diffusion MR examinations are able to pro-vide immediate and simple demonstration ofhyperacute cerebral ischaemia, before the ap-pearance of signal changes in MRI and/or den-sity changes in CT; however, it is not able to dis-tinguish between ischaemic penumbra, whichcould therefore benefit from recanalization

treatment, and irreversibly ischaemically dam-aged tissue.

MR spectroscopy and, in particular, spec-troscopic imaging can be of use in this sense,however it requires relatively long examina-tion times. Perfusion MR studies provide di-rect information on the status of cerebralparenchyma perfusion (depending on the ade-quacy of collateral circulation) and on tissuevitality and reversibility that is required for a


Fig. 1.70 - Spectroscopic study (a) of subacute ischaemia withmorphological MRI (T2-W FSE). The drastic reduction ofNAA concentration is evident.

a

b

suitable selection of patients for thrombolytictreatment.

It therefore follows that a multimodal solu-tion is required to solve the problem of acutecerebral ischaemia and to appropriately guidetreatment choices. The key to interpretingacute phase ischaemia is to combine differentMR and spectroscopic acquisition sequences.Diffusion/perfusion integration in particularenables accurate mapping, more precise grad-ing and more efficient treatment planning ofcases of cerebral ischaemia. These studies alsohave the advantage of being generally rapid toperform in association with basic MR examina-tions.

REFERENCES

1. Baird AE, Warach S: Magnetic resonance imaging of acutestroke. J Cereb Blood Flow Metabolism 18:583-609, 1998.

2. Barber PA, Darby DG, Desmond PM et al: Prediction ofstroke outcome with echoplanar perfusion and diffusionweighted MRI. Neurology 51:418-426, 1998.

3. De Boer JA, Folkers PJM: MR perfusion and diffusionimaging in ischaemic brain disease. Medica Mundi 41:20,1997.

4. Detre JA, Leigh JS, Williams DS et al: Perfusion imaging.Magn Reson Med 23:37-45, 1992.

5. Edelman RR, Siewert B, Darby DG et al: Quantitative map-ping of cerebral blood flow and functional localization withecho-planar MR imaging and signal targeting with alterna-ting radio-frequency. Radiology 192:513-520, 1994.

6. Graham GD, Blamire AM, Howseman AM et al: Proton ma-gnetic resonance spectroscopy of cerebral lactate and othermetabolites in stroke patients. Stroke 23:333-340, 1992.

7. Federico F, Simone IL: Prognostic significance of meta-bolic changes detected by proton magnetic resonancespectroscopy in ischaemic stroke. J Neurol 243:241-247,1996.

8. Federico F, Simone IL: Prognostic value of proton magne-tic resonance spectroscopy in ischaemic stroke. Arch Neu-rol 55:489-494, 1998.

9. Hacke W, Kaste M, Fieschi C et al: Intravenous throm-bolysis with recombinant tissue plasminogen activator foracute hemispheric stroke. The European Cooperative Acu-te Stroke Study (ECASS). JAMA 274:1017-1025, 1995.

10. Kidwell CS, Alger JR, Di Salle F et al: Diffusion MRI in pa-tients with transient ischemia attacks. Stroke 30(6):1174-1180, 1999.

11. Li TQ, Chen ZG, Hindmarsh T: Diffusion-weighted MRimaging of acute cerebral ischemia. Acta Radiologica39:460-473,1998.

12. Lovblad KO, Laubach HJ, Baird AE et al: Clinical expe-rience with diffusion-weighted MR in patients with acutestroke. AJNR 19:1061-1066, 1998.

13. Lovblad KO, Baird AE, Schlaug G: Ischemic lesion volu-mes in acute stroke by diffusion-weighted magnetic reso-nance imaging correlate with clinical outcome. Ann Neurol42:164-170, 1997.

14. Lutsep HL, Albers GW, DeCrespigny A et al: Clinical utilityof diffusion-weighted magnetic resonance imaging in the as-sessment of ischemic stroke. Ann Neurol 41:574-580, 1997.

15. Mathews VP, Barker PB, Blackband SJ et al: Cerebral me-tabolities in patients with acute and subacute strokes: a se-rial MR and proton MR spectroscopy study. AJR 165:633-638, 1995.

16. Ueda T, Yuh WT, Taoka T: Clinical application of perfusionand diffusion MR imaging in acute ischemic stroke. J MagnReson Imaging 10(3):305-309, 1999.


83

INTRODUCTION

Intracranial haemorrhages account for ap-proximately 20% of all cerebral ictuses relatedto vascular disease, with a higher prevalence ofintraaxial localizations (15%) as compared tothose principally within the subarachnoidspace (5%) (1, 6, 9). Although MRI is highlyspecific with regard to haemorrhagic lesions,CT remains the examination of choice, espe-cially in emergencies, in part due to the diffi-culty in managing acutely ill patients within theMR scanning unit.

Any physician who acquired an MRI unit inits early stages of clinical application will re-member the sense of confusion experiencedwith the first acute intracerebral haematomapatient, as initially diagnosed on MRI. In suchcases, the lesion MR signal was “ambiguous”,nearly devoid of the specific characterizationsseen on CT in patients with haemorrage. In theearly stages haemorrhage could appear quitesimilar to an ischaemic ictus, being differentiat-ed when possible by the differing topographyand morphology.

This impact conditioned the attitude of neu-roradiologists against the use of MRI in acutehaemorrhagic pathology for some years, andthis instinctive wariness has only partly been re-

conditioned by a clear working knowledge ofthe evolution of the MR signal of parenchymalhaemorrhagic collections (13, 15-18).

In this chapter, we will analyse the informa-tion that can be deduced from intracranialhaemorrhages using MRI, making a distinctionbetween intraaxial and subarachnoid formsdue to the difference in the anatomopathologi-cal and biochemical environment in which thephenomena that influence the haemorrhagicMRI signal occur.

SEMEIOTICS

Intraaxial haemorrhage

Intraaxial cerebral haemorrhages are seriousclinical events characterized by a variable alter-ation in the state of consciousness, an often se-vere neurological deficit and by the possible as-sociation with meningeal signs. Alongside thismore common presentation, there are more se-rious clinical forms such as sudden decerebra-tion as well as milder forms with relatively mi-nor effects on the state of consciousness and aless serious clinical deficit.

The most frequent cause of intraaxial haem-orrhage, which accounts for more than 50% of

1.7

MRI IN HAEMORRHAGE

L. Simonetti, S. Cirillo, R. Agati

cases, is systemic hypertension associated withintracranial atherosclerotic vessel alterations.Other causes, in order of frequency, are therupture of vascular malformations, coagulationdisorders, intratumoral haemorrhages (espe-cially neoplastic metastases and malignantgliomas), trauma and postsurgical/iatrogeniccauses.

Evolution-based semeiology

Neuroradiological semeiology based on thetime elapsed since the onset of the intraaxialbleeding is complex (2, 7, 8, 14, 19): with re-gard to CT, the observations are linked aboveall to the macroscopic and sub-macroscopicanatomopathological alterations of the haemor-rhagic focus, while with MR the imaging find-ings of haemorrhage must be integrated withvarying biochemical factors.

The various steps that take the haematic col-lection from the hyperacute phase, with aprevalence of oxyhaemoglobin, to the outcomeand reparation phase, in which the final break-down components such as haemosiderin pre-vail, and the consequent variations in the MRsignal are now well understood and catego-rized. It should be remembered that it was pre-cisely the need to explain the dynamic behav-iour of the MR signal of the haematoma thatprompted the reconsideration, proper correla-tion and accurate categorization of the stages ofhaemoglobin metabolism outside the vascularbed. It goes without saying that the state of thehaemoglobin within the haemorrhagic focus isof little importance from a diagnostic and ther-apeutic point of view, but it nevertheless pro-vides a very real stimulus for the neuroradiolo-gist to understand clearly this physiologicalprocess in order to properly interpret the im-ages.

The temporal evolution of the MR charac-teristics of blood is caused both by alterationsof the erythrocytes as well as the haemoglobinpresent under several differing conditions. Asfar as the red blood cells are concerned, mem-brane integrity, guaranteed under normal con-ditions by the ATPase/Na-K units dependent

on the membrane and powered by glycolyticenergy, is of great importance. Haemoglobin al-terations are influenced by various factors, in-cluding: pH, conditions of osmolarity, temper-ature, partial oxgen pressure (pO2) and themetabolic microenvironment along with theconcentration of the oxidizable sublayers. Bothoxygenated and deoxygenated haemoglobincirculate inside red blood cells; in such forms ofhaemoglobin, the heme contains bivalent iron.If the iron group is oxidized to form trivalentiron, the molecule (metahaemoglobin) loses itsability to bond oxygen; for this reason, throughthe pentoso-phosphate pathway, a considerablepercentage (10%) of the red blood cell’s cata-bolic energy is used to form reducing agents(NADPH and reduced glutathione) capable ofpreventing or correcting haemoglobin oxida-tion. The same reducing agents also performthe important role of controlling the peroxida-tion of the membrane lipids that would other-wise increase the osmotic fragility of the ery-throcytes. The remaining 90% of the glycidiccatabolism of red blood cells follows the gly-colytic pathway, which produces the ATP usedto fuel the Na-K dependent ATPase structures.The proper functioning of these membranepumps is indispensable for the maintenance oferythrocyte osmolarity and thus the normal bi-concave cellular shape. A sufficient glucosesupply is therefore required for several purpos-es: to maintain cellular osmolarity, to keep thehaemoglobin properly reduced and to avoidthe peroxidation of membrane lipids.

In the light of this, it is easier to interpret theblood’s relaxation parameter alterations usingMRI. In the hyperacute phase, in other wordsin the first 12 hours from onset, intraparenchy-mal haemorrhagic foci are composed of intactred blood cells with high oxygen saturation andtherefore containing oxyhaemoglobin. In theabsence of paramagnetic molecules or struc-tures, the MR relaxation times are longer thanthose of the surrounding tissue due to the localalteration in free water content and proteinconcentration. The resulting oxyhaemoglobin-dominant haemorrhagic lesion on MRI (Fig.1.71) is complex but includes: relative (as com-pared to normal brain tissue) minor hypoisoin-


tensity on the T1-weighted images, minor hy-perintensity on PD-weighted images, and mi-nor hyperintensity on the T2-weighted images(in truth, the relative intensity differentials ascompared to normal brain are quite small in allroutine MR acquisition sequences).

In the oxygen-dependent acute phase (12hours - 2 days), the pO2 within the extravasat-ed blood starts to drop fairly quickly, and con-sequently there is a reduction in the haemoglo-

bin’s oxygen saturation, with the eventual for-mation of deoxyhaemoglobin. Deoxyhaemo-globin, characterized by high magnetic suscep-tibility and enclosed in the finite intracellularspace of the erythrocyte, causes non-homo-geneity of the local magnetic field, thus result-ing in a loss of phase coherence of the residentprotons. This translates into a preferential fieldstrength -dependent enhancement of T2 relax-ation. Although deoxyhaemoglobin is para-magnetic, it does not influence T1 relaxationbecause its heme groups are contained in apo-lar pockets that prevent contact with water pro-tons. The presence of deoxyhaemoglobin in thehaemorrhagic lesion translates into (Figs. 1.72,1.73): relative hypo-isointensity on T1-weight-ed images, iso-hypointensity on PD-weightedimages and rather marked hypointensity on T2-weighted images.

The subacute, glucose-dependent phase (2-14 days) is characterized by two events that oc-cur in parallel but slightly out of phase with oneanother, partly sharing the same pathogenicmechanisms: the formation of metahaemoglo-

1.7 MRI IN HAEMORRHAGE 85

Fig. 1.71 - Hyperacute phase right intracerebral sub-Sylvianhaemorrhage (12 hours). Coronal T1-dependent scan (a) andaxial T2-dependent scan (b). The lesion presents as hy-pointense in T1 and non-homogeneously hyperintense in T2,where the notably hyperintense oedema halo in formation is al-so visible.

Fig. 1.72 - Acute phase intracerebral haemorrhage (38 hoursfrom onset) in a left thalamo-capsular location. Axial PD (a)and T2 scans: the lesion presents as non-homogeneously hy-pointense with a vast oedematous halo.

a

b

bin (methaemoglobin: 2-7 days) and erythro-cyte lysis (7-14 days).

Methaemoglobinization presupposes the ex-haustion of the oxide-reducing homeostasis ofthe erythrocyte systems due to a regional re-duction in glucose concentration, the blockageof the catabolitic pentose-phosphate pathwayand the progressive reduction of NADPH andreduced glutathione. In addition to an ex-tremely reduced concentration of glucose,haemoglobin oxidation to methaemoglobin isalso conditioned by a given pO2 of about 20mm Hg.

The pathogenesis of red blood cell lysis in-cludes: the exhaustion of erythrocyte ATP re-serves with the stoppage of the Na-K depend-ent membrane pumps and the osmotic swellingof the erythrocytes, the peroxidation of mem-brane lipids and the catabolization of the mem-brane phospholipids by tissue phospholipases.

Being intensely paramagnetic, methaemoglo-bin causes a reduction in T1 relaxation due tothe dipole-dipole interaction between the exter-nal shell electrons of the methaemoglobin andwater protons. The influence of methaemoglo-bin on T2 relaxation is identical to that de-scribed for deoxyhaemoglobin. Once erythro-cyte lysis has taken place, a loss of T2 relaxationenhancement occurs, as methaemoglobin as-sumes a homogeneous distribution, whichtranslates into hyperintensity of the MR signalon T2-weighted images. At the same time, theintensity on T1-weighted images increases dueto the greater T1 relaxation effects of the freemethaemoglobin as compared to intracellularmethaemoglobin.

To summarize, in the first week of thisphase (intact membrane methaemoglobiniza-tion), the MR signal characteristics of the in-tracellular methaemoglobin dominance withinthe haemorrhagic lesion can be classified asfollows: relative hyperintensity on T1-weight-ed images, hyperintensity on PD-weighted im-ages and hypointensity on T2-weighted im-ages. In contrast to this, once erythrocyte lysishas taken place, the extracellular methaemo-globin dominance within the haemorrhagedemonstrates: relative hyperintensity on T1-weighted images, hyperintensity on PD-de-pendent images and hyperintensity on T2-weighted images.

For purposes of completeness, we will nowdescribe MR signal alterations in chronic-phaseintraparenchymal haematomas (more than twoweeks), although, strictly speaking, this goesslightly beyond the temporal limits of this dis-cussion. The chronic phase of haematoma evo-lution is characterized by the phagocytosis of erythrocyte lysis products by microphagesaround periphery of the haemorrhagic collec-tion. Within the macrophages heme iron accu-mulates primarily within lysosome vacuoles in


Fig. 1.73 - Acute phase intracerebral haemorrhage in left tem-poral location: coronal T1- (a) and T2-dependent (b) scans:note the marked hypointensity of the lesion and the perilesion-al oedema.

a

b

the form of haemosiderin. The presence ofhaemosiderin causes increased T2 relaxationand therefore hypointensity on T2-weightedimages within the peripheral rim of the haem-orrhagic lesion that persists indefinitely. In

the meantime, methaemoglobin within thehaemorrhagic collection continues to causeMR signal hyperintensity on the T1- and T2-weighted images. Subsequently, as monthspass, methaemoglobin breaks down into de-rivatives that do not have T1 relaxation effects(Figs. 1.74, 1.75).

Bleeding cause-based semeiology

In addition to the diagnosis of the presenceof an intraaxial haemorrhage, MRI can alsosometimes provide information that indicatesthe underlying cause of the bleeding. Apartfrom arterial hypertension, and excluding trau-ma, intracerebral bleeding typically is causedby vascular malformations or richly vascular-ized intracerebral neoplasias. In such cases thesite, morphology, structure and number ofblood collections can vary. Therefore, using thisinformation together with the clinical picture,the neuroradiologist is able to suggest the like-ly cause(s) of bleeding. a) Site

The localization of intraaxial haematomas isrepresented, in order, by:– Nucleo-capsular haemorrhages (between

the basal ganglia nuclei and the internal cap-


Fig. 1.75 - Sagittal PD-dependent MRI scan: note the thin hy-pointense rim that surrounds the lesion, due to the presence ofhaemosiderin.

Fig. 1.74 - Left parietal haemorrhage in chronic phase (28days). Axial CT scan after contrast agent (a): hypodense le-sion with thin hyperdense rim. Axial PD-dependent MRscan: the lesion shows the characteristic hyperintense haema-tic signal.

a

b

sule: 50%). Nucleo-capsular haematomascan be subdivided into capsulo-lenticular(between the internal capsule and the lentic-ular nucleus [globus pallidus plus puta-men]), capsulo-thalamic (between the inter-nal capsule and the thalamus) and capsulo-caudate (between the internal capsule andthe caudate nucleus) haematomas. In mostcases the haematomas in this position areconsidered spontaneous, and are linked toarterial hypertension both as a cause of theinduced chronic vascular alterations as wellas the triggering cause of the acute haemor-rhage. Acute hypertensive crises can alsolead to haemorrhages at these locations.Small capsulo-caudate haematomas are anexception, as the rupture of small periven-tricular arteriovenous malformations moreoften causes them than does hypertension.

– Lobar haemorrhages (35%). These haem-orrhages are rarely spontaneous. Temporaland occipital lobe haematomas are usuallysecondary to arteriovenous malformationsor haemorrhagic infarcts, mainly due to ve-nous ischaemia. Frontal haematomas aregenerally caused by ruptures of aneurysmsassociated with the anterior communicat-ing artery or anterior cerebral artery. Alllobar haemorrhages can have a neoplasticorigin.

– Infratentorial haemorrhages (10%). Thesehaemorrhages can be subdivided into brain-stem and cerebellar bleeds. The former arefrequently caused by vascular malformationruptures, most commonly cavernous an-giomas; the latter are more typically associ-ated with tumoural bleeding or, less fre-quently, with aneurysm ruptures.

– Intraventricular haemorrhages (5%). Isolat-ed intraventricular haemorrhages devoid ofsigns of intraaxial haematoma formation arerare. They are generally secondary to therupture of small paraventricular or choroidplexus arteriovenous malformations.

b) Morphology and structureIntraaxial haematomas can be round or oval,

with well-defined margins, or alternatively ir-regular with dendritic margins or even withcompletely irregular boundaries having a some-

what map-like appearance. Haematoma mor-phology can be linked to either a vascular mal-formation/aneurysm or a spontaneous aetiolo-gy, however, haematomas with irregular mar-gins are more commonly encountered in pa-tients with blood dyscrasias.

The appearance of the haemorrhage can behomogeneous or heterogeneous, occasionallymanifesting a horizontal fluid-fluid level inhaemorrhages due to variations in the makeupof the blood clot. c) Number

Intraaxial blood collections tend to be singlein number. The finding of multiple haemor-rhagic foci, usually in a superficial lobar posi-tion (excluding those of traumatic origin),point in the direction of a diagnosis of a blooddisorder (including iatrogenic anticoagula-tion), multiple haemorrhagic neoplastic metas-tases (including melanoma) or dural venous si-nus thrombosis with venous infarcts/haemor-rhages.

Semeiotics based on technical MR parameters

MR tissue contrast in the presence of blooddepends to a great extent on the parameters ofthe image acquisition sequence used. In gradi-ent-recalled echo (GRE) sequences, the sensi-tivity to paramagnetic constituents is veryhigh. However, this sensitivity requires atten-tion to magnetic susceceptibility “border”artefacts at the interface of the petrous bonesand the paranasal sinuses with the brainparenchyma.

Fast Spin-echo (FSE) sequences differ fromconventional SE sequences in that they use atrain of 180° radiofrequency pulses, which gen-erate a set of echoes that are individually codedin the space of a single TR. The implications inbrain examinations are that the effects of mag-netic susceptibility dephasing are removed andthe effects of diffusion-induced signal loss arereduced. T2-dependent FSE sequences there-fore have a lower sensitivity to magnetically sus-ceptible blood products than do the correspon-ding conventional spin echo images. The use ofsupplementary GRE sequences or T2-weighted


conventional spin echo imaging sequences isrecommended in cases where clinical historysuggests possible cranial haemorrhage. Echo-planar Imaging (EPI) sequences are becomingincreasingly suitable for routine clinical appli-cations. They are very sensitive to magnetic sus-ceptibility in both conventional spin echo andGRE sequences.

Closing comments

The importance of understanding the MRsignal characteristics of intraaxial haematomaswithin the framework of the evolutional phaseof the individual blood collections should beunderlined: this knowledge is in part intendedto provide a means of interpreting MR images inpatients with an acute clinical ictus (stroke) whohave been inadvertently sent to MRI instead ofCT. The greater diagnostic contribution of MRIin patients with intracranial haemorrhage is inthe subacute and chronic phases. We refer hereto those cases in which the initial clinical andCT findings are ambiguous, thus creating prob-lems of differential diagnosis. In such instancesthe performance of an MR examination thatshows the MR signal characteristics specific forthe various evolving blood products dispels di-agnostic doubts.

One piece of additional information that canbe gleaned from MRI as compared to CT is theability of the former to link many “non-sponta-neous” haemorrhages with the underlyingpathological condition responsible for thebleed. The better relative sensitivity of MRI indiagnosing vascular malformations (Fig. 1.76),even in the presence of a haematoma, is wellknown. However, it is less well understoodthat, in order to be visible when haemorrhage ispresent, the vascular malformation must be of arather considerable size. In the presence ofacute or subacute haematomas, small vascularmalformations are easily overlooked on routineMR images, in part due to the distortion causedby the magnetic field; this applies for both con-ventional MR as well for MR angiography ex-aminations (Fig. 1.77). And, although MR an-giography is an important contribution to pa-

tient treatment planning, it should be comple-mented with a conventional angiographic ex-amination in the pretreatment phase of patientanalysis.

Subarachnoid haemorrhage

Haemorrhage into the subarachnoid space(subarachnoid haemorrhage: SAH) has a sud-den clinical onset with headache, nausea, vom-iting, varying degress of disturbance of con-sciousness, widespread cutaneous hyperaesthe-sia and severe meningeal signs. Clinical varia-tions can range from more subtle forms wherethe meningeal syndrome alone is present, tomixed cerebromeningeal forms associated withclinical symptomatology of the neurologicaldeficit type to more serious forms characterizedby coma.

The most frequent cause of SAH is aneurysmrupture, followed, in order of frequency by therupture of brainstem or cerebral arteriovenousmalformations, trauma, blood clotting disordersand, lastly, acute haemorrhagic necrosis of thepituitary gland (5).


Fig. 1.76 - Right temporal-occipital haemorrhage in subacutephase with arteriovenous malformation. Coronal PD-depend-ent scan: the haemorrhagic lesion is very clear, as is the malfor-mation nidus with its characteristic signal void.

Semeiology and variations based on time

MR semeiology of SAH is made all the morecomplex by the continuous alterations beingundergone by the blood with relationship tothe biological parameters of the subarachnoidspace (pH, pO2, glucose concentration). The

variation of these parameters follows differentrules that are less easily codified than those thatcharacterize intraparenchymal blood collec-tions (3, 4). For this reason, MRI generallyfinds little place in the evaluation of acutephase SAH, given CT’s greater sensitivity andrapidity, and its ease of access 24 hours a day.The interpretation of MR images in patientswith non-traumatic SAH is doubtlessly morestraightforward in the subacute and chronicphases, and its contribution grows with thepassing of time since the “acute” moment ofthe bleed as the diagnostic efficiency of CTdwindles. In reality however, even during theacute phase a well-planned and executed MRexamination can also allow a demonstration ofthe characteristic signs of SAH.

Variations in the relaxation parameters thatdistinguish the evolutional phases of haemor-rhagic collections are linked to the structuraland functional variations of erythrocytes andthe consequent conditions of haemoglobin oxi-dation and oxygenation.

In the subarachnoid space, erythrocyte andhaemoglobin alterations follow different dy-namics than those observed in intraparenchy-mal haemorrhages, in part due to the differentbiochemical-metabolic microenvironment. Thismakes it somewhat difficult to pinpoint the tem-poral limits of the phases of evolution of SAH.

In the hyperacute phase, there is no length-ening of proton density relaxation times incomparison to the surrounding CSF, but rathera slight shortening of T1 relaxation times dueto the increase in protein content; this subtlechange is often not detected due to the long re-laxation times of the CSF, which mask the the-oretical effects of the fresh blood, and conse-quently the T1-weighted MR images are usual-ly interpreted as being negative.

In the acute phase it is difficult to perceivethe reduction of T2 relaxation times character-istic to parenchymal blood collections, giventhat the CSF environment is an open system inwhich the focal variations of pO2 are slowed(relatively higher levels of pO2 are maintainedas compared to the cerebral parenchyma).And, as noted in the preceding paragraph, it isdifficult to evaluate small variations in relax-


Fig. 1.77 - Small left frontal intraparenchymal haemorrhage.Sagittal T1-dependent scan (a) TOF MRA (b). The image con-cerning the haematoma is obvious on the MRA reconstruction:this would prevent the visualization of any small arteriovenousmalformation present.

b

a

ation times in the environment of the CSF, andas a result the T2-weighted MRI tends to benegative.

During the acute phase it is sometimespossible to find some linear hyperintensity onT1-weighted images in an intrafissural loca-tion. Such observations, which indicate SAH,are interpreted to be clotting of the ex-travasated blood within the subarachnoidspace. Contact with the CSF is a sufficientstimulus to cause clotting of the blood pres-ent in the subarachnoid spaces. If we thenadd the fact that the retraction of the clotcauses dramatic variations in red blood cellconcentration and fibrin structure, we canthen explain how it is possible even in anacute phase to visualize SAH in some in-stances. Clotting is therefore the key to visu-alizing blood in the early phases of SAH whenusing conventional MR sequences. The limitof this semeiological element lies in the tem-poral, quantitative and topographic variabili-ty of clotting processes, the percentage ofblood in the CSF, the functionality of the clot-ting mechanisms, the site of the bleed and thebiochemical composition of the CSF microen-vironment.

In the subacute phase, a reduction in T1 re-laxation (hyperintensity on T2-weighted im-ages) caused by the presence of methaemoglo-bin is clearly visible. In the subarachnoid space,the reduction in glucose concentration, re-quired for methaemoglobinization and erythro-cyte lysis, also takes place at a slower pace thanthat observed in parenchymal blood collec-tions. This phase represents the period inwhich MRI reaches its peak sensitivity forSAH; this is made all the more important if weconsider that in this period, the CT density ofthe extravasated blood tends to decrease, thusconsonantly reducing the sensitivity of thistechnique.

In recent years, we have started to exam-ine SAH with MRI using FLAIR (fluid-at-tenuated inversion recovery) sequences (10,11). FLAIR images are obtained using an in-version recovery (IR) sequence that has longTI (time to inversion) and TE (time to echo).These sequences suppress the CSF signal, and

they produce images that are very heavily T2-weighted. This makes FLAIR particularlyuseful in identifying lesions on the surface ofthe hemispheres (and overlying subarachnoidspaces), within the basal subarachnoid cis-terns, around the brainstem and at the grey-white matter junction. On the basis of thesecharacteristics it is usually possible to detectSAH. SAH presents as high signal areas onFLAIR images and any associated intraven-tricular haemorrhage is also clearly visible.FLAIR is also useful in detecting acute SAHin the posterior fossa, which is difficult tostudy using CT due to the presence of scat-ter artefacts. FLAIR images have been shownto visualize SAH up to 45 days beyond theacute episode.

In the same manner as that mentioned in thepreceding section on intraparenchymal collec-tions, MRI can play an important role in theearly recognition of the vascular pathology re-sponsible for the SAH.

Closing comments

Given the numerous variables linked toMRI, CT remains the examination of choicein acute phase SAH diagnosis (12). However,in the subacute and chronic phases, the de-creasing sensitivity of CT corresponds withincreasing sensitivity of MRI for haemoglobinbreakdown products; in particular, chronicleptomeningeal haemosiderin deposits can berecognized even years after bleeding (superfi-cial siderosis).

And, MRI can play an important role in theearly recognition of the vascular pathology re-sponsible for the bleed. The continuousprogress made in MR angiography has recentlyled to a greater diagnostic reliability. In certaincases, MR angiographic examinations are cur-rently being proposed as the only presurgicalvascular evaluation in aneurysms responsiblefor SAH. However, more experience and fur-ther technical progress in MRI are required be-fore it becomes a routine procedure in order toprove the validity and efficacy of the method inthis area of diagnosis.


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version-recovery MR imaging. Radiology 203(1):257-62,1997.

11. Noguchi K, Ogawa T, Inugami et al: Acute subarachnoidhemorrhage: MR imaging with fluid-attenuated inversionrecovery pulse sequences. Radiology 1963:773-777, 1995.

12. Ogawa T, Inugami A, Fujita H et al: MR diagnosis of suba-cute and chronic subarachnoid hemorrhage: comparisonwith CT. AJR 165(5):1257-1262, 1995.

13. Osborne AG: Diagnostic Neuroradiology. Chapter 10. Mo-sby-Year Book, St. Louis, 1994.

14. Patel MR, Edelman RR, Warach S: Detection of hyperacu-te primary intraparenchymal hemorrhage by magnetic reso-nance imaging. Stroke 27(12):2321-2324, 1996.

15. Savoiardo M, Sberna M, Grisoli M: RM e patologia vasco-lare del sistema nervoso centrale. Rivista di Neuroradiolo-gia 1 (suppl. 1):95-100, 1988.

16. Thulborn KR, Atlas SW: Intracranial hemorrage. In: AtlasSW (ed). “MRI of brain and spine”. II Edition. Lippincott-Raven Publishers. Philadelphia, 265-313, 1996.

17. Triulzi F: Cerebral hemorrage: CT and MRI. Rivista diNeuroradiologia 3 (suppl.2): 39-44, 1990.

18. Vignaud J, Buolin A: Tomodensitometrie cranio-encefali-que. Ed Vigot Paris, 1987.

19. Zimmerman RA, Leeds NE, Naidich TP: Ring blush associa-ted with cerebral hematoma. Radiology 122:707-711, 1977.


93

INTRODUCTION

Some 80% of all cerebrovascular accidentsare caused by cerebral ischaemia and the re-maining 20% by cerebral haemorrhage (3).Most cases of ischaemia are brought on bythromboembolic complications within thelarge extracranial supraaortic vessels (only 20%are caused by cardiac embolism), and 90% ofthem affect the internal carotid, middle cere-bral or vertebral arteries (with a ratio of 10:5:2).

Consequential neurological deficits can becomplete with possibilities of death, partialwith permanent disability (25%) or transitory.In this last case, the risk of a second ischaemicepisode is very high, however the probability ofdeath or disability can be considerably reducedby antiaggregation treatment.

In ischaemic cerebrovascular events, ultra-sound is highly sensitive and specific with re-gard to both pathogenetic mechanism andsite, findings that can be easily documentedusing this method. In contrast to cerebralhaemorrhage, where ultrasound is not diag-nostic, it is fundamental to patients with tran-sient neurological deficit in determining thestrategy of primary and secondary preventionof subsequent ischaemic cerebrovascular acci-dents (2, 4, 6, 8).

PATHOPHYSIOLOGY

Vascular brain function impairment pres-ents clinically with a wide spectrum of signsand symptoms and is usually characterized bya relatively close correlation between theclinical observations and the ultrasound find-ings of the extracranial carotid vascular sys-tem.

Symptomatology of cerebral insufficiencycan be divided into four stages:– Stage I: stenosis or compensated occlusion;

the patient is asymptomatic.– Stage II: stenosis or not completely compen-

sated occlusion; the patient is symptomaticwith a transient cerebrovascular insufficien-cy (TIA, RIND).

– Stage III: multiple stenoses or total progres-sive occlusion; the patient is symptomaticwith a progressive stroke syndrome.

– Stage IV: multiple stenoses or complete oc-clusion; the patient is symptomatic with acomplete stroke.Ultrasound examinations are usually able to

establish the type and site of the extracranialvascular lesion responsible for the neurologicalpicture; that is, ischaemia caused by thrombo-sis or embolism and whether the latter origi-nates from an atherosclerotic plaque or the

1.8

ULTRASOUND

M. Impagliatelli, M. Pacilli, F. Nemore, S. Lorusso, M. Maiorano, T. Scarabino

heart (in this last case an echocardiographic ex-amination must be performed).

Clinical and medical imaging correlations canbe either positive (cerebral neurological sympto-matology corresponds to a vascular lesion demon-strated by ultrasound) or negative (no symptomswith a positive ultrasound examination). Thisclinical presence of signs and symptoms is in partbased upon the presence or absence of antero-grade cerebral blood flow and the competency ofthe collateral vascular pathways (which in turndepend on such variables as systemic blood pres-sure, pCO2, pO2 and packed cell volume).

The importance of the collateral vascularcircuits lies in the fact that they underlie a num-ber of different types of symptoms, even in thepresence of morphologically similar obstruct-ing lesions. These circuits usually develop pro-gressively, and for this reason sudden vascularocclusions cause more serious consequencesthan gradually developing ones.

The most important anastomotic network isthe vascular circle of Willis. The posterior ver-tebrobasilar vascular circuit compensates fordeficits in the two anterior carotid circuits bymeans of the posterior communicating arteriesand vice versa. The anterior communicating ar-tery on the other hand, connects the anteriorcirculation via this anastomosis between thetwo cerebral hemispheres.

In certain cases, due to vascular variations inthe circle of Willis, the collateral circulation ofthis network will not be complete due to devel-opmental atresia of one or more of the commu-nicating arteries. This anatomical variation con-stitutes an unfavourable prognostic factor incases of acquired cerebrovascular occlusion.

Other pertinent collateral circuits include:– the orbital branches of the external carotid

artery anastomosing with the ophthalmic ar-tery which in turn anastomoses with the in-ternal carotid artery;

– the branches of the external carotid arterysuch as the muscular branches of the occipitalartery, anastomosing with muscular branchesof the vertebral artery;

– the anastomotic branches between the sub-clavian artery and the external carotid arteryon the side of unilateral internal carotid oc-

clusion and the patent internal carotid arteryon the contralateral side;

– the leptomeningeal anastomoses betweenthe terminal branches of the principal cere-bral arteries (flowing from patent vesselsthrough their respective leptomeningealconnections in a retrograde direction intothe occluded vascular network);

– the anastomosis of vessels of the dura materconnecting branches of the external carotidartery with the internal carotid arteries andthe vertebral arteries;

– the intraparenchymal anastomoses betweenvessels within the basal ganglia; and

– the anastomoses between the anterior andposterior choroidal arteries.The formation of an efficient collateral net-

work is naturally negatively influenced by an-terograde cerebral vascular flow sustained byadequate systemic arterial pressure as well as bysome degree of patency in the remaining vascu-lar circuit.

The haemodynamic rule is that cerebral flowremains constant so long as mean arterial pres-sure is above 60-70 mm Hg. For lower arterialpressure values the blood flow drops, in partbecause the cerebral vascular bed loses its self-regulation capacity. In chronic hypertensivesubjects, the threshold values below whichcerebral flow starts to drop are higher thanthose in normotensive subjects.

In the regulation of cerebral flow, importantroles are also played by pCO2 (e.g., flow in-creases with hypercapnia), pO2 (e.g., its reduc-tion causes a drop in arterial oxygen saturationthat results in an increase in cerebral flow andthe extraction of oxygen from the blood). It isalso inversely proportionate to packed cell vol-ume, as a high packed cell volume reduces thebrain’s oxygen needs and the cerebral flow reg-ulates itself as a consequence.

TECHNIQUES

Ultrasound examinations of the vascular sys-tem can be divided into two techniques:– B-Mode echotomography: gives a picture of

the vessel and its walls; high frequency trans-


ducers (7.5-10 MHz) and high definition areused.

– Doppler-effect echotomography: dedicatedto the analysis of endovascular haemody-namic phenomena.This second group can be subdivided into

equipment with continuous emission of the ul-trasound band (CW or Continuous Wave) andpulsating emission (PW or Pulsed Wave). CWis a technique in which the transducer func-tions simultaneously as an emitting and receiv-ing probe and PW is a technique in which thetransducer functions alternatively as an emit-ting and receiving probe with a pulse repetitionfrequency (PRF) that can be regulated by theoperator.

CW equipment has the property that while iteasily identifies all vessels on the pathway of theultrasound emitted by the exploring probe, itcannot separate the signals from the various ves-sels, unless by means of technical intervention(e.g., when an artery and a vein superimpose up-on one another, the compression pressure exert-ed by the probe operator with the intrument in-terrupts the venous flow and permits the isola-tion of the arterial Doppler signal); moreover,with CW is not possible to discriminate thedepth from which the reflected signals originate.

PW appliances include:– Echo-Doppler (Duplex): in such appliances,

the positioning of the sample volume takesplace using the echotomography image as aguide. The transducers of these electronicprobes (convex, linear, sectorial) act in thesame way as do normal transducers used inB-mode ultrasound on all lines of vision withthe exception of one which functions alter-natively as an emitter and a receiver. In this,at a depth chosen by the operator, the sam-ple volume is positioned (within the vessel tobe examined) and velocitometric analysis isperformed (spectral analysis). This takesplace in real time and appears on the moni-tor by means of a system of Cartesian axes inwhich the time variable is on the abscissa,whereas the various frequencies (speeds) ap-pear on the ordinate. What is visualized isthe number of red blood cells that flow atany speed, corresponding to the width of the

Doppler signal. The flow moving towardsthe transducer is shown by the position ofthe spectrum above the base line, whereasthe flow moving away from the transducer iswritten below the base line.

– Echo-Colour-Doppler (ECD): This is a fur-ther innovative development of Duplextechniques. With this type of appliance, flowinformation is obtained from numeroussample volumes positioned throughout all orpart of the area explored, along each line ofvision of the image (not on one line alone).The Doppler signals gathered are subse-quently correlated by the computer with thecolour code that will indicate the flow direc-tion on red and blue chromatic scales: con-ventionally approaching flow is coded in redand the flow moving away is coded in blue.By selecting a precise line of vision and sam-ple volume one can obtain the flow spec-trum simultaneously.

– Power-Doppler (PD): This represents the lat-est development of the Colour-Doppler; itshows the width of the signal given by thedensity of the blood cells in movement irre-spective of the angle of incidence of the ul-trasound band and flow direction (Fig. 1.84).A further, innovative aid to ECD and PD in-

vestigations are the recently introduced ultra-sound contrast media (e.g., galactose mi-crobubble suspension administered endove-nously), which have the property of enhancingthe echo-reflectivity of the surrounding blood.They are currently frequently used in the eval-uation of the intracranial vessels (transcranialECD and PD) with the possibility of perform-ing three-dimensional reconstructions of the in-tracranial vasculature using lastest generationappliances (5).

Ultrasound exploration of blood vessels canbe either direct or indirect. In direct explo-rations, the probe is placed over the vessel to beexplored and the information received con-cerns that vessel. The vessels that can be exam-ined in the neck are the common carotid, ex-ternal carotid, internal carotid, subclavian andvertebral arteries, where it is possible to detectobstructions, stenoses, ectasias and alterationssuch as kinking and coiling.

1.8 ULTRASOUND 95

Information obtained from indirect explo-rations does not only concern the vessel ex-plored with the probe, but also haemodynamicvariations that take place up- and downstreamof it. Indirectly, using compression manoeu-vres, it is possible to evaluate the condition ofthe circle of Willis and of the intracranial seg-ment of the internal carotid artery. In particu-lar, it is also possible to explore, for example,the condition of the anterior communicating

artery (probe on the extracranial internalcarotid with simultaneous compression of thecontralateral common carotid artery) and theposterior communicating artery (probe on thedistal vertebral artery with compression of theipsilateral common carotid artery).

Using special indices (such as CR: carotid ra-tio; PPI: Perfusion Pressure Index; RI; resist-ance index, etc) it is also possible to obtain


Fig. 1.78 - 65 year-old male patient with hemiplegia of the leftside with acute onset. Fibroatheromasic plaque at the origin ofthe right internal carotid artery (a) with reduction in the vesseldiameter of more than 50% (b - short axis).

Fig. 1.79 - 79 year-old man with hypertension, diabetes and fib-rillation. Severely atheromasic common carotids with plaquesbulging into the lumen and marked wall alterations (a-b).

a

a

b

b

functional information on the degree of steno-sis, the state of resistance of the cerebral vascu-lar bed and the degree of elasticity of thecarotid tree as a whole.

In Doppler diagnosis of cerebrovascularemergencies, particular attention is paid to thediastolic speed (velocity) of the commoncarotid artery, analysed comparatively on the

two sides. In fact, a slight asymmetry of systolicvelocity can be a normal expression of a differ-ence in calibre of the two common carotid ar-teries. However, asymmetry of the diastolic ve-locity is always pathological and it alone is suf-ficient to diagnose an obstruction of the inter-

1.8 ULTRASOUND 97

Fig. 1.79 - (cont.) Fibroatheromasic plaque with irregular sur-faces in the right carotid bulb and the right internal carotidalong the entire extracranial stretch explored with max. reduc-tion in the vessel diameter greater than 65% (c - long axis, d -short axis).

Fig. 1.80 - 70 year-old male hypertensive patient, with dizzinessfollowing fall. Cerebral CT: left hemisphere ischaemic lacunae.Ulcerated fibrocalcific plaque on the rear wall of the leftcarotid bifurcation.

Fig. 1.81 - 45 year-old male patient with left-side hemiplegia.Thrombosis of the right internal carotid artery.

c

d

nal carotid artery. Low diastolic velocity of thetwo common carotids can be an indirect sign ofan aortic insufficiency or an expression of thearteriocapillary resistance downstream due toeither a reduced parietal compliance (such as isobserved in diabetic patients or in cases of ath-erosclerosis) or to global vascular compression(such as in cerebral oedema).

CLINICAL APPLICATIONS

Although the ECD technique was principal-ly developed in the previous decade, whenfaced with a cerebrovascular emergency it is agood rule to begin the exploration using a CWDoppler and complete it with a pulsed Doppler,including in some cases use of the B-mode tech-nique (2, 4, 6, 8).

A CW Doppler examination gives an accu-rate functional vascular analysis of haemody-namically significant stenosing lesions (stenosisequal to or greater than 70%) and of the occlu-sions of the supraaortic and the endorbital vas-cular structures. The reliability of this methodis very high, with a sensitivity of approximately92% and specificity of approximately 82%.

One particular application of the pulsedDoppler technique is the transcranial Doppler(including transcranial ECD and PD, Fig.1.85) (1), with which it is often possible topenetrate the bony barrier of the skull to ex-plore the large arteries of the circle of Willis.This is done by using compression manoeu-vres to evaluate the intra- and extracranial col-lateral circuits. It can also register severe in-tracranial vascular spasm even when it isasymptomatic and can follow the course ofarterial narrowing with serial recordings; inthis manner, invasive selective angiographymay be avoided and surgery can be under-taken in the critical phase of high flow ve-locity. Bilateral recordings of the flow veloc-ity in the anterior, middle and posterior cere-bral arteries can also aid in the comprehen-sion of flow modes in the collateral arteriesand in stenoses and occlusions of the intra-and extracranial carotid arteries.

With a simple echotomography or onecombined with a pulsed or Colour Doppler,the examination is more localized and is re-stricted to the extracranial vessels (7). This si-multaneously allows the collection of func-tional blood velocity data as well as informa-


Fig. 1.82 - 68 year-old female patient with left side hemiparesisand dizziness. Kinking of the left internal carotid artery withvelocitometric acceleration findings both in the internal carotidartery and downstream (left supraorbital artery).

Fig. 1.83 - 78 year-old female patient, hypertensive, diabeticwith left side hemiparesis with a duration of a few seconds.Coiling of the right internal carotid artery.

tion on the morphology of the vessel wall. Itcan identify both the surface of flat, non-haemodynamically significant atheromatousplaques (Fig. 1.78), and complicated plaques(haemorrhagic, ulcerated, calcified) (Figs.1.79, 1.80), which are usually stenosing andassociated with occlusive and preocclusivethrombus formation (Fig. 1.81). In this lastcase, PD has a higher sensitivity, specificityand diagnostic accuracy than does ECD, as itis able to detect the presence of a still accessi-ble lumen, even with an extremely slowedflow that cannot be detected by ECD (Fig.1.86). ECD therefore provides detailed evalu-

ations of the morphological alterations of thewall due to small and complicated plaques,and, on the basis of the alterations in echogenic-ity, it contributes to the definition of theiratheromatous, fibrous and/or calcific nature(in particular, cholesterine deposits and haem-orrhagic lesions of vessel walls are hypere-choic due to their low density, whereas fibro-calcific plaques are much more reflective). Italso makes it possible to directly visualize anyanomalies of the extracranial vessels, such askinking or coiling (Figs. 1.82, 1.83).

ECD permits a correct diagnosis of lesionsin 96% of cases and consequently has greatersensitivity than conventional selective angiogra-phy in identifying moderately stenotic lesionsand in understanding their nature. It also en-ables the recognition of subintimal haemor-rhages that are not shown on angiography aswell as small ulcerated plaques that sometimesare also difficult to visualize.

CONCLUSIONS

From a certain sense, ED is to a vasculo-pathic patient what the electrocardiogram is to

1.8 ULTRASOUND 99

Fig. 1.84 - Power Doppler of the carotid bifurcation.

Fig. 1.86 - Pseudo-occlusion of the internal carotid artery. ThePower Doppler is able to show a slight flow at an extremely re-duced speed.

Fig. 1.85 - Transcranial Echo-Colour-Doppler. Intracranial cir-culation viewed through the temporal window.

the cardiopathic patient, that is, it is the firstexamination to be performed upon the onset ofischemic signs and symptoms. When faced witha cerebrovascular emergency, once CT has dis-tinguished between haemorrhage and is-chaemia, ED is a reliable choice of primary im-aging modalities for determining the type andsite of extracranial vascular stenotic lesions andfor guiding subsequent therapy.

The three ultrasonographic techniques (CW,ECD and PD) are complementary to one an-other and very useful, in part due to their non-invasive nature. They are not however consid-ered a substitute for angiography, which atpresent remains essential for the definitivestudy of the intracranial blood vessels, especial-ly a focused therapeutic approach where in-travascular treatment is an option.

REFERENCES

1. Bazzocchi M, Quaia E, Zuiani C et al: Transcranial Dop-pler: state of the art. Eur J Radiol 27:141-148, 1998.

2. Bendick PJ, Brown OW, Hernandez D et al: Three-Dimen-sional Vascular Imaging using Doppler Ultrasound. Am JSur 176:183-7, 1998.

3. Bonita R: Epidemiologia dell’ictus. The Lancet 9:387-390,1992.

4. Dauzat M: Pratique de l’ultrasonographie vasculaire. Ed.Vigot Paris, 1986.

5. Postert T, Braun B, Pfundtner N et al: Echo contrast-enhanced three-dimensional Power Doppler of intracranialarteries. Ultrasound Med Biol 7:953-956, 1998.

6. Rabbia C, De Lucchi R, Cirillo R: Eco-Color-Doppler Va-scolare. Ed. Minerva Medica, 91-94, 1995.

7. Steinke W, Meairs S, Ries S, Hennerici M: Sonographic As-sesment of Carotid Artery Stenosis, comparison of PowerDoppler Imaging and Color Doppler Imaging. Stroke27(1):91-4, 1996.

8. Tonarelli A: Diagnostica per Immagini della carotide extra-cranica: Ecografia ed Eco-Doppler. Rivista di Neuroradio-logia 9 (suppl. 2):11-26, 1996.


101

INTRODUCTION

The development of neuroimaging tech-niques has in part been driven by the need todiscover and perfect methods for more rapidand accurate diagnosis of suspected cere-brovascular pathology. As a result, in recentyears diagnostic and therapeutic protocols havechanged by virtue of theses recent innovations.In addition, progress in the understanding ofcerebral ischaemic pathology has clearifiedmany of the physiopathological mechanisms as-sociated with ischaemic tissue damage, whichin turn have made it possible to develop morespecific and effective treatment options. Theneuroradiological diagnostic techniques avail-able in clinical practice today permit a non-in-vasive and definitive diagnostic evaluation asearly as the hyperacute phase of ischaemicstroke, in order to properly select those pa-tients that may best be amenable to treatmentwith thrombolytic agents (24).

In the neuroimaging diagnostic field, MRIplays a priority role given its many applicationsand higher sensitivity (82%) as compared toCT (60%) in the early detection of tissuechanges caused by an ischaemic event (15).That said, CT still plays a fundamental diag-nostic and screening role in hyperacute stroke

patients given that it is more sensitive that MRIin demonstrating the presence of haemorrhag-ic foci.

With the perfusion, diffusion, spectroscopyand MR angiographic techniques, MRI repre-sents an important arsenal for studying is-chaemic stroke (within the first six hours) andthe tissue changes caused by an occlusivethromboembolic event. The rational integra-tion of the various MRI methods available per-mits a non-invasive, rapidly acquired diagnosticanalysis of the patient presenting with signs ofcerebral ischaemia, especially when it is aimedat optimally selecting patients for a specifictreatment such as thrombolysis (24, 26).

MR angiography (MRA) in particular haswon itself a well-defined role in diagnosticprotocols evaluating cerebral ischaemia notonly as a screening method, but also as an al-ternative to selective digital subtractive an-giography (DSA) of the brachiocephalic andcerebral vessels. At present MRA constitutesan indispensable diagnostic method, whichwhen integrated with basic MRI is the meansof choice for studying the cerebral vessels withthe aim of locating the site of vascular stenosesand occlusions as well as their effects upon theunderlying brain tissue. Collectively the vari-ous MRI techniques are currently able to ac-

1.9

MR ANGIOGRAPHY

A. Carella, P. D’Aprile, A. Tarantino

quire high quality images of the intra- and ex-tracranial cerebral blood vessels that not onlysupply qualitative data, but also yield informa-tion on the relative velocity and direction ofthe blood flow.

TECHNIQUES

The techniques used are unenhanced time offlight (TOF) and phase contrast (PC) 2D and3D (two and three dimensional) MR angiogra-phy and contrast enhanced MR angiography(CE-MRA).

Time of flight (TOF)

The techniques based on the principles ofTOF MR angiography are widespread and areeasily performed at the same time as the basicMR scan. They are based on “inflow” phenom-ena capable of creating good flow-related con-trast enhancement between the signal of sta-tionary tissues and that of blood protons (i.e.,blood) in movement. On entering the imagingvolume under examination, the protons havenot yet been subject to spatially selective ra-diofrequency pulses and they produce a muchhigher signal than that given by stationary pro-tons within the imaging volume, which are par-tially saturated by previous radiofrequency(RF) pulses.

The degree of increase in flow signal de-pends on many parameters that are partly spe-cific to the tissues examined (T1 relaxationtime) and partly dependent on the acquisitionparameters used (TR, TE, flip angle, etc.), thetype of flow (velocity, turbulence, etc.) and onthe geometry of the acquisition volume in com-parison with the direction of the blood flow (1).

The 3D TOF technique is especially usefulin studying the arterial circulation, whereas the2D technique, which has a lower spatial defini-tion than 3D, is particularly useful in studyingslow (venous) flow. TOF techniques can besupplemented by techniques able to improvethe suppression of stationary background tissuesignal, thus increasing the relative contrast of

the flow signal using an additional “off reso-nance” RF pulse that acts on the stationary pro-tons, saturating them selectively in comparisonto those in movement that do not react to thispulse (Magnetization Transfer Contrast: MTC)(4, 6). Other possibilities of accomplishing thisare to reduce intravoxel dephasing and satura-tion of the spins with the tilted optimized nonsaturation excitation (TONE) and multipleoverlapping thin slab acquisition (MOTSA)techniques. In the TONE method, the flip an-gle is gradually increased as the flow proceedstowards the centre of the acquisition volume inorder to compensate for the reduction in longi-tudinal magnetization of the spins in move-ment, whereas the MOTSA technique uses anacquisition of multiple volumes that interleavewith one another (7, 16-18).

TOF techniques have limitations that aremainly characterized by two situations: the firstsource of error is caused by the presence in theacquisition volume of stationary tissues that canappear hyperintense (e.g., gadolinium enhance-ment, meta-haemoglobin, fat and oily sub-arachnoid contrast media) and that can there-fore be wrongly interpreted as blood flow sig-nal; the second source of error considers thepossibility that vascular structures may appearisointense and therefore not emit blood flowsignal using certain acquisition parameters.This latter situation can depend on a series oftechnical factors (e.g., TE, TR, flip angle, direc-tion of blood flow, thickness of the acquisitionlayer and acquisition volume). For example, theinadvertent use of a high TE value can be oneof the main causes of a lack of vascular signal;fortunately, many MR systems only allow a vari-ation in TE values within narrow limits.

It should also be stressed that in 3D-TOF ac-quisitions, the anatomical structure of interestmust be correctly positioned within the acquisi-tion volume, in other words in the lower third ofthe slab (where the inflow effect is highest).

Phase Contrast (PC)

This technique capitalizes upon the phaseeffects that occur when protons move along the


direction of a magnetic field gradient. PC MRangiography techniques allow the quantifica-tion of flow velocity and volume as well as thedirection of the blood flow. In general, thismethod entails long acquisition times with widefields of view, and it is therefore the techniqueof choice in the study of arteriovenous fistulasand AVM’s. In fact, PC and TOF MR angiog-raphy are complementary and provide for amore accurate diagnosis when combined.

Contrast Enhancement (CE)

Dynamic MR angiographic techniques usethe intravascular phase of a bolus of paramag-netic contrast medium (e.g., gadolinium) inject-ed intravenously, in association with the acqui-sition of ultrafast sequences dependent on T1relaxation times (9, 19, 22). The use of intra-venous contrast medium causes a significant re-duction in the T1 relaxation time of the bloodwith a considerable increase in the intensity ofthe blood flow signal as well as the relative con-trast between blood and the stationary tissues.It goes without saying that in order for the con-trast medium to have a maximum effect, it re-quires an optimal choice of the time interval be-tween the intravenous injection of the contrastmedium bolus and image acquisition.

The main drawback of this technique is anincrease in stationary tissue signal and the si-multaneous opacification of the veins. However,this limitation can be reduced by the use of veryshort scanning times (e.g., a partial K spacetechnique as in “key-hole” sequences) and byrapidly administering the contrast medium as abolus during data acquisition in order to ac-quire the images when the contrast mediumreaches its greatest intravascular concentration.

MR ANGIOGRAPHY OF THE SUPRAAORTIC VESSELS

Technique

In recent years MRA has enabled an accurateand non-invasive diagnostic analysis of the

supraaortic vessels, which together with Dopplerultrasound studies in the presurgical phase haslimited the use of invasive conventional DSA toselected cases.

Although PC MR angiography can be uti-lized to examine the supraaortic vessels, TOFtechniques are more commonly employed. Gen-erally speaking, for studies of the carotid bifur-cation a transverse acquisition plane with a 3D-TOF technique is used to reduce the saturationeffects, however, this technique has certain lim-itations due to its long acquisition times andconsequently the associated motion artefacts(14). The proposal made by Prince in 1994 (19)was therefore accepted with enthusiasm; theproposal involved using contrast-enhanced 3DMR angiography to capture the passage of a bo-lus of paramagnetic contrast material throughthe inaging volume in order to study thesupraaortic vessels. This led to the perfection ofa technique capable of examining the extracra-nial vessels including the aortic arch, the originsof the supraaortic vessels and the neck vessels(13, 23). In particular, extremely fast volumet-ric acquisitions are used directly in the coronalplane during the injection of the contrast medi-um bolus, over acquisition times of approxi-mately 15-30 seconds. In this technique, giventhat the signal is produced mainly by the ad-ministered contrast agent, it is mandatory to syn-chronize the image acquisition with the injec-tion of the contrast agent in order to obtainmaximum arterial filling during the central por-tion of acquisition. The advantage of thismethod lies in the speed of the examination andin the possibility of now covering the entirelength of the brachiochephalic vessels from theirorigins through their proximal intracranial seg-ments (Figs. 1.87, 1.88).

Clinical applications

The cervical carotid and vertebral arterieswere the first vascular segments for the applica-tion of MR angiography. Numerous studies ofMRA show its high sensitivity in detectingcarotid stenoses, 92-100%, with a specificity of64-100% (2, 5, 14).

1.9 MR ANGIOGRAPHY 103

Slow and turbulent flow can cause a signaldrop-out within the vessel under study, with aconsequent overestimation of the degree ofstenosis. This represents an important limita-tion in the use of standard 2D- and 3D-TOFMR angiographic techniques.

The recent introduction of CE 3D-TOFMRA has resolved certain problems concerningthe correct estimation of the degree of vascularstenosis and the evaluation of the origins of thesupraaortic vessels (Fig. 1.89). Recent studieshave shown the CE 3D-TOF technique to bemore accurate than standard 2D- and 3D-TOFacquisitions (14, 23).

Stenotic-occlusive atheromatous pathologyThe 3D-TOF MR angiographic technique is

currently considered the best available methodfor defining the morphology of stenotic-occlu-sive lesions of the carotid and vertebral arteries.

To avoid problems with the progressive satura-tion of the spins when using 2D- and 3D-TOFtechniques, one should preferably use an acqui-sition plane perpendicular to the longitudinalaxis of the vessel being examined; consequent-ly, both the carotid and the vertebral arteriesmust be examined in the axial plane (Fig. 1.90).The 3D-TOF technique can also be used with abolus injection of a contrast agent (gadolini-um), using rapid volumetric acquisitions in thecoronal plane (Fig. 1.91). The disadvantage ofthis technique is in its slightly invasive nature(linked to the intravascular administration ofgadolinium) and in its limited spatial resolutionas compared to the traditional 3D-TOF methodutilizing a transverse plane acquisition.

For stenoses greater than 70%, a signal drop-out at the stenotic segment is described in boththe 2D- and 3D-TOF MR angiographic tech-niques. In cases of preocclusive high grade


Figs. 1.87-1.88 - Dynamic MRA scan of the epiaortic vessels acquired in the coronal plane with high definition ultrafast T1 sequences(AT: 28 seconds); note the excellent demarcation from the emergence of the epiaortic vessels.

stenosis, the 2D-TOF technique may provemore effective than the 3D because its sensitivi-ty to slow flow makes it possible to identifyresidual flow distal to the narrowing, whereasthe 3D technique can give an erroneous pictureof occlusion with a complete absence of distalflow signal.

Vascular dissectionsStenotic-occlusive pathology of the internal

carotid artery and the vertebrobasilar vessels isbeing increasingly seen as cases presenting asneurological and neuroradiological emergen-cies. With regard to ischaemic strokes, particu-lar attention must be paid to the role of dissec-

tion of the cervical arteries. These dissectionsare often under recognized as they typically af-fect young patients who commonly lack theusual vascular risk factors (2%).

Increased diagnostic suspicion is often sug-gested by the appearance of headache, stiffneck, neck pain, Horner’s syndrome and dizzi-ness in the dissection of the vertebral artery.Carotid and vertebral dissections can be diag-nosed with relative ease using simple MR andMRA acquisitions (Fig. 1.92) (20). Levy et al(12) reported a sensitivity and specificity of95% and 98%, respectively, for the detectionof cervical internal carotid dissection.

Both T1- and T2-weighted spin echo (SE)images and the single partitions of 3D-TOFMRA permit the detection of the character-istic findings of vascular dissection, includ-ing the presence of a flow void in the resid-ual lumen and haemoglobin hyperintensitywithin the subintimal haematoma. An alter-native to the TOF method is a combinationof PC MRA and a comparative T1-weightedSE study with suppression of the fat signalfor the effective visualization of the intramu-ral thrombus.

With regard to dissections of the vertebralartery, although MR angiography is less sensitivethan that of the internal carotid artery, it is feltto be preferable to invasive selective conven-tional DSA as the double lumen caused by thesubintimal dissection can cause the detachmentof emboli in patients undergoing catheteriza-tion.

MR angiography plays an important role inthe follow-up of these lesions, which usuallysuccessfully heal after treatment with anticoag-ulants.

INTRACRANIAL VESSELS

Technique

The most frequently used technique forstudying the intracranial vessels is 3D-TOFMRA. The acquisition volume is oriented trans-versally and covers the vessels of the circle ofWillis and the proximal segments of the major


Fig. 1.89 - Dynamic CE MRA: presents a serrated stenosis ofthe right subclavian artery and a stenosis on the bifurcation ofthe right carotid artery.


Fig. 1.90 - Dynamic MRA: a) panoramic study of the epiaorticvessels; b) selective reconstruction of the left carotid bifurca-tion, which appears normal; c) selective reconstruction of theright carotid bifurcation in which one can observe the pres-ence of an atheromasic plaque at the beginning of the right in-ternal carotid artery. d) comparative study of the right carotidbifurcation with 3D-TOF technique and axial acquisitions:note a reduction in flow signal by the plaque; echo-Dopplerfinding: soft stenosing plaque at the origin of the right internalcarotid artery.

a

c

d

b

cerebral arteries; in order to obtain good spatialand contrast resolution, the thickness of the in-dividual scans must be relatively small (0.8 - 1.5mm). Optimal intravascular contrast is ob-tained using the variable flip angle technique

(TONE) coupled with transverse magnetiza-tion transfer (MTC) overlay for better suppres-sion of the perivascular stationary tissue signal(4, 16). For the separate study of the arterialand venous systems, it is necessary to correctlyposition prespatial saturation bands proximalto the flow signal to be eliminated.

In general, contrast agents are not used forstudying the cerebral vessels, with the excep-tion of certain cases where the intracranialpathology demands that intravascular contrastmaterial be specifically used for the study ofslow vascular flow.

CLINICAL APPLICATIONS

Stenotic-occlusive pathologyIn recent years the development and clini-

cal application of MRI in the study of is-chaemic stroke patients has provided much in-formation on cerebral perfusion (perfusionMR), metabolic integrity (spectroscopy MR),variations in cerebral diffusion coefficients(DWI) and information on the morphology ofthe intra- and extracranial vessels using MRangiography (2, 25).

In cases of ischaemic stroke, MR angiographyplays a potentially important role. In the hypera-cute phase of cerebral ischaemia, integrating themorphological and metabolic imaging informa-tion in cases of vascular stenosis or occlusionprovides all the data required to make specifictherapeutic choices (Figs. 1.93, 1.94).

MR angiography provides a good represen-tation of the first and second order vessels ofthe circle of Willis, but has limitations in thestudy of smaller vessels (Figs. 1.95, 1.96, 1.97,1.98). In addition to spatial definition, limita-tions include an accurate estimation of the de-gree of high grade stenoses and the accuratedistinction between high grade stenoses andfrank occlusions (8, 11).

The carotid siphon can benefit from an MRangiographic evaluation, although care must betaken to avoid errors in overestimation of thepathological changes due to the reduction inflow signal as a result of turbulence. Anotherproblem is posed in some cases by the flow tur-


Fig. 1.91 - Dynamic MRA scan of the epiaortic vessels: a) steno-sis on the bifurcation of the right carotid artery and occlusionat the start of the left internal carotid artery; b) the specificstudy using the 3D-TOF technique better demarcates the pres-ence and entity of the stenosis at the start of the right externalcarotid artery.

a

b

bulence present at vascular bifurcations, whichcan erroneously be interpreted as stenoses. Theadministration of contrast media (gadolinium)has been used to resolve these problems of par-tial signal loss.

Collateral pathways to the circle of Williscan be evaluated using the 3D-TOF techniqueby means of an appropriate arrangement of theselective prespatial saturation pulse; an alterna-tive is the PC method that provides informa-tion on the direction of blood flow (25).

Occlusive venous pathologyWith suspected venous thrombosis, MR

venography is the diagnostic examination ofchoice. This technique is used together with theconventional SE MR scan, which permits thedetection of associated parenchymal abnormal-ities (e.g., venous infarction) as well as the ab-normal signal of vascular thrombosis or the ab-


Fig. 1.91 - (cont.) – c) Another case, medium grade stenosis onthe right carotid bifurcation and serrated stenosis with presenceof plaque at the beginning of the left internal carotid artery; d ande) selective reconstruction of the carotid bifurcations.

c

d

e


Fig. 1.92 - Dissection of the left vertebral artery. a) Basic SE T2MR scan: left cerebellum ischaemic lesion; b and c) MRA: ab-sence of signal in the last stretch of the left vertebral artery; d) single base partition: presence of hypointense parietalthrombus, in acute phase, at the vertebral artery; e) check-upMRA (15 days later): partial recanalization of the vessel.

a

b

c

d

e

Fig. 1.92 - (cont.) f) Comparison with DSA.


f

a

b

c

Fig. 1.93 - Hyperacute phase ischaemia. a) Basic SE T2 MRI:negative finding; b) DW MR image; ischaemic lesion in left insu-lar-parietal location; c) MRA of the vessels of the circle of Willis:occlusion of the bifurcation of the left Sylvian artery.

sence of normal signal void within the dural ve-nous sinuses. Toward this same aim, T2-weight-ed SE images acquired perpendicular to thedural venous sinuses are recommended for amore accurate supplemental study.

In MR angiography, the high signal of thethrombus can give false negative results; insuch cases a comparative study using T1- andT2-weighted SE images and the application ofpresaturation bands, as well as use of the PC tech-


Fig. 1.94 - Hyperacute phase ischaemia. a) and b) TSE-HASTE images, a blurred swelling caused by the oedema of the cortex in aright parasagittal frontal position with small hyperintensities near the signal; c and d) DW images: widespread ischaemic focus in theterritory of the right anterior cerebral artery.

c

d

a

b

nique are in combination typically able to dis-pel diagnostic doubts (17).

AneurysmsIn the acute stage of subarachnoid haemor-

rhage, the examination of choice is CT, followed by invasive conventional selectiveDSA to reveal the presence of one or moreaneurysms and to visualize the anatomy of theindividual aneurysms; MRI and MRA have sec-ondary roles during this acute phase.

MRA is the examination technique of choicefor screening patients with family histories of

such potentially heritable pathology as theaneurysms associated with polycystic kidneydisease, or in cases where there is a relativelyhigh association of aneurysms such as aorticcoarctation (21). Studies performed thus farshow that MRA is able to detect 3-4 mmaneurysms with approximately 86-90% sensi-tivity, and with 100% specificity (3, 10) (Fig.


Fig. 1.94 - (cont.) e and f) MRA of the vessels of the circle ofWillis: occlusion at the start of the right anterior cerebral arteryand serrated stenosis in segment M2 of the right Sylvian artery.

Fig. 1.95 - Left insular-temporal-parietal ischaemic lesion: a) ba-sic SE T2 MRI; b) 3D-TOF MRA of the vessels of the circle ofWillis; occlusion in segment M2 of the left Sylvian artery.

e

f

b

a

1.99). Smaller aneurysms are often not visibledue to MR angiography’s limited spatial resolu-tion and because of the irregular flow dynamicswithin small aneurysms. And, when studyinggiant aneurysms the slow and turbulent flowcan reduce the intraluminal signal and cause an

underestimation of the dimensions of the lu-men of the aneurysm.

3D-TOF MRA has recently been used instudying aneurysms treated with Guglielmi’s


Fig. 1.96 - Left temporooccipital ischaemia: a) basic SE T2 MRI;b) MRA of the vessels of the circle of Willis: occlusion in the P1segment of the left posterior cerebral artery.

Fig. 1.97 - Right parietal ischaemia: a) basic SE T2 MRI; b) 3D-TOF MRA of the vessels of the circle of Willis: absence of flowsignal in the right carotid siphon with partial revascularizationof the right Sylvian artery through the circle vessels.

b

a

a

b


Fig. 1.97 (cont.) - c) MRA of neck vessels: occlusion at the be-ginning of the right internal carotid artery.

Fig. 1.98 - a) Basic SE T2 MRI; blurred signal hyperintensity inright occipital location; b) SE T1 image after gadolinium: non-homogeneous contrast enhancement due to blood-brain barri-er damage caused by the presence of an acute ischaemic area;c) MRA of the vessels of the circle of Willis: stenosis in theproximal segment of the right posterior cerebral artery.

c

a

b

c

detachable embolization coils. This has showna good correspondence between MRA and se-lective DSA with regard to the evaluation ofaneurysms occluded with coils. It has in factbeen possible to evaluate any residualaneurysm neck and flow within the residualaneurysmatic sack if present. However, to befair, certain vascular details are obviously lesseasy to evaluate in the single MRA partitions.

Arteriovenous malformationsGenerally speaking, MRA used in combina-

tion with MRI is sufficient for the detection ofmost cerebral arteriovenous malformations.The TOF MRA technique gives good documen-tation of the major arterial feeding arteries (Fig.1.100). Venous drainage and the central nidusare better studied using PC MRA. The use of in-travenous gadolinium improves visualization ofthe venous vascular components of AVM’s.

MRA also permits in-depth studies of thenidus, its dimensions and its relationship withthe surrounding neural tissue, which are im-portant elements for treatment planning. Thistechnique is also useful during follow-up aftertherapy; invasive selective DSA is neverthelessrequired in order to obtain precise images ofthe exact anatomical architecture and the dy-namic aspects of the AVM.

CONCLUSIONS

MRA is an important non-invasive methodfor studying the brachiocephalic and cerebralblood vessels. Its main application in neuro-radiological emergencies is for the evaluation


Fig. 1.99 - 3D TOF MRA of the vessels of the circle of Willis:presence of an aneurysm on the anterior communicating artery.

b

a

Fig. 1.100 - AVM: a) basic SE T2 MRI: numerous serpigenousimages with signal void in the left temporoparietal region; b) 3DTOF MRA: presence of a large AVM, supplied by branches orig-inating from the Sylvian artery and left posterior cerebral artery.

of cerebral circulation in suspected cases ofischaemic stroke or thrombosis of the duralvenous sinuses. In such cases, MRA can beperformed together with conventional MRIaimed at obtaining a rapid and complete di-agnostic analysis of the problem, thereby al-lowing optimal specific treatment choices tobe made. It is also widely used to screen forcerebral aneurysms in high risk groups, andmore recently to monitor aneurysms follow-ing treatment with Gugielmi’s detachable em-bolization coils.

It is important to underline the importanceof having access to high performance MRI sys-tems that allow the rapid execution of both thestatic conventional imaging as well as the an-giographic acquisitions.

REFERENCES

1. Anderson CM, Edelman RR, Turki PA: Clinical MagneticResonance Angiography. Raven Press New York, 1993.

2. Atlas SW: MR angiography in neurologic disease. Radio-logy 193:1-6, 1994.

3. Atlas SW, Sheppard L, Godberg HI et al: Intracranialaneurysms: detection and characterization with MR angio-graphy with use of an advanced post-processing techniquein a blinded-reader study. Radiology 203:807-814, 1997.

4. Atkinson D, Brant-Zawadzki M, Gilliam G et al.: ImprovedMR angiography: magnetization transfer suppression withvariable flip angle excitation and increased resolution. Ra-diology 190:890-894, 1994.

5. Bowen BC, Quencer RM, Margosian P et al.: MR angio-graphy of occlusive disease of the arteries in the head andneck: current concepts. AJR 162: 9-18, 1994.

6. Edelman RR, Ahn SS, Chien D et al.: Improved time-of-fligth MR angiography of the brain with magnetizationtransfer contrast. Radiology 184: 395-399, 1992

7. Furst G, Hofer M, Steinmetz H et al.: Intracranial stenooc-clusive disease: MR angiography with magnetization tran-sfer and variable flip angle. AJNR 17:1749-1757, 1996.

8. Heiserman JE, Drayer BP, Keller PJ et al.: Intracranial vascu-lar stenosis and occlusion: evaluation with tree-dimensionaltime-of-flight MR angiography. Radiology 185:667-673, 1992.

9. Kim JK, Farb RI, Wright GA: Test bolus examination in thecarotid artery at dynamic gadolinium-enhanced MR angio-graphy. Radiology 206:283-289, 1998.

10. Korogi Y, Takahashi M, Mabuchi N: Intracranial aneury-sms: diagnostic accuracy of MR angiography with evalua-tion of maximum intensity projection and surce images. Ra-diology 199:199-207, 1996.

11. Korogi Y, Takahaski M, Nakagawa T et al.: Intracranial va-scular stenosis and occlusion: MR angiography findings.AJNR 18:135-143, 1997.

12. Levy C, Laissy JP, Raveau V: Carotid and vertebral arterydissections: three dimensional time of fligth MR angio-graphy and MR versus conventional angiography. Radio-logy 190:97-103, 1994.

13. Levy RA, Prince MR: Arterial-phase three-dimensionalcontrast-enhanced MR angiography of the carotid arteries.AJR 167:211-215, 1996.

14. Litt AW, Eidelman EM, Pinto RS et al.: Diagnosis of caro-tid artery stenosis: comparison of 2D time of fligth MR an-giography with contrast angiography in 50 patients. AJNR12:149-154, 1991.

15. Mathews VP, Elster AD, King JC et al: Combined effects ofmagnetization transfer and gadolinium in cranial MR ima-ging and MRA. AJR 164:167-172, 1995.

16. Mattle HP, Wentz KU et al: Cerebral venography with MR.Radiology 178:453-458, 1991.

17. Mohr JP, Biller J, Hilal SK et al: Magnetic resonance ima-ging in acute stroke. Stroke 26:807-812, 1995.

18. Parker DL, Blatter DD: Multiple thin slab magnetic reso-nance angiography. Neuroimag Clin North AM 2:677-692,1992.

19. Provenzale JM: Dissection of the internal carotid and ver-tebral arteries: imaging features. AJR 165:1099-1104, 1995.

20. Prince MR, Grist TM, Bebatin JE et al: 3D contrast MR an-giography. Springer-Verlag (New-York) 1997.

21. Ruggeri PM, Poulos N, Masaryk TJ et al: Occult intracra-nial aneurysms in polycystic kidney disease: screening withMR angiography. Radiology 191:33-39, 1994.

22. Sardanelli F, Zandrino F et al: MR angiography of internal-carotid arteries:breath-hold gd-enhanced 3D fast imagingwith steady-state precession versus unenhanced 2D and 3Dtime-of-fligth techniques. J Cat 23:208-215, 1999.

23. Scarabino T, Carriero A et al: MR angiography in carotidstenosis: a comparison of three techniques. Eur J Radiol28:117-125, 1998.

24. Sorensen AG, Buonanno FS, Gonzales RG et al: Hypera-cute stroke: evaluation with combined multisection diffu-sion-weighted and hemodynamically weighted echoplanarMR imaging. Radiology 199:991-401, 1996.

25. Stock KW, Wetzel S, Kirsch E et al: Anatomic evaluationof the circle of Willis: MR angiography versus intraarte-rial digital subtraction angiography. AJNR 17:1495-1499,1996.

26. Warach S, Gaa J et al: Acute human stroke studied by who-le brain echo planar diffusion-weithted magnetic resonanceimaging. Ann Neurol 37:231-241, 1995.


117

INTRODUCTION

The relatively recent advent of sophisticatedimaging techniques such as CT and MR has dra-matically reduced the demand for conventionalinvasive selective cerebral angiography in radio-logical diagnosis. Despite the fact that conven-tional angiography is now considered comple-mentary to other techniques in neurologicalemergencies, it has been shown not to be com-pletely replaceable because there are certainquestions that angiography alone can answer.

In recent years, there has been a return to theuse of angiography based on the improvement inthe technique’s safety, speed and sophistication(e.g., hard- and software improvements, atrau-matic catheterization materials, and new low os-molarity contrast agents), and on the progres-sively increasing experience of vascular interven-tional radiology treatment techniques (8). Thislast factor has led to angiography being consid-ered as having a dual purpose: an instrumentused in both diagnosis and therapy.

CLINICAL INDICATIONS

The clinical indications for emergency an-giography are cerebral ischaemia and haem-

orrhage, as well as some forms of cranial trau-ma and thrombotic pathology of the venousstructures. The initial diagnostic evaluation isnevertheless left to non-invasive methodssuch as CT, MR and Doppler ultrasound,which are now able to satisfy the most urgentdiagnostic requirements. Generally speaking,angiography is presently used in those casesin which non-invasive techniques have ex-hausted their usefulness, and, above all, whentreatment using endovascular techniques isbeing considered.

Cerebral ischaemia

In cerebral ischaemia, depending on whetherit manifests itself as TIA or frank infarction, an-giography is not routinely used except in specif-ic cases during certain time periods followingthe ischaemic ictus.

a) Transient ischaemic attacks: TIA’s do notusually constitute an angiographic emergency;patients with TIA’s are typically subjected to an-giography only after a certain period of timeduring which the clinical evolution and the lessinvasive diagnostic techniques (e.g., ultrasound)have indicated the presence of a vascular lesionthat might be amenable to surgery. Although in-

1.10

CONVENTIONAL ANGIOGRAPHY

F. Florio, M. Nardella, S. Balzano, V. Strizzi, T. Scarabino

frequently encountered, angiographic examina-tions can be mandatory in patients sufferingfrom repeated ischaemic attacks and having anon-invasive imaging diagnosis of subtotal oc-clusion of one of the cervicocranial vessels; insuch cases urgent surgery or angioplasty may beable to prevent total vascular thrombosis.

b) Cerebral infarction: Angiography is rarelyused today in cases of frank cerebral infarction,and is in any case usually delayed until partialfunctional clinical recovery is observed.

Trends recently have pointed towards utiliz-ing very early angiographic examinations, with-in hours following the acute ischaemic event,when the clinical syndrome can be attributed toan arterial occlusion that may be susceptible totreatment using transcatheter fibrinolysis. Thisis one of the more recent innovations of inter-ventional neuroradiology, although its real clin-ical efficacy merits further investigation (2).

Cerebral haemorrhage

Angiography plays a more important role incases of cerebral haemorrhage.

a) Parenchymal haemorrhages do not usuallyrequire angiographic analysis when the originof the haemorrhage is thought to be sponta-neous (i.e., elderly patient with hypertension).However, when clinical and anatomical condi-tions favour a different aetiology for the haem-orrhage (e.g., relatively young patient, nor-motensive, atypical position, etc.), angiographybecomes mandatory and should be performedurgently, especially when the haemorrhage de-mands emergency surgery.

b) In cases of epidural/subdural haemor-rages emergency angiography has varying diag-nostic importance. It is unusual for posttrau-matic epidural/subdural haemorrages to gaindiagnostic benefit from angiography. Angiogra-phy can only be justified when associated le-sions of the cerebral vessels are suspected (e.g.,dissection or rupture of a vessel wall, posttrau-matic aneurysms, arteriovenous malforma-tions/fistulae).

c) Angiography has a different importancein the case of subarachnoid haemorrhage. With

its often abrupt onset and typical clinical pic-ture, subarachnoid haemorrhage is the mostfrequently encountered of the potential neuro-logical angiographic emergencies.

Thrombosis of the cerebral veins and dural venous sinuses

This type of pathology, now somewhat rare,can require emergency angiography when in-tracranial hypertension dominates the clinicalpicture. In such cases, angiography is used toconfirm the clinicoradiological suspicions.However, while the cranial dural venous sinus-es are more critically assessed angiographically,digital subtraction angiography (DSA) is onlycapable of providing indirect information onthe thrombosis of cortical venous structures(e.g., slow arterial and venous circulation, areasof paucity of venous vessels, presence of collat-eral venous circulation).

TECHNIQUES

Angiography performed in emergency con-ditions is relatively difficult and requires a cer-tain degree of experience as it is almost alwaysperformed in less than ideal circumstances.This difficulty is due both to the patient’s stateof consciousness and ability to cooperate aswell as to the gravity of the clinical picture,which requires the utmost rapidity of angio-graphic examination execution and immediateinterpretation. The use of conventional angiog-raphy has been much improved by the adventof modern DSA appliances with high spatialdefinition (1024 x 1024 matrix). DSA allows,above all, reduced examination times, while themarked simplification of the radiographic tech-nique has made it possible to limit the totalamount of contrast medium required for eachindividual injection. In addition, the use of lowconcentration, low osmolarity, non-ionic con-trast agents has reduced the potential contrastagent toxicity risk. In short, DSA has evolvedinto the a much simpler imaging modality withless risk to the patient.


The only drawback of DSA is its sensitivityto even the slightest patient motion; this re-quires complete patient immobilization, whichis typically only possible with deep sedation orgeneral anaesthesia. If there are no specific con-traindications, such as underlying cerebralhaemorrhage, minimal heparinization can beundertaken. With these exceptions, no otherparticular patient preparation is usually re-quired.

Patient vital functions and neurological sta-tus should be monitored constantly during theexamination, and the patient should be keptunder observation for 12-24 hours after theprocedure. In the absence of contraindica-tions, the angiogram is performed throughtransfemoral access. Other routes of access(e.g., axillary, common carotid arteries) have ahigher risk of local complications. Preliminaryarch aortography used to explore the largesupra-aortic arterial branches is preferable ingeneral and specifically indispensable for iden-tifying vacular variations and ostial/proximalatherosclerotic lesions. In order to study theaortic arch and its branches, the left anterioroblique projection is used with an angulationof 15-20 degrees; generally speaking, 20-25 mlof contrast medium are required with a flowrate of 10-15 ml/sec delivered over 1-2 sec-onds (total contrast volume: 25-50 ml). Stud-ies of the carotid bifurcation require bothoblique projections in order to project the in-ternal carotid free from the external carotidartery, as well as to study the walls and lumenof the vascular structures circumferentially.Although panoramic imaging of the cranialvasculature can be useful as a preliminary ap-proach to locating major lesions and toanalyse overall haemodynamic balance of flowbetween the cerebral hemispheres, selectivecatheterization of the cerebral vessels is almostalways essential. Each arterial injection exam-ined requires at least the two orthogonal pro-jections during DSA; in many cases obliqueprojection imaging also needs to be performedin order to properly define the pathology.Each individual injection usually requires notmore than 6-9 ml of contrast medium deliv-ered at a rate of 6 ml per second (more in

cases of arteriovenous malformation or largearteriovenous fistula). In latest generation an-giographic appliances, the examination is fa-cilitated by improvements such as rotationalangiography or even 3D angiography (20).

APPLICATIONS

We will examine the dual diagnostic andtherapeutic role of angiography in ischaemicand haemorrhagic pathology, and omit traumaand thrombotic pathology of the venous struc-tures, which are more rarely observed at emer-gency diagnostic cerebral angiography.

Diagnostic role

In cases of ischaemia and haemorrhage, an-giography is usually principally responsible foridentifying the vascular lesion(s) responsiblefor the clinical syndrome and for definitivelydetermining the plan for therapy.

a) Cerebral ischaemia: Regardless of whetherit involves transient ischaemic attacks or frankinfarction, the principle role of DSA is simplyto identify the vascular lesion(s) responsible forthe ischaemia. Further goals include the analy-sis of the degree of the stenotic/occlusivepathology and an estimation of its haemody-namic significance, exclusion of the presence ofother lesions that could affect treatment andprovision of a complete picture of cerebralhaemodynamics. Another important factor isthe characterization of such lesions: whetherthey are atherosclerotic, dysplastic (e.g., fibro-muscular dysplasia) or related to trauma (e.g.,arterial dissection); and whether there are asso-ciated complications (e.g., intraluminal throm-bus, ulceration of atherosclerotic plaques) (Fig.1.101). In actual fact, today there are a numberof examination techniques available (Echo-Colour-Doppler, MR angiography, CT angiog-raphy and SPECT), which alongside angiogra-phy contribute to this global evaluation and fi-nally to the formulation of treatment choices.

b) Cerebral Haemorrhage: In the presenceof haemorrhages, cerebral angiography plays a

1.10 CONVENTIONAL ANGIOGRAPHY 119


Fig. 1.101 - (a-e) Cerebral ischaemia. (a-c) selective catheterism of the common carotid artery. In (a) plaque at the start of the inter-nal carotid artery, with “rose thorn” image due to ulcer (arrow); kinking in the precranial stretch (small arrows); in b) irregular plaque(ulcerated). (d-e) Ultrasound of the carotid bifurcation. In (d) marked intimal thickening with flat plaques (arrowhead); in (e) coarsesclerocalcific plaque (arrow).

a

c d e

b

more complex role. Nevertheless, in cases of in-traparenchymal haemorrhage, when performedcorrectly using proper techniques, angiographyis able to identify or exclude the existence ofassociated underlying aneurysms or vascularmalformations.

With AVM’s, utmost attention must be paidto determining the arterial feeders, venousdrainage and other singular anatomical andhaemodynamic characteristics of the malforma-tion (Fig. 1.102). This information is essentialfor treatment planning and for optimally choos-ing between surgery and transcatheter embolictherapy.

The recent interest in intraoperative angiog-raphy made possible by the new portable andmanageable DSA appliances have allowed toconduct angiographic examinations directly onthe operating table. This approach could proveinvaluable in immediate preoperative, intraop-erative and postoperative evaluations of vascu-lar malformations in patients with intra-parenchymal haemorrhage.

In the presence of subarachnoid haemor-rhage the use of angiography is even more im-portant and is essential in most cases to de-termine the optimal surgical approach. An-giography is the most suitable method for di-rectly demonstrating the cause of the bleed(e.g., aneurysm or malformation) in such cas-es. At present, MR angiography and CT an-giography can identify large and many of thesmaller aneurysms; however, in patients withsubarachnoid haemorrhage, negative MR an-giography does not rule out the presence ofan underlying aneurysm or vascular malfor-mation. Therefore, although invasive selectiveangiography is not completely devoid of risks,at the present time it remains the most sensi-tive angiographic technique. Selecting thetime at which to perform the examination isparticularly difficult, and is much dependentupon the presence or absence of arterial va-sospasm and the timing of surgery. Perform-ing angiography in the period during whichvasospasm is most likely to be present (3-10days after the bleed) can lead to a masking ofthe presence of the aneurysm sack due to non-filling. The decision as to whether to perform

angiography either in the early phase (dayone) following subarachnoid haemorrhage orlater (two weeks) depends upon the decisionof the surgical team and the patient’s clinicalcondition. This examination requires experi-ence and diligence, paying particular attentionto detail. It should also be pointed out that incertain situations, despite the utmost care inangiographic examination execution and in-terpretation, the study can be negative due topartial or total thrombotic occlusion of theaneurysmal lumen or to the persistence of thearterial vasospasm (18). Angiography permitsan evaluation of the size of the aneurysm, itsshape and its neck (Fig. 1.103). Angiographyis also required to evaluate the entire cerebralarterial system both to search for other possi-ble aneurysms as well as to perform a com-plete presurgical haemodynamic assessment.To this end, it can be useful to perform cross-compression of the contralateral cervicalcarotid artery during carotid injections in or-der to study the cross-filling, and therefore thecollateral circulatory capacity, of the elementsof the circle of Willis.

Therapeutic role

The interest and utility of interventional radi-ology is increasing in the neuroradiological field,especially in certain emergency situations whereit can provide support for or even replacementof traditional therapeutic approaches.

Cerebral ischaemia: In cerebral ischaemia,the principal therapeutic use of angiography isselective intraarterial fibrinolysis and percuta-neous angioplasty.

a) For some years now, selective intraarter-ial fibrinolysis has been used in treating acuteischaemia of the lower extremities as well asother regions of the body (e.g., renal, mesen-teric, coronary ischaemia). This has occurredprimarily because of the introduction of new,efficient fibrinolytic drugs that are easy to han-dle and have low incidence of untoward sideeffects. Its use in the treatment of cerebral is-chaemia, which in industrialized countries ac-counts for the third largest cause of death and


is the most common cause of lifetime disabil-ity, is now available in many centres world-wide.

Treatment must be begun within 6-8 hoursfrom onset of the ischaemic ictus, once an-giography has demonstrated the obstructivenature of the ischaemia. A microcatheter is in-troduced via the transfemoral route into theoccluded artery; the distal tip of the catheteris positioned in contact with the thrombusand injecting from 200,000 to 1,000,000Urokinase; 1/3 of the total amount of the doseis administered as a bolus, and the remainderas a continuous infusion over the subsequent1-2 hours. The main hindrance to the wideruse of this technique is the extreme sensitivi-ty of the cerebral tissue to anoxia, whichleaves a very small time margin between on-set and the start of treatment, and the poten-tial risk of peripheral non-cerebral and cere-

bral haemorrhagic complications (Fig. 1.104).The procedure requires a high degree of spe-cific physician experience and a high level oforganization of the medical and paramedicalteam involved. It is therefore typically onlyperformed in highly specialized centres and inselected patients. However, statistics revealencouraging figures for this technique. By re-specting rigid patient selection criteria, re-canalization of the occluded vessel varies from44% to 100% of cases, and partial or total re-gression of the clinical picture is observed in31% - 100% of cases (3, 7, 22).

b) Until recently, percutaneous angioplasty,has found fertile ground in areas of the bodyoutside the brachiocephalic region. The con-tinuous technical evolution of the materialsused (e.g., small calibre PTA catheters, thin-ner guide wires and flexible stents), the expe-rience gained in other body regions and the


Fig. 1.102 - (a-c) Intraparenchymal haemorrhage. a) CT: volu-minous intraparenchymal haematoma in right temporoparietalposition of recent onset, with intraventricular expansion. (b-c)Selective catheterism of the right internal carotid artery, earlyand late arteriographic phase of same case: arteriovenous mal-formation (arrow) sustained by branches of the middle cerebralartery and the rear choroid arteries, with venous drain throughascending superficial veins (arrowheads).a

b c

perfection of medical support have made itpossible to extend PTA to the supraaortic ves-sels, albeit with application and selection cri-teria that are yet to be universally accepted. Itmay be that PTA is not absolutely required inhyperacute emergency situations, however, it

may be useful to perform this therapeutic pro-cedure in a timely manner subacutely in pa-tients with rapidly worsening transient is-chaemic syndromes, when preceding angiog-raphy demonstrates the presence of a severestenosis that is felt to be responsible for the


Fig. 1.103 - (a-d) Subarachnoid haemorrhage. a) CT: subarachnoid blood expansion, at the occipital region of the cortical sulci (ar-rows). b) selective catheterism of the left vertebral artery (same case): small aneurysm of the left posterior cerebral artery, near to thestart of the temporooccipital artery (arrow). c) selective catheterism of the left internal carotid artery: small sac-shaped aneurysm ofthe anterior communicating artery (arrow). d) selective catheterism of the left internal carotid artery: aneurysm of the anterior com-municating artery (arrowhead); spasm of the anterior cerebral artery (arrow).

a

c

b

d

clinical picture; in such cases one may logical-ly predict the vessel’s rapid evolution to com-plete occlusion and perhaps resulting frankcerebral infarction. In some specialized cen-tres, PTA of the supraaortic vascular branch-es is performed at the origins of the supraaor-tic vessels (Fig. 1.105) and within the vertebralarteries, the extracranial and sometimes eventhe intracranial segments of the internalcarotid arteries (Fig. 1.106), and the first or-der branches of the major cerebral arteries. Al-though experience in this field is still some-what limited, it is widely held that PTA rep-resents a valid alternative to thromboen-darterectomy, at least in patients who are athigh surgical risk or who present with stenosesthat are difficult to access surgically; however,it may well become more widely used as moresophisticated materials and instruments aremade available.

Recent statistics have shown that PTA en-ables the recovery of vascular patency in morethan 90% of cases; in the remaining 10% amodest residual stenosis remains. The frequen-cy of intra- or postangiographic complicationsis relatively low (minor infarction: 1.6%, majorinfarction: 0.9%), as is the procedural deathrate (0.4%) (1, 5, 6, 10-12, 19).

It should also be pointed out that emer-gency PTA can sometimes be performed onpatients with subarachnoid haemorrhagecaused by cerebral aneurysm rupture, wherethe clinical picture is dominated by the is-chaemia caused by the vasospasm. It has beenfound that the arterial spasm responds well todilation. Such patients are first treated with in-traarterial papaverine (150-300 mg in 100 cm3

of physiological solution injected over 30 min-utes) using a microcatheter that is introducedinto the cerebral artery as far as the vascularspasm to be treated. In cases where papaver-ine treatment is unsuccessful, PTA is used first(Fig. 1.107) (4, 13, 14, 17).

In cases of subarachnoid haemorrhage, PTA’slargest contribution to interventional radiology isin the percutaneous treatment of cerebralaneurysms using Guglielmi detachable coils(GDC). This widely used treatment is the mostrecent and perhaps the most fascinating and


Fig. 1.104 - (a, b) Intraarterial fibrinolysis. a) selective catheter-ism of the left vertebral artery: acute thromboembolic occlu-sion of stretch V3, with impossibility of viewing the basilarstem and the posterior circulation (arrow tips). b) check-up af-ter fibrinolytic treatment: complete recanalization of the verte-bral artery with opacification of the basilar stem and posteriorcircle (arrowheads)

a

b

promising interventional radiological techniquein the neurological field. Through femoral arteri-al access, selective vascular catheterization intothe specific vessel off of which the aneurysm orig-inates is performed; using a microcatheter to se-lectively enter the lumen of the aneurysm, GDC’sare introduced into the sack until a preferablycomplete occlusion is obtained. The technique’sdegree of invasiveness, if compared to surgical

clipping, is far lower and the procedure is far eas-ier for patients in any condition to tolerate. How-ever, patients to be subjected to this treatmentmust be carefully chosen. The best results are ob-tained for small diameter aneurysms with narrownecks (90% success rate with low mortality andmorbidity rates) (Fig. 1.108).

Obviously, this kind of procedure achievesthe best results when practiced under ideal


Fig. 1.105 - (a-d) Angioplasty of the left subclavian artery. (a-c) Aortogra-phy in early and late stages: suboccluding stenoses at the start of the leftsubclavian artery (arrow); in a and b, non-opaque homolateral vertebral ar-tery; c) late opacification, against the stream of the homolateral vertebralartery (theft) (arrows). d) Check-up after angioplasty (same case): completedilation of the stenotic tract (arrow); swift opacification of the homolateralvertebral artery (arrows).

a b c

d

conditions; however, it can still be used inemergency situations. According to Moret, of124 cases presenting with subarachnoid haem-orrhage related to ruptured aneurysms, 21 weretreated in emergency conditions (17%), with aglobal success rate of coil embolization of 79%(9, 15, 16, 21).

CONCLUSIONS

In short, cerebral angiography offers awide range of practical opportunities for usein the field of neurological emergency, andthe role of this technique applied to variousclinical situations is extremely varied. How-ever, it should be pointed out how the role ofangiography has changed in recent years bothwith regard to use in emergency and routineclinical conditions, thanks mainly to the in-vention of new imaging techniques. Angio-graphic semeiotics itself has also changed,and unfortunately a portion of its refined se-meiological knowledge has gradually beenforgotten. At the same time, the angiograph-ic radiologist’s role has also changed. From acertain point of view his or her task has be-

come increasingly straightforward due to thetechnical advances made in angiographic ap-pliances, and the sophistication of the instru-ments used have made angiographic examina-tions safer and more patient tolerable. In ad-dition, newer imaging techniques have great-ly simplified angiography’s diagnostic role.

However, from other points of view, the ra-diologist’s task has become more complex, duein part to the vast range of imaging techniquescurrently available. The imaging specialist’s ap-proach to any type of pathology has now be-come multidisciplinary, which makes obtainingsufficient expertise and experience with all thevarious diagnostic techniques and then choos-ing the optimal diagnostic-therapeutic pathwaysomewhat taxing.

However, the powerful development of in-terventional radiology has also made the ra-diologist’s task more delicate by requiring athorough knowledge of both routine andemergency clinical problems, a continuousupgrading of his knowledge of appliancesand instruments that are themselves under-going constant evolution, and familiarity withthe use of a vast number of pharmacologicalpreparations.


Fig. 1.106 - (a, b) Angioplasty of the internal carotid artery. Selective catheterism of the right internal carotid artery. 33 year-old pa-tient with history of cerebral ischaemia. a) Segmentary stenosis at the passage between the extra- and intracranial tract, probably of afibrodysplasic nature (arrow). b) Check-up after angioplasty (same case): complete resolution of stenosis.

a b


Fig. 1.107 - (a, b) Angioplasty of the middle cerebral artery. a) Selective angiography of the right internal carotid artery: serrated spasmpost SAH of the M1 stretch of the middle cerebral artery (arrow) in patient operated for an aneurysm on the posterior communicat-ing artery. b) Check-up after papaverine + PTA: complete resolution of the spasm with patent vessel of a good calibre (arrow tip).

Fig. 1.108 - (a, b) Aneurysm embolization with Gugliemi’s detachable coils. a) Selective angiography of the left vertebral artery: 1 cmaneurysm of the apex of the basilar artery (arrow). b) Check-up after embolization: complete occlusion of the aneurysmatic sack withwell-compacted spirals (arrow tips).

a b

a b

REFERENCES

1. Borgey WM, Demasi RJ, Tripp MD, et al: Percutaneoustransluminal angioplasty for subclavian artery stenosis. TheAmerican Surgeon 60: 103-106, 1994.

2. Bozzao L, Fantozzi LM, Bastianello S et al: Ischaemic su-pratentorial stroke: angiographic findings in patients exa-mined in the very early phase. J Neurol. 236: 340-342, 1989.

3. Edwards MT, Murphy MM, Geraghty JJ et al: Intra-arterialcerebral thrombolysis for acute ischemic stroke in a com-munity hospital. AJNR 20: 1682-1687, 1999.

4. Elliot JP, Newell DW, Lam DJ et al: Comparison of balloonangioplasty and papaverine infusion for the treatment ofvasospasm following aneurysmal subarachnoid haemorrha-ge. J Neurosurg 88: 277-284, 1998.

5. Florio F, Balzano S, Nardella M et al: Terapia translumina-le delle lesioni stenosanti dei tronchi epiaortici. Radiol.Med 86, 302-307, 1993.

6. Florio F, D’Angelo V, Nardella M et al: Displasia fibromu-scolare dell’arteria carotide interna: angioplastica percuta-nea. Radiol. Med 84, 796-801, 1992.

7. Gonner F, Remonda L, Mattle H et al: Local intra-arterialthrombolysis in acute ischemic stroke. Stroke 29: 1894-1900,1998.

8. Grzyska U, Freitag J, Zeumer H: Selective cerebral intraar-terial DSA. Complication rate and control of risk factors.Neuroradiology 32: 296-299, 1990.

9. Guglielmi G, Vinuela F: Intracranial aneurysms Guglielmielectrothrombotic coils. Neurosurg. Clinics North America3: 427-435, 1994.

10. Henry M, Amor M, Henrry I et al: Percutaneous translu-minal angioplasty of the subclavian arteries. In: Tenth in-ternational course book of peripheral vascular intervention.Europa Edition. Paris, pp. 617-627, 1999.

11. Henry M, Amor M, Henry I et al: Angioplasty and Stentingof the Extracranial Carotid Arteries. In: Carotid angiopla-sty and stenting. ISCAT ed. Europea pp. 267-280, 1998.

12. Higashida RT, Tsai FY, Halbach VV et al: Transluminal an-gioplasty for atherosclerotic disease of the vertebral and ba-silar arteries. J Neurosurg 78: 192-198, 1993.

13. Livigstone K et al: Intraarterial papaverine as on adjunct totransluminal angioplasty for vasospasm induced by subara-chnoid haemorrage. AJNR 14: 346-347,1993.

14. Milburn JM, Moran CJ, Cross DT et al: Effect of intraarte-rial papaverine on cerebral circulation time. AJNR 18:1081-1085, 1997.

15. Moret J, Boulin A, Castaings L: Endovascular treatment ofberry aneurysms by endosaccular occlusion. In: Nacci G,Scialfa G: Atti 3° meeting neuroradiologico potentino:Neuroradiologia terapeutica, pp. 10-14, Ed. C.S.E. Potenza1991.

16. Murayama Y, Vinuela F, Duckwiler GR: Embolization ofincidental cerebral aneurysms by using the Guglielmi deta-chable coil system. J Neurosurg 90: 207-214, 1999.

17. Polin RS, Coenen VA, Hansen CA: Efficacy of transluminalangioplasty for the management of symptomatic cerebralvasospasm following aneurysmal subarachnoid hemorrha-ge. J Neurosurg 92: 284-290, 2000.

18. Redfern RM, Zygmunt S, Pickard JD et al: The natural hi-story of subarachnoid haemorrhage with negative angio-graphy: a prospectie study and 3 year follow-up. Br J Neu-rosurg 2: 33-41, 1998.

19. Sivaguru A, Venables GS, Beard JD et al: European carotidangioplasty trial. J Endovasc Surg 3: 16-20, 1996.

20. Smith TP: Radiologic intervention in the acute stroke pa-tient. J Vasc Intervent Radiol 7: 627-40, 1996.

21. Vinuela F, Duckwiler G, Mawad M: Guglielmi detachablecoil embolization of acute intracranial aneurysm: periope-rative anatomical and clinical outcome in 403 patients. JNeurosurg 86:475-482, 1997.

22. Zeumer H, Freitag HJ, Grzyska U et al: Local intraarterialfibrinolysis in acute vertebrobasilar occclusion. Neurora-diology 31: 336-340, 1989


II

HEAD INJURIES

131

Overall, trauma represents the most fre-quent cause of death and permanent disability,with an annual incidence of 0.2-0.3% and withpeak incidence in the 15-24 year age band (1).In the United States alone, approximately 2million head injuries occur annually, of whichsome 10% are fatal. Approximately 5-10% ofsurvivors experience neurological deficits ofvarying degrees (1, 4, 5). The most commoncauses of trauma are road accidents, firearm in-juries, falls and assaults.

The brain lesions resulting from cranialtrauma are usually classified as being eitherprimary or secondary, according to how di-rectly they correlate to the traumatic event (4,20, 22, 29). Primary lesions include fracturesof the skull, extraaxial haemorrhages (e.g.,epidural haematoma, subdural haematoma andsubarachnoid haemorrhage) and intraaxial le-sions (e.g., diffuse axonal injury [DAI], corti-cal contusion, deep grey matter injury and in-traventricular haemorrhage). Secondary lesionsare constituted by pathological processes thatoccur due to the brain’s response to the pri-mary trauma and are generally more clinicallydevastating than primary ones. Secondary brainlesions include internal cerebral herniation, dif-fuse cerebral oedema, infarction and secondaryhaemorrhage (4, 20, 22, 29). Yet other lesionsare the result of sequelae of severe cranial trau-

ma; these changes are represented by pneu-mocephalus, CSF fistulae, leptomeningealcysts, lesions of the cranial nerves, diabetes in-sipidus secondary to pituitary axis injury, cor-tical atrophy and encephalomalacia (9).

In recent decades, considerable progress hasbeen made in the diagnosis and management ofcranial trauma patients. The application ofComputed Tomography (CT) has resulted in arevolution in head injury diagnosis, making itpossible to detect cases suitable for surgicaltreatment in a rapid, non-invasive manner (6, 7,11, 12, 14). Its near-universal availability in hos-pitals, the speed with which examinations canbe conducted, the general absence of con-traindications to emergency patient scanning,and its sensitivity in diagnosing haemorrhagiccollections make CT the imaging technique ofchoice for the initial assessment of patients withacute head injuries (4, 22, 32, 33). Further ad-vantages offered by this technique are found inits high spatial resolution allowing the possibil-ity of documenting even the thinnest fracturesand those located in critical positions such asthe base of the skull or the temporal bone, andin identifying small splinters of metal or tinyfragments of bone displaced into the cranialcavity (24, 31). The drawbacks of CT includeits limited sensitivity in studying small traumat-ic lesions in the inferior posterior fossa or else-

2.1

CLINICAL AND DIAGNOSTIC SUMMARYG. M. Giannatempo, T. Scarabino, M. Armillotta

where adjacent to the base of the skull, theselimitations being principally due to bone arte-facts generated by the technique. CT also has arelatively low sensitivity in the identification ofsmall non-haemorrhagic lesions of the cerebralcortex, white matter and brainstem (4, 10, 20,21, 23). However, these limitations do not pre-vent CT from identifying the nature, size andsite of the most clinically significant acutephase traumatic brain lesions and from decid-ing whether or not surgical intervention is re-quired (4, 22, 32, 33).

Magnetic Resonance Imaging (MRI) plays alimited role in the acute phase of cranial trau-ma, given its higher cost, relatively limitedavailability, longer examination times, lowersensitivity in recognising fractures, patient con-traindications (internal electronic pacemakers,etc.) and the practical difficulty of effectivelymonitoring patients with severe clinical condi-tions requiring external support devices (4, 8).MR is also limited by problems encountered inrecognising acute phase haemorrhages (e.g.,oxy- and deoxyhaemoglobin within hyperacutehaemorrhages) and small bone fragments dislo-cated into the skull. The use of MR in emer-gency situations also entails certain intrinsicrisks, for example those linked to the difficultyin ascertaining the presence of electronic pace-makers in unconscious trauma patients.

Technological progress has to some extentreduced the drawbacks associated with longexamination times and the difficulties in usinginstruments to monitor the patient’s vital pa-rameters during the MR examination. The useof fast scanning sequences (e.g., fast spin-echo,gradient-echo, echo-planar) has considerablyreduced the amount of time required to per-form MR studies, to the point where it is nowpossible to perform a basic MR scan in lessthan ten minutes. This scan protocol may in-clude a T1-weighted spin-echo sequence, a T2-weighted fast spin-echo sequence and a T2*-weighted gradient-echo sequence, the latter be-ing particularly sensitive to haemorrhagic ex-travasations. It must also be pointed out thatconsiderable progress has been made in the de-velopment of new non-ferromagnetic alloysemployed in the manufacture of electronic

medical instruments used for vital parametermonitoring and life support, so that they arenow compatible with MRI (4, 8).

MRI has greatest diagnostic sensitivity inmany of the very cases in which CT encounterssome of its greatest limitations. Given itsgreater sensitivity in the diagnosis of diffuseaxonal injury (DAI), small cortical contusionsand primary and secondary traumatic brain-stem lesions, MRI is also used as a complementto other imaging methods in the acute phase oftrauma, especially in patients with clinicalsigns and symptoms but with minor or absentCT findings (4, 20, 21). MR examinations arealso suitable in subacute and chronic phasecranial trauma for the purpose of evaluatingsecondary lesions and other sequelae.

In the area of cranial trauma diagnosis, digi-tal angiography currently plays only a marginalrole and is principally utilized for cases inwhich traumatic vascular lesions are suspected(e.g., vascular dissections, lacerations, occlu-sions, pseudo-aneurysms and arteriovenous fis-tulae).

NEURORADIOLOGICAL PROTOCOLS

Although any diagnostic approach must betailored to suit the requirements of each pa-tient, some general guidelines can be identifiedto aid in the establishment of which techniqueis most suitable. Defining an efficient and effi-cacious diagnostic protocol requires compro-mising between the choice of a technique guar-anteeing high diagnostic sensitivity and the lim-itations imposed on the number and complexi-ty of the diagnostic examinations that can beperformed.

Although CT is the examination techniqueof choice in cranial trauma, not all authorsagree on the necessity of performing CT inasymptomatic patients with previous minorcranial traumatic incidents, the need for com-plementing CT examinations with MR scans inpatients with intermediate or serious head in-juries and the real contribution of traditionalskull x-rays in patients with head injuries of anydegree.

132 II. HEAD INJURIES

The choice of a specific imaging techniqueto be employed must be preceded by a defini-tive clinical evaluation of the patient. The mostcommonly used method for evaluating head in-jury patients is the Glasgow Coma Scale (GCS),based on a progressive score attributed to thepatient’s ability to open his/her eyes, performmovements and verbally respond to externalstimuli (13, 22, 28) (Tab. 2.1). The degree ofseverity of the trauma is classified in three cate-gories according to the GCS score: mild traumafor a GCS score of 13-15; moderate trauma fora GCS score of 12-8 and severe trauma for GCSscores lower than 8.

Patients with mild head trauma (GCS 13-15)usually complain of headaches and transientmental confusion or disorientation (30) and, bydefinition, they do not exhibit persistent prob-lems with consciousness (30). Some authorshold that it is sufficient to keep patients withsuch mild degrees of cranial trauma under ob-servation, and furthermore that they do not re-quire imaging studies (18). On the contrary,others believe that mild head injuries warrant ata minimum a CT examination, because despitethe paucity of symptoms, traumatic brain le-sions may be observed (19, 27). In a recent sur-vey conducted on 1,170 mild cranial trauma pa-tients (GCS = 15), CT demonstrated the pres-ence of brain lesions in 3.3% of cases, of which18 in number were intracranial bleeds; in 1.8%the CT examination altered the treatment pro-gramme, and in four cases surgery was per-formed (19). The same authors also stressed theprognostic value of a negative CT examination:in the same patient sample, none of the patientswith negative CT scans experienced clinical de-terioration. The authors therefore believe thatit is not necessary to keep asymptomatic mildhead trauma patients under observation in thesetting of negative CT findings (19). Patientswith mild trauma can reveal skull fractures, as well as extraaxial and intraparenchymalhaematomas, lesions that are usually clearlydocumented on CT images. Although MR isslightly more sensitive than CT in demonstrat-ing extraaxial haematomas, those that are notdetected by CT are small and generally do notrequire surgery (4). The diagnostic sensitivity of

MR is clearly superior to that of CT in cases ofsmall, non-haemorrhagic lesions (e.g., DAI,bland cortical contusions), but the recognitionof this type of lesion in minor head trauma pa-tients does not alter the therapeutic manage-ment nor the clinical outcome (18, 30).

Patients with moderate (GCS = 8-12) andsevere (GCS< 8) head trauma share a numberof clinical and therapeutic characteristics, andfor the sake of simplicity they will be consid-ered as a single group (4). It should be point-ed out that before commencing any diagnos-tic examination, the stabilization of the pa-tient’s respiratory and circulatory systemsmust be ascertained, ensuring the freedom ofthe airways (with intubation, if necessary), cer-vical spine stabilization (in case of underlyingfracture/subluxation), respiratory function(face mask with high flow O2; controlled ven-tilation if the patient is intubated) as well astheir haemodynamic condition (e.g., identifi-cation and treatment of serious internal andexternal haemorrhaging; volemic restorationwith isotonic solutions or plasma expanders).


Tab. 2.1 - Glasgow Coma Scale (GSGS)

Best Eye Response• Eyes open spontaneously• Eye opening to verbal command• Eye opening to pain• No opening of eyes

Best Motor Response• Obeys commands• Localising pain• Withdrawal from pain• Flexion to pain• Extension to pain• No motor response

Best verbal Response• Oriented• Confused• In appropriate words• Incomprehensible sounds• No verbal response

Mild cranial trauma GCS = 13 - 15Moderate cranial trauma GCS = 9 - 12Severe cranial Trauma GCS = 1 - 8

Once the patient’s clinical stability has beenascertained, the neurological examination maycommence with the evaluation of the GCS,pupillary analysis and the evaluation of later-alizing signs, as well as with a general clinicalexamination for the identification of any oth-er non-cranial traumatic lesions. Patients withmoderate and severe head injuries usually suf-fer from disorders of consciousness, often as-sociated with focal neurological deficits. Insuch cases, the fundamental question to beanswered is whether the patient has an in-tracranial haematoma that requires surgery; atpresent CT is the only technique that is ableto exclude this type of lesion rapidly and withsufficient reliability.

Once the need for emergency surgery hasbeen eliminated, certain authors recommendperforming an MR examination during thefirst two weeks of the traumatic event in pa-tients with moderate to severe head injuries.MR has a far greater sensitivity than CT indiagnosing DAI, small cortical contusions(especially when non-haemorrhagic) andbrainstem lesions, conditions that usuallydemonstrate minor or completely negativeCT findings that may contrast considerablywith the impaired clinical picture. In suchcases, MR permits a more accurate evalua-tion than does CT with regard to the extentof the involvement of the encephalon and thebrainstem, thus offering important informa-tion on possible clinical evolution and out-come (3, 5).

It should be remembered that althoughclinical indicators such as the GCS are usefulinstruments in establishing the patient’s clini-cal condition, they do not provide significantinformation on the actual lesion(s) underlyingthe signs and symptoms, the prognosis or thepatient’s clinical evolution. Low GCS scorescan be obtained from a number of differentbrain injuries that ultimately are responsiblefor vastly different clinical evolutions. Prior tothe advent of MRI, diagnostic studies had lit-tle impact on prognosis; for example, many au-thors have highlighted the poor prognostic val-ue of CT findings (2, 3, 12). CT’s poor sensi-tivity in documenting non-haemorrhagic le-

sions of the brain is believed to be partly re-sponsible for the poor correlation between CTfindings and clinical evolution, which appearto be much better correlated with MRI find-ings (3).

In particular, the number of DAI lesionswould appear to be inversely correlated withthe GCS score in the long term; whereas 80%of patients without DAI recover well, only27% of those with more than 10 lesions havea good prognosis (3). Conversely, the numberof cortical contusions and the presence of iso-lated subdural or epidural haematomas do notappear to be statistically correlated with clini-cal evolution, unless associated with significantmass effect (e.g., transtentorial cerebral herni-ation and brainstem compression) (3). Signs ofbrainstem compression and intrinsic brainstemlesions typically suggest a very severe progno-sis, especially when observed in combination.

It should be pointed out that most au-thors agree that it is not necessary to per-form skull x-rays for the purpose of diag-nosing fractures (15, 17, 20, 25, 26). Thepresence or absence of fractures is often notindicative of the gravity of the underlying in-jury of the brain. Skull fractures can in factbe isolated and are not necessarily associat-ed with intracranial haematomas; converse-ly, the absence of fractures does not excludethe possibility of serious brain damage: in25-30% of patients with moderate and se-vere trauma and brain lesions, the skull isnot fractured (16). Fractures shown on x-rays do not therefore necessarily indicatebrain damage, nor is the absence of suchfractures reassuring with regard to the pa-tient’s normality (15, 17). In short, the diag-nosis of fractures is not as important as isthe identification of depressed fractures, in-tracranial dislocation of bone fragments,fractures in critical positions such as thetemporal bone and base of the skull (whichcan be associated with fluid fistulae and vas-cular lacerations or fistulae) and associatedintracranial lesions (especially intra- and ex-traaxial haematomas). In all such cases, CToffers diagnostic potential that is far superi-or to conventional x-ray examinations.


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26. Snoek J, Jennet B, Adams JH: Computerized tomographyafter recent severe head injury in patients without acute in-tracranial hematoma. J Neurol Neurosurg Psychiat 42:215-225, 1979.

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28. Teasdale G, JennettB: Assessment of coma and impairedconsciousness: a practical scale. Lancet 2:81-84, 1974.

29. Weisberg L., Nice C.: Cerebral computed tomography.W.B. Saunders, Philadelphia, pp 321-343, 1989.

30. Williams DH, Levin HS, Eisenberg HM: Mild headinjury classification. Neurosurgery, 27:422-428, 1990.

31. Wilson AJ: Gunshot injuries: what does a radiologist needto know? Radiographics 19:1358-1368, 1999.

32. Wysoki MG, Nassar CJ, Koenigsberg RA et al: Head trau-ma: CT scan interpretation by radiology residents versusstaff radiologists. Radiology. 208(1): 125-8, 1998.

33. Zee CS, Go JL: CT of head trauma. Neuroimaging Clin NAm. 8(3): 525-39, 1998.


137

INTRODUCTION

Trauma constitutes the most frequent causeof death and permanent disability in the west-ern world (3, 20). For example, each year in theUnited States of America alone, some 2 millionincidents of head injury occur (9), representingthe most frequent cause of death among chil-dren and young adults (3, 20). Annual mortali-ty from head injuries is estimated to be 25 per100,000 population and is four times higher inmales than females (2, 4). In the United States,20-50% of head injuries are the result of roadtraffic accidents, 20-40% of firearm injuries,and assault or falls in the remainder (2, 4). Fallsare particularly dangerous in children underten years of age and the elderly, representingapproximately 75% of all head injuries in thepreschool population (2, 4).

Head injuries can be classified as open orclosed, depending on whether or not the duramater is intact (11, 12, 26). Closed cranial trau-mas are the more frequent of the two types andproduce violent accelerations of the brain tis-sue, which are responsible for tissue contusionand vascular laceration at both the site of the di-rect trauma as well as on the opposite side.Among other injuries, skull fractures, extracere-bral intracranial haemorrhages and parenchy-mal lesions are typically observed alone or in

varying combinations. Open head trauma in-cludes lesions of the skull such as depressedfractures associated with interruptions of thedura mater, and intracranial lesions secondaryto the action of penetrating foreign bodies ordislocated calvarial fracture fragments.

Brain lesions can also be divided into primaryand secondary categories according to howclosely they are linked to the traumatic event (3,20, 22, 26). Primary lesions include skull frac-tures, extraaxial haemorrhages (e.g., epiduraland subdural haematomas and subarachnoidhaemorrhages) and intraaxial lesions (e.g., dif-fuse axonal injury [DAI]), cortical and deep greymatter contusion [bland or haemorrhagic], andintraventricular haemorrhage) (Tab. 2.2). Sec-ondary lesions are caused by pathologicalprocesses that arise from the brain’s response tothe trauma, as a complication of the primarytraumatic brain lesions or as neurological in-volvement associated with systemic extracranialtrauma (Tab. 2.3). In general, the secondarytypes of trauma are more clinically devastatingthan are the primary brain injuries. They aregenerally caused by compression of the brain,cranial nerves and blood vessels against the bonycranial structures and the non-expandable duralmargins. Secondary brain injuries include cere-bral herniations, diffuse cerebral oedema, infarc-tion and secondary haemorrhages (3, 20, 22, 26).

2.2

CT IN HEAD INJURIESG.M. Giannatempo, T. Scarabino, A. Simeone, A. Casillo, A. Maggialetti, M. Armillotta

In the study of acute head injuries, CT cur-rently represents the diagnostic methodologyof choice (3, 7, 20, 22, 28). Its ability in dis-tinguishing between minor differences in tis-sue density, its high spatial definition, capaci-ty to demonstrate even very subtle or critical-ly positioned (e.g., base of the skull, temporalbone) fractures, fast scanning times and com-patibility with life support devices all con-tribute to making CT the most suitable tech-nique in acute phase head injury evaluation (3,7, 20, 22, 29).

TECHNIQUES

Despite the speed with which CT must beperformed in emergency conditions, head in-juries warrant the observance of certain techni-cal and methodological parameters that ensurediagnostic efficiency and the reproducibility ofthe results in the event of serial evaluations (14,22, 29).

Caution is required when positioning the pa-tient on the CT bed, taking care that any tubesand electrode cables are sufficiently long to en-able suitable scan table indexing during thescan. Particular care must be observed in posi-tioning the patient’s head in the supine posi-tion: the chin must be extended in order to pre-vent breathing difficulties. And, to prevent apotential cervical spinal cord injury resultingfrom a suspected or occult unstable spinal col-umn fracture-dislocation, immobilization of thehead and cervical spine should be undertaken.

The CT examination begins with a projectiondigital scanogram that includes the cervicalspine. This serves to define the scanning limitsfor an evaluation of skull vertex fractures, grosssubluxations and fractures of the cervical spinalcolumn, gross soft tissue alterations and for therecognition of any radioopaque foreign bodies.The CT scan gantry should be oriented alongthe orbitomeatal plane, or alternatively along theso-called horizontal “German plane” parallel tothe hard palate, and should be directed in sucha way as to avoid if possible sectioning throughany metal foreign bodies (e.g., dental fillings,etc.) that might be likely to cause beam-harden-ing artefacts (5, 7, 22, 29). The examination con-tinues with contiguous 5 mm-thick axial slicesthrough the structures of the posterior fossa andthen concludes with a stacked series of 10 mm-thick axial slices through the cranial vertex tocover the supratentorial structures (5, 7, 22, 29).

For small lesions or in order to visualize frac-tures at the base of the skull, the acquisition of2-3 mm sections is recommended. Coronalscans may be required at a later point beyondthe emergency period in order to identify or ex-clude fractures at the base of the skull, the bonyorbit and the petrous bone, and for visualizationof parenchymal or bony lesions adjacent to thevertex. It should also be pointed out that coro-nal scans require optimal patient cooperationand should only be performed when it is ab-solutely certain that there are no fractures/insta-bility of the cervical spine or at the atlanto-oc-cipital junction.

When an otorrhagia or acute paralysis of thefacial nerve suggests a fracture of the temporal


Tab. 2.2 - Primary traumatic cranioencephalic lesions.

1) Fractures

2) Intraaxial lesionsa) diffuse axonal injury (damage)b) cortical contusionc) intraparenchymal haematomad) intraventricular haemorrhagee) lesions of the deep grey matterf) brainstem lesions

3) Extraaxial lesionsa) epidural haematomab) subdural haematomac) subarachnoid haematomad) subdural hygromae) vascular lesions

Tab. 2.3 - Secondary traumatic cranioencephalic lesions

1) Cerebral herniation2) Diffuse cerebral oedema3) Posttraumatic ischaemia4) Posttraumatic infarction

bone, the examination must be completed witha detailed study of the petrous bone using thinslices (1-2 mm), a reduced field of view (FOV)and utilizing bone reconstruction algorithms(14, 24, 29).

Generally speaking the examination shouldbe filmed/reviewed using window and level val-ues that permit an optimal viewing of the cere-bral parenchyma (e.g., 100 H.U. window and40-50 H.U. level), and those that also enable vi-sualization of the bony structures (e.g., 2000-3000 H.U. window and 500-700 H.U. level). Incertain cases, especially for the visualization ofthin epidural or subdural haemorrhages, it isadvisable to film the examination with windowvalues equal to 200-350 H.U. and level valuesequal to 40-80 H.U. in order to distinguish themildly hyperdense blood collection from theadjacent bony hyperdensity (9, 15, 22, 28).

The intravenous administration of iodine con-trast medium does not significantly improve thediagnostic sensitivity of the examination in casesof cranial trauma; in fact, it can conceal intracra-nial haemorrhage, causing minor blood collec-tions to be overlooked. The administration ofcontrast agents is also usually avoided as it canproduce renal injury or even potentially worsenbrain function in patients with traumatic cerebrallesions. However, the utilization of contrast mediacan be useful in certain limited cases when betterdefinition of the dural venous sinuses is desired,better visualization of chronic isodense subduralhaematomas is necessary, and above all, in orderto document simultaneous underlying pathologysuch as neoplasia or AVM’s. Of course, intravas-cular contrast media are required for performingCT angiography in cases where there is a suspi-cion of posttraumatic intracranial vascular pathol-ogy (e.g., vascular lacerations, arteriovenous fistu-lae and posttraumatic pseudo-aneurysms). In allof these cases, MR may be more sensitive and issometimes preferable to CT.

Modern CT appliances with spiral (helical)scanning capability greatly reduce the time re-quired for scanning, these units acquiring theentire scan volume in just a few seconds; whenacquired in sufficiently thin sections (e.g., 1-2mm) these scans can then subsequently be re-constructed in different spatial planes (1, 10,

22, 24). Helical scans are most useful in caseswhere scanning time must be reduced to a min-imum, such as in children or in non-coopera-tive patients. It can also be very helpful whenthere is a suspicion of lesions of the orbit or thefacial skeleton in which it is possible to quicklyobtain high resolution two- or three-dimen-sional reconstructions (1, 10, 24).

It is useful, however, to stress that spiral CTexaminations can sometimes produce imagesthat simulate non-existent pathology, such asminor subdural haematomas, in part due to thepartial volume averaging effects along the z-ax-is of scanning. This kind of artefact appearsprincipally along sloping surfaces such as theskull-brain interface over the frontoparietalconvexity (1, 10, 22).

Another type of artefact associated with spi-ral CT that can simulate a chronic subduralhaematoma is the so-called “stairstep” artefactthat produces images with hypodense peripher-al areas, especially at the skull vertex (1, 10, 22).Such problems can be partly or completely re-solved by reducing the collimation, the recon-struction interval, the scan bed’s index speedand/or the tube rotation speed (22). Recent re-search shows that traditional, non-helical CT issuperior to spiral CT with regard to the sig-nal/noise ratio, in visualizing the interface be-tween white and grey matter and in observinglow contrast, small, complex structures (e.g.,the internal capsule) (1).

In summary, the use of spiral CT in cases ofcranial trauma should be restricted to thosecases in which scanning time must be as brief aspossible, instances in which a three-dimension-al study of the bony structures is required orwhen CT angiography of intracranial circula-tion is necessary.

SEMEIOTICS

PRIMARY TRAUMATIC LESIONS

Skull fractures

Skull fractures associated with cranial trau-ma are common and are discovered in approx-

2.2 CT IN HEAD INJURIES 139

imately 60% of all cases (20). The presence ofa fracture is not necessarily significant with re-gard to the clinical severity of the trauma, nordoes the absence of a fracture exclude the pos-sibility of severe brain damage; records showthat in 25-35% of patients with severe traumaand underlying brain injury, no fracture ispresent. For this reason, many practitionersfeel that x-rays aimed at diagnosing skull frac-tures are superfluous with reference to patientcare (16, 20, 25). In addition to the parietal,frontal and occipital areas, skull fractures canaffect the vertex or base of the skull. And, de-pending on the intensity of the force applied,they can be classified as linear fractures usual-ly caused by lesser forces (Fig. 2.1), and com-minuted and depressed fractures typicallycaused by greater forces (Fig. 2.2) (16, 17, 22,25, 29). Fractures of the skull base can becaused by superficial or penetrating trauma,the caudal extension of a fracture of the cal-varia, or alternatively, the upward transmissionof traumatic forces along the vertebral column.Although CT is sensitive in detecting thesetypes of lesions, thin, linear fractures and thoseoblique/parallel to the plane of section can gounnoticed (16, 17, 25). However, the practicalimportance of fracture recognition is second-ary, as efforts are principally concentrated onthe search for associated intracranial lesions.Linear fractures are often associated withepidural and subdural haematomas, whereasdepressed fractures are more frequently associ-ated with focal parenchymal lesions adjacent tothe bony lesions (20).

In more severe cases, such as in open headinjuries that are often consequences of knifeor firearm wounds, fractures may be associat-ed with a laceration of the dura mater and apenetration of bone fragments, air or foreignbodies into the cranial cavity (3, 20, 27). In thestudy of such open head injuries, CT permitsthe accurate localization of foreign bodies orbone fragments in large part due to their rela-tive high density (Fig. 2.3). CT also provides adetailed picture of the spatial characteristicsof depressed fractures (Fig. 2.4) and at thesame time, documents any related cerebral le-sions.

Lesions of the dura mater at the base of theskull, associated with fractures of the adjacentbone, can be complicated by a CSF fistula for-mation, with consequent oto- and/or rhinor-rhea (Fig. 2.5). In such cases, the site of the fis-tula can be suggested by means of a detailedstudy of the bone using high resolution CT.This study should be performed employing ax-ial slices to study fractures of the posterior wallof the frontal sinuses and the petrous bone,and coronal acquisitions to study ethmoid frac-tures and also to supplement the evaluation ofpetrous fractures.

In addition, fractures of the paranasal sinus-es, the mastoid cells or the middle ear may re-sult in the introduction of air into the sub-arachnoid spaces or the cerebral ventricles(pneumocephalus) (8, 27). These conditionscan occasionally behave as space-occupying le-sions (e.g., pneumatocele formation) when avalve mechanism is formed at the dural lacera-tion resulting in a considerable increase in thevolume of intracranial air, and therefore will re-quire treatment (Fig. 2.6).

Intraaxial lesions

Diffuse axonal injury

Diffuse axonal injury (DAI) is one of themost common primary brain lesions associatedwith severe trauma and accounts for approxi-mately 48% of all traumatic intraaxial injuries(3). DAI typically results from abrupt accelera-tions or decelerations or when violent rotation-al forces obtain causing a differential inertia be-tween grey and white matter, between the cere-bral hemispheric connecting structures or with-in the diencephalon and brainstem with conse-quential axonal stretching, twisting and tearing(3, 20). Clinically, DAI is characterized by a lossof consciousness beginning immediately at thetime of the trauma which can evolve into a co-ma that is often irreversible (3, 13, 22). DAI isthe most severe of all primary brain lesions, be-ing ahead in degree of severity of that of corti-cal contusions, intraparenchymal haematomasand extraaxial haemorrhages. Pathoanatomically,


ball-shaped deformations of the damaged axonscan be observed; the lesions are not usuallyhaemorrhagic, although in 20% of cases theycan be associated with small haemorrhages re-sulting from the rupture of penetrating arterialvessels (3). DAI usually occurs in one of threetypical positions: the cerebral hemisphericwhite matter, the corpus callosum and the dor-solateral aspect of the midbrain. More precisely,in approximately two thirds of cases the lesions

are located at the subcortical grey-white matterjunction in the frontotemporal region, 20% arelocated in the corpus callosum (especially thebody and the splenium), and less frequently thealterations affect the dorsolateral side of thebrainstem tegmen, the internal capsule, the thal-amus and the caudate nucleus (20). During theearly phases of a traumatic injury, the CT pic-ture is often normal despite the fact that theclinical status is that of a seriously compromised


Fig. 2.1 - (a-d) Recent head injury. Irregular hypodense cortical-subcortical areas are observed bilaterally in the frontal lobes; hyper-dense haemorrhagic material is noted in the occipital horns of the lateral ventricles (a-b). Also seen is a frontal bone fracture line (c).

a

b d

c

patient; research indicates that alterations canonly be documented by imaging in 20-50% ofpatients with DAI (3, 20, 24). The alterationsthat can be documented by CT consist of smallhaemorrhages and hypodense lesions that affectthe corpus callosum and the grey-white matterjunction of the cerebral hemispheres (Fig. 2.7).Small haemorrhages also occur in the internalcapsule, in the periventricular grey matter andin the dorsolateral quadrants of the brainstem,the latter being a somewhat vulnerable area inpatients subjected to angular accelerations-de-celerations. Although MRI also underestimatesthe real extent of axonal damage in DAI relativeto the pathoanatomical findings, it is currentlythe most sensitive imaging technique available(3, 20, 21).

Cortical contusion

Cortical contusion is the second most fre-quent form of parenchymal lesion followingDAI and represents approximately 45% ofall intraaxial primary traumatic injuries (3,20). Unlike DAI, cortical contusion is lessfrequently associated with loss of conscious-ness and occurs following a violent traumaticshaking injury of the cerebral tissue (3, 13). Itcan occur secondary to linear accelerations ofthe cerebrum that produce the typical coupand countercoup parenchymal contusions, oralternatively after angular accelerations thatproduce cortical contusions resulting fromcollisions of the brain against the inner sur-face of the skull. As the grey matter is farmore vascularized than the white matter, cor-tical contusions tend to be more frequentlyhaemorrhagic than do those lesions associat-ed with DAI (7, 29). Pathoanatomically, thesecontusions are characterized by isolated ormultiple foci of focal or linear microhaemor-rhages of the cortical gyri. The lesions may beassociated with focal oedema resulting fromalterations of the permeability of the regionalcapillaries and the walls of involved glialcells. Petechial lesions, which are often com-bined with overlying bony skull fractures,tend to expand into more widespread haem-orrhagic foci that often manifest 24-48 hoursafter the trauma (3, 20, 29). Because the le-sions are caused by the impact of the cerebralparenchyma against the surrounding bonystructures, most contusions are located incharacteristic locations. In approximatelyhalf of all cases, the lesions are situated with-in the temporal lobes (especially in thepoles), over the lower surface of the frontallobes and in the cortex surrounding the Syl-vian fissure (Fig. 2.8).

The CT appearance of cortical contusionsvaries in part with the manner in which the le-sions evolve over time. At the onset, the CTpicture can be negative because the lesions areinitially isodense, and therefore are impossibleto distinguish from the surrounding healthyparenchyma. In other cases, early stage contu-sions appear as small hypodense areas often in-


Fig. 2.2 - (a, b) Demonstrated is a depressed fracture of theright parietal bone.

a

b

termingled with small hyperdense haemorrhag-ic foci.

In serial CT scans performed 24-48 hoursfollowing the trauma, the lesions become moreobvious due to the increase in oedema and theresulting enlarging mass effect. The traumamay also be responsible for frank damage to theintracerebral vessels with consequent progres-

sive haemorrhagic extravasation (7, 29). There-fore, it is important that repeat CT scans beperformed within the first 24 hours of the ini-tial trauma to reassess the condition of thebrain for possible intervention.

In such cases the CT shows areas of mixeddensity due to a combination of hyperdensehaemorrhagic foci often in combination with


Fig. 2.3 - (a-d) Open head injury caused by firearm, examined using a soft tissue (a, b) and bone (c, d) algorithm. One can clearly ob-serve the bullet entrance hole (b, d) in a left paramedian parieto-occipital location, the bullet’s pathway that ends against the fracturedparietal bone (a-c), various metal and bone fragments which appear hyperdense a right parietal subdural haematoma, midline shift tothe left and obliteration of the cortical sulci (a, b).

a

c

db

confluent hypodense non-haemorrhagic areas(Fig. 2.8 a, b). The haemorrhagic componentgradually resolves and disappears completelywithin 2-4 weeks (Fig. 2.8 c, d), whereas theoedematous areas may persist for longer peri-ods before complete recovery; alternatively, ir-regular areas of hypodensity may remain indi-cating residual encephalomalacia (Fig. 2.8 e, f),and in some cases parenchymal cavitation oc-curs (3, 20).

Traumatic intraparenchymal haematoma

Intraparenchymal haematomas are usuallycaused by combined torsion and compressionforces applied to the intraparenchymal vessels,causing them to rupture; less frequently they area consequence of direct vascular damage in-


Fig. 2.4 - (a, b) Open head-facial injury caused by road trafficaccident. Multiple fractures of the left orbital, ethmoidal andfrontal bones are noted, with fluid within the ethmoid air cellsand frontal sinus (a, b).

Fig. 2.5 - Fracture of the left petrous bone, with fluid within themastoid air cells (arrows).

a

b

Fig. 2.6 - Frontal head injury caused by road traffic accidentwith fractures of the walls of the right frontal sinus and the for-mation of an air-fluid level.

curred from penetrating injuries. These haem-orrhages vary in dimension from a few mm toseveral cm and occur in 2-16% of all head injurypatients (3). Haematomas can occur acutely,typically due to primary vessel rupture, or mayappear sometime after the trauma, as a result ofthe confluence of multiple small laceration-con-tusion foci; CT scans performed in such casesimmediately after the traumatic incident may becompletely negative. Unlike patients with DAI

or cortical contusion, trauma patients with sin-gle intraparenchymal haematomas may not loseconsciousness; in 30-50% of cases these pa-tients remain lucid for the entire duration ofthe clinical outcome (3, 15). Signs and symp-toms in parenchymal haematomas and theirclinical evolution are similar to those observedin extraaxial haematoma patients, with the ex-ception of large or temporal lobe haemorrhagesthat have an unpredictable outcome; evenwhen small, these haematomas can cause brain-stem damage due to associated transtentorialherniation (3, 7, 29).

Intraparenchymal haematomas usually oc-cur in the same or nearly the same position inwhich the primary trauma was applied to thecranium as a typically well-circumscribed hy-perdensity with or without a rim of perilesionaloedema, depending upon the time of the CTacquisition relative to the traumatic incident(acute: no perilesional oedema; subacute: per-ilesional oedema; Fig. 2.9). These haematomasare frequently observed within the frontal andtemporal lobes. Up to 60% of cases are asso-ciated with extradural haematomas, either epi-or subdural in location. If the haematoma de-velops in a periventricular position, it can rup-ture into the cerebral ventricles. Larger haem-orrhages result in considerable mass effect andhave the added risk of downward transtento-rial internal herniation of cerebral and brain-


Fig. 2.7 - (a-c) Diffuse axonal injury (damage). Multiple hyper-dense foci are observed with haemorrhage and compression ofthe white-grey matter junction bilaterally (arrow heads).

a

b

c

stem tissue through the tentorial incisura, oreven the possibility of herniation of the cere-bellar tonsils through the foramen magnumlater in the process of haemorrhagic expan-sion. Clinically it is not always easy to distin-guish intraparenchymal haemorrhage fromDAI or parenchymal contusion; this differen-tial diagnostic difficulty probably accounts forthe marked variability in the clinical evolutionstatistics as reported in the literature (3). Theprognosis for isolated intraparenchymal haema-tomas is fairly good, but worsens considerablywith increasing degrees of mass effect or whenit is associated with DAI or haemorrhages in-to the basal ganglia.

Intraventricular haemorrhage

Traumatic intraventricular haemorrhage issomewhat uncommon and is only present in 1-5% of closed head injuries; it is usually a con-sequence of particularly severe trauma andtends to be associated with DAI and traumaticlesions of the deep grey matter and brainstem.The clinical prognosis is generally poor (3, 13,20, 22). CT shows hyperdense intraventricularcollections, which may or may not have associ-ated fluid-fluid levels. Intraventricular haemor-

rhages are occasionally seen in combinationwith choroid plexus haematomas, haematomasof the deep grey or white matter and subarach-noid haemorrhage (Fig. 2.22c).

Traumatic lesions of the deep grey structuresand the brainstem

This type of lesion is caused by stretchingand torsional forces that cause the rupture ofsmall perforating vessels, or by the direct im-pact of the dorsolateral surface of the brain-stem against the tentorial incisura. These le-sions are less frequently observed than those

mentioned in the preceding sections and repre-sent approximately 5-10% of primary traumat-ic pathology (3, 20, 22). They are associatedwith severe clinical states, and usually have un-favourable prognoses. Depending upon theclinical severity, CT can be entirely negative ormay show relatively minor findings, includingsmall haemorrhages in the areas of the brain-stem surrounding the cerebral aqueduct and inthe basal grey nuclei. As compared to CT, onMRI these types of lesions appear relativelymore clearly.


Tab. 2.4 - Comparison between subdural and epidural haematomas

EPIDURAL HAEMATOMA SUBDURAL HAEMATOMA

Incidence 1-4% of trauma cases; 10-20% of all trauma cases;10% of fatal trauma cases 30% of fatal trauma cases

Aetiology Associated fractures in 85-95% of cases; Tearing of the cortical veins of the ponsLaceration of middle meningeal

artery/dural venous sinus in 70-80% of cases.

Site Between skull and dura mater; Between dura mater and arachnoid mater;Crosses the dura mater Crosses the cranial sutures but not the dura mater;

but not the cranial sutures; 95% are supratentorial;95% are supratentorial 5% are bilateral

5% are subtentorial;5% bilateral

CT findings Biconvex (lens) shape; Acute: 60% hyperdense;Shifts the white-grey matter interface; 40% mixed (hyper-/hypodense)

66% are hyperdense; Subacute: isodense;33% are mixed (hyper-/hypodense) Chronic: hypodense

Crescent shape;

Extraaxial traumatic lesions

Epidural haematomas

Overall, epidural haematomas are present in1-4% of head injury cases, and in 10% of fatalcranial head injuries. These injuries are quiterare in patients over 60 years of age, because ofthe increased adherence of the parietal duramater to the overlying inner table of the skull(Tab. 2.4).

Epidural haematoma patients may presentwith few or minor signs and symptoms. In al-most 50% of all cases there is a typical intervalof mental lucidity between the traumatic eventand the onset of severe neurological deteriora-tion or coma (3, 13). In 10-30% of cases, theimaging findings may first appear and evenprogress over the first 24-48 hours followingthe traumatic incident (20, 22).

Epidural haematomas are situated betweenthe dura mater and the internal bony table of theskull, and they are almost always associated withskull fractures (Fig. 2.10). On occasion,parenchymal countercoup lesions may be ob-served on the side of the cranium opposite to theprimary traumatic blow (3, 20, 22). Thesehaematomas are often secondary to lacerationsof the middle meningeal artery (when in the tem-poroparietal region), or more rarely, tears of thecranial veins such as the diploic and meningealveins, and the dural venous sinuses. In this lattercase, the epidural haematoma straddles the mid-line when the sagittal venous sinus is involved(direct coronal acquisitions or scans reconstruct-ed in the coronal plane may be required for pre-cise demonstration); alternatively, the epiduralhaemorrhage may extend between the supra-and infratentorial compartments, if the lateraldural venous sinuses are involved. Arterially fedepidural haematomas are typically observed inthe acute phase because they grow under arteri-al blood pressure, thus compressing the brainand resulting in early downward internal cere-bral herniation coupled with rapid clinical dete-rioration and eventual coma (7, 29). Venousepidural haematomas are usually small by com-parison as the accumulation of blood takes placeunder relatively low venous pressure. Larger ve-

nous epidural haematomas are typically seenwhen resulting from the rupture of one of thelarger dural venous sinuses. The CT density ofthe extraaxial blood collection depends in partupon the phase in which the haematoma is im-aged. In the acute phase, epidural haematomasappear as homogeneously hyperdense lesions,with a biconvex or lens shape; the varying masseffect can be observed in the contralaterally dis-placed ventricular and extraventricular CSF


Fig. 2.8 - (a-f) Temporal evolution of contusive haemorrhagicfocus. (a-b) CT examination a few hours following trauma: ir-regular haemorrhagic foci are seen in both frontal lobes and inright temporal-parietal region with the obliteration of the ipsi-lateral Sylvian fissure cistern.

a

b

spaces (Figs. 2.10 and 2.11). Rarely epiduralhaematomas can have an isodense appearanceimmediately subsequent to the traumatic inci-dent, if imaging is undertaken before the freshblood clots (another cause may be a very anaemicpatient).

In certain cases of venous epidural haema-toma, CT examinations conducted immediatelyafter the trauma may reveal little, whereas thehaematoma appears only 2-3 days later. This delay

in the appearance of the haemorrhage is due tothe fact that in venous epidural haematomas theinjured veins bleed relatively slowly; alternatively,a delay in epidural haemorrhage from a trauma-tized arterial source may occur because blood canonly flow into the epidural space after resolutionof the trauma-induced arterial spasm. Thehaematoma can also be dampened by the mass ef-fect of overlying brain contusion. In the case ofpersistent bleeding within an extraaxial blood col-lection, the haematoma can appear of mixed den-


Fig. 2.8 (cont.) - (c-d) Follow up after 3 weeks: The hyperdense haemorrhage has been almost completely resolved, whereas the hypo-dense component is still clearly visible; a subdural hygroma has accumulated on the left side. (e-f) Follow up after 6 weeks: There is par-tial resolution of the hypodense component, a residual of which persists in a right frontal region; the hygroma on the left side remains.

c e

d f

sity due to the presence of non-clotted new bloodalternating with older clotted haemorrhage (7,29). In subacute forms, as in the case of bleedingcaused by the rupture of the dural venous sinus-es, the density of the clotted haemorrhage variesin part according to the resorption of the solidblood constituents (Fig. 2.12).

Acute epidural haematomas represent themost urgent of all cases of cranial trauma. Theyrequire swift treatment before irreversibleparenchymal damage occurs, caused by thecompression of brain structures, especially thebrainstem. Although rare (5% of extraaxialhaematomas), extradural haematomas in theposterior fossa are potentially the most worri-some and tend to demonstrate the most rapidcompromise of patient vital functions. As anadditional factor, the compression of the aque-duct of Sylvius may cause acute obstructive hy-drocephalus resulting in progressive supraten-torial mass effect and accelerated downwardtranstentorial internal cerebral herniation.

Subdural haematoma

Subdural haematomas (SDH’s) are one ofthe most life threatening events that can occur


Tab. 2.5 - Post-traumatic sequelae of head injuries

1) - Cortical atrophy2) - Encephalomalacia3) - Pneumocephalus4) - Leptomeningeal cyst formation5) - Cranial nerve lesions6) - Diabetes insipidus (pituitary injury)7) - Hydrocephalus (communicating or obstructive)

Fig. 2.9 - An acute post-traumatic intraparenchymal haematomain observed in the right temporal-occipital area.

Fig. 2.10 - (a-b) A large epidural haematoma is seen in left tem-poral-parietal region (a) associated with an overlying skull frac-ture (b).

a

b

following head injuries, having a 50-85% mor-tality rate (20) (Tab. 2.5). They occur in 10-20% of all cases of cranial trauma and are fre-quent in the elderly with underlying brain atro-phy and large intracranial subarachnoid spaces,and in physically abused children who have

been subjected to strong shaking (i.e., “shakenbaby syndrome”) (3, 6, 20, 23). In elderly pa-tients they may arise in the absence of a trau-matic episode (18, 19). If the haematoma is iso-lated and small, symptomatology may be absentor minor (e.g., headache). However, the SDH isoften associated with DAI and/or severe masseffect, and patients therefore tend to be clini-cally compromised, with low Glasgow ComaScores; in up to 50% of cases, patients appearflaccid or even decerebrate (13).

SDH is a collection of blood in the subduralspace between the external surface of the lep-tomeninges and the dura mater secondary to thelaceration of veins (in particular the veins in-volved are those that join the cerebral corticalveins and veins of the pons with the dural si-nuses), or in the more severe forms, secondaryto or associated with underlying cortical lacera-tion. SDH’s can occur at any age, but are mostfrequently observed in patients aged 60-80 yearsbecause of the greater mobility of the brainwithin the skull secondary to senile atrophy andtherefore the greater ease with which veins rup-ture upon acute traumatic stretching of the at-tached cortical venous structures (18, 19).SDH’s are more frequent than are epiduralhaematomas and are relatively more often asso-ciated with contusion-type injuries rather thanskull fractures. This relationship is useful in pre-dicting patient prognosis and in part explainswhy the overall intracranial mass effect is largerthan are the actual dimensions of the SDH. Dis-tinctions are made between the acute (i.e., with-in 3 days from the trauma), subacute (i.e., with-in 3 months) and chronic (i.e., more than 3months) forms of SDH. In the acute phase, sub-dural haematoma appears as a hyperdense, sick-le-shaped extraaxial lesion (Fig. 2.13); in somecases there may be a medial beak at the level ofthe pterion, where it penetrates the anterior andlateral aspects of the Sylvian fissure between theopercula of the frontal and the temporal lobes.Atypical configurations may be encountered invery large SDH’s (Fig. 2.14a) or in the presenceof fibrous bands traversing the subdural spaceresulting from previous trauma or inflamma-tion; these cases of SDH can take the form of abiconvex lens or a multilocular appearance.


Fig. 2.11 - Axial CT shows an epidural haematoma with bicon-vex lens shape, in right parietal region with compression of thecerebral parenchyma and midline shift.

Fig. 2.12 - Axial CT reveals a small right frontal subacuteepidural haematoma with mixed hypodense and hyperdensecomponent, concomitant extracranial haematoma.

Subsequently, due to the effect of the me-tabolism of the protein content of haemoglo-bin, SDH’s initially become isodense (e.g., be-tween the 7th and 21st day following the trau-matic incident) (Fig. 2.15), and then evolve in-to a generally hypodense lesion (Figs. 2.16,2.17) relative to the density of the underlyingbrain tissue. In practice, an SDH can also be

isodense or hypodense outside of this predictedphase density pattern if the patient is anaemic,or if the systemic blood is diluted with iatro-genically administered fluid; conversely, chron-ic SDH’s can show progressive hyperdensitydue to interim haemorrhage(s) which can beasymptomatic and unprovoked by recurrenttrauma (i.e., spontaneous) (Fig. 2.16). In cer-


Fig. 2.13 - Axial CT demonstrates an acute subdural haematomaalong the left hemisphere convexity with right shift of the mid-line structures and compression of the left lateral ventricle. [a),b) axial CT].

Fig. 2.14 - Bilateral subdural haematomas. There is a biloculat-ed acute-subacute subdural haematoma on the right side (a), aheterogeneous appearance of the two haematomas with fluid-fluid levels (b), and presence of haemorrhagic components ofdifferent ages. The left sided subacute subdural haematoma isalmost isodense as compared to the underlying brain and istherefore somewhat difficult to visualise. [a), b) axial CT].

aa

b

b

tain cases in the subacute or chronic phases, ablood-fluid level can be observed followingblood clot liquefaction, perhaps contributed toby haemorrhagic sedimentation (hypodensitysuperiorly and iso- or hyperdensity inferiorly)(Fig. 2.14b). In some cases, haemorrhagicevents are followed by blood clot organization,which gives the crescent image a layered curvi-linear appearance, with the older, hypodensecollections on the medial and lateral marginsand the more recent haematomas showing a relatively denser core; complex, crescent-shaped layers of varying density, representinghaematomas and membranes of different ages,may subsequently occur.

In rare cases SDH’s can reabsorb sponta-neously, although some increase in volume andbecome chronic in duration. The eventual evolu-tion depends in part upon the hyperosmolarity ofliquefied blood products, as well as on whetheror not new bleeds have occurred over the inter-im. The sites of SDH’s are usually supratentorialand especially over the convexity; due to the lackof barrier to progression at this level, the ex-travasated blood easily extends along the entirehemicranium. If the SDH is situated at the ver-tex, it can go unnoticed on axial slices, and there-

fore coronal scans are required in appropriatecases (Fig. 2.18). If unilateral, SDH’s are accom-panied by a contralateral shift of the midlinestructures and the lateral cerebral ventricles (Fig.2.19); if bilateral, these extraaxial haemorrhagescause compression of the ventricles that assume a


Fig. 2.15 - Subdural haematoma. Axial CT shows a subacuteright frontal subdural haematoma is noted that is isodense andassociated with obliteration of the cortical sulci, displacementof the corticomedullary junction away from the overlying skull,leftward shift of the midline structures and compression of theadjacent lateral ventricle.

Fig. 2.16 - Subdural haematoma. Axial CT reveals and unusualappearing left frontoparietal subdural haematoma with a hy-perdense acute haemorrhagic component layering posteriorly.The left lateral ventricle is compressed by the haematoma andthe contralateral lateral ventricle is dilated. [a), b) axial CT].

a

b

thinner, elongated and parallel appearance (Fig.2.20). In both instances, the characteristic findingis the disappearance of the underlying corticalsulci and the displacement of the superficialbrain parenchyma away from the bony innertable of the skull. For the demonstration of theseSDH’s, especially when the haemorrhage is iso-dense, it is important to identify the correspon-ding cortico-medullary junction and the digita-tions of the white matter that penetrate into thegyral folds. The centrum semiovale usually has a

convex lateral margin; however, in the presenceof an SDH this margin becomes flattened, con-cave or irregularly distorted. If the cortico-medullary junction is not visible, a bolus injectionof contrast medium administered during the scanmay be useful in identifying the cortical surfaceand delineating the border of an isodense SDH.This image enhancement method can document


Fig. 2.17 - Bilateral subdural haematomas. Axial CT shows bi-lateral hypodense subdural haematomas. [a), b) axial CT].

Fig. 2.18 - Subdural haematomas. Axial and coronal CT showssmall, chronic subdural haematoma over the convexity of thebrain is observed which is better seen on coronal scans. [a) ax-ial CT; b) coronal CT].

a

b

a

b

a thin line of enhancement at the brain surface(perhaps due to compression ischaemia), a focaltraumatic rupture of the blood-brain barrier, vi-sualization of a membrane related to the priorhaemorrhage or prominent enhancement of di-lated cortical veins.

SDH’s do not cross the midline because thesubdural spaces on the two sides of the crani-um do not communicate. These haematomasare occasionally observed beneath the tempo-ral lobe within the middle cranial fossa and un-der the occipital lobes extending along the ten-torium cerebelli, and are often difficult to seewith axial slices alone. In these instances, sup-plemental coronal slices are helpful for visuali-zation.


Fig. 2.19 - Subdural haematoma. The axial CT shows a rightfrontoparietal subdural haematoma with associated mass effectupon the adjacent cerebral parenchyma, which causes a subfal-cian herniation of the cingulate gyrus and the compressed rightlateral ventricle. The left lateral ventricle is dilated due to a CSFobstruction at the level of the left foramen of Monro.

Fig. 2.21 - Subarachnoid haemorrhage. Hyperdensity is notedwithin the cortical sulci over the left cerebral hemisphere. Smallhaemorrhagic cortical contusions are also seen, the largest ofwhich can be observed in the right temporal region (arrow-head). [a), b) axial CT].

Fig. 2.20 - Bilateral subdural haematomas. The CT study showslateral ventricles that are thinned, elongated and parallel to oneanother. The left sided subdural haematoma is almost isodenseas compared to the underlying brain.

a

b


Subarachnoid haemorrhage (SAH)

SAH’s typically occur after severe cranialtrauma and are usually associated with haemor-rhagic parenchymal contusions (Figs. 2.21 and2.22) (3, 29). Traumatic SAH’s are usually some-what insignificant from a clinical point of view,being linked pathologically to the rupture ofsmall cortical vessels that traverse the subarach-noid space. These haemorrhages are seen as hy-

perdense collections of blood in the sulci, fis-sures and cisternal spaces, especially around theSylvian fissure and the interpeduncular cistern(Figs. 2.21 and 2.22) (20, 22).

The site of the SAH is often somewhat dis-tant from that of the trauma because the bloodtends to diffuse within the subarachnoidspaces. In some cases the blood can reach theventricular system, due to retrograde flowthrough the foramina of Luschka and Ma-

a

c d

b

Fig. 2.22 - Posttraumatic intraventricular haemorrhage, pneumocephalus, and cerebral oedema. Bilateral eyelid haematomas are seenassociated with subcutaneous emphysema (a). Intracranially are observed subarachnoid (b) and intraventricular haemorrhage (a), airbubbles in the CSF spaces (c) and the widespread oedema within the right cerebral hemisphere (d). [a)-d) axial CT].

gendie. The ability of CT to detect SAH is di-rectly related to the quantity of extravasatedblood as well as to the time from the traumaticincident; the SAH can be negative if the CTscan is performed some days after the event.SAH’s can sometimes be falsely simulated incertain particularly severe cases of diffuse cere-bral oedema, in which the brain appears rela-tively hypodense in comparison to the underly-ing dura mater and neural tissue (20).

Subdural hygroma

A subdural hygroma is an extraaxial collec-tion of CSF caused by the extravasation of thisfluid from the subarachnoid space through atraumatic tear in the arachnoid mater (Fig.2.23). The acute form is particularly frequent inchildren and less so in adults (6, 23). Subacute

and chronic forms can be seen following sur-gery performed to treat severe head injuries. Insuch cases, the hypodense subdural collectionis either located in the region of the operationor alternatively on the opposite side due to anex vacuo mechanism following the evacuationof a contralateral haematoma. The differentialdiagnosis includes chronic, hypodense SDH.

Traumatic vascular lesions

Traumatic cerebrovascular lesions aresomewhat rare, but are probably less infre-quent than reported in the medical literature(3, 9, 20). In certain cases these lesions canbe asymptomatic or have a clinical onsetsometime after the initial traumatic incidentand can therefore be overlooked on routineimaging studies in patients having undergonetrauma. In other cases the presence of othercraniocerebral lesions related to trauma canconceal the presence of related underlyingvascular lesions, as both clinical symptomsand imaging findings may be attributed to other dominant traumatic parenchymalpathology such as DAI, intraparenchymalhaematomas or extraaxial haematomas. CT isa most useful technique for identifying pa-tients with an increased risk of vascular le-sions such as those with fractures at the baseof the skull extending into the bony internalcarotid canal, the sphenoid bone, and thepetrous pyramid of the temporal bone andthe basiocciput. Of course, it should bepointed out that the presence of fractures insuch sites does not necessarily indicate thepresence of associated vascular lesions (7, 29).

The internal carotid artery, which is the mostfrequently affected vessel in cranial trauma, canundergo dissection due to the forced extensionand torsion of the neck or due to the direct lac-eration of the arterial wall by a skull base frac-ture; this is especially true with trauma to theregion directly adjacent to the anterior clinoidprocesses and the bony internal carotid canal(9). In certain cases the adventitia of the carotidartery wall can remain intact and thereby de-velop a pseudo-aneurysm (3, 9, 20). Other pos-sible cerebrovascular lesions related to the trau-ma include dissections, lacerations and frankvessel occlusions, which may or may not be as-sociated with perivascular haematomas.

Another pathological entity connected withbrain trauma is the formation of arteriovenousfistulae. The most typical site is a fistula be-tween the internal carotid artery siphon and thecavernous venous sinus, usually a consequenceof the fracture of the central skull base. In such


Fig. 2.23 - Posttraumatic subdural hygroma. The axial CTshows a left sided frontal posttraumatic subdural hygroma.

cases, one suggestive indirect sign on imaging isthe CT finding of an enlarged, arterialized su-perior ophthalmic vein.

CT is very accurate in demonstrating frac-tures of the base of the skull, whereas greaterdiagnostic sensitivity in demonstrating traumat-ic vascular lesions can be obtained with MR or

MR angiography examinations (3, 20). In se-lected cases where such traumatic cerebrovas-cular lesions are suspected on the basis of non-invasive imaging studies and clinical informa-tion, selective cerebral angiography is requiredto clearly define the diagnosis and to suggestoptimal treatment options.

SECONDARY LESIONS

Internal cerebral herniation

Bony and dural structures grossly subdividethe cranial cavity into functional supra- and in-fratentorial compartments. Internal cerebralherniations are a mechanical shift of the cere-bral parenchyma, cerebrospinal fluid and theattached blood vessels from one compartmentto another. These alterations are the most com-mon secondary effects of expanding intracra-nial processes. Based on the site and directionof the shift, they can be divided into subfalcian,transtentorial (ascending and descending),cerebellar tonsillar and transphenoid (ascend-ing and descending) in type. Patients with in-ternal cerebral herniations are usually in com-promised clinical states that only permit the useof axial CT acquisitions, which are not the mostsuitable for viewing craniocaudal shifts of thecerebral parenchyma. Therefore, due attention


Fig. 2.24 - Posttraumatic cerebral swelling. The CT demon-strated diffuse posttraumatic cerebral swelling is seen withobliteration of the basal subarachnoid cisterns and superficialcortical sulci, compression of the 3rd ventricle and reduction insize of the lateral ventricles. The midline structures are notshifted, and there are no focal haemorrhages are present. [a),b), c) axial CT].

a

b

c

must be paid to gleaning the indirect signs ofinternal cerebral herniation (3, 20).

Subfalcian and descending transtentorialherniations are the most common subtypes. Asubfalcian herniation is defined by a shift of thecingulate gyrus across the midline, traversingbelow the free margin of the falx cerebri. As theshift progresses, the compressed ipsilateralcerebral ventricle becomes thinner, while thecontralateral ventricle dilates as a consequenceof CSF obstruction at the level of the foramenof Monro (Fig. 2.19). In addition, distalbranches of the anterior cerebral artery are alsoshifted towards or across the midline, and, inthe most severe cases these vessels can be com-pressed against the free edge of the falx cerebri;this in turn may result in secondary ischaemiaor infarction due to pressure-occlusion of thepericallosal or callosomarginal arteries.

Descending transtentorial herniations consistof a medial and caudal shift of the uncus and theparahippocampal gyrus of the temporal lobebeyond the free margin of the tentorium cere-belli. This results in an asymmetric appearanceof the peripontine cisterns and the cerebello-pontine angle, which are widened on the side ofthe mass lesion due to a contralateral shift of thebrainstem; the contralateral cisterns are conso-nantly narrowed by both the lateral shift as wellas the downward herniation of cerebral tissue.The anterior choroid, posterior communicatingand posterior cerebral arteries are also dis-placed medially and downward and can becompressed against the free edge of the tentori-um cerebelli with resulting ischaemia or infarc-tion of the occipital lobe if severe. In rare cases,compression of the perforating vessels emergingfrom the arterial circle of Willis can cause is-chaemia and infarction in the basal cerebral nu-clei. Other possible complications of transtento-rial herniations include periaqueductal brain-stem necrosis, brainstem haemorrhage (i.e.,Duret haemorrhages) and direct contusion ofthe cerebral peduncle(s) due to traumatic im-pact against the free edge of the tentorium cere-belli (i.e., Kernohan’s notch) (20).

Ascending transtentorial herniations aremore rare, and are defined by the cranial shiftof the cerebellar vermis and parts of the superi-

or-medial aspects of the cerebellar hemispheresthrough the tentorium incisura. This in turn re-sults in compression of the superior cerebellarand superior vermian cistern and the upperfourth ventricle. If severe, hydrocephalus maydevelop due to the compression of the aque-duct of Sylvius.

Tonsillar herniations are usually caused byan increase in mass effect within the posteriorfossa, which causes a downward displacementof the cerebellar tonsils through the foramenmagnum. It is estimated that up to half of alldescending transtentorial herniations and ap-proximately two-thirds of ascending transten-torial herniations are associated with tonsillarherniations at some point in the evolution ofthe herniative process.

Descending transphenoid herniations areproduced by a posterior and downward (cau-dal) shift of the frontal lobe beyond the marginof the greater wing of the ipsilateral sphenoidbone, with backward displacement and com-pression of the Sylvian fissure, the middle cere-bral artery and the temporal lobe on the sameside. Conversely, in ascending transphenoidherniations, the frontal lobe is pushed upwardsand anteriorly, to extend above the margin ofthe greater wing of the sphenoid.

Posttraumatic diffuse cerebral oedema

Diffuse cerebral oedema with generalizedswelling of the brain occurs in up to 10-20%of all severe head injuries; this is encounteredmore commonly in children and can be eitherunilateral or bilateral (Figs. 2.24, 2.25). Uni-lateral diffuse cerebral oedema is associatedwith ipsilateral subdural haematoma forma-tion in 85% of cases and with epiduralhaematoma in 9% of cases; it is an isolatedfinding in only 4-5% of cranial trauma pa-tients (3, 20). Despite the fact that it can de-velop in just a few hours in the most seriouscases, it usually evolves over a period of 24-48 hours. Posttraumatic diffuse cerebral oede-ma is caused by an increase in the water con-tent of the brain and/or an increase in in-travascular blood volume, both of which can


be precipitated by a number of factors. Thisis a severe clinical condition and is fatal in ap-proximately 50% of cases (20). The CT pic-ture is characterized by a generalized obliter-ation of the cerebral cortical sulci and the in-tracranial subarachnoid spaces of the suprasel-lar and perimesencephalic cisterns (e.g., am-biens and quadrigeminal), and the cerebralventricles appear thinned and compressed.

The brain appears diffusely hypodense, witha loss of the distinction of the grey-white

matter interface. The cerebellum is generallyspared and can appear relatively hyperdense ascompared to the cerebral parenchyma which isisodense. In the later stages of evolution in se-vere cases, diffuse cerebral oedema is often ac-companied by transtentorial internal cerebralherniation (3, 20, 22).

Posttraumatic cerebral ischaemia and infarction

The herniation of brain parenchyma acrossthe falx cerebri and through the tentoriumcerebelli is the most common cause of post-traumatic infarction. The occipital lobe is theterritory most frequently affected by ischaemicevents, which are usually associated with herni-ation of the temporal lobe through the tentori-al incisura, with consequent compression-oc-clusion of one or both of the posterior cerebralarteries (3, 20). The second most common areaof infarction associated with cranial trauma isthe vascular territory of the anterior cerebralbranches contralateral to the traumatic mass le-sion, to include the pericallosal and callosomar-ginal arteries, consequent to subfalcian hernia-tion of the cingulate gyrus. More rarely, infarctsmay occur in the basal ganglia due to the com-pression of the choroid, lenticulostriate andthalamoperforating arteries against the struc-tures at the base of the skull (7, 29).

Another category of important secondarymanifestations of brain injuries is that of post-traumatic haemorrhages related to direct injuryof larger arteries and veins. The caudal shift ofthe upper portion of the stem in transtentorialherniations can cause a compression of the per-forating vessels in the interpeduncular cistern.This in turn causes small haemorrhagic foci,which can be confluent, in the tegmen (i.e.,Duret haemorrhage), which must not be con-fused with the rarer primary haemorrhagic con-tusion lesions in the dorsolateral portion(s) ofthe midbrain resulting from collision of thebrainstem with the free edge of the tentoriumcerebelli. As an additional factor in descendingtranstentorial herniations, the impact of thecerebral peduncle contralateral to the traumat-ic mass lesion(s) against the free edge of the


Fig. 2.25 - Posttraumatic cerebral oedema. The CT revealsposttraumatic cerebral oedema is observed associated with dif-fuse hypodensity of the white matter and obliteration of theSylvian and perimesencephalic cisterns, a reduction in the sizeof the ventricular system and small intraparenchymal righthaemorrhages in the right frontal region.

a

b

tentorium cerebelli may cause oedema, is-chaemia and/or haemorrhagic necrosis of thisstructure which results in focal atrophy thatmay take the gross form of a notch (i.e., Ker-nohan’s notch). Clinically this may result inhemiparesis ipsilateral to the side of the pri-mary traumatic effects; this is known by theterm “false localizing sign” because it occurs inthe peduncle contralateral to the supratentorialtraumatic mass effect (20).

POSTTRAUMATIC SEQUELAE

The most common sequelae of severe cranialtrauma include cortical atrophy, encephaloma-lacia, pneumocephalus, CSF leaks (i.e., fistu-lae), leptomeningeal cysts, cranial nerve lesionsand diabetes insipidus (Tab. 2.8).

Encephalomalacia is characterized by foci ofcerebral parenchyma loss in the area of the con-tusion and by diffuse cortical atrophy (3, 20).Encephalomalacic foci appear on CT as hypo-dense areas, often associated with varying de-grees of dilation of the adjacent cerebral ventri-cles and overlying cortical sulci.

Skull base fractures with interruption of thedura resulting in direct communication of thecranium with the paranasal sinuses, can lead tointracranial air collection(s) (i.e., pneumo-cephalus). This is easily detected using CT be-cause of the extremely low attenuation coeffi-cient of air (Figs. 2.3, 2.22) (8). Air limited tothe epidural space tends to remain localizedand does not vary in position with the place-ment of the head; conversely, air localized tothe subdural space tends to move its principalfocus with head movements (20). Subarachnoidair is typically multifocal, non-confluent, has a“bubble-like” appearance and is often localizedwithin the cerebral sulci. Posttraumatic intra-ventricular air occurs in association with frac-tures at the base of the skull with lacerations ofthe dura mater. Intravascular air is only rarelyobserved and is usually detected only in casesof fatal trauma.

CSF leaks are a consequence of fractures ofthe base of the skull in 80% of cases (20). Typ-ically they are frontally positioned with CSF

draining via a fistula into the ethmoid or thesphenoid paranasal sinus, and in 20% of casesthey are complicated by meningitis, which ifuntreated can in turn lead to the formation ofcerebral abscess or extraaxial empyema (20).Clinical onset of a posttraumatic CSF leak usu-ally occurs within a week of the initial trauma,but can develop as late as several years after theevent. High resolution coronal acquisition CTis the examination of choice to identify the as-sociated skull base fracture, although the visu-alization of the fistula is often difficult or im-possible to achieve. Positive contrast CT or MRcisternography may be required to prove thepresence and pinpoint the location of the fistu-la preoperatively.

Cranial fractures can later cause lepto-meningeal cysts. These cysts are typically limit-ed to children, occurring months to years afterthe cranial trauma. They are associated withunderlying meningeal lacerations and theoreti-cally result from an interposition of meningealtissue within the space of the fracture line ofthe overlying calvaria at the time of the trau-matic event. Sometimes known as an “expand-ing posttraumatic fracture”, CSF pulsationshave been hypothesized to be the mechanism ofcyst accumulation as well as fracture expansion.

Diabetes insipidus is an infrequent sequelaof cranial trauma, most commonly seen in in-fants as a result of birth trauma. Diabetes in-sipidus can be a direct result of either descend-ing transtentorial herniation causing hypothala-mic infarction or pituitary stalk transection oc-curring at the time of the traumatic event.

Posttraumatic paralysis of one or more ofthe cranial nerves, especially the second, third,fourth and sixth nerves and the second divisionof the fifth cranial nerve, are typically due tocranial base fractures that involve the cav-ernous venous sinus and the apex of the orbit.The third cranial nerve can also be affected in-dividually by transtentorial herniation of thetemporal lobe, whereas the fourth cranial nervecan be injured by compression against the freemargin of the tentorium cerebelli during vio-lent shaking movements of the head.

One final sequela to cranial trauma is hydro-cephalus, usually secondary to intraventricular


haemorrhage or traumatic adherence of themeninges over the cerebral convexity, the basalcisterns or the aqueduct of Sylvius. This iscaused by an inflammatory meningeal reactionto the effects of the trauma and the presence ofblood products with consequent defective CSFresorption.

CONCLUSIONS

The advent of CT and its progressive tech-nological improvement have revolutionized thediagnosis and clinical management of acute cra-nial trauma patients, resulting in early accurateanalysis and swift evidence-based treatment ofpotentially fatal head injuries. Unenhanced CTis the examination technique of choice in thesecases as it is quickly accomplished, readilyavailable and does not require ancillary studiesusing other imaging technologies in most cases.

The spiral (helical) CT technique is princi-pally useful in those cases in which the exami-nation must be performed within an extremelylimited time frame and in cases in which three-dimensional acquisition is necessary for multi-planar reconstruction of fractures of the orbitand the facial skeleton or CT angiographicstudies of the intracranial vessels. Otherwise,standard CT acquisitions are preferred for theiraccuracy and absence of artefacts.

The use of IV contrast media is restricted tothose rare cases in which a CT angiographic ex-amination is needed when posttraumatic vascu-lar pathology is suspected. Intrathecal positivecontrast cisternography coupled with either CTor MRI may be required to analyse the pres-ence and focus of a CSF fistula preoperatively.

One important limitation of the use of CT isthe difficulty in detecting small parenchymal le-sions located in the posterior fossa or at base ofthe skull, principally because of beam harden-ing artefacts typically present. However, thisproblem is of little practical significance clini-cally in the acute stage of trauma, as suchpathology seldom requires surgical interven-tion.

It should be noted that MRI is more sensi-tive than is CT in detecting small cortical con-

tusion lesions at the grey-white matter inter-face, DAI, extracerebral haematomas (especial-ly when hypodense) and primary and second-ary brainstem lesions. However, these changesare relatively minor and do not usually demandoperative therapy in the emergency time frame.On the other hand, MRI can be a useful com-plement in the acute phase of cranial trauma inpatients with significant clinical findings but noor few CT observations. And finally, MRI is thetechnique of choice in the evaluation of thesubacute and chronic phases of symptomatichead injury.

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24. Rhea JT, Rao PM, Novelline RA: Helical CT and three-di-mensional CT of facial and orbital injury. Radiol ClinNorth Am 37:489-513, 1999.

25. Shane SA, Fuchs SM: Skull fractures in infants and pre-dictors of associated intracranial injury. Pediatr Emerg Ca-re. 13(3):198-203, 1997.

26. Weisberg L., Nice C: Cerebral computed tomography.W.B. Saunders, Philadelphia, pp 321-343, 1989.

27. Wilson AJ: Gunshot injuries: what does a radiologist needto know? Radiographics 19:1358-1368, 1999.

28. Wysoki MG, Nassar CJ, Koenigsberg RA et al: Head trau-ma: CT scan interpretation by radiology residents versusstaff radiologists. Radiology. 208(1):125-8, 1998.

29. Zee CS, Go JL: CT of head trauma. Neuroimaging Clin NAm. Aug; 8(3):525-39, 1998.


163

INTRODUCTION

Trauma is the most common cause of deathamong children and infants, of which head in-juries account for some 60%. The mortality andmorbidity rates concerning primary lesions andposttraumatic sequelae in patients with head in-juries have been considerably reduced by theadvent of computed tomography (CT), which isstill the examination technique of choice in theacute phase, thanks to the rapidity with which itcan be performed, the ready availability of theimaging equipment and the absence of con-traindications (6, 25, 29). The drawback of thistechnique is the difficulty encountered in de-tecting smaller lesions, which are often locatedat the grey-white matter junction or in the vicin-ity of bone (e.g., temporal and frontal lobepoles, posterior fossa). In certain cases, the pa-tient’s clinical condition can be quite in contrastwith the information yielded on their respectiveCT examinations (4, 7).

Due to its greater sensitivity in detectingthese types of lesions, magnetic resonance im-aging (MRI) can be used as a complement to oreven a substitute for CT in some instances (5,10, 14, 16, 18, 19, 24, 26). This said, perform-ing an MR examination in the acute phase oftrauma can prove somewhat difficult and en-tails a number of risks. These drawbacks,

which will be discussed briefly below, makeMR a technique of secondary importance in theoverall imaging evaluation of head injuries (12).

DRAWBACKS

Intrinsic limits

The intrinsic limits of the MR technique con-sist in the absolute contraindication of examiningsubjects having ferromagnetic foreign bodies orelectronic device implants (e.g., cardiac pace-makers). This problem becomes important inpolytrauma patients, who may have acquiredmetal splinters from the traumatic event itself,and even more so in subjects with disorders ofconsciousness in whom it is not possible to re-construct an accurate medical history with regardto previous surgical or prosthetic implant proce-dures (22, 9). It is therefore necessary if possibleto determine the compatibility of any metallicforeign materials that are known or suspected tobe present before exposure of the patient to thestrong magnetic fields inherent in MRI.

Semeiological limits

The semeiological limits of MRI during theacute phase of cranial trauma include its lower

2.3

MRI IN HEAD INJURIESM. Gallucci, G. Cerone, M. Caulo, A. Splendiani, R. De Amicis, C. Masciocchi

sensitivity as compared to CT in identifyingbony fractures of the skull, especially smallones, and acute intracranial bleeds (1, 30).Whereas in CT the densitometric value of theblood is due primarily to the quantity of thehaemoglobin protein component, in MRI theintensity of the signal depends in large part on

the magnetic properties of the iron containedin blood, or rather, on the electronic configura-tion that the hemoglobin iron assumes duringevolution of the haemoglobin breakdownprocess (2). Therefore, although CT is clearlyable to detect a hyperacute phase haemorrhageas an obvious area of hyperdensity due to the


Fig. 2.26 - Hyperacute mesencephalic haemorrhage. CT (a) shows the haemorrhage as a hyperdense area in comparison with the sur-rounding brain tissue. The MRI examination conducted in the acute phase shows the haemorrhage to be isointense on T1-weightedsequences (b) and hyperintense on T2-dependent, FLAIR and turbo spin echo (TSE) (c, d) sequences because blood cannot be dis-tinguished from oedema in this phase on the basis of MRI (i.e., oxyhaemoglobin).

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b

c

d

high concentration of haemoglobin, MRI inthis same phase has characteristically poor sen-sitivity, as the blood (oxyhaemoglobin) has notyet undergone metabolic transformation to aparamagnetic species (Fig. 2.26).

It is only in the acute period, after approxi-mately 12 hours after the event responsible forthe bleed, that the first of a series of haemoglo-bin breakdown products starts to form inamounts that will alter the MR signal. This newspecies, deoxyhaemoglobin, causes a shorten-ing of T2 time, and, to a greater extent T2*,thus creating local inhomogeneities in the mag-netic field generated by the MR unit. On theother hand, red blood cell lysis and the block-age of the respiratory chain in haemorrhagescause an increase in the quantity of free waterand therefore an increase in T2 and protondensity signal, with consequent balancing ofthe T2 shortening, effect and a possible con-cealment of the hypointensity linked to thepresence of intracellular deoxyhaemoglobin.As the magnetic susceptibility effect and there-fore T2* shortening is directly proportionate tothe square of the intensity of the static magnet-ic field, by using high field MR appliances andsequences particularly sensitive to T2* (e.g.,gradient echo sequences, echo-planar samplingtechniques) it is possible to resolve the problemand achieve dominant T2 shortening effects onimaging (i.e., focal reduction of the MR signalwithin subacute haemorrhages).

Another limitation posed by MRI is the factthat it requires relatively longer examinationtimes than does CT. Time is critical in the diag-nostic management of critical cranial traumapatients. In addition, these patients frequentlyare unable to consciously cooperate for thelong examination times inherent in MRI, there-by often resulting in motion artefacts. Recentprogress in technology has largely made it pos-sible to overcome such limits with the use ofhigh field equipment having ultrafast acquisi-tion sequences, that allows to obtain single sliceimages in less than one second (9, 20) (Fig.2.27b).

However, it should be remembered that inacute head injury patients the fundamentalquestion to be answered is whether emergencysurgery is required. In almost all cases thisquestion is answered by CT, which is efficientin depicting significant haematomas or frac-tures of surgical interest. MRI is doubtlesslymore sensitive in identifying subtle haemor-

2.3 MRI IN HEAD INJURIES 165

Fig. 2.26 (cont.) - An MRI examination conducted three dayslater shows an area of hyperintense signal on T1-weighted se-quences (e) and hypointense signal on T2-weighted sequencesas a result of haemoglobin breakdown products (i.e., deoxy-haemoglobin). [a), b), c) axial CT; d), f) axial T2-weightedMRI; e) axial T1-weighted MRI].

e

f

rhagic collections and small intraaxial lesionsrelated to the traumatic incident, but such find-ings have no relevance with regard to emer-gency treatment (17, 23, 27). In any case, theseminor imaging findings can be detected usingMRI once the immediate life-threatening prob-lems have been addressed and the patient hasstabilized.

SEMEIOTICS

Primary intraaxial traumatic lesions

Contusions and laceration-contusions repre-sent approximately 45% of all head injuries.They occur as a consequence of the impact ofbrain tissue against the inner table of the skullor dural insertion of the cranium. This traumatends to cause related lesions in the poles of thefrontal and temporal lobes and within thebrainstem (22, 25). MRI is generally more sen-sitive in detecting these types of lesions than isCT due to the proximity of the traumatic alter-ation to the bony structures (i.e., CT beamhardening effects obscure this pathology) (15).A distinction must be made between simplenon-haemorrhagic contusions and haemor-rhagic or laceration-contusions.

Simple (non-haemorrhagic) contusions are ar-eas of tissue characterized by the presence ofoedema in the acute phase and by necrotic-en-cephalomalacic evolution in the chronic phase.MR is estimated to be up to 50% more sensi-tive than is CT in identifying simple contusions,which appear as hyperintense on T2-weightedsequences, typically affecting the surface layersof the cortical gyri. The sensitivity of MR is fur-ther increased by the use of FLAIR sequences;T1-weighted sequences by comparison are oflittle benefit in the acute phase in simple con-tusions (Fig. 2.28).

Laceration-contusions (haemorrhagic contu-sions) differ from simple contusions by the pres-ence of a haemorrhagic zone within the contu-sion. In this type of lesion, CT can have greaterspecificity than MR, which is often not able todifferentiate between haemorrhagic and non-haemorrhagic lesions (Figs. 2.26, 2.29, 2.30). As


Fig. 2.27 - Multiple contusive and lacerative haemorrhagic cere-bral foci in the acute phase. The T2-weighted sequence (a) showsmultiple areas of signal hyperintensity within which haemor-rhagic components cannot be distinguished. The long scan timeoften results in motion artefacts. The echo-planar sequence (b),which is more sensitive to T2*-weighted tissue, enables the iden-tification of areas of hypointense signal caused by the presence ofsubacute haemorrhage (deoxyhaemoglobin). Motion artefactscan also be reduced by obtaining the acquisition in approxi-mately 500 msec. [a) T2-weighted MRI; T2*-weighted MRI].

a

b

mentioned previously, the use of high field ap-pliances with sequences sensitive to T2* in-crease MR’s specificity, thereby enabling theidentification of haemoglobin breakdown prod-ucts within the haemorrhagic focus (Fig. 2.27).

Axonal injury is caused by axonal shear le-sions that occur with linear or torsional inertialforces, which are common in instances of highspeed trauma. They have preferential sites inspecific areas of the brain that are particularly


Fig. 2.28 - Cerebral contusions. T2 fast spin echo (FSE) and FLAIR sequences demonstrate that the latter prove more sensitive inidentifying contusive foci, even of very small dimensions. The superior identification of the subdural haematoma with FLAIR se-quences is also noted. [a), c), d) T2-weighted MRI; b) FLAIR MRI].

a

b

c

d

sensitive to these kinds of force in traumaevents, including: the white grey-white matterinterface, the border between the superficial

mantle and the deep grey matter structures(junctional lesions), the midline commissures(especially the corpus callosum: commissural


Fig. 2.29 - Hyperacute cerebral haemorrhage. CT and T2-weighted MRI images show that in the hyperacute phase onlyCT is capable of showing the haemorrhagic component of theright temporal-insular shear-contusive focus. [a) axial CT; b)axial T2-weighted MRI].

Fig. 2.30 - Contusion-shearing injury. T2-weighted MRI se-quences highlight multiple grey-white matter junction axonal(a) callosal commissure lesions (b, c), lesions in the basal gan-glia (c, d) and brainstem lesions (e). However CT alone is ableto demonstrate the presence of any haemorrhagic component(f). [a)-e) axial T2-weighted MRI; f) axial CT].

a

b

a

b

lesions) and the brainstem (7, 13). These le-sions are usually ovoid in shape with their lon-gitudinal axis directed parallel to the directionof nerve fibre bundles, and having dimensions

ranging from a few millimetres to 2 cm; theselesions are usually not haemorrhagic.

Junctional lesions are believed to be the mostfrequently observed type of traumatic cerebral


Fig. 2.30 (cont.).

e

f

c

d

injury and are usually located in the poles of thefrontal and temporal lobes. Neuropathological-ly, the lesion is characterized by the transectionof the nerve cell’s axon, with subsequent Wal-lerian degeneration of the distal axon processand associated swelling of the nerve cell body.Junctional lesions only affect the grey-whitematter interface in the basal ganglia in 4.5% ofcases and usually have a focus in the thalamus;in these cases at least 50% of lesions are haem-orrhagic, in part because of the rich vascular-ization of such tissue. The explanation for thispreferential injury site lies in the difference be-tween the relative kinetic energy of white mat-ter versus grey matter, partly due to their dif-ferent specific weights. Therefore, in the case ofabrupt acceleration-deceleration, the two sub-components come to a stop at different times,thus resulting in linear tears at their interface.MR is up to three times more sensitive than isCT in identifying such junctional lesions, typi-cally demonstrating focal hyperintense areas onT2-weighted sequences having an ovoid shapeand located at the border area between whiteand grey matter (Fig. 2.30). The sensitivity ofMR can be further enhanced by the use ofFLAIR sequences, which typically make it pos-sible to visualize even the smallest lesions (Fig.2.31). Once again, the use of high field magnetsand T2*-dependent sequences makes it possi-ble to detect haemorrhagic components whenpresent (Fig. 2.32). However, it must be re-membered that although the identification ofthis type of lesion is not important for reasonsof emergency treatment, it can be a significantfactor in later prognostic and legal analyses.

Commissural lesions affecting the axonal fi-bres of the corpus callosum typically occur incases where the brain has been subjected togreater degrees of trauma, often of a torsionalnature. This torsion injury results from differ-ential forces applied to the corpus callosumwhen a different rotational kinetic energy ob-tains within one cerebral hemisphere as com-pared to the contralateral one during accelera-tion-deceleration trauma. The falx cerebri canact as a contributory factor in the traumatic ef-fects, causing mechanical compression of thecingulate gyrus, by inducing vascular lesions via

trauma to the adjacent pericallosal artery or bydirect contusion or even a slicing of the corpuscallosum as it collides against the posterior ex-


Fig. 2.31 - Shearing injury. The FLAIR MRI sequence (b) ismore sensitive than the T2-weighted FSE sequence (a) in iden-tifying even very small junction lesions (reprinted by M. Gal-lucci et al., 9)

a

b

tent of the free edge of the callosum. The neu-ropathological picture is always that of a tran-section of the involved nerve fibres. The most

common sites involved in this pathologicalprocess are the splenium and posterior body ofthe corpus callosum, in large part because ofthe proximity of these areas to the posteriorfree margin of the falx cerebri. The MR semei-otics are similar to those described for junc-tional lesions (Fig. 2.30).

Brainstem lesions constitute the clinicallymost serious form of axonal damage and can bedivided into primarily non-haemorrhagic neu-ronal and primarily haemorrhagic microvascu-lar lesions. Neuronal lesions, which are usuallymore severe from a clinical point of view, mostfrequently represent a transection of nerve fi-bres of the ascending sensory pathways, or morerarely, injuries of the fibres of the descendingmotor pathways. They are generally caused fol-lowing torsion trauma due to the same mecha-nisms described for commissural lesions. Theselesions tend to be round morphologically. TheMR signal semeiology is typically identical tothat seen in junctional lesions. These lesions areusually located in the dorsolateral portion of thepons and midbrain (Fig. 2.30). Primary haem-orrhagic microvascular brainstem trauma, orDuret lesions, occur following the tearing of theperforating branches of the basilar artery or theproximal portion of the posterior cerebral ar-tery. The most frequent location for this type ofhaemorrhagic lesion is the ventral midline por-tion of the brainstem. This type of lesion is of-ten associated clinically with a “locked-in” syn-drome. With regard to the MR signal character-istics, the same comments apply as those madeabove for haemorrhagic lesions.

The superior sensitivity of MR as comparedto CT in the identification of brainstem lesionsis further increased because of the obscuringeffects of the beam hardening artefacts presenton CT within the posterior fossa (Fig. 2.33).

Primary extraaxial traumatic lesions

Primary extraaxial traumatic lesions accountfor approximately 45% of all head injuries. In-cluded in this category are subarachnoid haem-orrhage, epi- and subdural haematomas, andsubdural hygromas.


Fig. 2.32 - Haemorrhagic shearing injuries. Unlike FSE T2-weighted sequences, gradient recalled echo sequences whichare more sensitive to T2* effects, are able to distinguish thepresence of a haemorrhagic components within very small grey-white matter junction shearing injuries. [a) T2-weighted MRI;b) T2*-weighted MRI].

Subarachnoid haemorrhage consists of local-ized or diffuse haemorrhage within the sub-arachnoid space. These haemorrhages rarely oc-cur as isolated lesions but instead are more fre-quently associated with extraaxial haematomasor cerebral laceration-contusions (3, 4, 28). Adistinction can be made between primary andsecondary subarachnoid haemorrhage. Primarysubarachnoid haemorrhage results from thesubarachnoid rupture of small pial-cortical sur-face vessels, from the tearing of bridging veinstraversing the subarachnoid space or from theposttraumatic rupture of arteriovenous malfor-mations or cerebral aneurysms. Secondary sub-arachnoid haemorrhage, on the other hand, iscaused by the rupture of a subdural haematomaor a cerebral laceration-contusion into the sub-arachnoid space.

Routinely, CT is undoubtedly the examina-tion of choice when subarachnoid haemorrhageis suspected. However, MR is more sensitivethan CT in detecting the smaller subarachnoidbleeds, because it is able to identify the pres-ence of small quantities of blood in the sub-arachnoid space if FLAIR sequences are used.In cases of massive primary subarachnoidhaemorrhage, MR examinations performed inthe acute phase combined with MR angiogra-

phy (MRA) can potentially identify the AVM oraneurysm responsible for the bleed.

Subdural haematomas can be either primary,due to the rupture of superficial bridge veinsor small, superficial cortical arteries, or sec-ondary, when the presence of an intracerebralhaematoma with a leptomeningeal margin re-sults in a rupture of the blood into the subdur-al space (8). The rapid diagnosis of acute sub-dural haematomas in head injury patients isquite important, as surgical evacuation withinthe first 4 hours reduces the death rate in suchpatients by 30%. Yet again, when acute sub-dural haematoma is suspected, CT representsthe technique of choice in head trauma pa-tients. Subdural haematomas that are visual-ized on MRI but not seen on CT are usuallysmall and of no surgical significance (Fig.2.34). However, the discovery of small subdur-al haematomas can be important in distin-guishing these lesions from other types ofpathology, or alternatively in cases of legal orforensic interest, in which case MRI is the im-aging technique of choice because of its higherrelative sensitivity overall.

Acute subdural haematomas reveal charac-teristic MR signal, including isodensity on T1-weighted sequences and hyperintensity on PDand T2-weighted sequences indicating princi-pally oxyhaemoglobin. The presence of clotswithin the subdural haematoma can be respon-sible for an inhomogeneity in the signal, theseclots appearing hyperintense on T1 sequencesand hypointense on T2-dependent sequences(i.e., the combined effects of clot consolidationand deoxyhaemoglobin).

Extradural or epidural haematomas are bi-convex haemorrhagic collections with smooth,distinct margins, situated between the internaltable of the skull and the dura mater. Thesehaematomas are most commonly caused by therupture of the middle meningeal artery or oneof its branches, or less frequently, rupture ofthe posterior meningeal artery, one of the duralvenous sinuses or the diploic vessels of the cal-varia. Epidural haematomas are usually en-countered at temporobasal or temporoparietalsites, and in most cases (85-90%) are associat-ed with fractures of the adjacent skull. With re-


Fig. 2.33 - Shearing injury. Identified on this T2-weighted FSEsequence is a small posttraumatic lesion of the posterior medul-la oblongata, following attempted suicide by hanging.


Fig. 2.34 - Haemorrhagic contusion, subdural haematoma and skull fracture. The CT examination (a, b) shows a haemorrhagic con-tusion associated with a small subdural haematoma (small solid arrows). The MRI conducted using T1- (c) and T2- (d) weighted se-quences more clearly shows the thin subdural haematoma located adjacent to the overlying bone (small solid arrows). CT (b) allowsmore direct identification of small associated bony fractures, although fractures may also be visible on MRI (arrowheads). (reprintedfrom M. Gallucci, et al., 9) [see Fig. 2.36].

a

b

c

d

gard to the identification of extraduralhaematomas, the sensitivity MRI is similar tothat of CT, but MRI is more accurate. This isprincipally due to the ability of obtaining mul-tiplanar acquisitions on MRI that inherentlyhave a greater probability of visualizing even

small bleeds without artefact, and the difficultyencountered with CT in the detection of thinhyperdense collections of blood adjacent tobone (Fig. 2.29). However, CT does permit thesimple identification of associated bone frac-tures when present. In any case, the thin ex-


Fig. 2.35 - Left-sided cerebellar contusion. An MRI examination conducted in the hyperacute phase shows the presence of oedemain a left-sided cerebellar contusion (a, b). The MRI follow up conducted 15 days later documents the partial resolution of the oede-ma within the cerebellar contusion on the left. (a, b) (reprinted from M. Gallucci, et al., 9)

a

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tradural collections that may be missed on CTbut are visible on MRI do not require surgicalintervention. Once again, legal and forensic in-terests may demand an MR examination inspite of these observations.

A tear of the leptomeninges and inner ormeningeal layer of the cranial dural mater dur-ing head trauma can result in the passage ofCSF into the subdural space. The resulting for-mation of a fluid collection, that is isointensewith the fluid in all MR acquisitions, is knownas a subdural hygroma (8). Subdural hygromastypically are not large and therefore producelittle mass effect upon the underlying cerebraltissue, although exceptions are occasionally en-countered.

Acute secondary traumatic lesions

These secondary complications arise at afairly early stage in the evolution of head trau-ma, assume their own clinical importance andcan eventually come to dominate the patient’sclinical condition.

Cerebral swelling of a diffuse nature occursin association with 10-20% of all severe headinjuries, having a greater incidence in children.This type of brain swelling usually occurs inconnection with a primary traumatic lesion ofthe cranium that in 85% of cases is a subduralhaematoma. Diffuse cerebral swelling occurs asan isolated lesion in only 5% of cases of headtrauma. It typically appears within 4-48 hoursof the traumatic incident and represents an in-crease in cerebral volume in part due to diffusevascular paralysis (i.e., loss of cerebrovascularself-regulation) with a consequential increase in


Fig. 2.36 - Posttraumatic right-sided cerebellar infarct. T2-weighted MRI shows the presence of a cerebellar infarct in theterritory of the right posterior inferior artery. The frontal MRAexamination reveals a thinned, string-like incomplete MRI flowsignal within the right vertebral artery. A T1-weighted scan ofthe neck, carried out 4 days after the traumatic event, shows adissection of the right vertebral artery with intramural hyperin-tensity (open arrows) due to the presence of methaemoglobin.(reprinted from M. Gallucci, et al., 9)

the cerebral blood pool. Cerebral swelling istherefore different from cellular or cytotoxicoedema (see below) of the cerebrum, which iscaused by an increase in free water in the intra-cellular compartment, or vasogenic edemawhich is a result of leakage of fluid from the

vascular system into the extracellular compart-ment (21, 7, 27). The swelling can be mono-hemispheric or bihemispheric. Monohemi-spheric swelling tends to a more serious prog-nosis due to the greater incidence of internalcerebral herniation associated with this sub-type. The overall mortality in cases of diffusecerebral edema is approximately 50%. CT andMRI have similar sensitivity in diagnosing cere-bral swelling. From a semeiological point ofview, both techniques show a compression ofthe lateral ventricles and an effacement of thecerebral sulci over the cranial convexity. In theabsence of complications or associated trau-matic effects, no signal alteration on MRI canbe identified in these cases on T2-weighted se-quences.

Whether focal or diffuse, as it is linked to anincrease in the amount of free water, cytotoxicand vasogenic cerebral oedema translates onMRI into a reduction of signal intensity on T1-weighted images and in an increase in signal in-tensity on PD- and T2-weighted sequences.The gradual resolution of the oedema in thedays following the trauma can be well docu-mented on MRI, with a parallel resolution ofthe T2-dependent hyperintensity of the oede-matous brain tissue.

Vascular lesions. Trauma can cause the lacer-ation, compression or dissection of the largevessels in the head and neck or of the intracra-nial vessels, and consequentially this can resultin ischaemic or haemorrhagic lesions of thebrain (9, 11, 13). The semeiotics of these sec-ondary ischaemic traumatic lesions is no differ-ent than that described for primary ischaemiclesions. In such cases, MRI has an advantageover CT in that it is able to integrate into onebasic examination the documentation of boththe ischaemic lesion by means of MRI, as wellas the responsible abnormality of the vascularsystem by means of MRA (Fig. 2.36).

Internal cerebral herniations typically occurin association with cases of posttraumatichaemorrhage in which the collections exertsufficient mass effect to result in the dramaticdislocation of brain tissue within the skull.Herniations are usually transfalcian, transten-torial, transphenoid or transalar in location,


Fig. 2.37 (cont. of 2.36) - Basal ganglia cytotoxic oedema. T2-weighted MRI shows hyperintensity within the basal gangliaand cerebral cortex signal consistent with cytotoxic oedema ina case of brain death. (reprinted from M. Gallucci, et al., 9).

however, internal herniations can and do occurin the cerebellar tonsils and inferior vermisdownwardly through the foramen magnum.The multiplanar capability of MRI and itsmore clear visualization of the posterior fossastructures routinely make it more informativethan CT for the evaluation of this type ofpathology.

Brain death. The literature contains someexperiences with the MR angiography tech-nique that demonstrate the absence of flow inthe intracranial circle in the event of braindeath (9, 21).

Our experience, associated with a review ofthe literature, identifies a number of imagingparameters seen in cases of brain death follow-ing cranial trauma. These findings include aloss of the gray-white matter distinction, lowsignal intensity within the cerebral cortex andbasal ganglia related to brain oedema (Fig.2.37), absence of vascular enhancement afterIV contrast medium administration attributedto the absence of intracerebral flow, and an ab-sence of MR flow signal in the main intracranialarterial structures (e.g., carotid siphons, middlecerebral arteries).

CONCLUSIONS

The observations in this chapter show thatMRI is generally more sensitive than is CT inidentifying the acute primary and secondary in-juries associated with cranial trauma. However,this is counterbalanced by the intrinsic limits ofthe technique and the difficulties inherent inthe clinical management of the patient withacute head trauma.

These limitations have recently been at leastpartially overcome by technological progresswith regard to reduced MR scanning times andthe better differentiation of haemorrhagic andnon-haemorrhagic lesions on MRI in the acutephase of head trauma. This is in turn counterbal-anced by the insurmountable incompatibility ofmany metallic life support appliances with themagnetic fields present in and near the MRI unit.

In summary, MRI is now more widely ap-propriately utilized in acute cases of cranial

trauma than it was even a few years ago. Nev-ertheless, CT still remains the undisputed tech-nique of choice for use in most acute phasetrauma patients due to the relative rapidity withwhich it can be performed, the ready availabil-ity of the equipment required and its compati-bility with the life support systems often re-quired by trauma patients.

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21. Osborn AG: Diagnostic Neuroradiology. Mosby YearBook, St. Louis 1994. Cap. 8.

22. Passariello R: Elementi di tecnologia in radiologia e dia-gnostica per immagini. Cromac, Roma 1990.

23. Pierallini A, Pantano P, Zylberman R et al: Valutazione RMcon sequenze FLAIR e FFE del carico lesionale in pazien-

ti affetti da gravi traumi cranici chiusi. Rivista di Neurora-diologia 10:57-60, 1997.

24. Piovan E, Beltramello A, Alessandrini F et al: La Risonan-za Magnetica nei traumi sub-acuti e cronici. In: PellicanòG, Bartolozzi A (eds): La TC nei traumi cranio-encefalici.Ed. del Centauro, 153-171, Udine 1996.

25. Scotti G, Pieralli S, Righi C et al: Manuale di neuroradio-logia diagnostica e terapeutica.

26. Sklar EM, Quencer RM: MR application in cerebral injury.RCNA 30(2):353-56, 1992.

27. Splendiani A, Gallucci M, Bozzao A et al: Ruolo della Ri-sonanza Magnetica nello studio dei traumi cranici acuti ecronici: studio comparativo con tomografia computerizza-ta. In: Pardatscher K.: Neuroradiologia 1989. Ed. del Cen-tauro, Udine 1989.

28. Yoon HC, Lufkin RS, Vinuela F et al: MR of acute suba-rachnoid hemorrhage. Am J Neuroradiol 9:404-5, 1988.

29. Zimmerman RA, Bilaniuk L, Gennarelli T et al: CranialCT in the diagnosis and management of acute head trau-ma. Am J Radiol 131:27-34, 1975.

30. Zimmerman RD, Heier LA, Snow RB et al: Acute intra-cranial hemorrage. Intensity changes on sequential MRscans at 0.5 T. Am J Neuroradiol 9:47-57, 1985.


179

INTRODUCTION

Head injuries in the industrialized worldconstitute an important growing social andmedical problem. On the basis of the clini-cal picture, these injuries are divided intomajor and minor. Unfortunately, the severetype accounts for a large part of all head in-juries and most frequently affects theyounger sector of the population, otherwisecharacterized by the highest life expectancy.The improvement of diagnostic techniques,especially Computed Tomography (CT), aswell as neurosurgical techniques, have great-ly reduced the death rate associated with thistype of trauma, thus underlining the impor-tance of early and accurate diagnosis in pa-tient outcomes.

In emergencies involving facial trauma,many conventional radiological techniqueshave been replaced by spiral CT, which can beperformed more rapidly, achieved with greateraccuracy and with reduced patient discomfort,and accomplished at lower overall cost (8). Theefficiency with which spiral CT examinationscan be performed makes it possible to examinepatients with serious facial injuries in accidentand emergency wards. This is an important as-pect in the instance of polytrauma patients,

where several CT scans can be performed insuccession within a very brief timeframe. Thesuperior quality of spiral CT over alternativetechniques is also due in part to the reductionin motion artefacts (including breathing arte-facts), the use of safer intravascular contrastagents and the better quality of multiplanar re-constructions achieved from high resolutionprimary spiral image sets. Spiral CT is a reliableand rapid method of obtaining vital informa-tion and therefore improving treatment plan-ning in seriously ill patients; this has resulted ina reduction in the utilization of traditional radi-ography in examining the head and neck in cas-es of trauma.

TECHNIQUES

For a diagnostic approach in acute and non-acute head trauma cases, it can be useful to di-vide patients into three groups based upon theseverity of the clinical condition, each of whichhas a different diagnostic procedure associatedwith it: the patient in high grade coma with as-sisted breathing; the non-cooperative patient inlow grade coma; and the awake and co-opera-tive patient with or without focal neurologicaldeficits.

2.4

CT IN FACIAL TRAUMA

S. Perugini, S. Ghirlanda, A. Fresina, M.G. Bonetti, U. Salvolini

1) Patient in high grade coma with assistedbreathingThe patient must be laid supine on the im-

aging examination table, with the head in a po-sition that keeps the cervical spine slightly hy-perextended without forcing. When possible,the CT study should begin with a lateralscanogram (Fig. 2.38a) that includes both thefacial structures as well as the cervical spine.The cervical spine is included because severehead injuries are often associated with traumat-ic lesions of the spine, an area that is difficult toevaluate clinically due to the presence of coma(Fig. 2.38b).

It has been proposed by some practitionersthat several scanograms with different projec-tions (anterior-posterior and right and left45°obliques) be acquired in addition to the lat-eral in order to exclude the possibility of find-ing gross vertebral fracture-dislocations thatmay influence patient care (10). The wide-scaleintroduction of the spiral CT technique has en-couraged this practice, where it has in part re-placed conventional x-rays in screening investi-gations of head and neck trauma patients. It isimportant to emphasize that in some subjectswith facial injuries, associated spinal traumamay be overlooked. A recent study conductedon 582 consecutive patients revealed 6 cases ofcervical spine injury (approximately 1%), mostof which were clinically unsuspected at the timeof initial patient investigation (5).

In cases where the cervical spine is suspect-ed of injury, systematic examination of the cer-vical spine can be undertaken with spiral CT atthe same imaging session during which the fa-cial structures are being analysed (1). In twopublished reports evaluating polytrauma in-volving the head and neck, 32 patients out of 88(9) and 20 patients out of 58 (34%), respec-tively, were found to have traumatic cervicalspine lesions.

Another reason why spiral CT is being in-creasingly used in facial injuries is because themultiplanar and 3D reconstructions made pos-sible with this technique are very useful instudying the facial skeleton and skull (2-4). Spi-ral CT also makes it possible at the same timeto demonstrate foreign bodies in more than one

plane using these multiplanar reconstructions(6). Finally, spiral CT is important because ofits association with CT angiography.

These additional advantages offered by thespiral technique have reinforced CT’s role inscreening facial injuries, even in the era ofMRI (7). This is especially true with regard tothe high definition analysis of complex bonyanatomy such as that found in the orbits. Spi-ral CT is also considered a suitable techniquefor the screening of facial injuries due to itsrelative low cost (11). As always, however, CTstudies must not overshadow the importanceof the physical examination, in order not toobtain results that could prove to be mislead-ing (12).


Fig. 2.38 - Cervical spine fracture. a) A scout view of the cervi-cal spine. b) The CT scanogram identifies a C5 fracture.

a

b

The preferable scan plane is the neuroocularplane (Fig. 2.39), which usually coincides withthe plane of the hard palate or with the Frank-furt plane. This plane can almost always be de-termined from the lateral scanogram. It ispreferable for the following reasons:

1. Simultaneous craniofacial imaging is pos-sible: the facial skeleton, to include the orbits,can be scanned at the same time as the brain.As traumatic lesions of the face are frequentlyassociated with concomitant injuries to thebrain, this technique avoids having to delay adetailed study of the facial skeleton to the dayssubsequent to the initial patient imaging evalu-ation in the emergency room.

2. This plane allows for a more accurate ex-amination of the frontobasal and cervicooccip-ital regions, frequent sites of associated trau-matic lesions.

The scans can begin at the vertex of the cra-nium and proceed downwards toward the skullbase, to include the cervical-occipital junction.Contiguous 10 mm-thick slices are utilizedmaking it possible to identify the presence ofintracranial lesions potentially requiring surgi-cal intervention (e.g., extradural haematoma,subdural haematoma, hydrocephalus). Thescan then proceeds with the study of the struc-tures of the posterior cranial fossa and the or-bitofacial area, using 5 mm-thick contiguousslices.

2) The non-cooperative patient in low grade comaThis is the most frequent clinical condition

encountered in acute trauma patients. Becausepatients in low grade coma are not coopera-tive or are unable to cooperate, performing the

Fig. 2.39 - Neuro-ocular plane. a) A CT scanogram in lateralprojection with indication of the neuro-ocular plane. A-B = linejoining the orbital roof and floor. C-D = line joining the medi-an point of A-B with the sphenoid jugum (neuro-ocular plane).b) The line that passes through the ocular lens, optic nerve, op-tic canal and occipital cortex in the neuro-ocular plane. c) Notethat the neuro-ocular plane virtually coincides with that of thehard palate.

2.4 CT IN FACIAL TRAUMA 181

CT examination is a challenge and may requirepatient sedation or even general anaesthesia. Ittherefore follows that the clinical physicianmust determine whether performing the imag-ing examination is essential for management ofthe patient before proceeding. Patient condi-tion permitting, a rapid CT examinationshould be conducted with contiguous 10 mm-thick scans, starting in the lowermost aspect ofthe posterior cranial fossa and using very shortscan times. The images thus obtained, al-though not high resolution, do make it possi-ble to exclude large intracranial space-occu-pying processes related to the trauma.

3) The awake and cooperative patient with orwithout focal neurological deficitsThis clinical category tends to be seen in pa-

tients with minor head or facial injury and se-quelae. Once again, the use of the neuroocularplane is preferable for the examination of thefrontal and temporal lobes as well as for thestudy of the orbitofacial region. Slice thicknesscan vary from 2-10 mm: 10 mm for studying thesupratentorial compartment of the cranium, 5mm for the posterior fossa structures and 2 mmfor the orbitofacial region.

The spiral CT technique recommendedfor the study of the facial skeleton is as fol-lows: slice thickness: 3 mm; interval: 3 mm(pitch of 1); reconstruction slice thickness:1.5 mm (alternatively for lower resolution re-constructions: 5 mm slice thickness); inter-val: 5 mm (pitch of 1); interval layer recon-struction: 2.5 mm.

In CT studies of the facial skeleton it is alsopossible to perform a more rapid study usinglow mA. This low technique yields good spatialinformation at the expense of densitometric da-ta. However, the latter is typically of little prac-tical importance in cases of facial injury.

The CT study of the facial skeleton mustideally include a direct coronal scan. This scanshould be performed with caution due to thepossibility of associated but unsuspected orundiagnosed injuries of the cervical spine. Es-pecially in acute trauma patients, it is thereforebetter to use coronal reconstructions, re-formed from the high resolution axial image

section set. The information thus obtained isless detailed than that obtained with directcoronal scans, but it is usually diagnostic in allbut the most subtle cases of injury to the facialskeleton.

One must not underestimate the importanceof a complete series of reconstructions in threedimensions, reformed from the high resolutionaxial image section set. While the diagnosis ofspecific trauma can be made from the axial sec-tions, the reconstructions show the most severefractures and dislocations of the face in multi-ple planes, thereby greatly assisting in surgicalplanning.

Of course, in awake and cooperative pa-tients, the imaging investigations must be guid-ed by clinical information. Any ocular or facialposttraumatic deformity, loss of vision, diplop-ia, ocular reflex disorder, and/or facial anaes-thesia or hyperaesthesia merits an imagingstudy of the facial skeleton and cranium.

Most CT examinations are performed with-out the administration of intravascular contrastagents. Using contrast media only lengthens thetime required to perform the examination, usu-ally without adding any information in the trau-ma patient. Contrast is only administered inhighly selected cases, for example: in the pres-ence of considerable mass effect without thedemonstration of a focal mass lesion; when ex-tracerebral collections are suspected that areisodense to the cerebral parenchyma (e.g., sub-acute subdural haematoma); in cases of traumacomplicated by a cerebral and or meningeal in-fectious process; or in instances of posttrau-matic carotid-cavernous fistulae having a char-acteristic clinical picture.

Finally, it must be emphasized that the directCT scans as well as the reconstructions shouldbe filmed and examined utilizing both bonyand soft tissue windows.

SEMEIOTICS

Traumatic craniofacial pathology can be divid-ed into two separate but related groups: cranialinjuries, and facial injuries. In clinical practice, theassociation between these two subtypes of head


injury is quite frequent. Cranial trauma has beendealt with previously in a separate chapter.

FACIAL INJURIES

Fractures of the facial skeleton can involvethe mandible or the maxilla. Fractures of thelatter can be divided into isolated or com-plex subtypes. Isolated fractures involve onefacial component only and are typicallycaused by low energy trauma, whereas com-plex fractures involve more than one com-ponent and are usually associated with highenergy trauma.

1. Fractures of the mandibleDue to its anatomical position, the mandible

is often the site of trauma caused by either di-rect or indirect forces. Mandibular trauma caneither be isolated or associated with other headinjuries. The most widely used of the manyfracture classification systems makes a distinc-tion between simple, compound, comminuted,complicated, ingrained, greenstick and patho-logical fractures.

By definition, simple fractures do not com-municate with the external environment, un-like compound fractures, that have an exter-nal or open surface with the mouth and/or theskin. Comminuted fractures have more thanone fracture line and consist of one or morebony fragments. A fracture is termed compli-cated when it affects nerves, vessels or the tem-poromandibular articulation. Ingrained frac-tures indicate that there is no dislocation ofthe various fracture fragments. Greenstickfractures are defined by a bony structure hav-ing a frank distracted fracture on one corticalsurface, while the opposite side presents a bentbut not fractured cortex; these fractures aremost frequently encountered in children in thesubcondylar region. Lastly, a fracture is classi-fied as pathological when it occurs in an areathat has been weakened by past abnormality(e.g., infectious, neoplastic), or when it occursspontaneously or in the face of minor trauma.

Descriptions of mandibular fractures mustalways focus on the substructure of the

mandible under discussion: the condyle (intra-or extracapsular, subcondylar); the choronoidprocess; the neck, the angle, or the body; the in-cisor (parasymphyseal); the symphysis; or thealveolar process. The direction of the fractureand any dislocation of fragments should also berecorded.

Traditional radiography (e.g., mandibular x-rays, pantomography, intraoral radiographs)is usually sufficient for diagnosing traumaticmandibular lesions. However, CT is suitable asa complementary imaging technique, especiallyin the study of the temporomandibular joint, asit provides good visualization of dislocations ofthe mandibular condyle and the condition ofthe masticatory muscles.

CT examinations are usually performed inthe axial plane with thin slices, and supple-mented with multiplanar reconstructions(e.g., coronal, sagittal, oblique and three-di-mensional). Reconstructions are necessary forthe diagnosis of fractures in the axial plane,such as those of the glenoid cavity. As notedin the foregoing sections, direct coronal scansshould be avoided in acute trauma patientsbecause of the frequent association of headand face injuries with instability of the at-lanto-axial articulation or traumatic cervicalspine lesions.

2. Simple fractures of the maxillaThe most frequently encountered simple

fractures are those of the nasal bone, the or-bito-malar-zygomatic complex and those of thebony orbit.

Fractures of the nasal bonesNasal fractures are the most common of

all facial fractures. Traditional radiography issufficient for obtaining all the informationnecessary in these cases, although CT is alsosensitive in the demonstration of nasal frac-tures, and can be useful if posttraumatic sur-gical reconstruction is being considered (Fig.2.40).

Fractures of the zygomatic archZygoma fractures are also frequently en-

countered, due to the prominent superficial po-


sition within the face and its relatively delicateconstitution. The fractures of this region can bedivided into isolated fractures of the zygomaticarch or so-called “tripod” fractures.


Fig. 2.40 - Broken nose as part of a complex facial fracture. A2 mm axial CT image (a-b) yields a reasonable resolution re-constructed sagittal image (c) from which the axial (d, e) andcoronal (f, g, h) images of the nasal bones are reconstructed.This results in optimal demonstration of the fractures.

a

d

e

f

h

b

c

Fractures of the zygomatic archThe zygomatic arch is constituted by the zy-

gomatic process of the temporal bone and thezygomatic process of the zygomatic (i.e., malar)bone. The traumatic involvement of this struc-ture is well documented by both standard radi-ography as well as CT, which makes it possible

to view the depression or dislocation of fracturefragments, the relationships of the arch to thedeep structures (e.g., masticatory muscles andchoronoid process) and to exclude the involve-ment of the nearby structures (e.g., the glenoidcavity of the temporal bone, orbit and maxillarysinus).


Fig. 2.41 - Tripod fracture of the left cheekbone, with medial and inferior displacement of the orbital-malar-zygomatic complex. Ax-ial CT images (a, b), reconstructed coronal CT section (c) and three-dimensional reconstructions (d, e, f) show the mildly depressed,fractured zygomatic arch and lateral orbital-maxillary sinus walls.

a

b

c

d

e

f

Tripod fracturesThese are also termed malar fractures, frac-

tures of the zygomatic-maxillary complex orfractures of the zygomatic complex and are char-acterized by the fracture and/or diastasis of thezygomatic-maxillary, zygomatic-frontal and zy-gomatic-temporal sutures or the underlyingbony components. Therefore, these fractures af-fect the orbital structures and the maxillary sinus

(Fig. 2.41a-c). This type of fracture can be com-posed or decomposed, with lateral, medial, pos-terior and/or inferior dislocation of the orbito-malar-zygomatic complex (i.e., depressed frac-ture).

CT performed in the axial plane must besupplemented with direct coronal acquisi-tions or reconstructions from a high resolu-tion axial slice set in order to see the in-


Fig. 2.42 - Orbital study technique. 2 mm (a) or 1mm-slices (b). The optic canal (c) may be documented well with high resolutionoblique-coronal reconstructions (d, e).

a

b

c

d

e

volvement of the adjacent soft tissues (e.g.,extraocular orbital muscles, structures withinthe pterygomaxillary fossa) and bony struc-tures as well as to better define the disloca-tion of the orbito-malar-zygomatic complex inthe three spatial planes (Fig. 2.41d-f). Amongother clinical manifestations, the involvementof these nearby structures can cause: limita-tion of mandibular motility due to interfer-ence of the orbito-malar-zygomatic complexwith the choronoid process; limitation of oc-ular motility; loss of vision with the opticnerve at the orbital apex.

Fractures of the bony orbitOrbital trauma can cause: visual compro-

mise due to involvement of the optic nerve;diplopia caused by lesions to the extraocularmuscles or due to alterations of the oculomotornerves; cosmetic alterations (e.g., exo- andenophthalmus). The mechanism of the orbitaltrauma includes: direct trauma; extension of afracture of the adjacent connected bony struc-tures; and “blow-out” fractures, which involvethe thinner orbital wall structures, in particularthe medial wall and floor.

Orbital fractures can involve a part or theentire rim of the bony orbit. CT is withoutdoubt the single imaging examination thatprovides the largest amount of informationon both the bony as well as the intra- andextraorbital soft tissue components of theorbit. A CT investigation angled to the neu-roocular plane is preferred for studying theoptic nerve and canal and is fundamental toimaging of the orbit as a whole. The CT slicethickness should be 2 mm, with 1 mm sec-tions acquired at the level of the optic canal(Fig. 2.42); fast scanning times and low mAcan be used to obtain good spatial defini-tion.

The CT examination must be supplement-ed with direct or reconstructed coronal sec-


Fig. 2.43 - Orbital floor blow-out fractures. a) neuro-ocularplane of study; b, c) axial CT sections passing through the or-bit show discontinuity of the right orbital floor and soft tissuewithin the roof of the right maxillary sinus. c

b

a

tions in order to visualize the orbital floor androof and to better document their relationshipto the extraocular muscles (Fig. 2.43), and toexclude the entrapment of these muscles with-in a linear fracture (esp. orbital floor blow-outfractures). In this manner, diplopia when pres-ent can be clinically considered to be fromother causes. CT also makes it possible toidentify intraorbital or intraocular foreignbodies, orbital emphysema (Fig. 2.44) and in-traorbital haematomas.

3. Complex fractures of the maxillaThis type of fracture can be divided into Le

Fort fractures and nasal-ethmoid midface frac-tures.

Le Fort fracturesHorizontal complex facial fractures are clas-

sified according to Le Fort criteria, which areas follows:

a. Le Fort 1: involves the lower portion ofthe midline anteriorly and the posterior-later-al wall of the maxillary sinus(es), with exten-sion into the distal part of the pterygoidprocesses.

b. Le Fort 2: involves the medial nasofrontalregion, the maxillary sinuses (with the zygomat-ic bone spared), and the base of the pterygoidplates posteriorly.

c. Le Fort 3: involves the medial nasofrontalregion and the orbito-malar-zygomatic com-plex laterally.


Fig. 2.43 (cont.) - d) A reconstructed coronal CT section shows the soft tissue within the roof of the maxillary sinus adjacent to theinferior rectus muscle. e), f) Direct coronal sections better show the orbital floor and the herniation of orbital material into the sub-jacent maxillary sinus. g) A second case showing a larger orbital floor fracture on the right side with depression of bone and soft tis-sue into the roof of the maxillary sinus.

d

f

ge

In clinical practice, these fracture types tendto be more complicated, but they can always betraced back to one of these three categories. Tomake this more interesting, a Le Fort fractureof one type may involve one side of the face on-ly, and be associated with a different type of LeFort fracture on the opposite side.

Direct axial CT with multiplanar recon-structions without doubt offers an accuratespatial representation of bony fracture-disloca-tions while also analyzing involvement of theadjacent bony and soft tissue structures.

Nasal- ethmoid midface fracturesVertical fractures of the face are usually

complex, involving the facial midline struc-tures from the nasal bone junction with theplanum ethmoidale through to the hardpalate. As described above, high resolutionaxial CT with multiplanar reconstructionsmakes it possible to clearly visualize such frac-tures as well as any related cerebral complica-tions (Fig. 2.45).


Fig. 2.44 - Posttraumatic orbital lesions. The CT examinationshows air within the left orbit (a), and an intraocular metallicforeign body on the right side, localised accurately with CT inthe axial plane (b) as well as with CT reconstructions (b1, b2,b3); residual intraocular air (c) following extraction of the for-eign body using a magnet.

c

b1

b2

b3

a

b

REFERENCES

1. Beirne JC, Butler PE, Brady FA: Cervical spine injuries inpatients with facial fractures: a 1-year prospective study. IntJ Oral Maxillofa Surg, 24(1 Pt):26-29, 1995.

2. Buitrago-Tellez CH, Wachter R, Ferstl F et al: 3-D CT forthe demonstration of findings in compound skull injuries.Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr,160(2):106-112, 1994.

3. Gentry LR, Manor WF, Turski PA et al: High-resolutionCT analysis of facial struts in trauma: 2. Osseous and soft-tissue complications. AJR , 140(3):533-541, 1983.

4. Kassel EE, Noyek AM, Cooper PW: CT in facial trauma. JOtolaryngol, 12(1):2-15, 1983.

5. Kirshenbaum KJ, Nadimpalli SR, Fantus R et al: Unsuspectedupper cervical spine fractures associated with significant headtrauma: role of CT. J Emerg Med, 8(2):183-198, 1990.

6. Mauriello JA Jr, Lee HJ, Nguyen L: CT of soft tissue injuryand orbital fractures. Radiol Clin North Am, 37(1):241-252, 1999.

7. Maya MM, Heier LA: Orbital CT. Current use in the MRera. Neuroimaging Clin N Am, 8(3):651-683, 1998.

8. Novelline RA, Rhea JT, Rao PM et al: Helical CT in emer-gency radiology. Radiology, 213(2):321-339, 1999.


Fig. 2.45 - Complex facial fracture. The CT study shows a comminuted hard palate fracture (a), a fracture of the vomer (b), posteri-or extension of the fracture as far as the medial wall of the cavernous venous sinus on the right (c) and a right paramedian sagittalfracture of the ethmoid bone, extending into the optic canal (d).

a c

b d

9. Nunez DB Jr, Zuluaga A, Fuentes-Bernardo DA et al: Cervi-cal spine trauma: how much more do we learn by routinelyusing helical CT? Radiographics, 16(6):1307-1318, 1996.

10. Perugini S, Bonetti MG, Ghirlanda S et al: Technical note:CT scout views of the cervical spine in severely head-inju-red patients. Skeletal Radiol, 25:247-249, 1996

11. Rhea JT, Rao PM, Novelline RA. Helical CT and three-di-mensional CT of facial and orbital injury. Radiol Clin NorthAm, 37(3):489-513, 1999.

12. Thai KN, Hummel RP 3rd, Kitzmiller WJ et al: The roleof computed tomographic scanning in the managementof facial trauma. J Trauma, 43(2):214-217, 1997.


III

INTRACRANIAL HYPERTENSION

195

INTRODUCTION

The skull and bony structures of the spineand cranium combined with the cerebral andspinal meninges form a relatively rigid con-struction of protection for the brain, cere-brospinal fluid (CSF) within the subarachnoidspace and the craniospinal arteriovenous sys-tem. Alterations in the form of an increase inthe volume of brain parenchyma, the CSF orthe vascular components, or alterations of thebony compartment that contains them can giverise to a progressive increase in intracranialpressure.

The terms intracranial hypertension (ICH)and hydrocephalus do not define the same en-tity, but rather refer to a variation in the con-tainer-content relationship in the first case, andin the second case to an accumulation of CSFwith a dilation of the cerebral ventricles; how-ever, in the latter instance, there will also besome degree of necessarily associated ICH.ICH patients usually present the classic sign-symptom triad of headache, vomiting and pap-illary elevation (7, 9).

The headache has particular semeiologiccharacteristics, as it usually occurs upon awak-ening and has a frontal location. It is believedto be caused by the traction exerted on the

meningeal neural structures both within themeninges as well as within the related vascularstructures. Not only the parietal meningovascu-lar structures are involved, but also innervatedare the dura mater of the skull base, the walls ofthe dural venous sinuses and the bridgingveins.

Vomiting is also manifested clinically in themorning, similarly upon awakening, and beforethe patient has eaten. It is not preceded by veg-etative signs such as nausea or ptyalism (exces-sive flow of saliva) and is almost always associ-ated with headache. The pathogenic mecha-nism responsible for the vomiting in cases ofICH is still unknown, however it has been ob-served that the headache subsides partially af-ter the episode(s) of vomiting.

Bilateral ocular papillary elevation is causedby hypertension of the CSF pathways, accom-panied by an increase in the CSF pulse pressuretransmitted to the optic nerve head. This pul-satile pressure increase is directly broadcastedto the optic nerve trough of the optic subarach-noid space via the meningeal sheaths that coatthe entire length of the optic nerve, therebycausing a progressive vascular compression-congestion of the optic nerve head and outwardphysical bulging of the optic papilla into therear of the globe.

3.1

PATHOPHYSIOLOGY AND IMAGING

M.G. Bonetti, T. Scarabino, R. Rossi, A. Ceddia, U. Salvolini

Minor signs and symptoms of ICH include:1) Diplopia: Diplopia is caused by a paresis

of the 4th cranial nerve as a consequence of thepressure increase, which injures the fragile ab-ducens nerve;

2) Eyesight impairment: Protracted oedema,compression and expansion of the optic nervehead cause regressive phenomena entailing per-manent damage and resultant atrophy, ulti-mately terminating in an impairment of eye-sight. In extreme cases amaurosis occurs, aprocess that is almost always irreversible.

3) Endocrinological alterations: ChronicICH is associated with a reduction in functionof the hypophysis, with resultant alterations inhormone production (e.g., FSH, LH, TSH,ACTH, GH) and changes in the gland’s re-sponse to physiological and pharmacologicalstimuli.

4) Disorder of recent memory: This nonspe-cific sign is almost always present in patientswith long clinical histories of minor intracranialpressure elevations. The deficit would seem toaffect the recall of recent events, rather thanmemory of chronological order or long-termmemory.

There is a wide range of possible underlyingpathological conditions responsible for theICH, such as neoplastic, vascular, inflammatory,toxic, metabolic, traumatic or hormonal causes.This chapter deals with the physiopathology ofintracranial hypertension, cerebral oedema,pseudotumor cerebri and hydrocephalus.

THE PATHOPHYSIOLOGY OF INTRACRANIAL HYPERTENSION

The intracranial space is divided by the ten-torium cerebelli into the supratentorial and sub-tentorial compartments, which communicatewith one another via the tentorial incisura. Thisintracranial space is completely occupied by sol-id or fluid components, including the brain, thesubarachnoid space and cerebrospinal fluid,and the blood and attendant vascular walls; itscontent is considered uncompressible: varia-tions in intracranial pressure are closely de-

pendent on and correlated with variations inthese solid and fluid subcomponents.

Over a wide variety of pathological as well asnormal physiological situations (normal health,changes of posture, some forms of illness, etc.)the quantity of blood present in the intracranialspace does not undergo significant overall vol-ume alterations. The blood exiting the craniumvia the outgoing venous system guarantees suf-ficient space for the arterial blood that entersthe skull with each systolic cycle, thus consti-tuting a self-regulating mechanism of cerebralblood flow. This flow self-adjusts to intracranialpressure changes in order to guarantee steadyblood flow to the brain.

Normal intracranial pressure

In order to clearly understand normal varia-tions in intracranial pressure (ICP), a few simplemodels will be discussed as examples (10). Fig.3.1a illustrates a patient in the lateral decubitusposition, with a spinal tap needle within the lum-bar subarachnoid space. The plane of the needlepasses through the midsagittal plane of the spineand skull. In the case of the cranium being opento atmospheric pressure, the fluid pressuremeasured in the spine is equal to the distance be-tween the middle sagittal plane and the upper-most lateral wall of the cranial meninges.

When the patient is in the vertical position(Fig. 3.1b) the hydrostatic column of CSF ap-proximately equals the distance between thepoint in which the spinal tap is positioned andthe top of the cranial meninges if it is open tothe influence of atmospheric pressure. Howev-er, if the skull is excluded from the direct actionof atmospheric pressure but instead is imaginedto be completely closed, there is no change inpressure on the passage from the horizontal tothe vertical position (Fig. 3.1c), because in thiscase the spinal portion of the system alone issubject to the action of atmospheric pressure.

Fig. 3.1d illustrates a normal person in a sit-ting position with the same lumbar subarachnoidneedle in place. One can observe how the meas-urement of pressure reaches that expected of thecervico-thoracic junction level, thus showing tobe lower than it would have been if the intracra-

196 III. INTRACRANIAL HYPERTENSION

nial space had been open to the direct influenceof atmospheric pressure, and greater than itwould be were the system completely closed.

This series of experiments demonstrates thatthe intraarachnoid craniospinal system cannotbe considered a completely closed system, as itis in contact with atmospheric pressure throughthe craniocerebral blood vessels. For the mostpart this pressure effect is transmitted throughthe veins that lead from the skull base or fromthe peridural venous plexus at the level of theforamen magnum.

When measuring CSF fluid pressure, the val-ues recorded at lumbar level are greater thanthose obtained from the cervical area, which are,in turn, higher than those recorded directly at anintracranial level. In normal subjects, the bal-anced hydrostatic point is situated at the cervi-cal-thoracic junction: it remains the same whenmeasured in either the horizontal or vertical po-sition. The zero pressure point is situated crani-ad to this in the cervical region of the spine. Nor-mal intracranial pressure values fall between 9and 13 mm Hg, and therefore values higher than15 mm Hg are considered pathological.

The pressure-volume ratio

The various phenomena that occur in thevolumetric alterations of the intracranial com-ponents are linked to physical laws expressedby the pressure-volume ratio (4).

Intracranial hypertension is the result of anincrease in the total absolute intracranial vol-ume of the contained soft tissue and fluid com-ponents. This volume increase may be causedby expansions in the volume of the cerebralparenchyma, circulating blood or CSF, eithersingularly or in combination. ICH does not ap-pear immediately in response to a gradual, mi-nor increase in volume of one of these con-stituents, as the other components of the systemare able to compensate to a certain degree, thusmaintaining the total volume at a constant level.

The Monro-Kellie doctrine establishes thatbecause the volume within the skull is not ableto increase, there is a fixed relationship be-tween the various intracranial constituents.Therefore, if normal intracranial pressure is tobe maintained, an increase in volume of one ormore of these components or the developmentof a space-occupying lesion can only take placeif there is a reduction in the volume occupiedby the others.

As alterations in the volume of the intracra-nial nerve tissue can only be very slight, it fol-lows that the larger compensatory alterationstake place at the expense of the volume of theCSF and/or the circulating blood within thecraniospinal system. It is estimated that thesupratentorial structures can absorb approxi-mately 50% of such volume alterations, thesubtentorial structures 20% and the spinalcompartment 30%. Any pathological process

Fig. 3.1 - See text.

3.1 PATHOPHYSIOLOGY AND IMAGING 197

a

b c d

that alters the volume of these compartmentsreduces their total compensatory power.

Generally speaking, the CSF compartment inparticular has a relatively high capacity for ab-sorbing increases in intracranial pressure. How-ever, this capacity is contingent on the conditionthat the pressure increase takes place graduallyand slowly. In part this is due to the high resist-ance of the arachnoid villi to CSF filtration;when this CSF-venous drainage rate limit isreached, the intracranial pressure will rise. Thesystem’s fluid reabsorption capacity can at themost guarantee a CSF drainage rate of 1 ml/perminute. It therefore follows that an expansion,for example, of a subdural haematoma may notprecipitate signs of intracranial hypertension ifit forms sufficiently slowly.

The opposite is true for the vascular com-partment, which has very little reserve spacewithout circulatory insufficiency arising withinthe brain. However, what reserve there isadapts very rapidly, thanks to the direct con-nection of the cerebrovascular network withthe systemic circulation.

Fluctuations in cerebral blood flow are gov-erned by a number of factors such as carbondioxide levels, adenosine, potassium, pro-staglandins and anaesthetics. Numerous medi-cines, such as xantine, hypertonic saline solu-tions and hyperosmotic solutions can also in-crease cerebral blood flow. After a certain pointis reached, an increase in cerebral blood flowcauses an increase in intracranial pressure.

In healthy subjects, intracranial pressure ap-pears to be controlled and maintained within arelatively narrow range from moment to mo-ment by minor alterations of CSF volume.However, when intracranial hypertension islong-standing and considerable (e.g., cerebraloedema, intracranial space-occupying lesion,etc.), the resulting hypercapnia induced bythese conditions causes an increase in intracra-nial pressure in part due to the reduced amountof fluid available for reabsorption.

To summarize, the abovementioned com-pensation mechanisms therefore have a varyingrole in intracranial pressure homeostasis. Theintracranial volume occupied by pathologicalalterations can be obtained at the expense of

the CSF volume, the amount of endovascularblood or, to a lesser extent, the brain’s intracel-lular and interstitial water content. However,whereas prolonged mass effect upon the braincan produce a reduction in the amount of braintissue water, variations in the parenchymal cel-lular tissue component are practically negligi-ble. Moreover, although intraparenchymalblood volume can represent a small buffer re-serve, realistically it is the intracranial CSF flu-id content that is the most important buffervolume when intracranial alterations occur.

Intracranial pressure waves

Temporary intracranial pressure readings arenot accurate in revealing the real characteristicsof pressure waves. However, measurementsrecorded over a long period of time show a mi-nor pulse-type pattern, due primarily to the ef-fects of breathing and cardiac activity (5).

Three types of pressure wave alterations aredescribed in patients with intracranial hyper-tension. The smallest waves, termed subtypes Band C, are accentuations of physiological phe-nomena: the C wave represents the breathingcomponent, whereas the B wave is an expres-sion of cardiac activity. The A wave, the onlyone of pathophysiological importance, can bedivided into two forms:

1) rhythmic pressure fluctuations, with in-tervals of 15-30 minutes;

2) plateau waves, which last for longer peri-ods of time.

The former have a frequency of 2-4 cyclesper hour, they begin spontaneously from an av-erage or moderately high pressure base andreach levels of 60-100 mm Hg, before returningto their baseline values. The latter often exceeda value of 100 mm Hg and represent, likerhythmic waves, a serious prognostic index ofimminent serious cerebral consequences.

The relationship between intracranial pressure and CSF production

The CSF produced by the choroid plexusesis not a mere plasma filtrate, but rather an ac-tive fluid body tissue (e.g., certain electrolytes


have higher concentrations than does the sys-temic blood) that functions in part via the ac-tion of carriers and pumps.

Increases in intracranial pressure cause a re-duction in the cerebral perfusion pressure,which in turn results in a reduction of superfil-trate production by the choroid plexuses byhindering the activity of the active transportcarriers and fluid pump. CSF production ceas-es at an intracranial pressure of 22-25 mm Hg.

The consequences of intracranial hypertension on cerebral circulation

Intracranial hypertension has a direct effectupon cerebral perfusion. An increase in in-tracranial pressure would cause a halt of theblood cerebral blood flow when arterial and in-tracranial pressure become equal, were it notfor the intervention of two compensatorymechanisms: arteriolar-capillary vasodilatationand an increase in systemic arterial pressure.

The first of these mechanisms is a cere-brovascular self-regulation mechanism causedby a parietal vessel reflex that acts on the mus-cular fibres of the vessel wall, relaxing themwhen the pressure inside the vessels drops; a lo-cal increase in CO2 and metabolic acids have avasodilatory effect.

The increase in systemic pressure is a result ofa bulbar (i.e., brainstem) reflex triggered bybrainstem ischaemia and would only seem tocome into play once the cerebrovascular self-reg-ulation mechanisms have failed. The latter areefficient up to intracranial pressure values of 50-60 mm Hg, beyond which passive vasodilatationoccurs. Increases in intracranial pressure thentake place until complete circulatory arrest ulti-mately occurs.

Mechanical consequences of intracranial hypertension

By altering the mechanisms that keep in-tracranial pressure within normal limits, in-tracranial space-occupying lesions have an ef-fect on cerebral perfusion but my also inducedisplacements of the cerebral tissues within thecranial cavity.

In childhood, intracranial hypertension takeslonger to manifest itself than it does in adults be-cause of the elasticity of the immature skull. Theabsence of cranial suture closure allows a degreeof expansion of the bony structure of the cal-varia of the skull when an increase in intracranialpressure occurs, whereas this adaptability nolonger exists in adults having a rigid skull.

The matters discussed thus far may suggestthat an increase in intracranial pressure is dis-tributed uniformly inside the skull and is there-fore borne equally by the various parts of theneuraxis. However, this is not true for two rea-sons: the majority of lesions causing intracranialhypertension are focal in nature, and, the cere-bral parenchyma has mechanical propertiesthat are similar to both those of elastic solids aswell as those of viscous fluids.

The nervous tissue adjacent to a mass under-goes deformation, and the pressures are distrib-uted in various ways: they are high in the vicin-ity of the lesion and gradually diminish with dis-tance, thus creating pressure gradients underwhich the nervous tissue is displaced. Theseshifts of the nervous tissue, favoured by theoedema that reduces the viscosity of theparenchyma, may result in internal cerebral her-niations. Neoplasia, abscesses, haematomas andother space-occupying lesions may cause thesedislocations of the contents of the cranium.

When intracranial hypertension associatedwith mass formation occurs, initially the mostimportant factor to recognize clinically is notthe nature of the cause, but rather the presenceor absence of internal cerebral herniation. Themanner in which these shifts occur is more orless similar irrespective of their cause, althoughthey vary with the site, size and rapidity withwhich the space-occupying lesion evolves.

In the initial stages, any expanding lesionexerts uniform pressure on the surrounding tis-sues. These forces are opposed by others, forexample the cerebral tissue itself and the hy-drodynamic resistance of the CSF-containingventricles that oppose resistance to deforma-tion from compressive forces. Another oppos-ing force is the cerebral vascular system and thecontained arterial pressure, as these arteriesconstitute a sort of skeleton for the surround-


ing cerebral tissue. In addition to the arteries,the veins, nerves and meninges also oppose thistype of pressure.

It should also be remembered that the falxcerebri and the tentorium cerebelli divide theskull into three compartments and provide fur-ther opposition to the dislocating effects of masslesions. This division of the intracranial spaceallows displacements of the brain parenchymaunder the effect of space-occupying processesonly in certain directions, including: within thesame compartment, from one supratentorialcompartment to another, beneath the falx cere-bri, downward or upward through the tentorialhiatus, and from the posterior cranial fossadownward into the spinal canal through theforamen magnum.

In the presence of a space-occupying lesion,a sequence of compensation mechanisms canbe described. Initially, the subarachnoid spacesadjacent to the lesion are compressed, with aflattening of the superficial gyri, distortion ofthe ventricular cavities and a deformation anddislocation of the nearby arteries and veins.This is followed by a second phase in which thevolume of the brain tissue involved increasesdue to oedema, and the CSF spaces are nolonger able to compensate for the primary andsecondary mass effect. Any further compensa-tion requires a shift of parenchymal tissue fromone anatomical compartment to another, withthe consequent development of internal cere-bral herniation.

Subfalcian herniations are observed in as-sociation with dominant hemicranial lesions;the degree of brain dislocation beneath thefalx varies according to the original site andsize of the mass lesion. For example, massesthat originate in the frontal regions are morefrequently associated with this kind of hernia-tion as the falx cerebri is less broad anterior-ly and consequently the free space below isgreater than that posteriorly, where the falxand the splenium of the corpus callosum arein closer proximity. This type of cerebral her-niation involves the supracallosal and cingulategyri, the corpus callosum, the anterior cerebralarteries and their branches, the frontal hornsof the lateral ventricles and the midline cere-

bral veins. The third ventricle is also shiftedacross the midline.

Axial herniations take place through the ten-torial hiatus in either an upward or downwarddirection. This type of internal herniation caus-es a distortion and compression of the brain-stem. When downward and the mass effect issufficiently large, the herniation may also affectthe lower cerebellum, which can be displacedthrough the foramen magnum.

Temporal herniations involve the medial partof the temporal lobe and in particular the hip-pocampus and the uncus, which can herniate ei-ther unilaterally or bilaterally. This herniationstretches the oculomotor nerve, compresses theposterior cerebral artery and can impinge on thecerebral peduncle on one or both sides. Theseevents are followed by secondary lesions includ-ing oedema and haemorrhage.

Temporal herniations therefore threatenfunctions regulated by the brainstem, includingvigilance, muscle tone, voluntary motion andvegetative functions. A unilaterally expandingtemporal mass lesion is less favourable than abilateral one because it can cause temporal her-niation at an earlier stage in the mass formingprocess.

Downward cerebellar herniations are ob-served as a complication of expanding process-es in the posterior cranial fossa and may occurin two forms that are often associated. In thefirst type, the cerebellar tonsils are thrust to-wards the upper spinal canal through the fora-men magnum. In the second type, the upperpart of the cerebellar vermis (i.e., culmen) her-niates upwards through the tentorial hiatus,thus pushing the lamina quadrigemina and themidbrain forwards. The resulting injury to thebrainstem depends in part upon vascular com-pression and secondary ischaemia of the upperbrainstem.

Finally, internal cerebral herniations can ob-struct the subarachnoid cisterns, thus prevent-ing the free circulation and proper drainage ofCSF. Above the level of the herniation, in-tracranial pressure tends to increase, whereasbelow it it is normal or only slightly raised.These differentials in CSF pressure add to thevector of thrust and thus worsen the herniation.


This in part explains why in such cases a lum-bar puncture can precipitate a worsening of theclinical status.

The relationship between intracranial pressure and cerebral function

Many patients with obstructive hydro-cephalus or pseudotumor cerebri show modestsigns of cortical compromise in the presence ofhigh intracranial pressure, the degree of whichdepends in part upon whether or not the cere-brum in such patients was normal prior to theonset of the pathological event. The situation issomewhat different in patients with pre- or co-existent parenchymal lesions, such as neoplasiaor contusions. In addition, an increase in ICPdue to the volume of the mass, cerebral oede-ma and/or vasodilatation secondary to hyper-capnia combine with local cerebral hypoperfu-sion, the function of the brain adjacent to theexpanding lesion can be compromised witheven relatively low elevations of ICP (e.g., 15-25 mm HG).

In summary, an increase in ICP causes mal-function of cerebral function through four relat-ed mechanisms: a generalized reduction of cere-bral blood flow, a compression of the tissue sur-rounding the focal mass with local cerebral mi-crocirculatory compromise, brainstem compres-sion and an internal herniation of brain tissue.

PATHOPHYSIOLOGICAL CLASSIFICATION

The general causes of intracranial hyperten-sion can be summarized as an increase in vol-ume of one or more of the intracranial soft tis-sue components: the parenchyma, the CSF vol-ume and the blood volume.

ICH Resulting From Cerebral Oedema

Cerebral oedema (13) is defined as an in-crease in the volume of the encephalon causedby an increase in its water content. This content

may be focal or generalized. When widespreadand severe it can be associated with neurologi-cal signs and may ultimately result in internalcerebral herniation. Cerebral oedema can bedivided into a number of different types, in-cluding: vasogenic, ischaemic, cytotoxic and in-terstitial related to hydrocephalus. Cerebraloedema is usually accompanied by intracranialhypertension, but there are exceptions, espe-cially when the degree is minor.

On CT scans cerebral oedema is character-ized by an area of hypodensity as compared tothe parenchyma. On MR oedema is hypointenseon T1-weighted images, more intense than CSFand less than the parenchyma. On T2-weightedscans, the relative hyperintensity of oedemavaries, and, depending on the protein content, itcan appear more or less intense relative to CSF.

Vasogenic oedema

Vasogenic oedema is the most commonform of cerebral oedema and is typically associated with neoplasia, abscesses, intra-parenchymal haematomas and traumatic con-tusion. It is caused by an increase in the per-meability of the blood-brain barrier and usu-ally affects the white matter with a resultingincrease in density/intensity between whiteand grey matter on medical imaging. These al-terations are due to an increase in the volumeof the extracellular fluid.

Vasogenic oedema is easily discernible inthe white matter as it generally spares the greymatter and exerts mass effect on the ventricu-lar structures (Fig. 3.2). After IV contrastmedium administration, a curvilinear or gyralpattern of enhancement can often be observedalso related to the increase in blood-brain per-meability.

Ischaemic oedema

Ischaemic oedema is the result of a cere-brovascular accident. The pathological processinvolves both white and grey matter with a lossof differentiation on imaging between the two


(Fig. 3.3). It causes the nerve cells to swell andan increase in the permeability of the blood-brain barrier. This type of oedema is both intra-and extracellular and consists of a plasma ultra-filtrate that includes proteins. On imaging thesealterations demonstrate peripheral contrast en-hancement and mass effect.

Cytotoxic oedema

Cytotoxic oedema is most frequently causedby an ischaemic-hypoxic insult such as preced-ing cardiopulmonary arrest. Less frequently itmay be related to water intoxication, the de-compensation syndrome in dialysis patients, di-


Fig. 3.2 - Vasogenic oedema caused by malignant cavitary glial neoplasm. The MRI study shows extensive oedema involving the whitematter surrounding the neoplasm. Note the mass effect upon the lateral cerebral ventricles and the irregular mural contrast enhance-ment. [a), b) T2-weighted, c) unenhanced T1-weighted, d) and T1-weighted MRI following IV gadolinium (Gd) administration].

a c

b d

abetic ketoacidosis, purulent meningitis, severehypoglycaemia and methanol intoxication.

Brain swelling occurs within all cellular com-ponents of the cerebrum (e.g., neurons, glia,ependyma, endothelial cells), in both white andgrey matter, with an increase in the total intra-cellular water content. Neuroradiologically,findings are most frequently observed in thecerebral and cerebellar cortex, the basal ganglia,the hippocampus and the vascular watersheds.The thalami and brainstem tend to be spared.

Mass effect when present results in ventricu-lar compression and the effacement of the CSFspaces (e.g., sulci, basal cisterns). Due to re-duced cerebral perfusion, there may be no en-hancement after IV contrast medium adminis-tration.

Interstitial oedema related to hydrocephalus

This type of oedema is observed in obstruc-tive hydrocephalus and is caused by thetransependymal passage of fluid from the ven-tricles to the periventricular white matter, with

consequent interstitial oedema. It is typicallysymmetric surrounding the anterolateral por-tion of the lateral ventricles (Fig. 3.4).

The grey matter is normal, and there is no ab-normal enhancement after contrast medium ad-ministration. These periventricular alterationsregress following proper ventricular shunting orspontaneous resolution of the hydrocephalus.

ICH RELATED TO ABNORMAL CSFPHYSIOLOGY

Pseudotumor cerebri

Pseudotumor cerebri is a condition (13) hav-ing an undefined pathogenesis that usually af-fects young, obese patients with or without hy-percorticism and menstrual disorders. It is typ-ically observed in females that are otherwisehealthy. Electroencephalograms are normal,and the mental status is intact.

Signs and symptoms associated with pseudo-tumor cerebri include headache, nausea, vomit-ing and diplopia. Bilateral papilloedema is pres-ent, and visual loss is documented in one-thirdof cases, which becomes permanent in one ofeight patients. The diagnosis is determined fromlumbar punctures showing an increase in CSFpressure and from neuroradiological studiesthat exclude the presence of hydrocephalus,mass-forming processes and thrombosis of thedural venous sinuses.

In approximately 36% of cases, CT andMRI are negative; in the remainder, the follow-ing findings may be seen: a small ventricularsystem and a failure to visualize the basal cis-terns; small ventricular system with normal vi-sualization of the basal cisterns; empty sella tur-cica; and enlargement of the sheaths of the op-tic nerves. With normalization of fluid pres-sure, the ventricular and periencephalic fluidspaces return to normal.

HYDROCEPHALUS

CSF (3) is secreted by the choroid plexuses,especially those within the lateral cerebral ven-


Fig. 3.3 - Hemispheric cerebral infarction. Unenhanced axialCT demonstrates a large hypodense area in the vascular distri-bution of the right anterior and middle cerebral arteries associ-ated with mass effect.

tricles. CSF is a clear, colourless fluid containingvery few cells (approximately 2 per mm3) and lit-tle protein (normal range: 25-40 mg/100 ml). Ithas a different ionic composition as compared toplasma, as active secretion mechanisms such ascarriers and pumps contribute to its production.

Interposed between the capillary blood ofthe choroid plexuses and the intraventricularCSF is a blood-fluid barrier, which is perme-able to water, oxygen, carbon dioxide and to alesser degree to electrolytes, but is imperme-

able to cellular and protein components of theblood. Certain drugs (e.g., acetazolamide,furosemide) and metabolic and respiratory al-kalosis reduce CSF production.

Once produced, CSF passes from the lateralventricles, through the foramina of Monro intothe 3rd ventricle and from there through theaqueduct of Sylvius into the 4th ventricle. Fromthe 4th ventricle, the CSF passes through theforamina of Luschka and Magendie, to reachthe subarachnoid spaces of the skull base.


Fig. 3.4 - Neoplasm of the cerebellar vermis with obstructive hydrocephalus. The MRI examination shows a contrast enhancing mass(a) likely originating within the cerebellar vermis that compresses the 4th ventricle and has resulted in obstructive hydrocephalus (b).The T2-weighted images reveal transependymal extravasation of CSF into the periventricular white matter (c, d).

a c

b d

Thereafter the CSF passes into the anteriorpericerebellar cisterns and surrounds the brain-stem. CSF therefore generally follows two path-ways, one medial and one lateral.

Along the medial pathway, it reaches theprepontine, interpenducular, suprasellar, chias-matic and terminal laminar cisterns, until arriv-ing at the subfrontal regions. Then it reachesthe superior sagittal sinus, through the inter-hemispheric spaces. Simultaneously, it flowsupward through the pericerebellar, laminaquadrigemina and pericallosal cisterns untilreaching the region surrounding the superiorsagittal sinus. Along the lateral pathway, the flu-id passes from the interpeduncular, prepontine,ambient and suprasellar cisterns into the Syl-vian fissures, and from there through the sub-arachnoid spaces over the cranial convexity.

In these locations over the cranial convexityare the arachnoid villi of the Pacchionian granula-tions, which are essential for the proper reabsorp-tion of CSF into the venous blood of the dural ve-nous sinuses. This absorption partly depends up-on the hydrostatic pressure gradient between theCSF and blood of the dural sinuses. When thisgradient is sufficient, the microtubules of thegranulations remain open and permit the passageof CSF towards the bloodstream. If, however, thedifference in pressure is very high, the tubulesclose, thus preventing the reabsorption of fluid.

In addition to this reabsorption mechanism,limited absorption apparently takes place alongthe perineural sheaths of the cranial and spinalnerves, through the surfaces of the neuraxisbordering upon the subarachnoid space andthrough the ventricular ependyma.

The total volume of CSF within the sub-arachnoid spaces in normal adults is approxi-mately 120-160 ml, and 30-40 ml is presentwithin the cerebral ventricles. The intraventric-ular CSF pressure is 712 cm of water, and thelumbar pressure is 8-18 cm of water.

Hydrocephalus: diagnostic morphological aspects

The term hydrocephalus is used to describeany condition in which an abnormal increase in

the volume of CSF occurs within the cranium.There are four possible types (1, 8, 11).

In obstructive hydrocephalus, there is ablockage to the passage of CSF through theventricular cavities and outlets, with a dilationof the ventricular spaces proximal to the ob-struction. Frequent causes are neoplastic andnonneoplastic mass-forming lesions; anotherrelatively common aetiology is fibrotic adhe-sions secondary to inflammatory and haemor-rhagic processes. The CSF obstruction may oc-cur at the level of the foramina of Monro (e.g.,neoplasia, inflammatory processes), the 3rd ven-tricle (usually neoplasia), the cerebral aqueductof Sylvius (e.g., congenital atresia, inflammato-ry stenoses), posthaemorrhagic adhesions, or inthe 4th ventricle (e.g., neoplasia, craniocervicalmalformation, infection or subarachnoid haem-orrhage).

From an imaging point of view, obstructivehydrocephalus is characterized by a symmetricdilation of the ventricular system proximal tothe point of obstruction. Characteristic is therounded appearance of the dilation of thefrontal horns, with a reduction of the angle be-tween the medial walls of the frontal hornsthemselves (<100 degrees). If involved in theprocess, the 3rd and 4th ventricle are also dilat-ed. The basal subarachnoid cisterns are eithernormal or mildly encroached upon, as are thesuperficial cerebral sulci, which are either ab-sent or smaller than usual.

Unilateral obstruction of one of the forami-na of Monro causes the distension of one later-al ventricle only. Such obstructions may be in-termittent if the obstructive process is valvular,with clinical manifestations of headache, nau-sea and vomiting. Characteristically, theseepisodes resolve rapidly when and if CSFdrainage is restored. On the other hand, if bothforamina of Monro are involved, the obstruc-tive hydrocephalus is limited to the lateral ven-tricles.

An obstruction of the aqueduct of Sylviuscauses supratentorial triventricular dilation(i.e., the 3rd ventricle and lateral ventricles).Aqueductal stenosis is a frequent cause of hy-drocephalus in infancy and the early stages ofchildhood. As at this age the cranial sutures are


not yet fused, macrocrania develops. If, howev-er, hydrocephalus develops in late childhoodafter closure of the sutures, the enlargement ofthe skull is absent or at most modest. In adultsthe aqueduct is more frequently compressed bya tumour (e.g., periaqueductal astrocytoma)(Fig. 3.5).

If the 4th ventricle or its outlets are obstruct-ed, all the other parts of the ventricular systemare distended. Obstruction of the foramen ofMagendie can be caused by a developmental

malformation (e.g., Arnold-Chiari malforma-tion [Fig. 3.6], platybasia and basilar invagina-tion, atlantooccipital fusion, etc.) or alternative-ly a peri- or intraventricular tumour. The foram-ina of the 4th ventricle can also become non-patent due to a granulomatous ependymitis,caused for example, by the tubercle bacillus. Anentrapped 4th ventricle refers to a simultaneousobstruction of the aqueduct of Sylvius and theforamina of Luschka and Magendie, with a con-sequent distension of its cavity (Fig. 3.7).

In decompensated obstructive hydro-cephalus, the transependymal passage of fluidis more evident in the anterior-lateral portion ofthe frontal horns, and on CT has a reduction inperiventricular density with regular margins (oran increase of signal on T2-weighted MR im-ages, Fig. 3.4).

In communicating hydrocephalus there is alack of fluid reabsorption due to the thrombo-sis of the venous sinuses, malfunction of thearachnoid granulations or poor circulationwithin intracranial subarachnoid spaces due to meningitis, meningeal carcinomatosis or fol-lowing a subarachnoid haemorrhage. Blood,pus, meningeal metastases or adhesions maymechanically obstruct the fluid circulation path-


Fig. 3.5 - Mesencephalic tuberculoma with obstructive hydro-cephalus. The MRI shows a contrast enhancing mass lesion ofthe posterolateral midbrain resulting in stenosis of the aque-duct of Sylvius and obstructive hydrocephalus. [a) axial T2-weighted and b) sagittal T2-weighted MRI; c) coronal T1-weighted MRI following IV Gd].b

c

a

ways in the basal subarachnoid cisterns and/orinvolve the arachnoid granulations. The con-nection of the cranial subarachnoid space to thespinal subarachnoid space may remain patent.

After a certain time, chronic inadequate flu-id reabsorption can produce an enlargement ofthe ventricles without an attendant increase influid pressure (normotensive hydrocephalus).In acute hydrocephalus, the CSF is reabsorbedvicariously by the minor resorption systems,firstly by the transependymal pathway, with theappearance of typical findings of hypodensityon CT and hyperintensity on T2-weighted MRIin the periventricular white matter (Fig. 3.8).This absorption pathway is more permeablethan the normal one and permits the passagethrough the periventricular white matter ofeven large protein molecules.

In communicating hydrocephalus, the dila-tion starts from the anterior and temporal horns,followed by the occipital horns and the 3rd ven-tricle. The 4th ventricle is not necessarily dilated.Occasionally, dilated sulci can also be observedin hydrocephalus associated with a block of thesubarachnoid spaces over the cranial convexity.


Fig. 3.6 - Type II Arnold Chiari malformation with obstructivehydrocephalus The MRI examination demonstrates cerebellartonsillar ectopia, fourth ventricular outlet obstruction and hy-drocephalus. In addition, there is right occipital encephaloma-lacic porencephalic cyst and cervicothoracic syringohydromyelia.[a) sagittal T1- weighted cranial MRI; b) sagittal T1-weightedcervical MRI; c) axial T2-weighted cranial MRI]. b

a

c

In hypersecretory hydrocephalus, there is anincrease in the production of CSF (beyond thenormal 0.3-0.4 ml/minute) in the choroidplexuses due to infection or the presence of achoroid plexus papilloma.

Lastly, in ex-vacuo ventricular enlargementthere is a passive increase in the ventricularand extraventricular CSF spaces without an in-crease in the intraventricular fluid pressure.This type of ventricular enlargement is due toa generalized atrophy of the brain parenchy-ma (Fig. 3.9). Generalized atrophy results in asymmetric dilatation of the ventricular system,which may principally involve the lateral ven-tricles although the 3rd ventricle may also beaffected. If there is atrophy of the structuresof the posterior fossa, the 4th ventricle will al-so be passively enlarged. The angle betweenthe frontal horns is always greater than 110 de-grees. The basal subarachnoid cisterns and thesuperficial cerebral sulci can be normal, how-ever they more frequently are widened in syn-chrony with the overall atrophy.

Functional diagnosis

CT and MRI are excellent techniques for il-lustrating the morphological characteristics of

hydrocephalus as well as the presence of theunderlying pathology when this pathologicalchange is a mass. However, both techniqueshave limitations in their ability to directlydemonstrate the obstructing element to CSFcirculation resulting from adhesions of inflam-matory or haemorrhagic origin.

Radionuclide myelocisternography (12) ormyelocisternal-CT with water-soluble contrastmedium can be used to study CSF circulation,subject to the intrathecal spinal introduction ofthe tracer or contrast agent (e.g., 111-In DTPAand Iopamiro 300, respectively) and subse-quent serial imaging in order to follow theprogress of the agent through the subarachnoidspaces of the cranium.

In normal subjects, the basal subarachnoidcisterns show presence of the tracer or con-trast by the first to third hour, and the Sylvianfissures at the fourth to sixth hour. The sub-arachnoid spaces over the cranial convexityare normally opacified by the 12th hour, andmore completely at the 24th hour. In normalsubjects, the cerebral ventricles are neveropacified. The imaging appearance of thecerebral ventricles in normal subjects dependsin part upon the age of the patient. CSF opaci-fication is more rapid in children, typicallydisappearing by the 24th hour, than in the eld-erly, in whom opacification over the convexitycan persist beyond the 48th hour.

The radioisotopic technique can also beused to study CSF/plasma clearance of the trac-er by means of a series of blood samples. Innormal subjects, this will give the followinghaematological activity values as a percentageof the dose injected: 2nd hour: 1.6%; 6th hour:10%; 24th hour: 33%; 48th hour: 41%.

The study of cerebrospinal fluid circula-tion and CSF/plasma clearance in normoten-sive hydrocephalus enables some prognosticindication for the efficacy of the treatmentwith surgically placed shunts. This shunt op-eration proves to be effective in clinical prac-tice in patients with normotensive hydro-cephalus, in whom myelocisternal scintigra-phy shows a constant, early and persistentopacification of the cerebral ventricles afterthe 48th hour.


Fig. 3.7 - Trapped 4th ventricle with hydrocephalus. T1-weightedMRI showing a trapped 4th ventricle associated with obstructivehydrocephalus in a patient with tuberculous meningitis.

Potentially important diagnostic informa-tion can also be supplied by prolonged andcontinuous pressure monitoring of ventricularfluid using a catheter or by Katzman’s lumbarinfusion test. The latter technique involves thecontinuous infusion of the lumbar subarach-noid space with a physiological solution at aspeed of 0.8 ml/minute; in normal subjectsthere is an increase in fluid pressure up to a

plateau of approximately 20 mm Hg afterabout 30 minutes. In CSF reabsorption disor-ders such as hydrocephalus there will be amarked and early increase in CSF pressurevalues.

If the subarachnoid spaces, typically at aspinal level, are isolated from one another dueto a blockage of CSF circulation at some point,the CSF below the blockage will undergo an


Fig. 3.8 - Normotensive communicating hydrocephalus. The MRI images show a thin margin of hyperintensity representing chronicgliosis surrounding the lateral ventricles in a patient with clinically diagnosed chronic normotensive communicating hydrocephalus,not transependymal extravasation of CSF. [a, b) proton density-weighted MRI; c, d) T2-weighted MRI].

a c

b d

abnormal increase in cells (i.e., Froin’s syn-drome), while that above the obstruction willhave a normal cell and protein content.

Clinically, the Queckenstedt test (i.e., jugu-lar compression test) (2) is usually sufficient toestablish whether there is a partial or total CSFobstruction. With the patient in a lateral decu-bitus position, a lumbar puncture is performedand fluid pressure is measured. In normal con-ditions this pressure alters in synchrony withpulse and breathing. In normal subjects CSFpressure alters in a very marked and rapidlyreversible manner with abdominal compres-sion. The mechanism for this is via an increasein intraabdominal pressure originating from atemporary blockage of the spinal veins, in turnresulting in an increase in intraspinal fluidpressure; this demonstrates that there is no obstruction in the subarachnoid space at thespinal level.

If this abdominal compression test confirmsthat the subarachnoid space is not obstructed,and in the absence of intracranial hypertensionand an intracranial mass, one can perform theQueckenstedt manoeuvre by compressing bothinternal jugular veins simultaneously. This will

cause an increase in intracranial venous pres-sure with a resulting increase in intracranial flu-id pressure, which in normal conditions will betransmitted along the spinal subarachnoidspaces to the lumbar level of CSF pressuremeasurement. However, if there is a blockagein the spinal canal or at the cranio-cervicaljunction, the expected pressure increase willnot reach the pressure gauge. If the increase inCSF pressure at the level of the pressure gaugeis slow and incomplete in returning to normalonce the pressure on the jugular veins has beenremoved, an incomplete blockage can be as-sumed.

MRI is also capable of supplying importantinformation on spinal and intracranial fluidspaces and its circulation. In sectors of the sub-arachnoid space with high pulsatile CSFspeeds, the MR signal normally disappears dueto the flow void phenomenon. This can typical-ly be observed in the aqueduct of Sylvius, theforamina of Monro, the 3rd ventricle and in theregion of the foramen of Magendie.

A circulation blockage with CSF stasis willbring about a disappearance of this phenome-non. Using gradient-echo sequences combinedwith ECG gating, these phenomena can also bestudied dynamically with CSF flow measure-ments (6).

ICH RELATED TO VASCULAR CAUSES

A third cause of ICH is a relative increase inthe amount of blood contained in the cranialcavity. This form of ICH may involve the ve-nous or the arterial system. ICH may have a ve-nous cause when the circulation of the return-ing blood is obstructed, which can occur in cas-es of venous thrombosis associated with throm-bophlebitis of the dural venous sinuses, or ininstances of mediastinal compressive pathology.In this type of ICH, the venous congestion re-sults in a partial inhibition of normal CSFdrainage.

Increases in intracranial blood volume mayalso affect the arterial capillary sector of cere-bral circulation. In active vasodilatation, theeffect is usually due a local increase in CO2,


Fig. 3.9 - Ventriculomegaly with passive cerebral atrophy. Axi-al CT shows passive cerebral atrophy associated with ventricu-lomegaly.

which, irrespective of its origin ultimately re-sults in a vicious circle arising once intracra-nial hypertension has begun. In passive va-sodilatation there is a loss of cerebrovascularautoregulation as a consequence of a systemicacidosis. In this situation, the vessels becomepassively distended by the systemic bloodpressure.

AETIOLOGICAL CAUSES OF INTRACRANIAL HYPERTENSION

Intracerebral tumours represent the mostfrequent cause of intracranial hypertension. Be-yond the size of the mass itself, the principalpathophysiological mechanism involved inICH production in many neoplasms is oedema.However, not all tumours are equally produc-tive of oedema, the most oedema-inducing be-ing glioblastomas and neoplastic metastases.Low degree gliomas by comparison cause littleor no oedema, and when present it remains lo-calized to the immediate area around the lesion.Extracerebral tumours such as meningiomas,on the other hand, may become quite large be-fore causing ICH.

Expanding lesions localized to the subtento-rial compartment can lead to intracranial hy-pertension in part by CSF obstruction. Thistends to occur earlier in intraventricular tu-mours and those of the midline (e.g., medul-loblastomas and ependymomas) than in lateral-ly positioned tumours (e.g., neoplasia of thecerebellar hemispheres and the cerebellopon-tine angle), which typically cause a delayed in-crease in intracranial pressure.

Intracranial hypertension of a vascular causeis observed in a number of conditions. For ex-ample, in arterial hypertension, oedema can al-so occur as a result of paroxysmal hyperten-sion. Subarachnoid haemorrhages are alwaysaccompanied by an initial episode of intracra-nial hypertension due to a blockage of the CSFreabsorption pathways by the haemorrhage.The subarachnoid blood usually reabsorbswithout sequelae; however, if the haemorrhagehas been widespread or is a rebleed, subarach-noid adhesions can form with the possible de-

velopment of a secondary form of hydro-cephalus. Intraparenchymal haematomas withperilesional oedema behave as a mass forma-tion and can occasionally result in the onset ofICH. Intracranial pressure usually sponta-neously returns to normal with resolution ofthe haematoma.

Among the types of intracranial hyperten-sion of infectious origin, acute meningitis istypically associated with ICH. Pyogenic cere-bral infections are almost always oedema-in-ducing, and ICH is rarely absent in the acutephase. Viral encephalitis can also be accompa-nied by considerable cerebral oedema and re-sultant ICH.

Serious cranial trauma is often associatedwith varying degrees of ICH, due both to thepresence of an intraparenchymal haematoma inparenchymal contusion foci, as well as to relat-ed oedema and haemodynamic alterations. Infact, in the initial phase that follows trauma, anincrease in cerebral blood volume plays an im-portant role in the pathological increase in in-tracranial pressure.

ICH can also be observed in cases of intoxi-cation from carbon dioxide, lead, arsenic or fol-lowing allergic reactions.

In summary, while there are many potentialcauses of ICH, the majority are due to disordersof fluid dynamics that can be primarily attrib-uted to mass-forming processes as well as to ob-structions to CSF circulation due to haemor-rhagic, infectious or neoplastic involvement.

REFERENCES

1. Butler AB, McLone DG: Hydrocephalus. In Grossmann,Hamilton eds.: Principles of Neurosurgery, pp. 165-177.Raven Press, New York, 1991.

2. De Myer W: Tecnica dell’esame neurologico, pp. 415-429.Piccin ed., Padova, 1980.

3. Duus P: Diagnosi di sede in Neurologia. Casa ed. Am-brosiana, pp. 337-353, Milano, 1988.

4. Langfitt TW, Weinstein JD, Kassel NF et al: Trasmission ofincreased intracranial pressure. I. Within craniospinal axis.J Neurosurg. 21:989-997, 1964.

5. Lundberg N: Continuous recording and control of ventric-ular fluid pressure in neurosurgical practice. Acta Psychiat.Scand. 36 (S 149):1-193, 1960.

6. Mascalchi M, Ciraolo L, Tanfani G et al.: Cardiac-gatedphase MR imaging of aqueductal CSF flow. J. C.A.T.12:923-926, 1988.


7. Pagni CA: Lezioni di neurochirurgia. Cap. 13: Fisiopatologia eclinica della sindrome di ipertensione endocranica nei tumoricerebrali, pp. 203-214. Ed. Libreria Cortina, Torino, 1978.

8. Pagni CA: Lezioni di neurochirurgia. Cap. 11: L’idrocefalo,pp. 161-196. Ed. Libreria Cortina, Torino, 1978.

9. Papo I: Ruolo dell’ipertensione endocranica nella patoge-nesi del coma cerebrale traumatico. In Papo, Cohadon,Massarotti eds: Le coma traumatique, pp. 111-127. Livianaed., Padova, 1986.

10. Pollock LJ, Boshes B: Cerebrospinal fluid pressure. Arch.Neurol. Psychiatry 36:931-974, 1936.

11. Rao KCVG: The CSF spaces (Hydrocephalus and Atro-phy). In Lee, Rao, Zimmermann eds.: Cranial MRI andCT. 3rd ed., pp. 227-294, McGraw-Hill, Inc. New York,1992.

12. Staab EV: Radionuclide cisternography. In Freeman, John-son eds.: Clinical radionuclide imaging, pp. 679-703.Grune and Stratton, New York, 1986.

13. Weisberg L, Nice C: Cerebral computed tomography. Atext atlas. Cap. 13: Increased intracranial pressure, pp. 241-253. 3rd ed. W.B. Saunders Co., Philadelphia, 1989.


213

INTRODUCTION

The clinical onset of intracranial neoplasia istypically subacute and progressive, or charac-terized by episodes of epilepsy; however, it isnot infrequent for a tumour to present with anacute clinical syndrome, requiring emergencydiagnostic imaging. This need arises in cases as-sociated with an abrupt onset of intracranialhypertension, seizure or focal neurologicaldeficit. This acute onset can be caused by alter-ations that result in a progressive mass effect ofthe neoplasia upon the adjacent nervous tissueand subarachnoid spaces, including thechanges of perilesional oedema, haemorrhageand hydrocephalus.

The volume of the tumour can vary sudden-ly in response to involutional intrinsic tumoralphenomena such as necrosis or haemorrhage.These effects usually take place secondary tothe inadequacy of the neoplastic vascular archi-tecture, but can also be a result of the effects ofradio- or chemotherapy. In addition, in certaintumours such as astrocytomas, primitive neu-roectodermal tumours (PNET) and cranio-pharyngiomas, the formation and/or distensionof an internal cyst may take place very quickly.

Perilesional vasogenic oedema, a result ofthe primitive nature of the neovasculature of

the tumour, the intratumoral degenerative ef-fects described above and the effects of thesephenomena upon the surrounding neural tis-sue, increases the overall volume of the areainvolved and therefore causes an increase inthe so-called tumoral mass effect. The mostsevere consequence of neoplastic mass effectis internal cerebral herniation. Perilesionalvasogenic oedema is variably proportionateto the size of the tumour, its speed ofgrowth, its internal constitution including itsvascular supply, and the effects of the lesionupon the surrounding tissue. Therefore,small intraparenchymal metastatic lesions aretypically accompanied by substantial vaso-genic oedema, whereas benign tumours suchas meningiomas, which are slow-growing andextraaxial, often have no perilesional oede-ma unless they have grown through the over-lying pia mater of the underlying brain or have internal complication (e.g., intrinsicnecrosis).

Hydrocephalus, which can also be limitedto one or more ventricular cavities (i.e., causedby entrapment), is usually a result of the masseffect of the neoplasm; a typical example ismonoventricular hydrocephalus secondary tothe distortional parenchymal effect that caus-es effacement and ultimate obstruction of the

3.2

NEOPLASTIC CRANIOCEREBRAL EMERGENCIES

T. Tartaglione, C. Settecasi, G.M. Di Lella , C. Colosimo

foramen of Monro. Certain intraventriculartumours, or those adjacent to critical points ofCSF outflow (aqueduct of Sylvius), can be thedirect cause of subarachnoid space obstruc-tion. However, in such cases the hydrocephal-ic condition usually sets in slowly and symp-toms have a subacute although progressivepattern.

In this summarized introduction dedicatedto neoplastic emergencies, we will briefly con-sider examination technique, the key pointsof imaging findings and certain particularposttraumatic clinical and diagnostic situa-tions.

IMAGING EXAMINATION TECHNIQUE

True radiological emergencies are usuallyimaged first using CT due to the considerablespeed with which examinations of uncoopera-tive patients with serious conditions must becarried out. In addition, when the ictal symp-tomatology points to a haemorrhage, CT is theimaging technique having the greatest sensi-tivity.

However, in the case of cooperative pa-tients, and where available, MRI using fastsequences could become the technique ofchoice in neurological emergencies. Wideuser agreement attributes clear superiority toMRI over CT in recognising the lesion site,probable type, relationship to the adjacentstructures and therefore the true extent ofthe pathological process, in part due to itsmultiplanar nature and greater definition ofcontrast resolution. When useful, MRA se-quences, with or without paramagnetic con-trast media, make it possible to obtain a gen-eral vascular map of the area non-invasively,which is helpful for differential diagnosticpurposes as well as for surgical planning (2,13, 16). Nevertheless, MRA today is scarce-ly sensitive to neoplastic vasculature. Final-ly, the use of functional MR sequences maybe beneficial in some patients preoperative-ly, especially when the lesion is near neuro-logically sensitive areas such as the motor ar-eas of the cerebrum (2).

SEMEIOTICS

a) Recognition of the neoplastic nature and defi-nition of the site/origin of the lesionThe radiologist must be able to recognize

the neoplastic nature of the lesion and to defineits site with accuracy. In particular, the intra- orextraaxial site of the tumour and the relation-ship of the lesion with the surrounding sub-arachnoid spaces, the nervous and the vascularstructures must be discerned. Neoplastic le-sions are defined by the density/signal alter-ations as compared to the surrounding neuraltissue, the degree and pattern of enhancementafter IV contrast administration and its margin-al characteristics. The further definition of thesupra- or subtentorial position of the lesionguides the differential diagnosis and treatmentplanning (5, 13, 16).

b) Characterization of the pathological tissueThe majority of neoplastic lesions are char-

acterized by an increase in free water and there-fore a relative hypointensity on T1-weightedMRI, hyperintensity in PD- and T2-dependentsequences and a relative hypodensity on CT.Exceptions to these rules are those tumourswith a high cellular and a high nucleus/cyto-plasm ratio (e.g., PNET, germinoma, lym-phoma) that present signal degeneration in T2-dependent images and a relative hyperdensityin CT (Fig. 3.10). IV contrast medium adminis-tration is almost always used in the examinationof cerebral tumours and is only of somewhatlimited value in generally haemorrhagic lesions(2, 13, 16).

c) Detection of “acute” intraneoplastic alterationsCystic and necrotic areas are often pres-

ent within tumours, and it can sometimes beimpossible to distinguish between the twosubtypes. The cyst CT density and MR sig-nal characteristics depend on their contentand can vary greatly, although they are typi-cally characterized by marked hypodensityon CT and generally iso- hypointensity ascompared to CSF on MR sequences; the sig-nal and density generally increase with a risein protein content. As noted above, the dis-


Fig. 3.10 - Pineal region germinoma with obstructive hydrocephalus. A solid mass is seen in the pineal region characterised bymarked, homogeneous contrast enhancement. There is compressive obstruction the aqueduct of Sylvius resulting in obstructive hy-drocephalus. Also identified are associated signs of CSF hypertension revealed as transependymal extravasation of the CSF signalledby the broad margin of hyperintensity within the periventricular white matter on T2-weighted sequences. [a) axial CT following IVcontrast; b, c) axial proton density-, T2-weighted MRI; d) sagittal T2-weighted MRI].

3.2 NEOPLASTIC CRANIOCEREBRAL EMERGENCIES 215

ac

db

tinction between tumour cysts and necrosisis not often possible and is not always use-ful. That being said, necrosis is generallycharacterized by a heterogeneous content

with irregular, nodular walls and markedlyinhomogeneous contrast enhancement (Fig.3.11) (2, 13, 16). Intraneoplastic haemor-rhages include both microhaemorrhages and


Fig. 3.11 - Glioblastoma multiforme. The CT and MRI studies show a large, necrotic left hemispheric glioblastoma associated withextensive perilesional vasogenic oedema resulting mass effect and lateral subfalcian herniation. [a, b) unenhanced axial CT; c, d, b)PD-, FLAIR, T2-weighted MRI; f, g) T1-weighted axial and coronal MRI following IV Gd].

a

b d

c

macroscopic haemorrhages; these largerhaemorrhages occur in approximately 1-15%of all neoplasias (2, 16, 20). This haemor-rhagic frequency tends to increase within thesubgroup of malignant tumours and espe-

cially in cases of metastases and malignantgliomas (2, 10, 12, 19, 23). There are a num-ber of possible intraneoplastic causes ofhaemorrhage; among these are: primitive tu-moral neovascularization with a disorderlyendothelial proliferation and formation of ar-teriovenous shunts, rapid tumour growthwith subsequent ischaemic necrosis, releaseof plasminogens and vascular infiltration bythe tumour (2, 6, 11, 23, 24). The metabo-lism within haemorrhagic neoplasia is vari-able, but is generally lower than that ob-served in “benign” haemorrhages (1, 2).

Deoxyhaemoglobin, which is usually onlyfound in the acute phase of haematomas between7-72 hours from onset, can persist for weeks inintratumoral haemorrhages. Methaemoglobin,which forms in the subacute phase (i.e., 4-30days), remains along the peripheral rims ofhaematomas for months in neoplastic haemor-rhages. Haemosiderin, observed in the finalstage of haemorrhage evolution, is typically ab-sent. It is theorized that this altered evolutionof the haemoglobin derives from the low oxy-gen tension obtaining in tumours on which thepersistence of methaemoglobin depends (1, 7,8, 14, 15, 21). Therefore, the density character-


Fig. 3.11 (cont.).

f

ge


Fig. 3.12 - Malignant astrocytoma associated with subfalcian herniation. The images demonstrate a left frontal cortex haemorrhagiclesion with marked perilesional vasogenic oedema that compresses the ipsilateral ventricle and results in subfalcian herniation of thecontralateral midline structures. There are cystic, necrotic components with various haemoglobin species in different stages of break-down. After IV contrast medium administration irregular enhancement of the margins of the lesion is observed. [a) unenhanced ax-ial CT; b, c, d) axial T1-, PD-, T2-weighted MRI.

a

b d

c


Fig. 3.12 (cont.) - e) Axial T2*-weighted, f) axial T2-weightedand g) coronal T2-weighted MRI.

e

f

g

istics on CT and signal intensity on MRI of in-tratumoral haemorrhages differ somewhat fromthose of benign haemorrhages. In addition,neoplastic haemorrhages tend to appear moreheterogeneous and complex (Fig. 3.12). Non-haemorrhagic areas of solid tumour and cystic-necrotic components with blood-fluid levelsmay also coexist with tumour enhancement af-ter IV contrast medium administration. Finally,one last fundamental characteristic of many tu-mours is the persistence on imaging in thechronic phase of a marked hyperintense bandof signal intensity surrounding the haemor-rhage on long TR images due to vasogenicoedema (1, 2, 16, 18).

d) Vasogenic oedemaThe most frequent observation within the

cerebral nervous tissue surrounding a neo-plasia is vasogenic oedema. Vasogenic oede-ma causes an increase in intracranial volumeas well as that of the affected neural tissue.This oedema is hypodense on CT, hypoin-tense in T1-weighted sequences and hyper-intense on PD- and T2-weighted images. Asmentioned previously, the origin of theoedema does not depend so much on thesize of the neoplastic lesion as it does uponthe speed with which the tumour grows, thefundamental nature of the intrinsic angio-genesis and the integrity of the blood-brainbarrier (2, 5, 13, 16) (Fig. 3.12).

e) Internal cerebral herniationThe localized increase in cerebral volume

caused by the neoplasia itself, as well as byassociated haemorrhages, cysts, intratumoralnecrosis and/or vasogenic oedema can deter-mine the displacement of adjacent structures(cerebral, ventricular, subarachnoid spaces).The skull is divided by two large relativelyrigid meningeal structures, the falx cerebriand the tentorium cerebelli, into three sub-compartments. Depending upon the focus ofthe mass effect in relation to the tentorium,a distinction is made between supra- and sub-tentorial space; the falx represents an incom-plete separation between the cerebral hemi-spheres in the midline. The cerebral struc-


Fig. 3.12 (cont.) - h, i) axial and coronal T1-weighted MRIfollowing IV Gd].

i

h


Fig. 3.13 - Pilocytic astrocytoma. Identified is a mass lesion ofthe right cerebellar hemisphere characterised by a cystic coreand thick rim of solid tissue. The neoplasm compresses the 4th

ventricle and brainstem resulting in obstruction of the aque-duct of Sylvius aqueduct and obstructive hydrocephalus. This

in turn results in herniation of the midline inferior cerebellar structures caudally into the foramen magnum and cranially throughthe tentorial hiatus. [a, b) unenhanced axial CT; c) sagittal T1-weighted spin echo MRI; d) coronal inversion recovery T1-weight-ed MRI].

a

b

c

d


Fig. 3.14 - Anaplastic choroid plexus papilloma. The imagingstudies show an inhomogeneous mass lesion whose epicentre islocated within the left lateral ventricular trigone, characterisedby an enhancing solid nodule and a cystic component with thinmural contrast enhancement. There is some associated perile-sional vasogenic oedema. The sum mass effect results in minorlateral herniation of the midline supratentorial structures be-neath the falx cerebri. [a, b, c) axial T1-, T2-, PD-weightedMRI].

a

b

c

tures adjacent to a mass are pushed towardsregions of lesser resistance and tend to movetowards the pathways of communication be-tween the various endocranial subcompart-ments, resulting in so-called internal cerebralherniations. The compressive effect of an ex-panding hemispheric lesion can cause herni-ation of the paramedian cerebral structures,the lateral ventricles, the 3rd ventricle and theanterior cerebral artery and its immediatebranches below the falx cerebri towards thecontralateral hemicranium causing a subfal-cian herniation (Fig. 3.11, 3.12). A subfalcianherniation can in turn become complicatedby an infarction of the territory of the ante-rior cerebral artery branches involved. In ad-dition, uni- or biventricular hydrocephalusmay ensue due to the obstruction of theforamina of Monro as a result of parenchy-mal distortion phenomena.

An expanding process situated in one cere-bral hemicranium, especially if positioned inthe middle cranial fossa, may push the uncus ofthe temporal lobe medially and downward be-tween the free edge of the tentorium cerebelliand the ipsilateral cerebral peduncle into theperimesencephalic cistern; in the most severecases, the brainstem, ipsilateral posterior cere-bral and anterior choroid arteries and basalvein(s) of Rosenthal are compressed. This typeof internal cerebral dislocation is termed de-scending transtentorial herniation.

An expanding cerebellar hemispheric le-sion can compress the upper midline andparamedian structures of the posterior fos-sa, pushing them upward towards the tento-rial incisura, ascending transtentorial herni-ation, and simultaneously may dislocate thecerebellar tonsils and lower vermis down-ward through the foramen magnum, de-scending foramen magnum herniation (Fig.3.13).

Transtentorial herniations, be they descend-ing or ascending, may cause the infarction oftissue in the distribution of the posterior cere-


Fig. 3.14 (cont.) - d, e) Axial and sagittal T1-weighted MRI fol-lowing Gd].e

d


Fig. 3.15 - Postsurgical infection of surgical site. The surgical cavity demonstrates air with irregular contrast enhancement along theresection margins; hypodensity persists in the adjacent white matter due to persistent vasogenic oedema. The CT findings describedare of uncertain significance, as they are still compatible with expected postsurgical alterations, however the associated clinical find-ings (headache and high fever) suggest a probable infection of the surgical site. [a, b) unenhanced axial CT; c, d) axial CT followingIV contrast].

a

b

c

d


dFig. 3.16 - Postsurgical cerebritis. The CT examination shows diffuse hypodensity of the subcortical and deep white matter of theright cerebral hemisphere consistent with oedema, with inhomogeneous contrast enhancement and marked mass effect. The mass re-sults in compression of the ipsilateral ventricle, subfalcian herniation of the midline supratentorial structures and early dilation of thecontralateral ventricle caused by obstruction at the level of the foramen of Monro on the left side. The ipsilateral perimesencephaliccistern is obliterated due to downward internal herniation of the uncus of the temporal lobe. [a, b) unenhanced axial CT; c, d) axialCT after IV contrast].

a

b

c

bral arteries, the perforating arteries of the mid-brain and the upper cerebellar arteries. In ad-dition, obstructive triventricular hydrocephalusmay occur as a result of the parenchymal com-pression/distortion of the aqueduct of Sylviusby the herniative process.

Internal cerebral herniation is a seriouscomplication that may bring about a rapid es-calation of clinical signs and symptoms, andtherefore its neuroradiological recognition canprofitably alter the therapeutic approach. Itmust be underlined that the clinical expressionof severity of the herniation is in part directlyproportional to the rapidity with which itforms; in the presence of a herniation into theforamen magnum or a descending transtento-rial herniation, lumbar punctures are to beconsidered absolutely contraindicated in thatthey can result in a fatal compression of thebrainstem (4, 5, 17).

f) HydrocephalusThe effect of a tumour on CSF dynamics

must be evaluated and, in particular, hydro-cephalus must be recognized. The site of theobstruction must be established. The portionof the ventricular system situated proximal tothe obstruction undergoes distension whichcan be acute. The level of the obstruction isusually the foramina or pathways of commu-nication between the ventricles (e.g., foraminaof Monro, aqueduct of Sylvius), which arecompressed by the parenchymal distortion(Figs. 3.10, 3.13). In certain cases, neoplasiacan cause an entrapment of a small section ofthe ventricular section; one typical example isa neoplasm located within or near the ven-tricular trigone (Fig. 3.10), which causes en-trapment of the temporal horn of the lateralventricle (5, 13).

POSTTHERAPEUTIC NEOPLASTICEMERGENCIES

a) Postsurgical complicationsIn the postsurgical period, including after

stereotaxic biopsy, neuroradiological evalua-tion is often required to exclude early compli-

cations that may occur, including haemor-rhage (9), postsurgical oedema, acute hydro-cephalus and infection. In such cases the diag-nosis is often problematic because of the diffi-culties in distinguishing between neoplasticresidue, aseptic postsurgical reactive phenom-ena, and frank infection with cerebritis (Figs.3.15, 3.16), which may evolve into an abscess(3, 9).

b) Postventricular shunting complicationsThe complications of hydrocephalus shunts

include:1) Recurrence of hydrocephalus: A failure of

the shunt may be secondary to an obstructionof the shunt catheter, for example due to ablood clot, or to an interruption to the shuntsystem’s continuity due to a disconnection of acoupling or a fracture of the line.

2) CSF sequestration with a failure of drainage:Sequestration may occur in cases in which the tu-mour excludes part of the ventricular system onthe proximal end, or when a loculation of thedrainage fluid occurs on the distal end (i.e., theperitoneal cavity).

3) Hyperfunction of the shunt: This condi-tion precipitates an “overshunting” syndrome;this is associated with a considerable reductionin the dimensions of the ventricles, which aresometimes nearly completely collapsed (i.e.,“slit ventricle” syndrome). This situation canfurther be complicated by the formation of hy-gromas, and, in the most severe cases, subduralhaematomas that are often bilateral.

4) Infection: Infection may consist of simpleependymitis with periventricular enhancementafter IV contrast medium administration or ofmeningitis with generalized enhancement ofthe cranial leptomeninges.

REFERENCES

1. Atlas SW, Grossman RI, Gomori JM: Hemorragic intracra-nial malignant neoplasms: spin-echo MR imaging. Radiol164:71, 1987.

2. Atlas SW: MRI of the brain and spine. Spell Checking, The-saurus and Dictionaries, 1994.

3. Bayston R: Hydrocephalus shunt infection. Chapman andHall Medical, London, 1989.

4. Blinkov SM, Smirnov NA: Brain displacements and defor-mations. Plenum Press, New York-London, 1971.


5. Cittadini G: Manuale di Radiologia clinica, 2nd. ECIG, Ge-nova, 1983.

6. Davis JM, Zimmerman RA, Bilaniuk LT: Metastases to thecentral nervous system. Radiol Clin North Am 20:417, 1982.

7. Destian S, Sze G, Krol G et al: MR imaging of hemorragicintracranial neoplasms. AJNR 9:1115, 1988.

8. Gatenby RA, Coia LR, Richter MP: Oxygen tension in hu-man tumors: in vivo mapping using CT-guided probes. Ra-diology 156:211, 1985.

9. Horwit NH, Rizzoli HV: Postoperative complications in in-tracranial neurological surgery. Williams and Wilkins, Bal-timore-London, 1982.

10. Leeds NE, Elkin CM, Zimmerman RD: Gliomas of thebrain. Semin Roentgenol 19:27, 1984.

11. Little JR, Dial B, Belanger G, et al: Brain hemorrhage fromintracranial tumor. Stroke 10:283, 1979.

12. Mandybur TI: Intracranial hemorrhage caused by metasta-tic tumors. Neurology 27:650, 1977.

13. Marano P: Diagnostica per immagini, II vol. Casa EditriceAmbrosiana, Milano, 1994.

14. Neill JM: Studies on the oxidation-reduction of hemoglo-bin and methemoglobin. III. The formation of methemo-globin during the oxidation of autooxidizable substances. JExper Med 41:551, 1925.

15. Neill JM: Studies on the oxidation-reduction of hemoglo-

bin and methemoglobin. IV. The inhibition of spontaneousmethemoglobin. J Exper Med 41:561, 1925.

16. Osborne AG: Diagnostic Neuroradiology. Mosby YearBook, Inc, 1994.

17. Pagni CA: Lezioni di neurochirurgia. Edizioni LibreriaCortina, Torino, 1984.

18. Potts DG, Abbott OF, von Sneidern JV: National CancerInstitute Study: evaluation of computed tomography in thediagnosis of intracranial neoplasms. III. Metastatic tumors.Radiol 136:657, 1980.

19. Russel DS, Rubinstein LJ: Pathology of tumors of the ner-vous system, 5th ed. Williams and Wilkins, Baltimore-Lon-don, 1989.

20. Scott M: Spontaneous intracerebral hematoma caused bycerebral neoplasm: report of eight verified cases. J Neuro-surg 42:338, 1975.

21. Sze G, Krol G, Olson WL et al: Hemorragic neoplasms:MRI mimics of occult vascular malformations. Am J Radiol149:1223, 1987.

22. Zimmerman H: The pathology of primary brain tumors. Se-min Roentgenol 19:129, 1984.

23. Zimmerman RA, Bilaniuk LT: Computed tomography ofacute intratumoral hemorrhage. Radiol 135:355, 1980.

24. Zulch KJ: Brain Tumors. Their Biology and Pathology, 3rded. Springer-Verlag, Berlin, 1986.


229

INTRODUCTION

Cerebral angiography in the evaluation ofcranioencephalic tumours has a role that is de-termined to a great extent by CT and MRI as itis no longer required to diagnose the existenceof a lesion (7). However, selective cerebral an-giography is still utilized in cases where theneurosurgeon is considering emergency surgeryor another aggressive form of treatment.

Modern angiography is very different fromthe past, as the evolution in cauterization mate-rials and angiographic equipment have broughtabout vast improvements in the quality of theimages obtained while drastically reducing pa-tient risk. The innovations in equipment havewitnessed the introduction of digital acquisi-tion, storage and image display, thereby makingthe resulting examination yet more practical toperform and review (1-4, 6, 8).

The evolution of the imaging instrumenta-tion has coincided with the enormous techni-cal progress made in angiographic materials,such as increasingly small catheters with evergreater torsion control and thin walls with ex-tremely high mechanical resistance. It there-fore follows that what was once considered aprocedure associated with some degree of riskhas now become quite safe, benefiting from

the use of new contrast media, appliances andinstruments.

Neovascular architecture is characterized bycertain semeiological signs deriving from tradi-tional angiography, including: alteration of thecalibre, morphology and course of the vessels;presence of haemodynamic alterations; thepresence of arteriovenous microshunts; andpresence of a characteristic arteriolar-capillaryparenchymal blush. There are three possiblesubtypes of angioarchitectural alteration inneoplasia: typical pathological vascularization(e.g., meningiomas, gliomas); atypical patho-logical vascularisation and avascular lesions (5).

Pathological vascularization can originatefrom the intraaxial vasculature (e.g., internalcarotid and vertebrobasilar artery branches) orthe meningeal vessels (e.g., branches of the ex-ternal carotid artery). The type of vasculariza-tion depends on tumour type, however itshould be stressed that angiography, like allother imaging techniques, is not able to providea precise tissue diagnosis.

The table below shows a general classifica-tion of brain tumours as published by theWHO:– Neuroectodermal tumours (gliomas, medul-

loblastomas, ependymomas, papillomas, neu-rinomas)

3.3

ANGIOGRAPHY IN BRAIN TUMOURS

C. Piana, U. Pasquini

– Ectodermal tumours (craniopharyngiomas,hypophyseal adenomas)

– Embryogenic tumours (epidermoids, der-moids, teratomas)

– Mesodermal tumours (meningiomas, an-giomas, fibromas, chordomas, lipomas, os-teomas, sarcomas).

This angiographic discussion of brain tu-mours cannot exhaustively deal with all the var-ious types that can occur and will only detailthe most frequently encountered.

MENINGIOMAS

Semeiotics

Statistically, meningiomas are most frequentin females, with a ratio of 3:1 as compared tomales. With regard to other intracranial neo-plasias, they are the most common type with anoverall relative incidence that varies between20-25%.

The angiographic characteristics of menin-giomas vary with the histological type and spe-cific degree of vascularization. Minor distinc-tions are made between skull base menin-giomas and those of the convexity. Menin-giomas have preferential sites with frontal, pte-rional and parietal locations being the mostcommon, and they can be multiple.

During their development meningiomas de-form and compress the overlying neural andvascular tissues, some of which, such as the in-ternal carotid artery and cranial nerves withinthe cavernous sinuses, become enveloped with-


Fig. 3.17 - Meningioma of the left pterion. The imaging studiesreveal a left frontoparietal homogenously enhancing, broaddural based mass with perilesional oedema and neovascularityoriginating from the left middle meningeal artery. [a) unen-hanced CT; b, c) left external carotid, left middle meningeal ar-teriogram].

a c

b

in the confines of the tumour. They are suppliedby arterial branches that are usually hyper-trophic. These tumors demonstrate a patholog-ical circulation fed principally from meningealvessels that are usually quite regular with a dif-

fuse and homogeneous tumour blush in the lat-er phases of the serial angiographic study (Figs3.17, 3.18). The neovascular tumour circulationcan also be supplied from the pial arteries (i.e.,internal carotid or vertebrobasilar arteries).

3.3 ANGIOGRAPHY IN BRAIN TUMOURS 231

Fig. 3.18 - Invasive left frontal region meningioma. The skull x-ray demonstrates a large osteolytic lesion of the left frontal region. TheCT shows a hyperdense lesion invading the overlying skull and extracranial soft tissues. The angiogram of the left external carotid ar-tery reveals prominent neovascularity originating from branches of the left superficial temporal and middle meningeal arteries.[a) frontal radiograph; b), c) axial CT imaged with bone and soft tissue windows; d) left external carotid arteriogram].

a c

b d

In order to obtain a precise and completedocumentation of the vascular contributions tothe meningioma, it is mandatory to perform anangiographic examination that also includes allthe meningeal arteries that might potentiallycontribute to this supply. Angiographic exami-nations must also include a thorough search forvenous alterations (e.g., compressions and dur-al venous sinus invasion with stenosis or com-plete occlusion).

The circulation of meningeal sarcomas isquite different than that of benign menin-giomas and is characterized by reduced circula-tion times, in part due to the presence of arteri-ovenous fistulae. Given their site of origin inthe meninges, these tumours are also suppliedby intra- and extracranial meningeal branches.

Olfactory groove (Fig. 3.19) and cavernousvenous sinus meningiomas are less frequentand have typical appearances on CT and MRI.In the case of olfactory groove meningiomas,angiographic examinations rarely contributeadditional information. However, in the caseof cavernous venous sinus meningiomas, an-giography can show an encasement and re-sulting stenosis of the carotid siphon and aneovascularization with parenchymal blushoriginating directly from branches of thecarotid siphon itself. This observation pointsout the potential danger of surgical interven-tion and in some cases may suggest alternativetreatment (radiotherapy).

One last characteristic location that bearsdiscussion is the meningioma of the tentoriumcerebelli. In such cases the angiographic pic-ture is typical as it shows one or more hyper-trophic tentorial meningeal arteries originatingfrom the supraclinoid segment of the internalcarotid that flow toward the central core of thetumour, where the characteristic hypervascular-ization is noted.

Discussion

From these brief considerations it would ap-pear evident that the angiographic examinationof a meningeal lesion must be performed not somuch for diagnostic purposes, but rather to ob-

tain an accurate angiographic map of the lesionand surrounding tissues. There are two funda-mental reasons to accurately define this map: todemonstrate the type and degree of vascular-ization and to show the neurosurgeon the ves-sels that are to be isolated and coagulated.

Technological progress in recent years hasbrought about a new approach to the treatmentof meningiomas: embolization. This technique


Fig. 3.19 - Olfactory groove meningioma. The right internalcarotid arteriogram demonstrates neovascularity associatedwith a persistent parenchymal blush within a lesion in the ante-rior aspect of the skull base on the right side originating prin-cipally from ethmoid arterial branches. In addition, the rightophthalmic artery in hypertrophied as a result of the increasedflow in transit to the neoplasm. [a) frontal projection right in-ternal carotid arteriogram; b) lateral projection right internalcarotid arteriogram].

a

b

typically precedes surgery, as it results in adevascularization of the tumour permitting aconsiderable reduction in the surgical time pe-riod, a reduction in intraoperative bleeding andtherefore an overall reduction in surgical riskand complications. However, the embolic pro-cedure must be performed by an expert teamtrained specifically in interventional radiology.

GLIOMAS

Semeiotics

CT and MRI have altered the indications forcerebral angiography somewhat by permittinga precise determination of the location of thelesion as well as a clear depiction of its variouscomponents and gross internal structure. How-ever, visualization of the pathological neocircu-lation of the tumor still remains the province ofconventional angiography.

On angiographic examinations gliomas havedirect and indirect signs: direct signs are the ac-tual vasculature of the neoplasm and the indi-rect signs are shifts of the vascular structuressurrounding the tumour induced by its growth.This distinction between direct and indirectsigns derives from conventional angiographicsemeiology.

These direct angiographic signs are charac-terized by the specific afferent and efferent ves-sels, the appearance of the tumour vessels andthe circulation time of the tumour. The evalua-tion of the efferent vessels is also quite impor-tant in the diagnostic angiographic analysis ofbrain tumours; for example, the detection ofmedullary veins and deep venous drainage vir-tually excludes the possibility of an extraaxiallesion.

The regularity of tumour neovessels can bean element in favour of the relative benignancyof a lesion. Conversely, the irregularity of thevessels is usually associated with malignancy,and the presence of arteriovenous shunts al-most always indicates a malignant lesion.

Another distinctive characteristic of braintumours is the tumour circulation time: in anumber of lesions this circulation time is re-

duced due to the presence of arteriovenousshunts with early venous drainage. In other le-sions the tumour circulation time appears in-creased and the tumour blush persists withinthe lesion. Tumour circulation times are also in-fluenced by the presence of associated perile-sional oedema, the presence or absence of vas-cular spasm and the degree of resistance of thedraining veins (e.g., compression or completeobstruction of the draining venous structures).

Glioblastomas (Figs. 3.20, 3.21) are the sub-type of glioma that has the most varied angio-graphic findings. In part due to their high bio-logical activity, theses tumours typically revealangiographic characteristics that define a ma-lignant pathological circulation: a reduction in


Fig. 3.20 - Left temporoparietal glioblastoma multiforme. An-giogram of the left internal carotid artery reveals a prominentparenchymal blush and arteriovenous shunting typical of ma-lignant cerebral neoplasms.

circulation time, irregularity in the calibre ofvessels with very disorderly patterns, arteriove-nous fistulae and early venous drainage.

Other gliomas have different angiographicfindings, some presenting with a picture that ismore or less avascular. Even some quite hyper-vascular gliomas have areas that are avascularindicating necrosis or the presence of cysts orhaemorrhage within the tumour.

Benign astrocytomas (Fig. 3.22) and oligo-dendrogliomas only rarely have significantmacroscopic pathological neocirculation. How-ever, in certain cases some intrinsic vascular el-ements can be detected. When present, suchfindings can be interpreted as a greater or less-er degree of lesion malignancy.

OTHER CEREBRAL NEOPLASMS

Ependymomas and medulloblastomas candemonstrate a minor neovascularization; how-ever, these are not characteristic elements thatdefine these lesions. In choroid plexus papillo-mas (Fig. 3.23), the angiographic findings showa neocirculation composed of small vessels thatgive rise to a dense tumour blush. In these le-sions one observes hypertrophy of thechoroidal arteries from which the tumour ves-sels originate.


Fig. 3.21 - Left temporal lobe cystic glioblastoma. Angiogramof the left internal carotid artery shows mass effect in the ele-vation of the Sylvian vessels associated with a peripheralparenchymal blush.

Fig. 3.22 - Right parietal lobe astrocytoma. Contrast enhancedCT shows mural enhancement within a right parietal lobe sub-cortical mass lesion surrounded by much perilesional oedema.The angiogram of the right internal carotid artery demonstratesno hypervascularity. [a) axial CT following IV contrast; b) lat-eral projection right internal carotid arteriogram]

b

a

Discussion

The angiographic analysis of cranial neoplasiais important from the view point of the potentialneurosurgical therapeutic implications. Emer-gency angiographic examinations implicate theintention to perform interventional proceduresin order to reduce the vascularity of the lesionand are dictated by the patient’s clinical situation.

The exact representation of the tumour vas-cularity permits a proper and careful approach


c

d

e

a

bFig. 3.23 - Papilloma of the right choroid plexus. The contrastenhanced CT shows a homogeneously enhancing intraventric-ular mass. The right internal carotid arteriogram reveals a masslesion having neovascularity, associated with a tumor blush andarteriovenous shunting. [a) axial CT following IV contrast; b,e) frontal projection right internal carotid arteriogram; c, d) lat-eral projection right internal carotid artery arteriogram].

to stereotaxic biopsy, as it shows the course ofthe vessels to be avoided and tumour vessels.These observations potentially reduce the risksof a possible intratumoral haemorrhage.

Complete angiographic examinations facili-tate surgical intervention. However, in cases inwhich the lesion cannot be operated on, angiog-raphy may suggest alternative therapies such asradiotherapy and intraarterial chemotherapy.This latter technique is proving efficacious inthe treatment of particularly hypervascular le-sions; in such cases, the angiographic picturecan be correlated with considerable biologicalactivity, and therefore with greater pharmaco-logical sensitivity.

Lastly, in cases where the neurosurgeon doesnot intend to intervene, angiographic evalua-tions are of little or no value as the combinationof CT and MRI provide more than satisfactoryinformation concerning the type and locationof the lesion.

METASTASES

Given precise clinical and historical medicaldata, this type of lesion is usually not difficult tointerpret using CT and MRI. From a statisticalpoint of view, autopsy findings reveal brainmetastases in 24% of patients suffering fromtumours. The tumours that most frequentlyspread to the CNS include melanomas, lungcarcinoma, breast carcinoma, thyroid tumoursand leukaemia/lymphoma.

Although there is usually no diagnosticdilemma in diagnosing cerebral metastases onCT and MRI in the presence of multiple le-sions, this changes in the case of isolated lesionsthat are often cortical-subcortical in locationand may infiltrate the overlying meninges. Insuch cases, it may be necessary to perform anangiography in order to resolve differential di-agnostic problems between metastasis andmeningioma.

The angiographic picture of metastases(Fig. 3.24) is somewhat typical with the depic-tion of rather homogeneous neovascularity,which is most frequently supplied by a singlearterial branch. This neovascular circulation


Fig. 3.24 - Right temporoparietal parenchymal metastatic neo-plastic disease. Contrast enhanced coronal CT demonstrates anenhancing mass lesion adjacent to the skull on the right side.The right internal carotid arteriogram in the lateral projectionreveals an intensely hypervascular cortical lesion associatedwith a tumor blush and arteriovenous shunting. [a) coronal CTfollowing IV contrast; b, c) lateral projection right internalcarotid arteriogram].

a

b

c

has well-defined margins and persists in timeinto the venous angiographic phase. Typically asingle draining cortical vein is visible.

The lesion usually has a cortical or subcorti-cal location. In cases where the lesion infiltratesthe overlying meninges and bone of the skull,an examination of the meningeal branches is es-sential as the absence of supply of the tumourfrom these vessels permits differentiation frommeningioma.

Discussion

This brief analysis highlights the fact thatmultiple metastases do not necessarily requirean angiographic evaluation, as CT and MRI aresufficient for diagnosis. The principal excep-tion is that of isolated cortical lesions that infil-trate the overlying meninges and skull. As not-ed above, angiography can provide valuable in-formation in such cases in terms of differentiat-ing a metastasis from a meningioma.

CONCLUSIONS

Cerebral angiography has precise indica-tions in the light of new diagnostic and thera-peutic considerations; presurgical angiographicinvestigations are always required in order tofacilitate the surgical approach to the lesion bydemonstrating the afferent and efferent vascu-lar branches to the lesion. Angiographic studiesmay prove useful in subsequent intraarterialembolization or chemotherapy in conjunctionwith surgery or once it has been establishedthat surgery is not possible.

Cerebral angiography is considered super-fluous in the more benign or lower grade tu-mour types, in tumours of the posterior cranial

fossa and in tumour follow-up; in most of thesecases, CT and MRI are usually sufficient for di-agnosis and treatment planning.

MRA has a complementary diagnostic roleregarding information on hypervascular in-tracranial lesions. In particular, the recentlydeveloped techniques involving the injectionof a contrast medium bolus in order to betteridentify the arterial vascularization may proveuseful in the future. This makes it possible tovisualize some degree of the pathological neo-vascularization present in many malignant tu-mours. However, bolus contrast enhancedMRA does not yet possess the sufficient defini-tion to distinguish with certainty the smallerarteries; in addition, by its nature it lacks theability to selectively differentiate the variousvascular territories.

REFERENCES

1. Brant-Zawadki M, Gould R et al: Lane B.: Digital sub-traction cerebral angiography by intrarterial injection:comparison with conventional angiography. AJR 140, 347-353, 1983.

2. Chilcote WA, Modic MT, Pavlicek WA et al.: Digital sub-traction angiography of the carotid arteries: a comparativestudy in 100 patients. Radiology 130, 287-295, 1981.

3. Davis PC, Hoffman JC: Intraarterial digital subtraction an-giography: evaluation in 150 patients. Radiology 148, 9-15,1983.

4. Kelly W, Brant-Zawadzki M, Pitts LH: Arterial injection-di-gital subtraction angiography. J. Neurosurg. 58, 851-856,1983.

5. Leeds NE, Rosenblatt R: Arterial wall irregularities in intra-cranial neoplams: the shaggy vessel brought into focus. Ra-diology 103, 121-124, 1972.

6. Modic MT, Weinstein MA, Chilcote WA et al.: Digital sub-traction angiography of the intracranial vascular system:comparative study in 55 patients. AJR 138, 299-306, 1982.

7. Newton TH, Potts DG: Radiology of the skull and brain:angiography. Volume two/book 4. The CV Mosby Com-pany Saint Louis 1974.

8. Weinstein MA, Pavlicek WA, Modic MT et al: Intra-arterialdigital subtraction angiography of the head and neck. Ra-diology 147, 717-724, 1983.


IV

EMERGENCY NEURORESUSCITATION

241

INTRODUCTION

Toxic encephalopathy arises following the in-teraction between a chemical compound andthe Central Nervous System (CNS) (9). A widerange of chemical substances can be neurotox-ic, having mechanisms that affect the CNS ei-ther directly or indirectly by means of alter-ations to cerebral or systemic homeostasis in-duced by the substance in question. The maincauses of brain damage include: oxidative ener-gy depletion, deficit of the substrate for cerebralactivity, alterations in cell membrane integrity,enzyme deficit, alterations to the electrolyticequilibrium, and neurotransmission damage.

Toxic substances can be either endogenousor exogenous. Endogenous agents typically re-sult from congenital cerebral errors in metabo-lism; exogenous substances are classified as ex-ternal (i.e., when they are introduced into theorganism from outside) and internal (whenthey are produced by systemic metabolism er-rors and come into contact with the CNS viathe blood-brain barrier).

Neuroradiological emergencies are most fre-quently linked to external exogenous toxins.Intoxication requires immediate diagnosis andswift treatment in order to prevent brain dam-age becoming irreversible or fatal. Once therisk of death has been overcome, the contribu-

tion of diagnostic imaging and of MRI in par-ticular consists in the possibility of monitoringtreatment and the evolution of the neuroradio-logical picture over time.

In general, brain damage caused by toxinsinvolves both hemispheres, as there is no sidepreference. It is still unclear why some CNSstructures are affected to a greater extent thanothers, however it is probable that differencesin vulnerability and/or tissue affinity to the tox-ic substance are implicated.

It should be underlined that the clinical andneuroradiological findings do not always match,and even in cases of neuropathologically provenbrain damage diagnostic imaging techniquesmay provide falsely negative results.

ALCOHOLIC ENCEPHALOPATHY

Due to its low cost and ready availability, al-cohol is by far the most widespread drug in thewestern world. Given its marked neurotoxiccapacity, alcohol is probably the most com-monly encountered CNS toxin. The neurolog-ical pathology seen in alcoholics can only part-ly be attributed to the direct toxic effect of al-cohol and its metabolites, and some of the ae-tiological explanations are still unknown. Thefactors that are presumed to explain brain

4.1

TOXIC ENCEPHALOPATHYM. Gallucci, M. Caulo, G. Cerone, A. Splendiani, R. De Amicis, C. Masciocchi

damage include vitamin deficiency, hypogly-caemia, associated repeated cranial trauma,chronic liver failure and the presence of non-alcohol toxic substances that are present in al-coholic beverages. In chronic alcoholics, arte-rial hypertension, subarachnoid haemorrhage

and strokes are also more common than in average age-matched controls. Although notall alcohol-related neurological pathology re-quires management in emergency conditions,some do require immediate diagnosis andtreatment.

242 IV. EMERGENCY NEURORESUSCITATION

Fig. 4.1 - Extrapontine myelinolysis in an alcoholic patient. TheMRI demonstrates multiple areas of hyperintensity within thehemispheric subcortical hemispheric white matter, the deephemispheric white matter and the midbrain. [a) coronal FLAIRMRI; b, c, d) axial T2-weighted MRI].

a

b

c

d

Osmotic myelinolysis

Osmotic myelinolysis is a demyelinatingprocess that arises from a too rapid correctionof an existing state of hyponatraemia, which, inthe case of alcoholics, is induced by the impair-ment of ADH secretion caused by alcohol. OnMRI, these lesions appear as areas containing“excess water” that result in high signal intensi-ty areas in T2-weighted sequences and low in-tensity areas in T1-weighted sequences. Thesepure demyelinating forms do not manifest evi-dence of inflammation or blood-brain barrierdamage. For this reason, MRI shows no en-hancement following IV contrast medium ad-ministration.

A distinction is made between pontine andextrapontine myelinolysis. In the latter, themost frequent sites of demyelination are theputamen, caudate nucleus, thalamus and sub-cortical white matter. Less frequently, themamillary body, the tegmen of the midbrainand the white matter of the cerebellum mayalso be involved (Fig. 4.1). Central pontinemyelinolysis appears on MRI as a single sym-metric lesion that spreads to the pontineraphe and involves the transverse pontocere-bellar fibres and the long descending corti-cobulbar tracts (Fig. 4.2). The clinical aspectof this type of lesion is characterized by a flac-cid quadraparesis that may regress or alterna-tively evolve into a subsequent spastic formwith pseudo-bulbar paralysis. Osmotic myeli-nolysis is not always an alcohol-relatedpathology and may be caused by or connect-ed to many conditions in which there is a toorapid correction of a water and electrolyteimbalance. For example, this may also occurin dialysis patients (3, 18, 19, 29).

Wernicke encephalopathy

Wernicke encephalopathy is the conse-quence of a thiamine deficiency resulting eitherfrom reduced intake or from intestinal malab-sorption. This type of abnormal metabolismtypically occurs in subjects with congenitaltransketolase activity deficits. Thiamine deficits

cause a reduced use of glucose in the brain.This condition has an acute onset characterizedby ophthalmoplegia, ataxia and mental confu-sion. In the chronic phase patients may demon-strate a reduction in olfactory discriminationsecondary to midbrain lesions, whereas memo-ry disorders are related to injury to the mamil-lary bodies and the dorsomedial nuclei of thethalamus. Following thiamine therapy, the clin-ical situation may either improve or evolve intoKorsakoff’s syndrome. Korsakoff’s syndrome ischaracterized clinically by the impairment ofchronological fixation memory, learning abilityand the appearance of confabulatory attacks(i.e., amnesia with the appearance of false rec-ollections).

MR examinations using T2-dependent se-quences show abnormal high intensity areasin the involved white and grey matter witha characteristic topographic distribution.The affected areas include those surround-ing the 3rd ventricle: the massa intermedia,the floor of the 3rd ventricle, the mamillarybodies, the reticular formation and the peri-aqueductal region (Figs. 4.3, 4.4). In chron-ic forms one also observes a passive dilationof the third ventricle and atrophy of themamillary bodies.

The involvement of the mamillary bodies hasbeen demonstrated in 98% of autopsies per-formed on Wernicke sufferers. Using MRI it ispossible to demonstrate the involvement of themamillary bodies primarily in acute cases inwhich contrast enhancement of the mamillarybodies is observed. However, this finding is notconstant and is probably only present in cases inwhich there is endothelial necrosis with atten-

4.1 TOXIC ENCEPHALOPATHY 243

Fig. 4.2 - Two cases of pontine myelinolysis in alcoholic pa-tients. T2-weighted MRI shows a single hyperintense lesion ofthe pons in each case. [a, b) axial T2-weighted MRI].

a b

dant blood-brain barrier disruption. Neverthe-less, in such cases the finding of mamillary bodyenhancement can dispel diagnostic doubts (Fig.4.4). Certain authors have also documentedhigh signal intensity areas in the cortex of thecentral and precentral gyri.

In Korsakoff’s syndrome the neuropatho-logical and neuroradiological alterations arefocused on the dorsomedial nuclei of the thal-amus and the hippocampal formations. Injuryto these structures is associated with amnesicsymptomatology that defines the symptoms ofWernicke-Korsakoff syndrome (Fig. 4.5). Re-cent studies using PET and perfusion MR inthe thalamic and temporal regions of patientswith Korsakoff’s syndrome have shown bothreduced blood flow and metabolic activity inthese areas. In a similar manner to osmoticmyelinolysis, Wernicke’s syndrome is not nec-essarily alcohol-related and can be encoun-tered in other diet-related, deficiency-relatedor malabsorption pathology (Fig. 4.6) (1, 8, 10,11, 25, 29).

Marchiafava-Bignami disease

This rare disorder was initially described inmiddle-aged and elderly drinkers of red winehaving a high tannin content. For this reasonfor many years it was believed that the specificcause of the disease was Chianti wine, a theorythat has now been rejected. The most probable


Fig. 4.3 - Wernicke’s encephalopathy in alcoholic patient. CTonly rarely shows an area of hypodensity in the midbrain in cas-es of Wernicke’s encephalopathy, as in this case.

Fig. 4.4 - Wernicke’s encephalopathy in an alcoholic patient.Enhanced MRI shows contrast enhancement within the mamil-lary bodies bilaterally. More craniad T2-weighted scans showsabnormal hyperintensity within the posteromedial aspect of thethalami bilaterally and the hypothalamus. [a), b) T1-weightedMRI following IV Gd; c-e) PD- and T2-weighted MRI].

a-b

c-d

e

cause of the illness is an as yet unspecified nu-tritional deficiency. Clinical symptoms varyfrom convulsions to hallucinations and deliri-um, and in the terminal stages stupor and comamay be seen. The clinical diagnosis is problem-atic given the heterogeneity and non-specific

nature of the symptoms, and for this reason theuse of diagnostic imaging techniques is essen-tial. Marchifava-Bignami disease is character-ized by the necrosis and demyelination of themidline lamina of the corpus callosum and theinjury of other commissural fibres and thehemispheric white matter. MRI performed inthe sagittal plane in the chronic phase shows at-rophy of the corpus callosum and the presenceof multifocal necrotic areas characterized bylow signal intensity in T1-weighted sequencesand high signal intensity in T2- and PD-weight-ed sequences (Fig. 4.7) (2, 4, 22, 29).

Acquired hepatocellular degeneration (AHCD)

Acquired hepatocellular degeneration syn-drome is a complex illness characterized bychanges in consciousness, behaviour and per-sonality often associated with acute or chron-ic kidney disease or liver cirrhosis. It wouldappear to be linked to alterations in the me-tabolism of nitrogenated substances and alter-ations of the glutamate-glutamine ratio, withan increase in the synthesis of aromatic aminoacids and false neurotransmitters. The alter-ations visible on MRI are closely correlatedwith plasma ammonia levels, but do not seemto be linked to the degree of neuropsychiatric


Fig. 4.5 - Wernicke-Korsakoff syndrome in alcoholic patient.T2-dependent SE a) and PD-dependent sequences b). Wide-spread signal alteration in the dorsal-medial region of the thal-amus bilaterally and in the hypothalamus.

Fig. 4.6 - Wernicke’s encephalopathy in a malnourished 8-yearold child. T2-weighted MRI shows hyperintense periaqueduc-tal MRI signal alteration.

Fig.4.7 - Marchiafava-Bignami disease in alcoholic patient.Sagittal T2 weighted MRI shows marked thinning of the corpuscallosum associated with abnormal signal hyperintensity alongits entire course.

dysfunction or to electroencephalographic al-terations. In most cases, there is a widespreadshortening of the T1-dependent signal includ-ing hyperintensity of the basal ganglia; promi-nent involvement of the globus pallidus is typ-ical (Fig. 4.8). The caudate nucleus, pinealgland, subthalamic region and the midbrainaround the red nuclei may also be similarly in-volved. The reason for this signal alteration isnot yet clear, but it is thought to be connect-ed to a hyperplasia of the Alzheimer type IIastrocytes in association with neuronal necro-sis and the subsequent deposition of para-magnetic substances such as magnesium (10,12, 23, 29).

METHANOL INTOXICATION

There are a number of sources of methanol,which can be present in solvents, industrial liq-uids, perfumes and counterfeit spirits, thusmaking methanol intoxication relatively com-mon amongst alcoholics. It manifests clinicallyas general malaise and headache and mayprogress to stupor and coma. Necrotic areasare visible in the putamen as hypodense on CTscans and as high signal intensity on T2-de-pendent sequences in MR studies (Fig. 4.9).The appearance of these areas can also be af-fected by the presence of haemorrhagic infarc-tion. Other related necrotic areas can be identi-fied in the subcortical white matter and in thefrontal cortex (12, 28, 29).

ETHYLENE-GLYCOL INTOXICATION

Ethylene-glycol is typically present in paintsand glues but can also be encountered in foodpreservatives and as an alcohol substitute. In-gestion occurs accidentally or, more rarely, vol-untarily in the case of alcoholics. Neurologicalclinical symptomatology sets in after approxi-mately 12 hours of ingestion and is character-ized by a sense of inebriation and convulsionsprogressing to coma.

As with methanol intoxication, the toxic ef-fects are manifested as areas of necrosis thatprincipally affect the frontal cortex, the thalamiand the basal ganglia (Fig. 4.10) (28, 29).

INTOXICATION FROM NARCOTIC INHALATION

Toluene and methyl-ethylketone are lipophilicsolvents that are used in the chemical industryand that may be accidentally inhaled during pro-cessing. These substances are capable of causinga similar neurological, neuropathological andneuroradiological picture to those caused by oth-er voluntarily inhaled substances such as heroinand, more rarely, cocaine (in such cases the toxiceffect may be related to the substances withwhich the drugs are diluted). In cocaine and


Fig. 4.8 - Hepatocerebral degeneration in patient with cirrho-sis. The MRI demonstrates an abnormal area of high MRI sig-nal intensity in the globus pallidus bilaterally. [a) axial, b) sagit-tal T1-weighted MRI].

Fig. 4.9 - Alcoholic patient following consumption of a largequantity of methanol. Coronal T2-weighted MRI reveals highsignal intensity within the putamena and in the frontal subcor-tical white matter bilaterally.

ab

heroin sniffers, in an acute stage the neuropatho-logical and neuroradiological manifestations in-clude microinfarcts caused by toxic vasculitis. It

may also be possible to observe hypertensive en-cephalopathy (from cocaine) and hypotensive en-cephalopathy (from heroin) (Fig. 4.11), or rarerforms of vacuolating encephalopathy with foci ofdemyelination in the supra- and subtentorialwhite matter. Although in these cases the toxicagent has yet to be identified, it is theorized thata lipophilic substance present in the drug is re-sponsible (7, 15, 21, 27-29).

INTOXICATION FROM MEDICINES

Many of the medicines currently availablehave neurotoxic characteristics, includingchemotherapy drugs, which give can give riseto the most severe conditions.

Intoxication from Methotrexate

Methotrexate is usually administered intra-venously or via subarachnoid catheter, the lat-ter principally in the case of lymphoprolifera-tive disorders of the CNS. Although its neuro-toxicity has been proved, the pathophysiology


Fig. 4.10 - Glycol-ethylene intoxication. Axial CT showsmarked hypodensity of the thalami bilaterally.

a

Fig. 4.11 - Delayed post-hypoxic leukoencephalopathy,. MRI examination performed approximately three hours following admissionshows widespread MRI signal hyperintensity of the white matter of the centrum semiovale. Follow up MRI approximately 1 monthlater shows necrosis within the abnormal hemispheric white matter foci identified on earlier scans. This evolution is consistent withdelayed post-hypoxic leukoencephalopathy. As in this case, this phenomenon has been described in heroine addicts following expe-riencing acute cardiorespiratory depression. [a), b) axial T-2 weighted MRI on admission; b) axial T1-weighted MRI on admission;c), one month follow up axial T2-weighted MRI; d) one month follow up T1-weighted MRI].


b

c

dFig. 4.11 (cont.).

of the neurological damage caused by this drugis still controversial. The most commonly ac-cepted theory is that it causes a thickening ofthe endothelial walls of the cerebral vascula-ture, with consequent occlusion, ischaemia andnecrosis of the served neural tissue. Duringchemotherapy, this condition is believed to befavoured by concomitant radiation therapy.The MRI semeiotics vary from focal lesions todiffuse alterations of the white matter signal,mainly the deeper areas of the brain, havinghigh signal intensity on long TR sequences (Fig.4.12). On CT, the lesions appear hypodensewith the presence of hyperdense foci (i.e., calci-fied deposits) in the subcortical regions. TheMR appearance of the lesions that are hyper-dense on CT scans were evaluated usingFLASH MRI sequences and were found tohave low signal intensity. CT and MR findingstherefore show a picture of leukoencephalopa-thy with calcified deposits that are typical of thedisease (13, 17, 20, 23, 29).

Intoxication from Cyclosporin A (CsA)

Cyclosporin A is an immunosuppressivemedicine used in the prevention of so-calledgraft vs. host disease. Although the neurotoxiceffects of this drug have been determined, thepathophysiological mechanism is yet to bespecified. One theories of the most widely ac-cepted theories is that CsA causes arterial hy-pertension (90% of all patients treated), withconsequent similar neuropathological and neu-roradiological conditions to those of hyperten-sive encephalopathy; another, more recent the-ory states that CsA may cause damage to thecapillary endothelium with consequent vaso-genic oedema. This second theory would justi-fy the reversibility of the clinical and neurora-diological situation in CsA intoxication.

Clinically CsA intoxication is manifested asheadache, epilepsy, cortical blindness, visual hal-lucinations, trembling and cerebellar ataxia. MRexaminations show areas of high signal intensityon T2-dependent and FLAIR sequences, mostfrequently observed in the subcortical whitematter of the occipital lobes of the posterior por-

tions of the temporal and parietal lobes (16). Thelesions are frequently symmetrical, and they on-ly rarely show enhancement following IV con-trast agent administration. Recent observationsperformed using diffusion MR in cases of CsA


Fig. 4.12 - Methotrexate neurotoxicity. T2-weighted MRI, in apatient with disseminated cancer under treatment withmethotrexate, shows widespread hyperintense MRI signal al-terations within the hemispheric deep and subcortical whitematter consistent with chronic treatment related neurotoxicity.[a, b) axial T2-weighted MRI].

intoxication have shown that the altered signalareas are due to vasogenic rather than to intra-cellular oedema, thus supporting the direct en-dothelial damage theory. In 4 out of 14 cases ofCsA intoxication, Schwartz, et al (24) observedthe presence of cerebral haemorrhage, and inone case small focal areas of intraparenchymalhaemorrhage in the occipital lobes. The greymatter is also rarely involved (5, 23, 24).

CARBON MONOXIDE (CO) INTOXICATION

CO intoxication causes ischaemia-basedbrain damage in preferential positions that havebeen known for some time. CO’s affinity tohaemoglobin is 250 times greater than that ofthe oxygen with which it competes, thus reduc-ing haemoglobin’s capacity to capture, trans-


Fig. 4.13 - Acute carbon monoxide intoxication with cerebral necrosis. CT undertaken in the acute phase documents bilateral globuspallidus hypodensity and within the anterior frontal white matter on both sides. CT follow up approximately three weeks later revealsbilateral globus pallidus necrosis; MRI performed the same day as confirms globus pallidus necrosis and the frontal subcortical de-generative alteration. [a, b) acute phase axial CT; c) three week follow up CT; d) three week follow up T2-weighted MRI].

a-b

c e

d

port and release oxygen. The presence of car-boxyhaemoglobin shifts the haemoglobin’s dis-sociation curve to the left, and CO hampers cel-lular respiration as it bonds with cytochromeoxydase and generates hypertension due to the

myocardial dysfunction caused by the presenceof carboxyhaemoglobin in the heart tissue.

In the brain, it is typically responsible for bi-lateral necrosis of the globus pallidus (Fig. 4.13)and the hippocampal structures, and for eitherdiffuse or focal involvement of the white matter.The involvement of the white matter can becombined with that of the grey matter in themore distal vascular territories where capillaryproliferation (Fig. 4.14) can be observed patho-logically. CO intoxication may also have a spe-cific direct toxic effect upon the globus pallidus,which would justify such selective involvement.This observation derives from the fact that incases of non-CO-induced hypoxia, differentstructures such as the putamen, the caudate nu-cleus and the cerebral grey matter are typicallyinvolved. The interruption or delay in the trans-port of non-haematogenous iron through axonalstructures damaged by the ischaemic insult isprobably responsible for the low signal densitydetected in the basal ganglia on T2-dependentsequences (6, 14, 25, 26, 28, 29).

REFERENCES

1. Antunez E, Estruch R, Cardenal C: Usefulness of CT andMR imaging in the diagnosis of acute Wernicke’s encepha-lopathy. AJR 171:1131-37; 1998.

2. Bracard S, Claude D et al: Computerized tomography andMRI in Marchiafava-Bignami disease. J Neuroradiol 13:87-94; 1986.

3. Brunner JE, Redmond JM et al: Central pontine myeli-nolysis and pontine lesions after rapid correction of hypo-natremia: a prospective MRI study. Ann Neurol 27:61-7;1990.

4. Chang KH, Cha SH et al: Marchiafava Bignami disease: se-rial changes in corpus callossum on MRI. Neuroradiology34:480-2; 1992.

5. Debaere C, Stadnik T, De Maeseneer M: Diffusion-weigh-ted MRI in cyclosporin A neurotoxicity for the classifica-tion of cerebral edema. Eur Radiol 9(9):1916-8; 1999.

6. Dietrich RB, Bradley WG: Iron accumulation in the basalganglia following severe ischemic-anossic insult in chil-dren. Radiology 168:203-6; 1988.

7. Diez-Tejedor E, Frank A, Gutierrez M et al: Encephalo-pathy and biopsy-proven cerebrovascular inflammatorychanges in a cocaine abuser. Eur J Neurol 5(1):103-7; 1998.

8. Donnal JF, Heinz ER, Burger PC: MR of reversible thala-mic lesions in Wernicke syndrome. AJNR 11:893-5; 1990

9. Fazio C, Loeb C: Neurologia, Società Editrice Universo,Roma, 1994.

10. Gallucci M, Amicarelli I, Rossi A et al: MR imaging of whi-te matter lesions in uncomplicated chronic alcoholism, JComp Asst Tomogr 13:395-398, 1989.


Fig. 4.14 - Acute carbon monoxide intoxication with clinicora-diologic resolution. T2-weighted MRI on patient admissionshows swelling of the frontal lobe cortex, more prominent onthe right side, resulting from cytotoxic oedema. Follow up MRIperformed after clinical resolution reveals regression of thefrontal swelling. [a, admission T2-weighted MRI; b) follow upT2-weighted MRI].

a

b

11. Gallucci M, Bozzao A, Splendiani A et al: Wernicke en-cephalopathy: MR findings in five patients, AJNR 11:887-892, 1990.

12. Gallucci M, Caulo M et al: L’encefalopatia alcolica. AttiMeeting Scienze Neurologiche. Selva di Val Gardena,1999.

13. Genevresse I, Dietzman A et al: Subacute encephalopathyafter combination chemotherapy including moderate-dosemethotrexate in a patient with gastric cancer. AnticancerDrug 10(3):293-4; 1999.

14. Horowitz AL, Kaplan R: Carbon monoxide toxicity: MRimaging in the brain. Radiology 162:787-8; 1987.

15. Ikeda M, Tsukagoshi H: Encephalopathy due to toluenesniffing. Report of a case with Magnetic Resonance Ima-ging. Eur Neurol 30(6):347-9; 1990.

16. Jansen O, Krieger D et al: Cortical hyperintesity on protondensity-weighted images: an MR sign of cyclosporine-rela-ted encephalopathy. AJNR 17(2):337-44; 1996.

17. Kubo M, Azuma E, Arai S et al: Transient encephalopathyfollowing a single exposure of high-dose methotrexate in achild with acute lymphoblastic leukemia. Pediatr HematolOncol 9(2):157-65; 1992.

18. Laubenberger J, Schneider B, Ansorge O et al: Centralpontine myelinolysis: clinical presentation and radiologicfindings. Eur. Radiol. 6:177-83; 1996.

19. Lohr JW: Osmotic demyelination syndrome following cor-rection of hyponatremia: association with hypokalemia.Am J Med 96:408-12; 1994.

20. Lovblad K, Kelkar P et al: Pure methotrexate encephalo-pathy presenting with seizures: CT and MRI features. Pe-diatr Radiol 28(2):86-91; 1998.

21. Maschke M, Fehlings T, Kastrup O et al: Toxic leukoen-cephalopathy after intravenous consumption of heroineand cocaine with unexpected clinical recovery. J Neurol246(9):850-1; 1999.

22. Mayer JW, De Liége P, Netter JM: Computerized tomo-graphy and nuclear magnetic resonance in Marchiafava-Bi-gnami disease. J Neuroradiol 14:152-8; 1987.

23. Osborne AG: Diagnostic Neuroradiology. Mosby ed. St.Louis, Missouri, 1992.

24. Schwartz BR, Bravo MS, Klufas RA et al: Cyclosporine neu-rotoxicity and its relationship to hipertensive encephalopathy:CT and MR findings in 16 cases. AJR 165:627-31; 1995.

25. Shogry MEC, Curnes JT: Mamillary body enhancement onMR as the only sign of acute Wernicke encephalopathy.AJNR 15:172-4; 1994.

26. Silverman CS, Brenner J et al: Hemorragic necrosis and va-scular injury in carbon monoxide poisoning: MR demon-stration. AJNR 14:168-70; 1993.

27. Thuomas KA, Moller C, Odkvist LM et al: MR imaging insolvent-induced chronic toxic encephalopathy. Acta Ra-diol 37(2):177-9; 1996.

28. Valk J, van der Knaap: Toxic encephalopathy. AJNR 13(2):747-60; 1992.

29. Valk J, van der Knaap MS: Magnetic resonance of myelin,myelination and myelin disorders. Springer edition 1995.


253

INTRODUCTION

Coma is rightly considered to be the one ofthe most commonly occurring neurologicalemergency conditions. Coma can be the con-sequence of an entire spectrum of pathologi-cal conditions and thus requires equally variedbut quite specific treatment (8, 15, 16). Neu-roradiological studies are often the only realpractical option for initial diagnostic patientinvestigation, as the clinician may have accessto little or no information when the patient isadmitted.

In such situations, it is almost always Com-puted Tomography (CT) that assumes theleading role in the initial diagnostic, prognosticand therapeutic approach. The fundamentalquestion is whether or not there are docu-mentable intracranial neuroanatomical alter-ations, which, if present, can be subsequentlymonitored after the patient is admitted to theintensive care suite.

We will not deal in detail here with the en-tire spectrum of the intracranial pathology re-sponsible for causing coma, as they are dealtwith separately in the various chapters of thisvolume; instead, we will briefly outline the op-timal neuroradiological approach to be utilized

in patients in coma including: a) the modes ofinvestigation; b) the related technical variables;c) conditions causing acute focal lesions (9),and d) conditions causing diffuse brain impair-ment.

MODES OF INTRACRANIAL ANALYSIS

The neuroradiological evaluation can be di-vided into two clinical phases: the initial evalu-ation and the re-evaluation of the patient overtime. The aim of the initial evaluation is to de-tect or exclude focal alterations and to definethe overall status of the tissues within the in-tracranial compartment. As an example, therevelation of demonstrable focal cerebral le-sions eliminates clinical suspicion of a meta-bolic or toxic cause of coma, while the oppo-site can prompt and direct swift specific med-ical or surgical treatment. A typical example ofthis is the demonstration of an extracerebralhaematoma that requires immediate surgicalevacuation.

We will ultimately go on to describe the ele-mentary cerebral alterations implied in coma.However, first we intend to underline the im-portance of an overall evaluation of the in-

4.2

THE NEURORADIOLOGICAL APPROACH TO PATIENTS IN COMA

G.M. Di Lella, M. Rollo, T. Tartaglione, C. Colosimo


Fig. 4.15 - Epidural haematoma. The CT examination shows a biconvex blood collection over the right temporoparietal region asso-ciated with marked mass effect. Note the displacement of the surrounding parenchymal structures associated with leftward midlinesubfalcian herniation and compression of the right lateral ventricle. In the more caudal scan, ipsilateral downward herniation of theuncus is also clearly visible. In addition, there is a fracture in the right temporal bone, with minor fragment displacement. CT followup three months later documents encephalomalacia of the posterior temporal lobe, perhaps as a result of infarction secondary com-pression-occlusion of the posterior cerebral artery caused by the uncal herniation. [a1-2) initial axial unenhanced CT with brain win-dows; b1-2) initial axial CT with bone windows; c) three month follow up axial CT].

a1

b1

b2a2

tracranial compartment, which is subject toparticular pressure balances, the alteration ofwhich is often closely related to the patient’sclinical evolution and prognosis.

The importance of the effects of relativelysudden changes upon the contents of the in-tracranial compartment hinges upon its beinga “closed system” with a fixed volume. Thiscompartment has a strict relationship be-tween its rigid container (the skull) and itscontents (cerebral parenchyma, CSF andblood). Any condition that creates a changein intracranial pressure (ICP) will have a di-rect effect on what is visualized on CT and/orMR studies. An increase in ICP can altercerebral blood flow (CBF) and even com-pletely obstruct it when cerebral perfusionpressure (PP) is exceeded. Any alteration thatcauses an increase in intracranial contentsshows signs of mass effect on either CT orMRI. Mass lesions above all are defined bythe effacement and displacement of the in-tracranial fluid-filled spaces. The mass effect

and their corresponding CT/MR findings areinitially observed locally and subsequently ina more widespread manner. As cerebralswelling increases, the structures contained inthe expanding intracranial compartment aredisplaced beyond the boundaries of thatcompartment. Ultimately this may result ininternal cerebral herniation. In the case ofmonohemispheric swelling, this herniationmay occur below or beyond the falx cerebri(i.e., subfalcian herniation) or downwardthrough the tentorial incisura with disloca-tion of the uncus of the temporal lobe (i.e.,descending uncal herniation). In the case ofinfratentorial compartment swelling, portionsof the cerebellum and brainstem are pushedupward through the tentorial hiatus (i.e., as-cending transtentorial herniation) or down-ward through the foramen magnum into theproximal cervical spinal canal (i.e., descend-ing tonsillar herniation). This internal cere-bral herniation represents the displacement,distortion and compression of the involvedneural parenchyma and attendant vascularstructures.

The most severe and sometimes fatal effectof these internal cerebral herniations is dys-function of the brainstem, which can be im-paired in any of the descending uncal, ascend-ing transtentorial and descending forms oftonsillar herniation. The complete effacementof the cisternal spaces surrounding the brain-stem, the distortion/dislocation of the brain-stem and the direct demonstration of uncalherniation (Fig. 4.15) (i.e., medial and down-ward displacement of the uncus or unci) arequite common findings in patients in coma in-duced by acute, rapidly forming mass lesions,whatever the underlying cause. On axial CT,the signs of uncal herniation are typically eas-ily recognized, whereas herniations caused byexpanding subtentorial lesions may be less ap-parent; in this latter case the dislocation oc-curs in an upward caudocranial directionwhich has far less obvious findings on axialCT images (Fig. 4.16). In the case of ascendingtranstentorial herniations, one must search forthe disappearance of the superior cerebellarcisternal spaces and for the inversion, distor-

4.2 THE NEURORADIOLOGICAL APPROACH TO PATIENTS IN COMA 255

c

Fig. 4.15 (cont.).


Fig. 4.16 - Acute infratentorial ischaemic swelling. Unenhanced cranial CT demonstrates a large area of hypodensity in the cerebel-lar vermis and hemispheres bilaterally. Note the evidence of ascending transtentorial herniation: the tentorial hiatus and the ambientcistern are both effaced. Also note the acute obstructive hydrocephalus with signs of transependymal extravasation of CSF from thelateral ventricular margins. [a-e) unenhanced axial CT].

ac

db

tion or absence of the normally posteriorly directed convexity of the quadrigeminalplate/cistern. In the event of downward ton-sillar herniation, special attention must bepaid to the peribulbar CSF spaces and to thecisterna magna; with the progressive improve-ment in the quality of CT images, it is current-ly possible to observe clearly the downwarddisplacement of the cerebellar tonsils into theforamen magnum.

Compression of the parenchyma of the brainstem can have very severe clinical conse-quences, especially if acute. However, the effectof the internal cerebral herniation upon the re-lated blood vessels may also result in a consid-erable worsening of the neurological situation.This blood vessel involvement may result in ve-nous stasis and ischaemia, itself engendering afurther increase in cerebral swelling. This is thecase, for example, in ischaemic infarction with-in the territory of the posterior cerebral arteryconsequent to its compression-occlusion in theperimesencephalic segment caused by the di-rect external mass effect of the descending un-cal herniation (Fig. 4.15).

The pressure effects described can set inrapidly under the force of a large, rapidlygrowing haemorrhagic collection such as anepidural haematoma, however, more frequent-ly these observations are the result of a combi-nation of the primary mass lesion coupledwith related phenomena such as oedema,complications of ischaemia or widespreadbrain swelling engendered by vasospasm.Changes in the mass effect and the formationof internal cerebral herniation follow veryvariable chronological patterns that often donot correspond to objective clinical neurolog-ical signs that might otherwise be useful inevaluating evolution of the overall process. Di-rect measurements of ICP and its patternsover time using subdural or subarachnoidcatheters do provide one important objectiveparameter; however, this procedure is not al-ways possible, and it is only available in spe-cialized neurosurgery centres. This calls forfrequent CT re-evaluations, properly integrat-ed with other diagnostic techniques such asMRI or transcranial-echo colour Doppler, asrequired. Therefore, requests for frequent di-agnostic imaging checks by resuscitation staffmust not be considered superfluous on eithera clinical basis or in order to justify difficultICP measurements. The CT findings may infact change dramatically in the course of just afew hours, in a crescendo that can only becontrolled by swift implementation of appro-priate treatment.

With regard to serial re-valuation of theevolution of intracranial findings in patientswith coma, we must point out the signifi-cance of hydrocephalus associated with theprimary pathology. In the case of diffusebrain swelling caused by a principal insult(e.g., trauma, haemorrhage with vasospasm,etc.), the onset of hydrocephalus can havedramatic consequences. Therefore, it is nec-essary to make a correct diagnosis early in itsprogress, before marked ventricular dilata-tion occurs. The earliest signs of hydro-cephalus must be recognized, such as milddilatation and outward rounding of the mar-gins of the temporal horns of the lateral ven-tricles (Figs. 4.16, 4.17).


Fig. 4.16 (cont.).

e

TECHNICAL CONSIDERATIONS

The technical approach adopted when treat-ing patients in coma does not vary greatly fromthat generally applied in most cranial emergen-cies as has been described in the previous chap-ters. The general scheme uses CT as the initialexamination technique, backed up by MRIand, less frequently, by other techniques thatmay prove useful in patients in critical condi-tion.

CT is the preferred method of imaging in co-ma patients due to its very rapid examinationacquisition speeds, with single or multiple slicescanning times faster than one second in latestgeneration appliances; in addition to its gener-al diagnostic capabilities, it is also very sensitivein recognizing acute and hyperacute phase in-tracranial haemorrhages, in localizing the cra-nial compartment of the bleed (e.g., subdur-al/epidural, subarachnoid, intraparenchymal);finally it is almost universally available in the


Fig. 4.17 - Acute hydrocephalus in a case of spontaneous subarachnoid haemorrhage. Unenhanced cranial CT shows an intra-ventricular blood clot at the level of the foramina of Monro and the symmetrical subarachnoid haemorrhage. Also note the di-latation of the lateral ventricles, including the temporal horns, as a consequence of the obstructive hydrocephalus. [a-c) unen-hanced axial CT]

a

b c

various communities of industrialized regions(Figs. 4.15, 4.17, 4.19).

MRI maintains a secondary role, in part be-cause of its low sensitivity in demonstratinghaemorrhages in the early phases of evolution,its rather long scan acquisition times making itunsuitable for use in non-cooperative patientsand those in critical condition, and the stillrather scarce availability of MRI appliances insome hospitals and healthcare centres.

Despite these limits, in the near future it islikely that MRI will be more frequently appliedas scanning times are drastically reduced and asspecific techniques for early detection of cere-bral parenchymal haemorrhage become morereadily available.

One example of this technological advance-ment is the recent introduction of diffusiontechniques, which enable the very early detec-tion of cerebral ischaemia and other patholog-ical conditions characterized by cytotoxic/in-tracellular oedema utilizing very fast scanningtimes employing echo-planar acquisition se-quences. Diffusion imaging makes it possibleto detect parenchymal injury at a very earlystage, when CT images are completely nega-tive. In addition, diffusion imaging is equallysensitive in demonstrating posttraumatic dif-fuse axonal injury (Fig. 4.19) (4).

The rapid progress in MRI angiography andCT angiography (the latter especially since therecent introduction of multidetector appli-ances) has made it somewhat rare to have toresort to the use of invasive selective angiog-raphy in coma patients. Invasive angiographictechniques are currently primarily used fol-lowing the CT or MR diagnosis of vascularmalformations, where angiography remains im-portant for the fine definition of the angioar-chitecture of the documented malformation.While on the subject of vascular examinationsit should be pointed out that when monitor-ing coma patients, especially in resuscitationcentres, transcranial Doppler and transcranialecho-colour-Doppler may assume fundamentalroles due to their ability to evaluate and quan-tify CBF (3, 5).

These techniques can also be used to evalu-ate reductions in cerebral perfusion pressureand vasoparalysis in order to rebalance CBF onthe basis of ICP trends (1, 2).

ACUTE PRIMARY FOCAL CEREBRALLESIONS

Haemorrhage

In the acute phase, freshly clotted blood has adensity of approximately 70-80 H.U. It thereforeappears hyperdense in comparison to the sur-rounding cerebral parenchyma; however, whenfluid in consistency, newly extravasated bloodcan appear relatively isodense. Over time the CTdensity of the haematoma tends to decrease, with


Fig. 4.18 - Subacute cerebral infarction within the right middlecerebral artery territory. Unenhanced cranial CT shows wide-spread cortical-subcortical hypodensity in the right tem-poroparietal region. Moderate mass effect is present, as a resultof vasogenic oedema, represented by the effacement of the re-gional superficial subarachnoid spaces and the compression ofthe right lateral ventricle.

an eventual evolution towards hypo- isodensity, aphenomenon that begins in the outside layersand moves inward towards the centre of thehaematoma. The time required for the above-mentioned alterations depends on the size andsite of the blood collection; in general, parenchy-mal haemorrhages remain hyperdense for manydays and only appear frankly hypodense afterseveral weeks. The evolution of mass effect fol-lows a similar pattern: after a few hours, as oede-ma grows, the mass effect increases; in the ab-sence of treatment, mass effect reaches a peak af-ter 3-5 days, before gradually shrinking and dis-appearing, resulting in a loss of brain substancein late stages after many weeks or even months.

As mentioned previously, MRI at present isfar less sensitive relative than CT in its ability torecognize the hyperacute phase haemorrhages:oxyhaemoglobin present a nearly or completelyisointense signal in almost all image sequences(both T1- and T2-dependent sequences). Withthe subsequent transformation into methaemo-globin, MRI becomes more specific and sensi-tive than CT: initially the methaemoglobin thatis contained within the non-lysed red cells pres-ents a signal that is hyperintense on T1- andisointense on T2-weighted MR sequences,whereas subsequently, with the lysis of the redblood cells, extracellular methaemoglobin ap-pears hyperintense on all sequences. Lastly, the subsequent evolution of the bleed intohaemosiderin results in the haemorrhage be-coming hypointense on T2-weighted sequences.This is especially apparent if the acquisitions(e.g., gradient recalled echo) are sensitive to thepresence of paramagnetic substances (e.g.,haemosiderin and ferritin) (11).

Cerebral ischaemia

In the hyperacute phase, the CT and MR man-ifestations of cerebral ischaemia consist mainly incytotoxic oedema (Fig. 4.20); subsequently, from12-24 hours later, vasogenic oedema appears, en-larges and becomes more readily visible, this inpart due to mass effect (Fig. 4.16) (10, 13). EarlyCT signs of ischaemia are particularly evident inthe lentiform nucleus (when the deep territory of


Fig. 4.19 - Diffuse axonal injury (damage). Unenhanced cranialCT shows the presence of multiple, small cortical-subcorticaljunction haemorrhagic foci. These haemorrhages are an ex-pression of axonal shearing, some of which are not visible dueto the absence of bleeding. The parenchymal, and thereforefunctional, damage is often greater than predicted on the basisof CT alone. [a, b) unenhanced axial CT].

a

b

the middle cerebral artery is affected) due to thedisappearance of its normal physiological hyper-density. This finding, which can sometimes bevery slight, is strengthened by any finding of clearhyperdensity (thrombosis, embolism) in the lu-men of the first segment of the middle cerebral ar-tery; in the same manner, this CT hyperdense sig-nal can be observed in the basilar artery in casesof acute thrombosis/embolism.

Utilizing classic T1- and T2-weighted MRacquisitions in the initial phase of cerebral is-chemia, findings and sensitivity are similar tothose of CT. However, with new diffusionweighted sequences, both sensitivity and speci-ficity are far greater relative to CT and enable,when appropriate, the prompt application ofsystemic or selective intraarterial antithrombot-ic treatment.

Cerebral oedema

Cerebral oedema is a non-specific phenom-enon. Many events can cause intracellular cy-

totoxic oedema. Cytotoxic oedema, an expres-sion of cellular injury, principally involves thecerebral cortex and the basal nuclei of thecerebral hemispheres. Oedema generallyshows a relative reduction in density on CT, areduction in signal on T1-weighted MR andhyperintensity in T2-weighted sequences. Clin-ical practice has recently witnessed the intro-duction of T2-dependent FLAIR sequences(Fig. 4.22), on which abnormal signal alter-ations adjacent to the superficial and deep sub-arachnoid spaces are more immediately recog-nizable, thanks to the choice of parametersthat cancel out the CSF signal; these sequencesare currently the most sensitive in demonstrat-ing oedema and pathological tissue in generalin the acute phase of patient deterioration.Oedema can also be recognized by its mass ef-fect, however, this may be very modest in thecytotoxic phase; in this early time period, theoedema may appear on CT not as hypodensity,but simply as a loss of the slight normal physi-


Fig. 4.20 - Cytotoxic oedema. Unenhanced cranial CT reveals asubtle absence of the normal hyperdensity of the left putamenas compared to the contralateral structure, indicating the pres-ence of ischaemic cytotoxic oedema.

Fig. 4.21 - Brain death. Unenhanced cranial CT demonstratesbilateral subdural and subarachnoid blood collections. There isalso diffuse brain swelling, with loss of the grey-white matterdifferentiation, and bilateral compression of the cerebral ven-tricular system due to parenchymal oedema.


Fig. 4.22 - Global hypoperfusion. Unenhanced cranial CT performed 24 hours after a cardiac arrest during heart surgery documentsrelative isodensity of the lenticular nuclei bilaterally. Axial T2-weighted MRI 48 hours after the event reveals MRI signal hyperinten-sity within the lenticular nuclei. Axial T2-weighted and FLAIR MRI 3 weeks later demonstrates minor dilation of the ventricular sys-tem as a result of resolution of cerebral swelling, and an increase in the hyperintensity of the MRI signal of the lenticular nuclei. TheFLAIR image at 3 weeks shows hyperintense cortical-subcortical MRI signal alterations. [a) initial axial CT; b) axial T2-weighted MRIat 48 hours; c) axial T2-weighted MRI at 3 weeks; d) axial FLAIR MRI at 3 weeks].

a

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c

ological hyperdensity of grey matter in relationto the white matter (i.e., loss of grey-white mat-ter differentiation).

Solid/cystic/mixed neoplastic lesions

Patients with solid/cystic/mixed neoplasticlesions may also present acutely, because of asudden worsening in intracranial hypertension,due for instance to intratumoral haemorrhage(13), acute obstructive hydrocephalus or fol-lowing a seizure precipitated by the tumor. Thegeneral CT/MRI findings will not be dealt within this chapter, but once again the general ruleapplies that in such cases CT is suitable for theinitial diagnosis and analysis in emergency situ-ations, whereas MRI is better suited to morecomplete and definitive evaluation after theacute stage has passed.

WIDESPREAD INSULT/BRAINSWELLING

The main clinical and radiological aspectsappropriate to dealing with intracranial emer-gencies are dealt with in specific chapters, how-ever, we will here examine a number of differ-ent conditions that may present with coma withvarying aetiology. We will also demonstratehow, in addition to CT and MRI, important in-formation can be gleaned from their integrationwith other imaging techniques.

Both conditions resulting in widespreadbrain swelling (especially of traumatic aetiologyassociated with DAI) and those associated withvasospasm (especially that caused by subarach-noid haemorrhage) have important conse-quences on CBF (6, 7, 17). These lead to diffuseischaemic injury, with further brain swelling,greater increases in ICP and therefore a moremarked reduction in CBF. In the case of DAI(13), the primary injury is accompanied by theexacerbating effect of compression of and dam-age to the hypothalamic substructure that in it-self leads to a loss of vascular autoregulation.

Transcranial Doppler and transcranial echocolour-Doppler make it possible to monitor

variations in the speed of flow in arterial seg-ments undergoing vasospasm. In conditions ofnormal or slightly raised ICP, the increase inflow velocity (systolic or diastolic) representscompensation between the reduction in arterialcalibre and the perfusion downstream from thearterial narrowing. In conditions of significantincreases in ICP, a gradual increase in flow re-sistance occurs, with a drop in flow velocity(mainly diastolic) and a consequent reduction inoverall peripheral perfusion. DAI can affect thesubstance of the thalamus and the brainstem,tissues that are responsible for cerebral vascularautoregulation, a physiological phenomenonthat is aimed at maintaining CBF constant overa range of cerebral PP’s between 60 and 150mm Hg.

When cerebral PP drops below the minimumthreshold in a brain trauma patient, cerebral hy-poperfusion occurs as a result of progressivelyenlarging intracranial hypertension. Transcra-nial Doppler velocity measurements enable theidentification of an increase or decrease in cere-bral arterial flow speeds, which are generally inline with CBF alterations. CBF increases sec-ondary to increased flow velocity caused by va-soparalysis are responsible for an increase inICP and therefore the gradual, progressive de-crease in CBF ultimately leading to the condi-tion of cerebral vascular stasis (12, 17).

In recent years, establishing the diagnosis ofbrain death has gained particular importancebecause of the consonant importance in theharvesting of transplant organs from patients inirreversible coma. In addition to neurophysio-logical and metabolic tests, current regulationsalso require the certification of cerebral bloodflow arrest (cerebral vascular stasis).

In such situations, angiography and transcra-nial ECD can be used for this purpose. Angio-graphic examinations document the stoppage ofcontrast medium progression within the internalcarotid arteries and within the basilar artery, inthe absence of delayed opacification of the cere-bral arteries. Stasis of the arterial structures inthe infratentorial compartment typically followsthat of the supratentorial region (Fig. 4.21).

Another important clinicoradiological situa-tion to consider is the condition consequent to


widespread hypoperfusion (caused for instanceby massive coronary infarction or prolonged se-vere systemic hypotension) or to global hy-poxygenation (13) (for example following car-bon monoxide inhalation). The most frequent-ly affected areas are those with highest physio-logical oxygen demand, such as the basal nucleiof the cerebral hemispheres and the cerebralcortex. CT is usually negative immediately afterthe event, but may subsequently (Fig. 4.22) re-veal the disappearance of the normal physio-logical hyperdensity of basal nuclei and the differential density between grey and whitematter. On occasion, the only sign of suchpathology is a non-specific observation of brainswelling. MRI performed on the 2nd-7th day fol-lowing the inciting event documents withgreater certainty the alteration in signal of thebasal ganglia and later the typical corticalnecrosis having a gyriform (laminar) distribu-tion. Evolution towards a severe generalized at-rophy of the affected regions can ensue ratherquickly.

REFERENCES

1. Aaslid R, Lindegaard KF: Cerebral hemodynamics in tran-scranial doppler sonography. Aaslid R., Ed. Wien Springer-Verlag 60-85, 1986.

2. Aaslid R, Markwalder TM, Nornes H: Noninvasive tran-scranial doppler ultrasound of flow velocity in basal cere-bral arteries. J Neurosurgery 57, 769-774, 1982.

3. Ahman PA, Carrigan TA, Carlton D et al: Brain death inchildren: characteristics common carotid arterial velocitypatterns measured with pulsed doppler ultrasound. J. Pe-diatr. 110, 723-728, 1987.

4. Castillo M. et al: New techniques in MR neuroimaging.MRI Clinics of North America. Saunders 1998.

5. Chan CH, Dearden MN, Miller DJ et al: Transcranial dopplerwaveform differencies in hyperemic and nonhyperemic pa-tients after severe head injury. Surg. Neur. 38, 433-436, 1992.

6. Gean M: Head trauma. Raven Press 1994.7. Gentry LR: Current concepts in Imaging Cranio-facial

trauma. Neuroimaging Clinics of North America. Decem-ber 1991.

8. Grossmann RI, Younsem DM: Neuroradiology: the requi-sites. Mosby, St. Louis 1994.

9. Hachinskj V, Norris JW: Ictus. Athena editrice Roma 1988.10. Masakuni Kameyama, Masanori Tomonaga, Tadashi Aiba: Ce-

rebrovascular disease. Igaku-Shoin, Tokjo-New York 1988.11. Hayman LA: Nontraumatic intracranial hemorrhage. Neu-

roimaging Clinic of North America 2:1, 1992.12. Kassel NF, Sasaki T, Colohan Art et al: Cerebral vasospasm

following aneurismal subarachnoid hemorrage. Stroke 16,573-581, 1985.

13. Osborne A: Diagnostic neuroradiology. Mosby Year Book1994.

14. Osborne A: Handbook of Neuroradiology. Mosby YearBook 1991.

15. Scarabino T, Cammisa M: Urgenze cranio-spinali: diagno-stica per immagini. Ed. Liviana 1993.

16. Scotti G: Manuale di Neuroradiologia diagnostica e tera-peutica. Masson 1993.

17. Seckhar L, Wechsler LR, Yonas H, et al: Value of TCDexamination in the diagnosis of cerebral vasospasm aftersubarachnoid hemorrage. Neurosurg. 22, 813-821, 1988.


265

INTRODUCTION

The observation, clinical evaluation andprognosis of coma patients is always a de-manding matter and one that requires reliablediagnostic instruments capable of providinganswers in real time. This evaluation is furthercomplicated by the varying aetiology of comasof acute onset. Some of the most frequentcauses of coma include: head injuries, brain tu-mours, cerebrovascular lesions, meningitis, en-cephalitis and cerebral abscesses, epilepsy(postcritical coma), exogenous intoxication,endogenous intoxication (metabolic coma, se-vere hydroelectrolytic imbalances), respiratoryinsufficiency, and cardiocirculatory insufficien-cy. However, irrespective of the cause of thecoma, the pathophysiology of functional braindamage rests on dynamic factors whose evo-lution must be recognized and monitored withcare.

We believe that in neuroresuscitation,alongside the essential, accurate objectiveneurological examination and monitoring ofcardiorespiratory and metabolic functions,diagnostic examinations with medical instru-ments are finding an increasingly importantplace. It is now possible to study the manyaspects of cerebral pathophysiology using

neurophysiological (e.g.: EEG, evoked poten-tials), morphological (e.g.: CT, MRI) andfunctional (e.g.: PET, SPECT) methodsaimed at swiftly understanding events that al-ter the balance between the various compo-nents of the cranioencephalic system andcerebral perfusion.

Alterations in cerebral perfusion can bestudied using two possible categories of analy-sis: invasive (e.g.: measuring ICP; measuringthe jugular venous saturation of oxygen, SvjO2;conventional selective angiography) and non-invasive (transcranial Doppler [TCD] and ra-dionuclide scintigraphy of brain perfusion[SPECT]).

The introduction of SPECT into clinicalneuroresuscitation practice has made it pos-sible to obtain more rapid and accurate di-agnoses and make more certain prognosticjudgements. The most satisfactory resultshave been obtained in the examination ofpostanoxic coma, where perfusion parame-ters have proved reliable for guiding thera-py, and in cases of suspected brain death,where SPECT is useful in dispelling doubtsin either direction. In cases of posttraumat-ic coma or coma caused by stroke, brain per-fusion as determined by SPECT has enableda more certain prognostic prediction.

4.3

NUCLEAR MEDICINE IN NEUROLOGICAL EMERGENCIESM.G. Bonetti, P. Ciritella, G. Valle, T. Scarabino

MEASURING CBF

The brain is the organ that more than anyother requires a constant supply of oxygen andglucose transported by the blood (7). Measur-ing CBF makes it possible to visualize thehaemodynamic and pathophysiological conse-quences of intracerebral pathology.

At the current time, there are no valid alter-natives to the use of radionuclides to obtainquantitative flow measurements, especially inthe posterior cerebral fossa and brainstem. Theprincipal methods of the various techniques forstudying CBF with gamma-emitting radioactivetracers are shown in Table 4.1. In our experi-ence, we have used the repartition method utilizing hexamethyl propylene-amine-oxime(HMPAO) marked with 99mTc as a tracer.

The main steps of the technique we use areas follows (1, 3):

1. intravenous injection of a 99mTC HM-PAO;

2. when the fat-soluble HM-PAO moleculesare taken by the blood to the brain, they passthrough the blood-brain barrier, with a high ex-traction from the blood bed, and bond to thebrain tissue;

3. as a consequence the distribution withinthe brain is proportionate to the regional cere-bral blood flow (rCBF);

4. a bond between the HM-PAO mole-cule and the cerebral tissue forms and re-

mains constant for at least one hour (suffi-cient time in which to perform the SPECTexamination);

5. subsequent redistribution of the moleculein the white and grey matter.

The interpretation of the images obtainedusing brain SPECT with hexametazyme isbased on visual criteria (through a comparisonwith chromatic scales correlated with the lev-els of radioactivity recorded in the various ar-eas of the brain) and on the possibility of asemiquantitative study performed by compar-ing homologous areas with gamma-emissiondifferences higher than 12-16%. In particular,in all those cases in which a cerebral hemi-sphere, or part of it, is significantly different-ly perfused than the contralateral, it is possi-ble to calculate a perfusion ratio using the fol-lowing expression (2):

Perfusion ratio =Counts/pixel affected side x 100

Counts/pixel healthy side

The resulting value constitutes a measure-ment of the asymmetry between the two hemi-spheres.

SPECT also makes it possible to make amore accurate prognostic evaluation of the un-derlying problem, which is usually simply clas-sified into a favourable or unfavourable prog-nosis (Table 4.1).

Tab. 4.1 - Prognostic evaluation of cerebral lesions by SPECT.


Method Radiotracer Advantages/Disadvantages

Vascular Clearance 133Xe A: quantitative (if intracarotid injection)D: invasive

Dilution 99mTcO4 A: simple, easily available radiotracer

99mTc-albumin D: not quantitative99mTc-DTPA

Repartition 99mTc-HM-PAO A: steady state123I-IMP D: unknown uptake process

Good prognosis Bad prognosis

Meningeal lesions Focal lesionsNot focal lesions Many lesionsSmall lesions Large lesionsFew lesions Parietal lesionsOccipital lesions Brainstem lesionsFrontal lesions Cerebellar lesions

Temporal lesions

Tab. 4.2 - Prognostic evaluation of brain lesion using SPECT.

In our practice we use a rotating gammacam-era with a single dedicated head (GE 400 AC,Milwaukee, Wisconsin, USA) a few minutes af-ter an intravenous injection of freshly prepared950 MBq of 99mTc -HM-PAO (Ceretec, Amer-sham-Sorin, Saluggia, Italy).The following ac-quisition parameters are used: 64 planar imageswith a 1.6x zoom, 64 x 64 pixel matrix, radius ofrotation = 15 cm (on average), 20% symmetricwindow on photopeak of 140 keV of the99mTc, acquisition time 25-30 minutes and ageneral purpose parallel hole collimator.

During the examination the patient is venti-lated using a portable automatic respirator (Pu-ritan Bennet Companion 2801, USA), monitor-ing blood pressure with a portable electronicmodulus (Propaq 102, Protocol System Inc.Oregon, USA); ECG and the arterial saturationof O2 of the haemoglobin is determined with aperipheral digital detector.

CLINICAL USAGE OF HM-PAO SPECT

The study of brain perfusion in coma patientshas come to be part of routine clinical practice inour Resuscitation Centre in all those cases inwhich conventional neurophysiological and radi-ological techniques are inadequate in providing areliable prognostic estimate. The findings from anumber of coma patients are summarized in thetext below. For comparative purposes, Fig. 4.23shows a SPECT image for a normal brain.

Posttraumatic coma

SPECT’s superiority over CT in studyinghead injuries that do not demonstrate focal le-

sions consists mainly in its ability to detect patho-physiological cerebral perfusion alterations be-fore the appearance of gross injuries that CT candetect (8).

Cerebral ischaemia can be a consequence ofvasospasm occurring immediately after a trau-ma or following episodes of cardiocirculatoryinstability. This situation calls for serial studiesof cerebral flow in order to detect either in-creases or decreases in perfusion. CBF also cor-related with the final clinical outcome: persist-ently low CBF values have an unfavourableprognosis, whereas patients whose CBF rapidlyreturns to normal levels will typically have abetter recovery.

Another important aspect of CBF measure-ments is that SPECT highlights a reduction inflow that may be directly proportionate to thedegree of cerebral oedema. For example, an in-crease in cerebral oedema can reduce or evencompletely interrupt CBF.

Clinical CasePATIENT T.R.AGE 25 yearsDIAGNOSIS head injuryGCS on admission 5SAPS (Simplified acute Physiology Score) 8

Fig. 4.23 - Normal SPECT examination. SPECT examinationof the brain utilising 99mTC HM-PAO in a healthy subject forcomparison.

4.3 NUCLEAR MEDICINE IN NEUROLOGICAL EMERGENCIES 267

The CT examination (Fig. 4.24) was nega-tive for focal lesions; the BAEP’s determination(Brainstem Auditory Evoked Potentials) wasnormal. The scintigraphic study of cerebralperfusion in this patient showed (Fig. 4.25)multiple small perfusion defects in both cere-bral hemispheres, with good perfusion of thecerebral cortex. The patient came out of comaapproximately one month from the injury. Hewas subsequently referred to a functional reha-bilitation centre in order to complete the re-covery of neuromuscular activity.

Acute cerebrovascular pathology

To reiterate, in studies of rCBF in cere-brovascular disease, SPECT is able to docu-ment flow alterations at an early stage, within afew hours after the trauma. This is observed be-fore CT becomes positive, which in this stageoccurs in less than 1 case every 5. Serial rCBFstudies have considerable prognostic impor-tance: patients with limited perfusion defectssubsequently generally show complete or nearcomplete recovery, whereas almost 50% of pa-


Fig. 4.24 - Post-traumatic coma. Unenhanced CT shows no abnormality.

tients with diffuse areas of hypoperfusion, or es-pecially a complete absence of perfusion (4,5),have an unfavourable outcome as is shown inthe following case.

Clinical CasePATIENT A. G.AGE 75 yearsDIAGNOSIS right temporoparietal

haemorrhageGCS on admission 6SAPS 14

CT documented the presence of an extensiveright temporoparietal haemorrhagic focus withlateral ventricular compression and midlineshift (Fig. 4.26). SPECT demonstrated a largearea of perfusion absence involving the upperportion of the right parietal lobe that extendedmore caudally, frontally, medially and posterior-ly, thereby including the right subcortical greymatter structures. Overall, the remaining cere-bral cortical and subcortical structures ap-peared to be well perfused. Crossed cerebellardiaschisis was also present (Fig. 4.27).

A subsequent SPECT examination per-formed approximately one month from the first

study documented (Fig. 4.28): discreet im-provement of the perfusion in a right posterior-frontal region, immediately in front of thehaemorrhagic area; marked recovery of perfu-sion at the right temporal level, substantial nor-malization of the crossed cerebellum diaschisis.Overall, the picture showed a more or less com-plete recovery of perfusion within the areas ofischaemic penumbra surrounding the haemor-rhage. Nevertheless, the patient, who died ap-proximately 6 months after the stroke due tothe extent of the original focus, was unable torecover beyond the level of coma.

Postanoxic coma

The cerebral consequences of cardiocircula-tory arrest often determine the vital prognosisregardless of the success of the initial car-diopulmonary resuscitation. In fact, only 15-30% of patients with cardiopulmonary arrestsurvive either with or without neurological se-quelae (6).

Two separate clinical conditions precipitatedby cardiopulmonary arrest can be identified:global cerebral hypoxia and incomplete cere-bral ischaemia. The former is due to dimin-ished arterial oxygen content together with anincrease in cerebral blood flow requirementthat occur in acute respiratory insufficiency; thesecond is due to a reduction in the blood sup-ply to the brain with normal arterial oxygencontent that occurs in cases of shock and in in-tracranial hypertension (6).

The relationship between cerebral bloodflow, O2 transport (DO2) and cerebral oxygenconsumption (VO2) are shown in Table 4.3.Fortunately, there is a margin of safety that thebrain has in hypoxia or anoxia, because thequantity of O2 transported by the blood isequal to 2 or 3 times cerebral VO2. Cerebralperfusion SPECT in postanoxic coma thereforeshows impoverished cerebral blood flow, or ifthis is normal, depressed neuronal function,thus enabling the neuroresuscitator to con-struct a prognostic judgement while guidinghim in the implementation of a specific thera-peutic protocol.


Fig. 4.25 - Same case as in Fig. 4.24. Left hand images:SPECT images reveal multiple small perfusion defects. Righthand images: Another normal case is shown on the right forcomparison.

CBF x CaO2 = DO2CBF=5Oml/min/ 100 gCaO2 = 20 ml / 100 mlDO2 = 10 ml / min / 100 gVO2 = 3-5 ml / min / 100 g

CaO2 = arterial oxygen concentration

Tab. 4.3 - Relationship between CBF, O2 transport (DO2) andcerebral oxygen consumption (VO2).

Clinical casePATIENT T.AAGE 49 yearsDIAGNOSIS postanoxic comaGCS on admission 7SAPS 14

The first scintigraphic study in this patientdocumented a marked reduction in blood sup-


Fig. 4.26 - Acute cerebrovascular pathology. Unenhanced CT demonstrates a large intraparenchymal haemorrhagic focus associatedwith rupture into the ventricular system and ventricular dilatation.

ply throughout the cerebral cortex and in thesubcortical grey matter structures, withoutdemonstrating focal deficits. Cerebellum and

brainstem perfusion were generally well con-served (Fig. 4.29). A subsequent study (Fig.4.30) highlights the asymmetry of the peripher-al blood flow distribution between the twocerebral hemispheres with global hypoperfu-sion of the left hemisphere.

Finally, the third examination (Fig. 4.31) per-formed 15 days from the first, documented goodoverall cortical perfusion within both cerebralhemispheres and the disappearance of lateralizedflow asymmetries. The improvement in brainperfusion documented by SPECT correctly pre-dicted the patient’s gradual recovery from coma.


Fig. 4.26 - (Contd.).

Fig. 4.27 - Same case as in Fig. 4.26. Note that the SPECT im-ages reveal extensive perfusion defects and evidence of cere-bellar diaschisis.

REFERENCES

1. Avogaro F, Zamperetti N, Pellizzari A: Studio del flussoematico cerebrale. In: Trattato Enciclopedico di Anestesio-logia, Rianimazione e Terapia Intensiva, pp. 51-76. Piccined., Padova. 1991.

2. Choksey MS, Costa DC, Iannotti F et al: 99mTc-HM-PAOSPECT stuclies in traumatic intracerebral haematoma. J.Neurol. Neurosurg. Psych. 54: 6-11, 1991.

3. Costa DC, Ell PJ, Cullum ID et al: The in vivo distributionof` 99mTcHM-PAO in normal man. Nucl. Med. Com. 7:647-652, 1986.


Fig. 4.28 - Same case as in Figs. 4.26 and 4.27. The follow upSPECT examination shows an improvement in brain perfusion.

Fig. 4.29 - Post-anoxic coma. The SPECT study demonstratesdiffuse, bilateral marked reduction in perfusion of the cerebralcortex.

Fig. 4.30 - Same case as in Fig. 4.29. A SPECT follow up ex-amination conducted seven days later shows that the global hy-poperfusion of the left cerebral hemisphere persists. The CTstudy in this patient was negative (not shown).

Fig. 4.31 - Same case as in Figs. 4.29 and 4.30. Two weeks afterthe first examination, the SPECT images show good cerebralperfusion recovery.

4. Fayad PB, Brass LM: Single Photon Emission ComputedTomography in cerebrovascular disease. Stroke 26: 950-954, 1991.

5. Giubilei F, Lenzi GL, Di Piero V et al: Predictive value ofbrain perfusion single-photon emission computed tomo-graphy in acute ischemic stroke. Stroke 21: 895-900,1990.

6. Haberer JR, Hottier E: Encéphalopathies postanoxiques.Ann. Fr. Anesth. Réan. 9: 212-219, 1990.

7. Manni C, Della Corte F, Rossi R et al: La perfusione ce-rebrale in Anestesia e Rianimazione. Atti XLV Congr.Naz.le SIAARTI, pp. 1117-1127, Milano 8-12 ottobre1991.

8. Obrist WD, Gennarelli TA, Segawa H et al: Relation ofCBF to neurological status and outcome in head injured pa-tients. J. Neurosurg. 51: 292-297, 1979.


275

INTRODUCTION

Throughout mankind’s history, the conceptof death has changed constantly in parallel withthe scientific, cultural and social evolution ofthe various eras. Until the nineteenfifties, theinterruption of the heart beat or breathingmarked the point in time in which an individualwas deemed to be dead. With the introductionand dissemination of resuscitation techniquesas well as with the availability of total artificialrespiratory and cardiocirculatory support, it isno longer sensible to equate the time of deathwith the time of cardiorespiratory arrest. Infact, externally controlled respiratory and car-diocirculatory techniques have made it possibleto consider that a patient who is no longer ableto breath autonomously is nevertheless alive.

However, these cardiopulmonary resuscita-tion techniques may also allow a patient to con-tinue to be well oxygenated and maintain suffi-cient haemodynamic stability for limited peri-ods even when all cerebral functions have beencompletely and irreversibly lost. It thereforefollows that the confirmation of death cannotbe based on the observation or conservation ofautonomous cardiopulmonary activity alone.

Over the past thirty years this observationhas led to the introduction of the concept of

“brain death”, intended as a definitive andcomplete loss of all functions of the CNS. Inthe 1960’s the French school of medicine pro-posed the term coma depassée to describe thiscondition, however from a semantic point ofview the term is inaccurate because, as it indi-cates a state of brain death, it is no longer pos-sible to speak of coma. Coma in fact impliesthat brain activity is still present, albeit com-promised to a greater or lesser extent. It istherefore preferable to avoid such expressionsas “irreversible coma” but instead use the term“brain death” (BD) to indicate a subject whosecerebrum is no longer vital but whose car-diopulmonary function is still present.

By BD, we therefore signify the irreversiblearrest of all brain function, including that of thebrainstem, which is precisely the structurewhose loss of function is required for the veri-fication of brain death (14).

PATHOPHYSIOLOGY

The skull, a rigid and inelastic container,contains: brain substance, interstitial fluid, ar-terial and venous blood and the cerebrospinalfluid (CSF). Any variation in the volume of oneor more of these components must necessarily

4.4

DIAGNOSING BRAIN DEATHM.G. Bonetti, F. Menichelli, T. Scarabino, U. Salvolini

be compensated for by a variation in one of theother components in order to maintain total in-tracranial volume and pressure constant.

With progressive increases in volume, with-in certain limits, a slight and equally gradual in-crease in intracranial pressure (ICP) takesplace. A part of this compensation takes placeas a consequence of the cranial CSF being dis-placed into the subarachnoid space of thespinal canal (14). If the increases in volume aresufficiently large to exceed so-called cerebralcompliance, intracranial hypertension sets in,which if not treated can be life threatening.

The close relationship that exists betweenICP and cerebral blood flow (CBF) means thatany increase in intracranial pressure must cor-respond to an increase in venous and arterialpressure. This mechanism serves to prevent acollapse of the cerebral blood vessels and there-fore makes it possible to maintain adequatecerebral perfusion pressure (CPP).

There are cases in which this compensationmechanism is inadequate and in such instancesthe ICP increases beyond the limit required toensure adequate CPP. This occurs when nonspe-cific cerebral mass effect is not controlled or con-trollable using therapy, resulting in an increase inbrain volume within the rigid skull. This in turncauses a consequent compression of the intracra-nial vascular structures in order to gain addition-al intracranial space. In an attempt to compen-sate for this situation, a vicious circle is estab-lished whereby CBF rapidly increases, contribut-ing to further increases ICP and, ultimately, tofurther reductions in CPP.

At this point ICP, which can increase be-yond 40 mm Hg, prevents adequate CPP withconsequent anoxia and death of the brain with-in a very few minutes. The compressive effectof high ICP upon the cerebral vessels witheventual arrest of the blood flow correlateswith studies showing an absence of cerebralperfusion.

DIAGNOSIS

The diagnosis of BD is first and foremost aclinical one, the main signs being clinical coma,

together with the absence of brainstem reflexesand apnea. The main pathogenic factor leadingto BD is a severe state of brain swelling with aprogressive reduction and eventual completeinterruption of intracranial blood flow.

The further clinical criteria (16) for the diag-nosis of BD are the absence of spontaneous so-matic movements, total areflexia and an ab-sence of activity on the EEG as well as on thebrainstem auditory evoked potentials (BAEP).However, such findings can be mimicked byvarious causes such as intoxication from medi-cines, hypothermia and technical problemswith the recording equipment (14). For thisreason the Italian law (Law n. 578 of 29/12/93;Italian Ministry of Health Decree n. 582 of22/8/94) establishes that complementary inves-tigations aimed at highlighting the absence ofcerebral blood flow need to be performed inorder to prove BD (15, 18). However, ancillaryexaminations used for the confirmation of BDare only conducted if the usual clinical criteriaare unable to provide an unquestionable diag-nosis.

Transcranial Doppler (TCD) examinationscan be performed with ease at the patient’sbedside and can demonstrate the interruptionof arterial flow with a sensitivity that variesfrom 90% to 99%, and with a specificity thatapproaches 100%. In order to confirm a TCDdiagnosis of vascular stasis, it is recommendedthat the examination be repeated 30 minutesfollowing the first determination.

TCD can be used to diagnose BD (3, 8) (al-though it remains decidedly operator-depend-ent) on condition that the examination is car-ried out with both a supra- and subtentorial ap-proach while checks of systemic systolic bloodpressure insure that the recorded values do notdrop below 70 mmHg.

In cases of brain death, in addition to re-vealing the potential presence of focal lesions,computed tomography (CT) enables the detec-tion (21) of cytotoxic oedema secondary to is-chaemia- related diffuse cellular necrosis. Thisis responsible for the predominant hypodensityof the grey matter, with the disappearance ofthe grey-white grey matter differentiation. Thisis also accompanied by a reduction and eventu-


al disappearance of sulcal, pericerebral andventricular CSF spaces due to cerebral swelling(Fig. 4.32).

However, CT alone does not allow an un-questionable distinction between diffuseparenchymal insult and frank brain death. Theuse of spiral CT has been proposed as a methodthat may overcome this limitation. A demon-stration of the absence of cerebral blood flow(4), as required for the diagnosis of BD, is per-formed by means of the acquisition of images inthe arterial and venous phases after the admin-istration of intravenous contrast medium utiliz-ing a rapid bolus injection. This technique en-ables the measurement of blood flow, blood vol-ume, mean transit times and flow peak times ofthe cerebrum corresponding to the territories ofthe main arterial vessels, including the anterior,middle and posterior cerebral arteries (13).

CBF measurements can also be obtained byevaluating the distribution of inhaled xenon,which diffuses into the brain to form a variationin tissue density (10, 17).

It is also possible to visualize the arterial ves-sels directly by using the angio-CT technique.The administration of a bolus of intravenouscontrast medium is followed by a high spatialresolution volumetric acquisition, with resultsthat are similar to those obtained by conven-tional selective angiographic catheterization.

However, all the various possibilities of es-tablishing BD diagnosis by CT described abovehave yet to be validated for use for forensicpurposes.

Cerebral angiography by means of selectivearterial catheterization (Fig. 4.33), preferablyutilizing digital imaging equipment, has limita-tions in that it is invasive and cannot be per-formed in all centres (20). In the past this tech-nique has repeatedly been proposed as amethod for diagnosing BD. If this method isutilised, we suggest tailoring the examination toinclude a study of the supraaortic vessels and the intracranial circulation by a simplecatheterization of the ascending aorta, with in-jection of contrast medium at this point usingthe automatic injector. In order to certify BD,one must be able to demonstrate the absence offilling of the internal carotid arteries and the

4.4 DIAGNOSING BRAIN DEATH 277

Fig. 4.32 - Diffuse cerebral cytotoxic oedema in a patient withsubarachnoid haemorrhage. Unenhanced CT shows swelling ofthe brain with compression of the ventricular and subarach-noid spaces of the supratentorial compartment and posteriorfossa. Note also the disappearance of the grey-white matter dif-ferentiation indicating diffuse cytotoxic oedema.

vertebral arteries at the point where they enterthe skull together with normal filling of the ex-ternal carotid arteries (2, 5, 9). Being an inva-

sive technique, and given the known potentialfor the toxic effect of the contrast medium onorgans suitable for transplantation, certain


Fig. 4.33 - Brain death. Selective right carotid arteriogram reveals an absence of flow of contrast past the base of the cranium via theinternal carotid artery. Similar findings were observed in the left carotid and vertebral arteries (not shown).

doubts have been voiced concerning the use ofconventional cerebral angiography for verifyingBD (20).

Magnetic resonance imaging (MRI) easilydemonstrates diffuse cerebral oedema, even atan early stage, using T2-weighted or diffusion-weighted imaging sequences; MR spectroscopycan directly show the presence of lactic acid, anearly indication of cellular necrosis; MR an-giography can indicate the presence or absenceof flow in the cerebral veins and arteries. De-

spite the fact that MRI does present certain dif-ficulties in execution and has some clear limita-tions, the initial results would suggest furtherfuture investigation into its potential medico-le-gal use in the evaluation of BD (11, 12).

With regard to nuclear medicine methods, thestudy of cerebral perfusion with 133-Xenon,which is not readily available, does not enableevaluation of the deep brain structures and ishindered by artefacts caused by increased ex-tracranial flow (19). In addition, cerebral an-gioscintigraphy can be difficult to interpret, andimportantly, it is unable to study the vascularstructures of the posterior fossa (7, 19).

On the other hand, in our experience andthat of others, SPECT with HM-PAO hasproved to be simple to perform and interpret(1, 6). Additionally, it has made it possible todiagnose brain death at an early stage.

Using SPECT, the diagnosis of brain deathis made by demonstrating an absence of per-fusion throughout the brain. One example ofthis finding is shown in Fig. 4.34: absence ofdetection of the radionuclide in the brain; de-tection of radionuclide in the subcutaneousmuscular and bony tissues of the skull. In thesame case CT demonstrated the presence of adeep intraparencymal haematoma (Fig. 4.35).In another patient (scintigraphic planar scansin AP: Fig. 4.36; SPECT: Fig. 4.37), CT andMRI studies (Figs. 4.38-4.42) demonstratedthe presence of an intraparenchymal haema-


Fig. 4.34 - Brain death. SPECT scans reveal a complete absenceof cerebral and cerebellar perfusion. [a) axial a), sagittal b) andc) coronal SPECT].

a

b

c


Fig. 4.35 - Same case as Fig. 4.34. The CT images show only the presence of a deep intraparenchymal haematoma.

Fig. 4.36 - SPECT, CT and MRI comparison of brain death. Seetext.


toma, intraventricular and midbrain haemor-rhage and brain swelling. MRI also demostrat-ed a loss of grey-white matter differentiationand the absence of blood flow in the main in-tracranial vessels, suggested by a high in-travascular MR signal intensity.






Whichever methodology is embraced, it isrecommended that explicitly approved proto-cols are adopted in all hospitals were BD certi-fication is performed taking into account localsituations and conditions.

REFERENCES

1. Bonetti MG, Ciritella P, Valle G et al: 99mTc HM-PAObrain perfusion SPECT in brain death. Neuroradiology 37:365-369, 1995.

2. Bradac GB, Simon RS: Angiography in brain death. Neu-roradiology 7: 25-28, 1974.

3. Ducrocq X, Braun M, Debouverie M et al: Brain death andtranscranial Doppler: experience in 130 cases of braindeath patients. J. Neurol. Sci. 160: 41 -46, 1998.

4. Dupas B, Gayet-Delacroix M, Villers D et al: Diagnosis of

brain death using two-phase spiral CT. Am. J. Neuroradiol.19: 641-647, 1998.

5. Eelco FM, Wijdicks MD: The diagnosi of brain death. N.Engl. J. Med. Vol. 344, 16: 1215-1221, 2001.

6. Facco E, Zucchetta P, Munari M et al: 99mTc-HMPAOSPECT in the diagnosis of brain death.death. Intensive Ca-re Med. 24: 911-917, 1998.

7. Flowers WM Jr., Patel BR: Radionuclide angiography as aconfirmatory test for brain death: a review of 229 studies in219 patients. South Med. J. 90: 1091-1096, 1997.

8. Hadani M, Bruk B, Ram Z et al: Application of transcranialdoppler ultrasonographv for the diagnosis of brain death.Intensive Care Med. 25: 822-828, 1999.

9. Heiskanen O: Cerebral circulatory arrest caused by acuteincrease of intracranial pressure. Acta Neurol. Scand. 40: 7-59, 1964.

10. Johnson DW, Warren AS, et al.: Stable Xenon CT CerebralBlood Flow Imaging: Rationale for and Role in Clinical De-cision Making. Am. J. Neuroradiol. 12: 201-213, 1991.

11. Karantanas AH, Hadjigeorgion GM, Paterakis K: Contri-bution of MRI and MR angiography in early diagnosis ofbrain death. Eur. Radiol. 12 (11): 1210-6, 2002.

12. Kendall MJ, Patrick PB: MR diagnosis of Brain Death. Am.J. Neuradiol. 13: 65-66, 1992.

13. Kornig M, Kraus M, et al.: Quantitative Assessment of theIschemic Brain by means of Perfusion-Related ParametersDerived from Perfusion CT. Stroke 32: 431-437, 2001.

14. McL. Black P: Brain Death. N. Eng. J. Med. 299: 338-344,393-401, 1978.

15. Norme per l’accertamento e la certificazione di morte. Leg-ge 29 dicembre 1993. n. 578. Gazzetta Ufficiale della Re-pubblica Italiana, Serie generale - n. 5, of 8/1/94, pp. 4-5.

16. Pellizzari A, Digito A, Pellegrin C et al: Accertainento dimorte cerebrale: aspetti clinici. In Atti del 19° Corso Na-zionale di Aggiornamento in Rianimazione e Terapia Inten-siva, pp. 11-26. Piccin ed., Padova, 1990.

17. Pistoia F, Johnson DW, et al.: The role of Xenon CT mea-surements of cerebral blood flow in the clinical determina-tion of brain death. Am. J. Neuroradiol. 12: 97-103, 1991.

18. Regolamento recante le modalità per l’accertamento e lacertificazione di morte. Decreto del Ministero della Sanità22 agosto 1994, n. 582. Gazzetta Ufficiale della RepubblicaItaliana, Serie generale - n. 245, of 19/10/94, pp. 4-7.

19. Reid RH, Gulenchyn KY, Ballinger JR: Clinical use of Te-chnetium- 99m I IM-PAO for Determination of BrainDeath. J. Nucl. Med. 30: 1621-1626, 1989.

20. Salvolini U, Montesi A: Diagnostica angiografica di morte ce-rebrale. Annali Italiani di Chirurgia XLVII: 88-98, 1971-72.

21. Yoshikai T, Tahara T, Kuroiwa T et al: Plain CT findings ofbrain death confirmed by hollow skull sign in brain perfu-sion SPECT. Radiat. Med. 15: 419-424, 1997.



283

INTRODUCTION

Postsurgical craniospinal emergencies con-stitute an important aspect of neuroradiologybecause early, accurate diagnosis forms the ba-sis for rapid, optimally undertaken treatmentand potentially improved patient outcomes.The correct interpretation of cranial and spinalimaging studies requires an extensive knowl-edge of the underlying pathology as well as thespecific operative techniques used, making aclose cooperation between neuroradiologistand neurosurgeon imperative. The imagingfindings in postsurgical emergencies depend onthe site of the operation, the surgical techniqueand the clinical status of the patient.

As a general rule, the choice of the neurora-diological modality for the study of suchpathology depends primarily on specific clini-cal indicators. For acute phase evaluations ofthe skull, CT remains the diagnostic techniqueof choice. This is both because there are nocontraindications to the use of CT in patientswith metal cerebral aneurysm clips or in thepresence of patient support devices (as withMRI), as well as for the very short time periodrequired for performing the examination.

This being said, MRI is the most sensitivetechnique for use in spinal cord evaluation, in

particular for the evaluation of haemorrhage,oedema and ischaemia. Nevertheless, CT andtraditional radiography still play an importantrole in the evaluation of the spinal column it-self, such as the investigation of suspected post-surgical vertebral collapse or signs and symp-toms linked to the malpositioning or movementof implanted surgical spinal appliances.

It should be highlighted that the diagnosticsensitivity of both CT and MR in evaluating theskull and, especially, the spinal cord, is substan-tially reduced by the presence of artefactscaused by the ferromagnetic materials used orimplanted during surgical procedures (e.g.,clips, shunt catheters, plates, screws, rods andmetal residues from drilling and bone resec-tion). In order to minimize this phenomenon,fast spin echo sequences (44-46, 54) are used inMRI; because these acquisitions are less sensi-tive to magnetic susceptibility than are conven-tional sequences, there is a consequent reduc-tion in the artefacts induced by the ferromag-netic material. Moreover, these sequences areparticularly useful for studying the spinal sub-arachnoid spaces and the meningeal nerve rootsheaths.

In this chapter, we will outline the mostcommon postsurgical neuroradiological emer-gencies, discussing both those following cranial

4.5

POSTSURGICAL CRANIOSPINAL EMERGENCIES

T. Popolizio, A. Ceddia, V. D’Angelo, F. Nemore, N. Maggialetti, A. Maggialetti, T. Scarabino

surgery and those subsequent to spinal opera-tive procedures; emergencies secondary to hy-pophyseal surgery will be dealt with separately.

CRANIAL EMERGENCIES

The surgical approach to the cranium in-volves a surgical route of choice that does nothave a substantial impact on the possible com-plications that may ensue. Simplistically speak-ing, the operative techniques used are cranioto-my and craniectomy. In the former, the resect-ed bony operculum is repositioned after the op-eration, while in the latter it is removed fromthe skull.

Within a few hours after the operation, sev-eral things occur in the surgical site that do notcause concern from a clinical point of view. Forexample, small haematomas, extraaxial fluid orair collections and swelling of the extracranialsoft tissues (Fig. 4.43). These findings tend toresolve spontaneously within a few days of thesurgical procedure.

Haemorrhages

On certain occasions, the postsurgical out-come may be seriously complicated by acuteevents that significantly compromise the pa-tient’s clinical situation. Acute oedema andhaemorrhage are the most commonly observedemergencies, followed by hydrocephalus, infec-tions and infarct (39).

Haemorrhage occurring immediately aftersurgery is not rare, although the progressmade in surgical techniques and postsurgicalmanagement have minimized the frequency ofthis complication (7, 18, 52, 58). CT is un-doubtedly the technique of choice for theevaluation of postoperative haemorrhage, al-though tiny bleeds, such as those adjacent tothe vertex or base of the skull, may prove dif-ficult to visualize (7). Haematoma density de-pends on the packed cell volume as well as du-ration, and on blood concentration as well asprotein content. In severely anaemic patients,for example, it may be possible to encounter

only very slightly hyperdense or even isodensehaematomas, which are difficult to diagnoseon the basis of CT. On the other hand, clottingdisorders and other causes of repeated haem-orrhages may also profoundly alter the ap-pearance of haematomas (6, 59).

Intraaxial haemorrhages

A large number of pathogenic mechanismsmay be responsible for postsurgical intraaxialhaemorrhage (Fig. 4.44). These haemorrhagesmay be secondary to surgical procedures or tosystemic causes; in the case of the former, caus-es may include inadequate haemostasis, subto-tal removal of hypervascular neoplasia, directvascular trauma, postsurgical venous thrombo-sis, and rapid decompression in cases of in-tracranial hypertension (20). Systemic causes(18, 59) may include systemic perisurgical hy-pertension and clotting disorders (e.g., antico-agulation therapy, kidney and liver disease anddisseminated intravascular coagulation) (Fig.4.45). The removal of cerebral AVM’s maycause intraaxial haemorrhage; in such cases

Fig. 4.43 - Craniotomy alterations. Unenhanced axial CT showsexpected alterations of a recent prior craniotomy procedure toremove a left temporoparietal neoplasm.


bleeding develops because of a loss of a low im-pedence vascular bed in favour of normal cap-illary circulation. One may also observe thebreakthrough phenomenon, indicating thepresence of congestion of the cortical capillary

circulation with consequent vasogenic oedemadue to a breakdown of the blood-brain barrier(34, 51).

Although less frequently observed, postsur-gical haemorrhages may also present at a dis-tance removed from the surgical site (32, 37,38, 48). In fact, cases of cerebellar haemorrhagehave been observed following supratentorialoperations. In this case, the supine positioncould favour the stretching of the upper vermi-an veins and their tributaries, with the resultinglaceration of the wall; this process could be fa-cilitated by CSF overdrainage or by the in-tracranial influx of air through the postopera-tive drainage tube (59).

Extraaxial haemorrhage

Extraaxial haemorrhage may occur in theform of subgaleal, epidural and subduralhaematomas. The pathogenic mechanism mostcommonly underlying subgaleal haematomas isinadequate haemostasis during the reconstruc-tion phase of the muscular and subcutaneousplanes, which results in a blood collection be-low the surgical flap.

4.5 POSTSURGICAL CRANIOSPINAL EMERGENCIES 285

Fig. 4.44 - Postoperative intra-axial haemorrhage. Axial CT (a)shows extensive intraparenchymal haematoma in patient recent-ly operated on for large frontal meningioma (b). [a) postopera-tive unenhanced axial CT; b) preoperative T2-weighted MRI].

Fig. 4.45 - Spontaneous pontine haemorrhage. Unenhanced ax-ial CT demonstrates an acute pontine haematoma in a patientwith plasmacytopenia following the surgical removal of a neo-plastic metastatic deposit in the right temporal region.

a

b

Epidural haematomas, on the other hand,are typically caused by a failure to treathaemostasis of the dural mater. Less frequentlyepidural bleeding may be precipitated by ex-tended exposure of the dura mater with result-ant injury to this meningeal tissue ultimatelyleading to delayed haemorrhage (Fig. 4.46).

Subdural haemorrhagic collections are usu-ally a consequence of a sudden reduction inCSF volume that causes a negative pressureover the cerebral hemispheres. This in turn re-sults in the stretching and then laceration ofthe bridging cortical veins (25, 30, 57). Thesehaematomas may occur following seeminglystraightforward surgical procedures such asthe positioning of a ventricular shunt for non-specific hydrocephalus or as a consequence ofsudden decompression of obstructive hydro-cephalus during a posterior fossa mass resec-tion.

Cerebral oedema

Cerebral oedema may be caused by a num-ber of factors, such as surgical manipulations

that result in direct tissue trauma, vascularspasm, various alterations of venous drainageand fluid-electrolyte imbalances in the postop-erative period. Brain swelling usually beginswithin a few hours after the operation and lastsup to 3 to 4 days, before slowly spontaneouslyresolving (39).

The hypodensity and mass effect of oedemaas detected on CT scans may affect the areaclosely associated with the surgical procedure,or the entire hemisphere in which the operationwas performed. In certain circumstances, exter-nal herniation of cerebral tissue through thecraniectomy site may occur. In other cases ofmore massive swelling, internal herniation ofcerebral tissue may occur, such as in downwardtranstentorial or transfalcian herniations (8). Incases of complicated surgery in the posteriorfossa, cerebellar oedema may result in down-ward internal herniation of the cerebellar ton-sils through the foramen magnum (11, 28, 61).

Infections

Postsurgical infections may involve the sur-gical flap alone or may spread to the adjacentcerebral parenchyma (39). The infection ofthe surgical site represents a potentially veryserious complication (5). The first sign of aninfectious process on imaging is the progres-sive thickening of the meningogaleal complexwith intense enhancement of the inflamed du-ra mater (Fig. 4.47). Generally speaking, MRIis more sensitive to these changes than is CT(14, 23, 24).

Sterile inflammation within the first 24hours of the operation will cause benign, non-infectious dural enhancement as well as similarenhancement of the entire mengingogalealcomplex on MRI after the IV administration ofgadolinium (43). On CT, this type of postsurgi-cal enhancement usually will only be seen at theend of the first week after surgery. This normalpostsurgical enhancement may persist for anumber of months or even years on enhancedMRI examinations, but does not typically en-dure for more than six months on enhanced CTstudies (27).


Fig. 4.46 - Postoperative extra-axial haemorrhage. Unenhancedaxial CT reveals an acute epidural haematoma over the frontalconvexity in patient following surgery for ipsilateral tem-poroparietal meningioma.

Following craniotomy, the bone flap isdevascularized and therefore devitalized. Forthis reason, bacterial proliferation and conse-quently bony infection is facilitated (16). Stan-dard treatment of bone flap infection involvesthe removal of the infected bone and thedrainage of any associated suppurative collec-

tion that may have formed. In a similar mannerto haemorrhages, infectious collections may besubgaleal, epidural or subdural in location.

Intraparenchymal postsurgical infection oc-curs in a subacute phase following the opera-tive procedure. In such cases, physical signs ofintracranial hypertension or fever can representa clinical and neuroradiological emergency.

Cerebritis represents the initial stage of a pu-rulent brain infection, which if not treated mayevolve into a purulent abscess. Both cerebritisand abscess are associated with oedema andmass effect. On CT it is usually impossible todistinguish cerebritis from a sterile postsurgicalreaction, infarction or benign oedema. Howev-er, after the administration of contrast medium,early cerebritis will reveal minor degrees of en-hancement within the first few days followingthe operation. If not treated, this area will de-velop a necrotic core, which will show rim-shaped contrast enhancement on imaging. Ondelayed images (60-90 minutes), enhancementmay fill the centre of the abscess cavity (53).

Hydrocephalus

Postsurgical hydrocephalus may occur in upto 33% of patients subjected to craniotomy(28). In this case there is a slow, steady increasein intracranial pressure resulting in neurologi-cal signs and symptoms more typical of nor-motensive hydrocephalus than of acute in-tracranial hypertension (30, 34).

On the other hand, repeated (42) and exces-sive ventricular shunt drainage in cases of treat-ed hydrocephalus can generate the so-called“slit ventricle syndrome”. This is an acute-sub-acute syndrome characterized clinically byvomiting, headache and alterations of con-sciousness. On imaging, the lateral ventricles insuch cases are collapsed, thus giving the ap-pearance of slit-like ventricles (12, 17, 21).

Infarction

Causes of a postsurgical cerebral infarctioncan be found in factors closely linked to the op-


Fig. 4.47 - Infection of the surgical site in patient previously op-erated on for intracranial meningioma. Axial CT after contrastmedium administration shows extensive swelling and enhance-ment of the superficial soft tissues overlying the temporal sur-gical site which ultimately proved to be active infection.

a

b

eration itself (Fig. 4.48). The most frequentsurgical causes of infarction are the accidentalocclusion of arteries associated with cerebralaneurysms or with clips on the components ofcerebral AVM’s. The total or partial occlusionof an artery may also be caused by the use of abipolar coagulator during the removal of abrain tumour.

The ischaemic area can be adjacent to thesite of the operation, or alternatively can occurat a distance. In the latter case, the pathogenicmechanism may be laceration of the bridgingmeningeal veins due to rapid decompression ofcases of non-specific raised intracranial pres-sure, cerebral retraction or compression dur-ing surgery, marked systemic hypertension orprolonged hypoxia during the operation (2, 315, 39).

HYPOPHYSIS

Postsurgical emergencies following opera-tions on the hypophysis by the transsphenoidapproach are somewhat rare; most cases aredue to haemorrhage (intracerebral, subarach-noid and intraventricular), hydrocephalus,meningitis, marked pneumocephalus andcerebrospinal fluid fistula formation. Alter-ations of vision have also been observed fol-lowing prolonged surgical compression or di-rect surgical trauma to the optic chiasm,tracts or nerves. Operations requiring surgi-cal dissection that extends to the level of thecavernous venous sinus may injure the adja-cent cranial nerves. A rare complication oftranssphenoid surgery is the laceration orrupture of the cavernous segment of the in-ternal carotid artery, which may be rapidly fa-tal (36).

SPINAL EMERGENCIES

Postsurgical spinal emergencies can be di-vided into lesions of the neurological, bony orsoft tissues. In addition, spinal implant dys-function can also lead to clinical emergencies.This section has been divided into several parts

dedicated respectively to the upper cervicalspine (skull base-C2), the lower cervical spine(C3-C7), the thoracolumbar spine and the lum-bosacral spine. The type of operation and thetype of surgical approach commonly adopted(anterior, anterolateral, posterior) are discussedin each subsection (55, 56).

The upper cervical spine (skull base-C2)

Due to the particular mechanics of the at-lanto-occipital articulation, techniques for fix-ing and fusing the upper cervical spine are dif-ferent from those used in the lower areas of thespine (10, 19). The anterior approach can bebroken down into transoral, anterior retropha-ryngeal and anterolateral retropharyngeal.Each of these techniques presents surgical risksthat may potentially result in a clinical emer-gency (55).

The transoral approach has been reported toresult in infection in up to 59% of cases (40).Another complication is the creation of a pha-ryngeal fistula due to the dehiscence of the sur-gical incision.


Fig. 4.48 - Postoperative cerebral infarction. Unenhanced axialCT shows an extensive right hemisphere infarction associatedwith mass effect in patient recently operated on for aneurysmof the right internal carotid artery.

Complications affecting the spinal tissues in-clude CSF fistulae with associated anteriorpseudo-meningocele formation. The latter isdue to a dural tear. Pseudo-meningoceles onimaging appear as well-defined fluid collectionsthat extend along the intraspinal surgical tractinto the soft paraspinal tissues. Although onMRI it commonly demonstrates the same inten-sity as CSF, in certain cases it is possible to ob-serve fluid-fluid levels with the relative differ-ences in signal intensity being caused by thepresence of blood and other products (55).

In emergencies secondary to the malposi-tioning of vertebral screws, there can be directinjury to the neural structures adjacent to thesurgical site as well as to regional vascular struc-tures such as the vertebral arteries (22, 26).

Being extramucosal, the other approaches tosurgery in the upper cervical spine have lowerrates of postsurgical infections. However, giventhe close relationship that the surgical route haswith major vascular structures (e.g., anteriorvertebral arteries, ascending anterior pharyn-geal arteries, upper costo- thyrocervical branch-es), this still constitutes a relative risk. For ex-ample, retropharyngeal or lateral cervicalhaematomas may be observed, as well as the for-mation of pseudo-aneurysms secondary to sub-acute vascular ruptures due to the weakening ofthe wall of an overdistracted-compressed vesselduring surgery (4).

The posterior approach is generally used forthe reduction and subsequent fusion of the at-lanto-occipital articulation in order to correctatlantoaxial subluxation associated with insta-bility. This surgical route enables access to theforamen magnum, the posterior arch of the at-las, the spinous process of C2 and the laminaeand articular facets of C1-C2 (9).

Generally speaking, surgical emergencies areprincipally linked to pathology involving thenerves or the spinal cord. In such situations it ispossible to observe, preferably by MRI, fluidcollections, posterior pseudo-meningocele for-mation or the encroachment upon neurologicaltissue by bony or soft tissue abnormalities.

Complications from implanted surgical ap-pliances include incorrect positioning of thescrews within the lateral masses of C1-C2 ad-

versely affecting the nearby spinal nerves or thevertebral arteries. Moreover, in the event ofposterior C1-C2 stabilization procedures, thecollapse of the prosthetic implant or of thebone graft may result in varying degrees of cen-tral spinal canal stenosis with spinal cord com-pression.

In such cases, the diagnostic imaging tech-nique of choice is conventional radiographyfirst, to evaluate the bony spine and the spinalimplant, followed by MRI and then comple-mented by CT myelography in extraordinarycases in which the first two examinations donot answer the clinical questions (41).

The lower cervical spine (C3-C7)

Surgery performed upon the lower part ofthe cervical spine also includes anterior, antero-lateral and posterior approaches. Overall, theanterior and posterior routes are far more com-monly utilized than the anterolateral one, andwe will therefore focus our analysis of potentialsurgical complications on these (19).

In operations involving the anterior ap-proach, it is possible although rare to observearterial (e.g., carotid, vertebral, superior thy-roid arteries) and venous (e.g., internal jugularvein) lacerations, spinal cord injury and oe-sophageal and tracheal trauma. Overall, tempo-rary or permanent injury to the recurrent laryn-geal nerve has been described as the most com-mon postsurgical complication of anterior ap-proach cervical spine surgery (31, 60).

Acute postsurgical infections of the cervicalspine are rare. In such cases prominent epidur-al enhancement may be observed associatedwith mass effect and, if severe, spinal cord com-pression. In some instances, the intravenouslyadministered contrast medium may penetrateinto the intervertebral disk spaces at the levelsof surgery. It is important to note that neitherdisk space enhancement nor hyperintensity ofthe intervertebral disk on T2-weighted imagesof the operated region are to be considered ab-solute indicators of spinal infection in the im-mediate postsurgical period. Such observationsmay only be due to expected postoperative


oedema or the presence of blood at the surgicalsite. Related to these observations, within daysof the surgery MRI may reveal areas of alteredsignal at and near the operative site; such alter-ations, characterized by low MRI signal on T1-weighted images and high signal on T2-weight-ed acquisitions, indicate the presence of oede-ma and haemorrhage that may only be a physi-ological response to the normal trauma of sur-gery (19, 41).

Acute complications of anterior cervicaldiscectomy principally centre on the type ofthe surgical implant utilized, including themalpositioning of the fixation screws, due ei-ther to their being too long or to the acci-dental extension of the screws into the spinalneural foramina. An emergency observed inthe chronic phase relates to the fracture ofthe implanted spinal appliances (Fig. 4.49) as-sociated with the collapse of the surgical con-struct (26).

In cases of anterior fusion utilizing bonegrafts, the following neuroradiological emer-gencies may occur: collapse of the native bonegraft, collapse of a synthetic bone graft, over-distraction of the spine causing straightening oreven kyphosis of the cervical spinal curvatureas observed in the sagittal plane, and subsi-dence of the synthetic bone graft into thesupra- and subjacent vertebral body marrowspaces (Fig. 4.50).

Finally, we should point out the neuroradio-logical emergencies related to extrusions ofprosthetic materials, such as in the case of ex-pulsion of interbody bone grafts with compres-sion of the oesophagus and trachea. In suchcases, both MR and conventional radiographyare ideal imaging modalities for demonstratingthe problem (13).

The posterior surgical approach is the mostcommon technique for the decompression ofthe cervical spinal canal. This surgical route isalso typically used to stabilize complex frac-tures. Postsurgical emergencies commonly ob-served related to the posterior surgical ap-proach are characterized by injuries to thespinal or cervical spinal cord.

CSF leaks with pseudo-meningocele forma-tion are also observed at this level of the spine

in cases where the meninges are inadvertentlybreached. Finally, especially in cases of coagu-lation disorders, the formation of epiduralblood collections can present as clinical emer-gencies.

Other neuroradiological emergencies con-cern the surgical technique used in posteriordecompression. In cases of cervical laminecto-my, the extent of the removal of the vertebrallaminae can be insufficient, thus causing a pos-sible stenosis upstream and downstream fromthe bone decompression.

Lastly, in relation to cervical laminoplasty(with widening of the cervical canal leavingthe plates in place), the stabilization systemsused (plates and screws, bone grafts, metalwires) can recreate a condition of canal steno-sis with subsequent worsening of the clinicalsituation.


Fig. 4.49 - Fracture of surgical spinal appliance. A lateral radi-ograph of the cervical spine shows a fracture of the upper ver-tebral body screw in a patient with cervical myelopathy operat-ed on for spinal cord decompression and anterior fusion.

Emergencies linked to posterior instrumen-tation include the malpositioning of transartic-ular screws and those screws placed into thelateral masses of the cervical vertebral bodies,fractures of the posterior spinal facet joints, di-rect surgical injuries of the vertebral arteriesand impingement on the exiting spinal nervesand nerve roots.

The thoracic spine

As in other levels of the spine, clinical emer-gencies of the thoracic spine (19) depend onthe type of surgery performed and the surgicaltechnique used.

The anterior surgical approach to the tho-racic spine is best suited to the treatment ofneoplastic and infectious disease, and for the

management of complex problems such as sco-liosis. Potential complications that may requireemergency medical imaging studies includelung and pleural trauma, haemorrhage from in-juries of the intercostal arteries or the azygosvein and complications arising from injury ofthe lymphatic trunk. In such cases, the diag-nostic modality of choice is spiral CT per-formed either with or without the use of intra-venous contrast media.

Accidental penetration of the spinal meningesresulting in CSF leakage may cause fluid collec-tions in a pleural, extrapleural, posterior spinalsoft tissue or retroperitoneal location. In rare cas-es, haematomyelia may occur from direct traumaof the spinal cord (47).

The posterior approach to spinal surgery isutilized for laminotomy and/or laminectomyused for the treatment of spinal fractures, de-compression of spinal stenosis and neoplasticlesions (13). In addition, the posterior route isclassically used for the correction of skeletal de-formities, such as scoliosis.

The posterior surgical approach is alsomost commonly used for the stabilization ofthe thoracic spinal column. With regard tospinal surgical instrumentation, the samecomplications may occur in the thoracolum-


Fig. 4.50 - Collapse of spinal interbody bone graft in patientundergoing for diskectomy and spinal fusion. A lateral radi-ograph of the cervical spine shows postoperative intervertebraldisc space collapse at the C6-7 level following diskectomy andattempted bone graft placement.

Fig. 4.51 - Dislocation of surgical appliances following verte-bral collapse in patient with multiple myeloma operated on forposterior stabilisation. [axial CT].

bar spine as those outlined for the cervicalspine.

The most common radiological emergenciesare related to malpositioning of surgical im-plants. In such cases, poorly positionedtranspedicular fixation screws can injure the vas-cular and neural structures adjacent to the verte-bral pedicles or anterior to the vertebral bodies.Injuries to the thoracic or abdominal aorta (Fig.4.52), the intercostal arteries, the inferior venacava, the azygos vein, the thoracic spinal nervesand the thecal sack may occur. With malposi-tioning of translaminar surgical hooks, the mostcommonly recognized complication involves thecompression of the adjacent neural structures toinclude the spinal nerves and spinal cord.

Finally, dorsal epidural haematomas may beencountered, especially following decompres-sive laminectomies in patients with vertebralneoplasia or in those having coagulation disor-ders.

The lumbosacral spine

Anterior surgical procedures on the lum-bosacral spine, carried out via the retroperi-toneal or transperitoneal route are performedfor the removal of vertebral neoplasia, the treat-ment of spinal column infections and for ante-rior stabilization procedures in cases of spinaltrauma and degenerative disease.

Perhaps the most frequently encounteredclinical emergency is the formation of aretroperitoneal haematoma that may result incirculatory system shock. Other clinical emer-gencies not infrequently involve injuries of theregional soft tissues. In particular, trauma to thelarge retroperitoneal vessels (e.g., common iliacarteries, common iliac veins) may be seen (33,35). Lesions of the ureter can also be observed,as can perforations of the intestinal viscera andurinary bladder (34, 36, 47). Surgical neurolog-ical injuries and those linked to prosthetic mal-positioning are identical to those mentioned forthe thoracic spine (49, 50).

With regard to complications linked to theposterior surgical approach, the same observa-tions made previously in the cervical and tho-

racic spine sections apply in the lumbosacralspine concerning injuries of the lumbosacralroots and those of the thecal sack (e.g., CSF fis-tulae, pseudo-meningocele formation) (1, 29).

REFERENCES

1. Barron JT: Lumbar pseudomeningocele. Orthopedics13:608-609, 1990.

2. Bejjani GK, Duong DH, Kalamarides M et al: Cerebral va-sospasm after tumor resection. A case report. Neurochirur-gie 43 (3):164-8, 1997.

3. Bejjani GK, Sekhar LN, Yost AM et al: Vasospasm aftercranial base tumor resection:pathogenesis, diagnosis andtherapy. Surg Neurol 52(6):577-84, 1999.

4. Bell GR: The anterior approach to the cervical spine. InRoss J,ed. Neuroimaging Clinics of North America: Phila-delphia: WB Saunders 465-480, 1995.

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8. Bruce DA, Alavi A, Bilaniuk L et al: Diffuse cerebral swel-ling following head injuries in children: The syndrome ofmalignant brain edema: J Neurosurg 65:170-178, 1981.

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Fig. 4.52 - Over insertion of transpedicular screw with im-pingement upon the aorta. Axial T1-weighted MRI shows pen-etration of the transpedicular screw on the left side through theanterior cortex of the vertebral body associated with impinge-ment upon the abdominal aorta.

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34. Miller JD, Stanek A, Langfitt TW: Concepts of cerebralperfusion pressure and vascular compression during intra-cranial hypertension. Pro Brain Rse 35:411-32, 1972.

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36. Rajaraman V, Schulder M: Postoperative MRI appearanceafter transsphenoidal pituitary tumor resection. Surg Neu-rol 52(6):598-9, 1999.

37. Rao CVGK, Kishore PRS, Barlett J: Computed tomographyin the postoperative patient. Neuroradiology 19:257-263,1980.

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39. Rastogi H, Baazan III C, da Costa Leite C et al: The po-sttherapeutic cranium. In: Randy Jinkins J edt. Posthtera-peutic neurodiagnostic imaging. Philadelphia: JB Lippin-cott 3-39, 1997.

40. Richardson WJ, Spinner RJ: Surgical approaches to the cer-vical spine. In: White AH, ed. Spine Care. Baltimore: Mo-sby 1335-1350, 1995.

41. Ross JS, Masaryk TJ, Schrader M et al: MR imaging of thepostoperative lumbar spine: assesment with gadapentate di-meglumine. Am J Roentgenol 155:867-872, 1990.

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48. Shimizu S, Tachibana S, Maezawa H et al: Lumbar spinalsubdural hematoma following craniotomy: case report.Neurol Med Chir Takio 39(4):299-301, Apr 1999.

49. Slone MR, MacMillan M, Montgomery WJ et al: Spinalfixation: Part 2. Fixation techniques and hardware for thethoracic and lombosacral spine. Radiographics 13:521-543,1993.

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51. Spetzler RF, Wilson CB, Weinstein P et al: Normal perfu-sion pressure breakthough theory. Clin Neurosurg 25:651-72, 1978.

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61. Zimmerman RA, Bilaniuk LT, Dolinskas C et al: Computedtomography of pediatric head trauma: Acute general swel-ling. Radiology 126:403-408, 1978.


V

SPINAL EMERGENCIES

297

Given the variety of potential types ofpathology and their varied clinical presenta-tions, spinal emergencies are considered amongthe most challenging of all neuroradiologicalinvestigations. Spinal emergencies can be divid-ed into traumatic and non-traumatic causes andcan involve the spinal column itself and its re-lated bony, ligamentous and muscular tissues,as well as the intraspinal contents to include themeninges, spinal roots/nerves and spinal cord.

Non-traumatic spinal emergencies can origi-nate from a vast number of causes. These non-injury lesions of the spine are classified as be-nign/malignant neoplastic (primary or metasta-tic, including haematological malignancies) orinfectious-degenerative. Lesions of the spinalcontents may be extradural (e.g., haematoma,infection), intradural-extramedullary (e.g., pri-mary or secondary neoplasia) or intramedullary(e.g., infarction, haemorrhage, demyelinatingplaque formation) in location.

NEURORADIOLOGICAL PROTOCOLS

From a clinical point of view, the most im-portant crisis whatever the cause is the presen-tation of a patient with signs and symptomssuggesting compression of the spinal cord andthe spinal nerve roots. In this case, the neuro-

radiologist’s role is to identify the cause of theclinical presentation quickly so that decom-pression of the compromised neurological tis-sue can be undertaken in a timely manner: theearlier the diagnosis, the greater is the proba-bility of functional recovery following therapy.For this purpose a number of imaging methodscan be used, depending upon the specific clini-cal situation.

Conventional radiography is still consideredthe first technique of choice in spinal emergen-cies, despite the fact that it is not always con-clusive, especially in the more complex cases ofspinal pathology. Considering its low cost, uni-versal patient access and its rapidity and sim-plicity of execution, conventional radiographyprovides a general diagnostic evaluation, re-vealing the majority of pathological spinal con-ditions responsible for the compression of thespinal cord and the nerve roots.

The subsequent diagnostic imaging modali-ty chosen varies depending on the presence andnature of the neurological signs and symptomsindicating direct involvement of neural struc-tures. In cases where neurological symptomsare present, MRI is preferable to CT where it isavailable (1, 3-5, 9-11). By combining multipla-nar capabilities and high sensitivity to subtletissue abnormalities, MR provides a very thor-ough analysis of the spinal column, its contents

5.1

CLINICAL AND DIAGNOSTIC SUMMARY

T. Scarabino, M.G. Bonetti, M. Cammisa

and the perivertebral soft tissues. In general,MRI provides information non-invasively thatit currently unobtainable using other imagingtechniques.

Given its high sensitivity, MRI is capable ofvisualizing bone marrow abnormalities earlierthan other imaging techniques. In addition tolimited access in some areas, there may also bepractical drawbacks to the use of MRI, espe-cially in patients with acute vertebral collapseand spinal cord compression. Life support de-vices in such patients, for example, may pre-clude the use of MRI.

If MRI is unavailable or it is not technicallypossible, CT can provide useful information re-garding bony morphology, the central spinalcanal and the perispinal soft tissues (2, 4, 8).However, CT provides little data concerning thecontents of the central spinal canal. Neverthe-less, intervertebral disk herniations and verte-bral compressions/burst fractures of traumaticorigin are well visualized (7). In such instancesthe examination can be performed quickly,without having to immobilize the patient. In ad-dition, CT investigations can be extended to in-clude other organs and regions in polytraumapatients, providing results that are unquestion-ably superior to and more informative in mostcases than those obtained with conventional ra-diography. Of course, in order to avoid exces-sive irradiation the CT examination should befocused on limited levels of the spine by the pre-liminary identification of problem areas bymeans of x-ray or MRI, or on the basis of spe-cific localizing clinical signs and symptoms.

It is not always possible to clearly define thelocation of the pathology responsible for theclinical presentation. In such cases, MR is onceagain the most reliable examination technique,

as it clearly defines the spinal pathology re-sponsible for the neural compromise, analysingat once the epidural space, the intradural-ex-tramedullary space and the spinal cord (16). Torepeat, CT’s principal drawback in this regardis its inability to visualize the intradural struc-tures (7).

In conclusion, MRI currently represents anindispensable instrument in spinal diagnosis. Incertain cases it enables a complete diagnosticevaluation even when used alone. In other cas-es it can be combined profitably with otherconventional neuroradiological techniques tofacilitate a definitive diagnosis.

REFERENCES

1. Baleriaux DL: Spinal cord tumors. Eur Radiol 9(7):1252-1258,1999.

2. Brant-Zawadzki M, Miller EM, Federle MP: CT in the eva-luation of spinal trauma. AJR 136:369-375, 1981.

3. Han JS, Kaufman B, El Youse SJ et al: NMR imaging of thespine. AJNR 4:1151-1159, 1983.

4. Kaiser JA, Holland BA: Imaging of the cervical spine. Spi-ne 23(24):2701-712, 1998.

5. Keiper MD, Zimmerman RA, Bilaniuk LT: MRI on the as-sessment of the supportive soft tissue of the cervical spinein acute trauma in children. Neuroradiology 40(6):359-363,1998.

6. Klein GR, Vaccaro AR, Albert TJ: Efficacy of magnetic re-sonance imaging in the evaluation of posterior cervical spi-ne fractures. Spine 24(8):771-774, 1999.

7. Kretzschmar K: Degenerative disease of the spine: the roleof myelography and myelo-CT. Eur J Radiol 27(3):229-234,1998.

8. Lee CP, Kazam E, Newman AD: Computed tomographyof the spine and spinal cord. Radiology 128:95-102, 1978.

9. Modic MT, Weinstein MA, Paulicek W et al: MRI of thespine. Radiology 148:757-762, 1983.

10. Paleologos TS, Fratzoglou MM, Papadopoulos SS et al: Po-sttraumatic spinal cord lesions without skeletal or discaland ligamentous abnormalities: the role of MR imaging. JSpinal Disord 11(4):346-349, 1998.

11. Wilmink JT: MR imaging of the spine: trauma and degene-rative disease. Eur Radiol 9(7):1259-1266, 1999.

298 V. SPINAL EMERGENCIES

299

INTRODUCTION

The frequency of spinal trauma, which indeveloped countries affects 70% of cases underthe age of 40, has gradually increased over thelast 50 years. Typical causes of spinal trauma in-clude road traffic accidents (50%), sports ac-tivities (25%), occupational accidents (20%)and accidental falls (5%) (19).

Neurological injuries occur in 10-14% ofcases of spinal trauma; 85% of these cases pres-ent at the time of the trauma, between 5-10%originate shortly afterwards, and between 5-10% become evident at a later time (9). Diag-nostic and therapeutic advancements have in-creased patient survival rates; however, littlecan be done to reverse frank spinal cord injury.Improvements in survival rates have led to aparallel increase in the number of younger in-valids. It is in part for this reason that preven-tion, rapid diagnosis and proper patient man-agement are of paramount importance in mini-mizing neurological patient deficit (16).

Timely radiological diagnosis is fundamentalin the modern management of patients withspinal trauma. Mastery of this includes a thor-ough knowledge of the anatomy and biome-chanics of the spine, an understanding of themechanism of the trauma, experience in the

correct execution of radiological examinations,knowledge of the indications and limitations ofthe individual imaging techniques under con-sideration and a correct appreciation of the im-portance of the correlation between the imag-ing findings and the clinical signs and symp-toms.

Practically speaking, the spinal column hastwo functions: to facilitate stability and move-ment, and to protect the spinal cord and spinalnerves. Consequently, we have two separate yetclosely connected considerations when evaluat-ing the patient with spinal trauma: the spinalcolumn itself and the underlying neural andmeningeal structures. At the level of the presentstate of the art, medical imaging techniquesmake it possible to glean information concern-ing all components of the spine, including itscontents and the perivertebral tissues. Conven-tional radiology, CT and MRI are the tech-niques currently available, although the mostadvanced techniques do not necessarily repre-sent the best ones in every case (2, 12, 15).

Fundamental diagnostic information is pro-vided by conventional x-rays which, when com-plemented by conventional tomography, are thebest choice for evaluating acute trauma of thespinal column itself. Radiographic analysis alsomakes it possible to perform the examination in

5.2

CT IN SPINAL TRAUMA EMERGENCIES

S. Perugini, S. Ghirlanda, R. Rossi, M.G. Bonetti, U. Salvolini

a number of projections without moving the pa-tient. In addition, the entire spine as well as oth-er body parts can be examined at the same time.According to the literature, 43% of patientswith burst spinal fractures may have otherspinal injuries. Associated both distal and prox-imal traumatic spinal lesions are present in 10-17% of patients. For example, in patients withcervical injuries, 12% also have thoracic frac-tures and 3% reveal lumbar fractures.

With regard to conventional radiography,particular attention should be paid to evaluat-ing the following parameters in the patient withspinal trauma:

Vertebral alignment abnormalities:– reversal of normal spinal curvature– abrupt increase in the spinal curvature– alignment of the articular processes, lami-

nae, spinous processes, transverse processesand vertebral bodies

– widening of the interspinous/interlaminarspaces

Abnormalities of the perivertebral soft tissues:– enlargement of the retropharyngeal and

retrotracheal spaces– enlargement of the thoracic and lumbar

paraspinal spaces

Disk/Articular abnormalities:– abnormalities of the intervertebral disk

space– abnormalities of the posterior spinal articu-

lar facet processes (zygapophyses).

It is also necessary to evaluate spinal stabili-ty in patients with spinal trauma. The term in-stability in this context indicates a posttraumat-ic state of intersegmental hypermobility thatmay require surgical restabilization. In order toproperly discuss and study the spinal columnfor possible instability, the spine has been di-vided into three columns (6, 7): anterior col-umn, middle column and posterior column.Practically speaking, the involvement of a sin-gle column does not necessarily entail instabili-ty, however, the involvement of two adjacentcolumns usually does.

Recent studies (5) have identified five radio-logical signs of spinal instability associated withspinal injuries. These five signs can be summa-rized as follows:

1) anterior or posterior vertebral subluxa-tion greater than 2 mm

2) enlargement in the interlaminar space ofmore than 2 mm

3) enlargement in the joint space betweenthe articular facet processes; malalignment ofthe same a loss of contact between contiguousfacets

4) fracture involving the posterior cortex ofthe vertebral bodies

5) enlargement in the lateral dimension ofthe central spinal canal of more than 2 mm asmeasured by the interpedicular distance be-tween adjacent vertebrae.

It is also essential to know the mechanism ofthe trauma as well as the biomechanics of thespine, which make it possible to identify the ar-eas most at risk of injury. The highest risk areasare those sites at which a greater degree of mo-bility exists, such as the cervical and lumbarspinal segments, or where a junction exists be-tween a relatively mobile segment and one thatis less so or not at all (e.g., the cervico-thoracicjunction, the thoraco-lumbar junction, the lum-bo-sacral junction).

On the basis of the dynamics of trauma, it ispossible to recognize injuries caused by: simpleflexion, flexion-distraction, flexion disloca-tion, flexion and compression, simple exten-sion, extension-distraction, extension-disloca-tion, “shearing” forces, and rotation. Althoughthere is overlap between the various types,each of these traumatic mechanisms may causea particular type of fracture.

To summarize, when investigating traumaticlesions of the spine one must: understand themechanism of the trauma; ensure that the pa-tient is only moved once it has been determinedthat it is possible to do so with safety by expertpersonnel and preferably under medical guid-ance; remember that patients with spine traumanot infrequently have polytrauma and that neu-rological injuries can conceal involvement of in-ternal organs (e.g., the spleen); perform a pre-


liminary medical imaging investigation that willfocus clinical attention to relevant areas andsurvey the areas at highest risk; interrupt the di-agnostic evaluation if a lesion requiring emer-gency treatment is detected; demand that a spe-cialist interpret the medical images and that aradiologist be present when these examinationsare carried out.

TECHNIQUES

Although one must consider a technique’slimits and advantages (18), only thorough in-vestigations provide reliable diagnostic infor-mation. Naturally the imaging modality chosenand the parameters selected will vary accordingto the type of injury and the imaging equipmentavailable.

The CT investigation technique initially in-volves a lateral scanogram in the cervical, tho-racic and lumbar areas in order to centre theaxial sections of the spine and an anteroposte-rior scanogram in the thoracic spine in order tonumber the vertebrae. Axial sections are thenangled to the direction of the intervertebraldisk. A second set of stacked axial images arethen obtained using relatively thin sectionwidth and without space between the sections(this will enable multiplanar reconstructions tobe performed). For the cervical spine it is ad-visable to use a slice thickness of 2 mm, where-as at the thoracic and lumbar levels it is possi-ble to use slice thicknesses of up to 5 mm.Thicker slices will not reveal fractures or othertypes of injury due to the partial volume effect.The use of thin (2 mm) slices makes it possibleto obtain more reliable electronic reconstruc-tions on the coronal, lateral and oblique planes.The acquisition field of view (FOV) must bewide enough to cover the entire volume beingexamined (e.g., cervical spine: 25 cm; cervi-cothoracic: 35 or 50 cm; lumbar: 35 or 50 cm).The data postprocessing FOV must be of 15 or18 cm in order to be able to visualize the spinalcolumn as well as the perivertebral structures.Larger postprocessing FOV’s are used forstudying the surrounding tissues (e.g., lung, liv-er, kidney and spleen), especially when the clin-

ical situation or trauma dynamics suggest in-juries of these organs.

The introduction of spiral and multislice CTinto clinical practice has considerably expand-ed the diagnostic possibilities of CT. A majoradvantage of this technique is the ability of ac-quiring volume data rapidly, enabling subse-quent processing in multiple planes.

As a result, motion artefacts are reduced andone can obtain reconstructed images of excel-lent quality. These advantages make spiral CTparticularly well suited to studying acute trau-ma patients (17).

Conventional radiography, as compared toCT, has a sensitivity of 60%, a specificity of100% and positive and negative predictive val-ues of 100% and 85%, respectively (13). SpiralCT on the other hand has a sensitivity of 90%,a 100% specificity and positive and negativepredictive values of 100% and 95%, respec-tively (1, 11).

The spinal segment most at risk of injury intrauma patients is C1-2. A spiral CT of thisspinal segment is preferably performed at thesame time as the cranial CT (4, 20). Anotherhigh risk level is the cervico-thoracic junction,one that is often inadequately visualized withconventional x-rays (22). The CT screening ofthis level is also considered valid from an eco-nomic point of view (21). Overall, high resolu-tion spiral CT examinations offer a detailedanalysis of the spine, generating informationthat sometimes is of decisive importance intreatment planning (8, 10, 11).

An optimized spiral CT technique of thecervical spine includes: for routine imaging, aslice thickness of 3 mm (pitch 1) is used withsection reconstructions acquired at 1.5 mmintervals; for higher resolution imaging, aslice thickness of 1 mm with 1.5 mm intervals(pitch 1.5) is recommended with section re-constructions acquired at 0.75 mm intervals.At the thoracic and/or lumbar levels the spi-ral technique suggested is: for routine imag-ing, a slice thickness of 5 mm with 5 mm in-tervals (pitch 1), with reconstructions ac-quired at 2.5 mm intervals; for more detailedexaminations, the same protocol is used as forthe cervical spine.

5.2 CT IN SPINAL TRAUMA EMERGENCIES 301

However, CT principally focuses upon thebony structures. Obviously, the spinal cord isgenerally poorly visualized. When studying theCT images, the data must always be viewedwith windows suited to both bony structures aswell as the soft tissues. The investigation mustbe complemented by electronic reconstructionsin the sagittal, coronal and oblique planes. Ifpossible, three-dimensional reconstructions arealso performed.

INDICATIONS

Correct diagnostic medical imaging of thepatient with spinal trauma demands that thespine be examined in the sagittal and coronalplanes. Axial imaging alone is inadequate. Itshould also be pointed out that the clinical sta-tus of spine trauma patients varies greatly as dothe clinical and diagnostic priorities. Four dif-ferent clinical situations can be encountered:severe polytrauma patient in a coma, patientwith spinal cord damage not in a coma, patientwith radicular signs/symptoms, and patientwithout neurological deficits but with clinicalsuspicion of spine damage.

1) Severe polytrauma patient in a comaIn this case, and until proven otherwise, the

patient must be considered to have spine injury.The cranial trauma and the state of coma re-quire CT scanogram(s) extending from the topof the skull through the cervical spine in the lateral projection. With certain types of CTequipment, it is possible to obtain oblique projection scanograms. The current state ofscanography only permits the determination ofgross vertebral alignment alterations in thefrontal, lateral and oblique projections; in thelatter projection it is sometimes possible to seedislocations of the posterior spinal facet joints.The scanogram can also be used to evaluate thethoracolumbar spine, analysing the same in-juries as in the cervical spine.

Therefore, while at the current time thescanogram does not replace conventional radi-ography, it nevertheless can constitute the ini-tial examination in the spine trauma patient.

2) Patient with spinal cord injury not in a comaIn this case the CT should be performed in

patients when it is essential for emergency sur-gical planning and in patients where MRI is notpossible. Importantly, the CT examinationmakes it possible to discover if traumatic bonyencroachment into the central spinal canal ispresent (7).

3) Patient without neurological deficitCT should be performed in spinal areas

where conventional x-rays are inconclusive orin order to better define the extent of an injurydetected using x-rays.

4) Patient with radicular symptomsThe CT examination should focus on the

spinal level indicated by the clinical examina-tion in order to search for a traumatic abnor-mality giving rise to radicular compression(e.g., traumatic disk herniation, bony fracturefragment, vertebral subluxation).

SEMEIOTICS

CT provides an excellent analysis of thebony spinal structures. However, while frac-tures along the coronal and sagittal planes arewell visualized, fractures in the axial plane arepoorly identified. Dislocations in the axialplane can also be difficult to determine fromthe axial images. Nevertheless, multiplanar re-constructions when of high resolution qualitycan visualize these abnormalities in the axialplane, and lessens this limitation of CT. Finally,posttraumatic swelling of the paravertebral softtissues is well seen on CT examinations.

Radiography and CT

For descriptive purposes, vertebral columntrauma can be divided into: trauma of the prox-imal cervical spine (from the occipital condylesto C2) (case nos. 1, 2, 3, respectively, Figs. 5.1,5.2, 5.3); trauma of the mid-distal cervical spine(from C3 to C7) (case nos. 3, 4, 5, respectively,Figs. 5.3, 5.4, 5.5); trauma of the thoracolum-


bar spine (case nos. 6 and 7, respectively, Figs.5.6, 5.7).

Proximal (craniad) cervical trauma

Fractures of the occipital condyle are rareand are typically caused by vertical compres-sion; they are examined very well with thinslice CT; atlanto-occipital dislocation is usually

fatal and therefore rarely observed on radiog-raphy. In non-fatal cases, lateral projection x-rays show marked thickening of the periverte-bral soft tissues associated with atlanto-occip-ital dislocation.

C1 fractures can involve the anterior or pos-terior arch, and because C1 constitutes a bonyring, they are almost always seen in combina-tion. The mechanisms of trauma are essentiallyhyperextension (i.e., whiplash) or vertical com-


Fig. 5.1 - Acute cervical spine trauma. a), b) Axial CT of the cervical region includes the distance extending from the entire thicknessof the skull base to at least the bottom of C2, scanned with 2mm thickness or less slices. c), d) Contiguous axial sections show a com-minuted fracture of the anterior arch of the C1 with associated involvement of a lateral mass. The posterior arch of C1 is intact.

a c

b d

pression. Each of these causes a different typeof fracture: hyperextension trauma results in afracture of the posterior arch of C1, compres-sion trauma causes a fracture of both the ante-rior and posterior arches of C1. Posterior arch

fractures are clearly visible on both x-rays andCT images.

Fractures of the anterior and posterior archof C1, or Jefferson’s fractures, also result in thedislocation of the articular facets of C1 in rela-


Fig. 5.1 - (Cont.) e) A reconstructed sagittal section demon-strates the relationship between the anterior arch of the C1 andthe odontoid process. f1), f2) Reconstructed coronal sectionsshow the normal relationship between the occipital condyles(f2) and the lateral masses of C2 (f1); there is no lateral disloca-tion of the lateral articular masses of C2.

Fig. 5.2 - Acute cervical hyperextension trauma. a) Lateral x-ray of the cervical spine shows a hangman fracture associatedwith anterior subluxation of C2 and bilateral fractures of theposterior arch of C1. b) Lateral scanogram and c) d) axial CTconfirms the x-ray findings of the C1 and C2 fractures.

e

a

b

f1

f2


Fig. 5.2 (cont.) - c), d) oblique scanograms highlight the distal por-tion of the cervical spine at the cervicothoracic junction. e), f)Axial CT is performed initially with no angulation utilising 4 mmthick slices covering the entire cervical spine; this is then followedby a second set of axial CT scans utilising thinner slices (2 mm orless) extending from C1 to C3, angled generally to the cross-sec-tional plane of the longitudinal axis of the cervical spine. g) 2 mm-thick axial CT scans demonstrate the C1 and C2 fractures.

c

d

e

f

g

tion to those of C2. This alteration is clearly vis-ible on the open mouth anteroposterior projec-tion radiograph that is principally used forstudying the odontoid process. This projectionalso makes it possible to measure the degree oflateral dislocation of the articular facets which,if greater than 7 mm, suggests a rupture of thetransverse atlantal ligament. Axial CT makes itpossible to visualize the fractures, however theexamination must be performed using thincontiguous slices complemented by reconstruc-

tions in the sagittal and coronal planes in orderto show the subluxation of the articular facetprocesses.


Fig. 5.2 (cont.) - h), i) Sagittal reconstructions of the 4 m (h) andthe 2 mm (i) thick slides. Note the relative difference in spatialdefinition. j) A three-dimensional reconstruction clearly showsthe bilateral fractures of the posterior arch of C1 and confirmsthe integrity of the anterior arch.

Fig. 5.3 - Acute cervical spine trauma. a) Lateral x-ray of thecervical spine shows a fracture of the anterior-inferior corner ofC3 associated with a very minor retrolisthesis of C3 on C4.There is also a malalignment of the body of C2 with relation-ship to C1. b) Lateral CT scanogram proscribed to acquire ax-ial images extending from C1 to C4.

h

a

b

i

j

Dislocations between C1 and C2 in the sagit-tal plane are rare because the transverse liga-ment is both strong and resilient. However, ro-tary subluxations between C1 and C2 associat-ed with injuries of the articular capsule in theface of an intact transverse ligament may be en-countered. Such rotary dislocations result in atraumatic-acquired form of torticollis. CTmakes it possible to clearly identify the degreeof rotation between C1 and C2.

C1 fractures are often associated with C2fractures and these in turn are seen in combina-tion with fractures of the C7 spinous process.C2 fractures can involve the posterior arch, theodontoid process and the vertebral body. Frac-


Fig. 5.3 (cont.) - c) Axial CT showing a comminuted fracture ofthe right occipital condyle, d) rotation of the odontoid processwith relationship to C1 and e) a comminuted fracture of C2 atthe base of the odontoid process. f) Coronal CT reconstructionpoorly demonstrates the fracture at the base of the odontoidprocess. g) Sagittal CT reconstructions show the fracture at theodontoid base of C2 and the posterior dislocation of the C3vertebral body on that of C4.

c

d

f

g

e


Fig. 5.4 - Acute cervical spine trauma. a) Lateral cervical CTscanogram suggests the presence of rotation-subluxation in themid cervical spine. b) Right anterior-oblique scanogram show-ing the malalignment of the posterior aspect of the C6-7 verte-brae (arrows). c) Left anterior-oblique scanogram shows nor-mal alignment of the bony structures. d) Lateral x-ray confirmsthe finding of rotation of the distal cervical spine and shows thepresence of a fracture of the anterior-superior corner of C7 andretrolisthesis of C6 on C7.

a

c

d

b


Fig. 5.4 (cont.) - e) Anterior-posterior x-ray shows an abruptdeviation of the spinous processes of C6 and higher to the rightin relationship to the spinous processes of C7 and below. f), g)High resolution axial CT of the cervico-occipital shows a de-viation to the right of the C2 spinous process in the absence ofa fracture. h) A digital summation of the C1 and C2 images (f+ g = h) show a degree of atlanto-axial rotation, which ne-vertheless may within physiological limits. i) Fracture of the ri-ght C6 lamina and the right posterior articular spinal facet pro-cesses of C6-7.

e

g

h

i

f

tures of the body, caused by various types oftraumatic forces, are classified as three differenttypes, depending upon the site of the injury. C2fractures are associated with neurological in-juries in 20% of cases (2, 3).

Hyperextension C2 fractures, or hangman’sfractures, affect the pedicles bilaterally eithersymmetrically or asymmetrically and can be as-sociated with fractures of the inferior-anteriorcorner of the vertebral body itself; there is oftena related subluxation of C2 on C3. Radiographyin such cases will clearly demonstrate these

fracture-dislocations. CT must be performedusing thin slices, extending from the foramenmagnum through C4 and must be comple-mented by reconstructions in the sagittal andcoronal planes. CT is necessary when the pa-tient feels pain in the upper neck, when cervi-cal spine x-rays are negative or when radiogra-phy shows thickening of the perivertebral softtissues.

Limitations of CT include the often poor vi-sualization of linear fractures that developalong the axial plane of section. In this case it is


Fig. 5.4 (cont.) - j), k), l) Coronal reconstructions showing afracture of C7 (j), fractures of the lateral masses (k) and lateraldisplacement of the spinous process of C6 (l). m), n), o), p) Sa-gittal reconstructions: the reconstruction on the left side (m)demonstrates comminuted fractures of the posterior articularspinal facet processes; the reconstruction on the right side (p)shows normal relationships of the posterior articular spinal fa-cet processes; n-o) adjacent parasagittal reconstructions showthe fracture of the body of C7 and the greater intersegmentalrotational subluxation to the right of midline (n).

jm

n

o

p

k

l


Fig. 5.5 - Acute cervical spine trauma. a) Lateral radiographconducted shows anterior subluxation of C5 on C6, an increasein the interlaminar distance and dislocation of the posterior ar-ticular facets. b) Anteroposterior radiograph shows deviationof the spinous process of C5 to the right indicating a probablerotational dislocation. c, d) Right-oblique projection radi-ographs confirms the anterior dislocation of the articular facetsassociated with probable fracture of the pedicle of C5. d) Left-oblique projection radiograph shows a similar finding, but witha smaller displacement than that of the contralateral side. Notethe malalignment of the contralateral vertebral pedicles.

a

c

d

b


Fig. 5.5 (cont.) - e) Lateral CT scanogram . f) Axial CT showsasymmetric dislocation of the body of C5 with relationship toC6. g) Axial CT shows a fracture of the right pedicle of C5. h)Image summation technique including the bodies of C5 and C6showing the C5-6 anterior subluxation. i) Oblique-sagittal re-construction method from preceding axial image set.

e

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g

essential to supplement the examination withhigh resolution multiplanar reconstructionsand with conventional tomography.

Mid-distal (caudal) cervical spine trauma

Cervical spine trauma associated with minorspinal fractures does not in general result in

neural tissue injury, with the exception of casesin which there is underlying congenital-ac-quired stenosis of the central spinal canal.

In adults the mid-distal cervical region is thelevel of the spine that is most frequently affect-ed in cases of trauma. This is especially com-mon at the C5-C7 level (81% according toBerquist) (2, 3). Distal cervical spine traumaticinjuries are categorized according to the mech-anism of the trauma: hyperflexion, hyperexten-sion and axial compression.

Hyperflexion trauma: the forces that obtainin hyperflexion involve a distraction of the pos-terior ligamentous structures and a compres-sion of the anterior structures. Posterior dis-traction injuries can alter the spine’s stabilityeven in the absence of visible bony fractures. Insuch cases the spine radiographs only reveal anincrease in the interlaminar and interspinousspaces at one or more levels. This type of injurymay be associated with fractures of the articu-lar facets. These facet process fractures can bewell documented in oblique radiographic pro-jections or lateral conventional tomographicexaminations. The combination of such frac-tures with posterior ligamentous injury resultsin spinal instability.

X-rays are therefore fundamental to this di-agnosis, although CT can add important sup-plemental information, especially when thereare diagnostic doubts. As elsewhere in thespine, CT should always be performed usingthin sections, complemented with reconstruc-tions in the sagittal, coronal and oblique planes.

In hyperflexion trauma, fractures of the up-per-superior corner of the involved vertebra areoften observed. Should the flexion forces ob-tain with the neck in rotation, it can be possibleto have the same or similar fracture injury, butthere may be an asymmetric subluxation. Or-thogonal x-ray studies must therefore be sup-plemented with oblique projections.

Another type of flexion fracture that may af-fect the cervical spine is the so-called “teardropfracture” in which all three columns of thespine are involved in a characteristic triangularfracture of the vertebral body often associatedwith stenosis of the central spinal canal due toretropulsion of fracture fragments. This type of


Fig. 5.5 (cont.) - j), k) Parasagittal right and left reconstructionsthat show the asymmetric dislocation of posterior articular spi-nal facets.

j

k


Fig. 5.6 - Acute thoracic spine compression trauma. a) Lateralradiograph of the thoracolumbar junction shows compressionof T12 with poor definition of the T11-12 disc space. b) An-teroposterior radiograph showing an increase in the interpedic-ular distance of T12 as compared to the vertebrae above andbelow; this indicates the presence of a burst fracture of T12. c)Lateral CT scanogram confirms the fracture of T12 and showsthe anterior wedging of T8. .

a b

c


Fig. 5.6 (cont.) - d) Lateral scanogram annotating 5mm and e)lateral scanogram annotating 2 mm (e) slices. f), g) Sagittal mid-line (f) and paramedian (g) reconstructions using the 5mm axialsections show a reduction in the sagittal dimension of the cen-tral spinal canal caused by retropulsed bony fragments. h) Co-ronal reconstructions again show the vertebral burst fractureand the left lateral subluxation of the spine.

d

g

h

e

f

fracture should be differentiated from burstfractures that may be stable. CT enables the dif-ferentiation between these two types of fractureby showing the characteristic involvement ofthe three pillars in teardrop fractures.

Spinal cord injury in hyperflexion fracturesis common when there is a vertebral dislocationassociated with a subluxation of the posteriorarticular facets bilaterally, and in cases of tear-drop fractures. Cervical spinal nerve injuriesare more commonly observed in unilateral frac-ture-dislocations.

Hyperextension trauma tends to injure theposterior spinal elements in a compressivemanner, whereas the anterior elements are af-fected by distraction with avulsion of a frag-ment of the inferior-anterior corner of a verte-bral body associated with rupture of the anteri-or longitudinal ligament. This traumatic mech-anism can also result in vertebral subluxationwhich in turn is often linked with spinal cordinjury. Unlike hyperflexion injuries, hyperex-tension trauma can be associated with fracturesof the posterior bony elements of the spine.

Generally speaking, fracture-dislocations areunstable. A precise diagnosis of posttraumaticspinal instability is important for surgical plan-ning (14). Extension and rotation forces can in-jure both an articular mass as well as a lamina.This injury, which is difficult to document us-ing conventional radiography, is clearly visual-ized on CT. CT also makes it possible to deter-mine if any bone fragments have been dis-placed into the neural foramina.

Axial compression trauma of a severe degreeresults in burst fractures of the vertebral body.Fractures of the pedicles may also be seen. CTis excellent for demonstrating retropulsion ofbony fragments into the central spinal canal.Generally speaking, neurological injury is caused


Fig. 5.6 (cont.) - i), j), k) Multiplanar reconstructions using the2mm axial sections. The increase in spatial definition facilitatesthe demonstration of both the traumatic findings of the ante-rior spinal bony structures as well as the injury to the posteriorbony elements and their three dimensional relationships.

i

j

k


Fig. 5.7 - Acute lumbar hyperflexion trauma. a) Lateral CTscanogram shows a wedge fracture of L1. b, c) Axial CT sec-tions demonstrating a comminuted fracture of L1 and someretropulsion of bony fragments into the central spinal canal in-dicating a burst fracture. (1: anterior column; 2: middle col-umn; 3 posterior column) d, e) Sagittal reconstructions showthe posteriorly displaced fragment (e).

a

d

e

b

c

by this posterior displacement of bone with di-rect trauma to the spinal nerves/roots andspinal cord.

CT may also prove essential in differentiat-ing between certain types of fractures, for ex-ample in distinguishing between teardrop andburst fractures. CT must be performed usingthin slices, examining the vertebrae above andbelow the focus of the trauma. It is of vital im-portance to supplement the examination withimage reconstructions in the sagittal and coro-nal planes in order to better demonstrate thethree dimensional relationships of the spinaltrauma.

Trauma of the thoracic and lumbar segmentsof the spinal column

Most thoracolumbar spinal trauma (3, 5) oc-curs at and near the thoraco-lumbar junction,between T12 and L2. In this area there is ananatomical change in the orientation of the pos-terior articular spinal facet joints and a transi-tion from a relatively hypomobile spinal seg-ment to one with greater mobility.

The mechanisms of trauma are the same asthose described for the cervical spine, althoughthe majority of thoracolumbar injuries occur inhyperflexion.


Fig. 5.7 (cont.) - f) Three-dimensional (3-D) CT sagittal plane sectional reconstruction in the sagittal plane shows a relative increase inthe density of the vertebral marrow in three adjacent vertebrae (darker vertebral body shading), indicating that there is marrow com-pression and concentration of bony trabeculae. g) 3-D CT reconstruction demonstrating a superficial overview of the vertebral trauma.h), i) 3-D CT reconstruction of L1 shows the posterior vertebral body fracture, the central spinal canal stenosis and the widening of theposterior spinal facet joint articular space on the left side (arrows).

f h

g i

Flexion trauma entails a compression of theanterior structures and a distraction of the pos-terior spinal-perispinal tissues. Anterior com-pression results in wedge-shaped compressionfractures of the vertebral body, burst fractures,fracture-dislocations and distraction-fractures,depending in part upon the forces applied. Dis-traction-fractures may affect the articular facetprocesses or laminae.

Anteroposterior and lateral x-rays make itpossible to identify the vertebral compressionas well as burst fractures. In some cases, therelevant alterations can be quite minor, suchas a slight curve of the anterior margin of thevertebral body or condensation of the bonytrabeculae. Multiple, adjacent compressionfractures are common. In compression frac-tures, a loss of structural integrity of the pos-terior vertebral cortical surface can be sus-pected when the anterior height of the verte-bral body is reduced by more than one-halfthat of the rear.

CT demonstrates the posterior retropulsionof bony fragments in cases of burst fractures,the dimensions of the central spinal canal andneural foramina, and documents fractures ofthe posterior bony elements.

Fractures caused by flexion forces can resultin intersegmental subluxation, especially at thethoraco-lumbar junction. When there is an in-volvement of the posterior and middle columnsat the lumbar level, the fracture-dislocation isunstable. However, such instability is onlyrarely observed in the thoracic spine due to thestrong paravertebral muscles, the connectedribs and the orientation of the posterior spinalfacet joints.

Vertical compression trauma resulting inburst fractures is most commonly observed atthe thoraco-lumbar junction. Using conven-tional x-rays it is possible to show the compres-sion and fragmentation of the vertebral body,including disruptions of the posterior vertebralcortical margin. However, CT shows the in-volvement of the posterior vertebral cortex bet-ter than conventional x-rays and makes it pos-sible to visualize any migration of fragments in-to the central spinal canal. CT also makes itpossible to highlight fractures of the posterior

bony spinal elements that can indicate spinalinstability.

Single burst fractures of vertebral bodies areassociated with fractures at other levels thatmay or may not be contiguous in up to 43% ofcases. An imaging survey of the entire spinalcolumn is therefore imperative once a burstfracture is identified.

Hyperextension trauma is not commonly en-countered in the thoracolumbar spine. Whenthis is the mechanism of the trauma, isolatedfractures of the spinous and transverse process-es may be encountered. In the lumbar spine thelatter can be associated with renal trauma.

In cases of torsion trauma CT reveals evensmall fractures of the articular facet processes,on the condition that thin contiguous sectionsare used.

CONCLUSIONS

In cases of spinal trauma, CT provides addi-tional information to that obtained by conven-tional x-rays, thus permitting a more sensitiveexamination of the bony structures of thespinal column. Nevertheless, CT investigationsare only carried out after x-rays have shown orsuggested an injury. Contiguous, thin, stackedCT sections must be acquired in order to ob-tain optimal sagittal, coronal and oblique planereconstructions. CT also reveals traumatic le-sions of the adjacent soft tissue structures, how-ever these abnormalities are typically gross;subtle injuries will be overlooked on CT.

REFERENCES

1. Berne JD, Velmahos GC, El-Tawil Q et al: Value of com-plete cervical helical computed tomographic scanning inidentifying cervical spine injury in the unevaluable blunttrauma patient with multiple injuries: a prospective study. JTrauma, 47(5):896-902, 1999.

2. Berquist TH: Spinal trauma. Da: Trauma Radiology. Editedby Mc Cort – Churchill Livingstone: 31-74, 1990.

3. Berquist TH, Cabanella ME: The spine. Da: Imaging of theorthopedic trauma. Edited by TH Berquist – Raven Press:93-206, 1992.

4. Cusmano F, Ferrozzi F, Uccelli M et al: Upper cervicalspine fracture: sources of misdiagnosis. Radiol Med,98(4):230-235, 1999.


5. Daffner RH, Deeb ZL, Goldeberg AL et al: The radiologi-cal assessment of post-traumatic vertebral stability. SkeletalRadiol, 19:103-108, 1990.

6. Denis F: The three column spine and its significance in theclassification of the acute thoraco-lumbar spinal injuries.Spine, 8:817-831, 1983.

7. Denis F: Spinal instability as defined by three-column spineconcept in acute spinal trauma. Clin Orthop, 189:65-73, 1984.

8. El-Khoury GY, Kathol MH, Daniel WW: Imaging of acuteinjuries of the cervical spine: value of plain radiography,CT, and MR imaging. AJR, 164(1):43-50, 1995.

9. Guareschi B: Le lesioni traumatiche vertebrali. Da A.P.C.:Rivisitiamo la radiologia tradizionale. L’urgenza radiologi-ca, pp. 39-50.

10. Katz MA, Beredjiklian PK, Vresilovic EJ et al: Computedtomographic scanning of cervical spine fractures: does itinfluence treatment? J Orthop Trauma, 13(5):338-343,1999.

11. LeBlang SD, Nunez DB Jr: Helical CT of cervical spine andsoft tissue injuries of the neck. Radiol Clin North Am,37(3):512-532, 1999.

12. Leite CC, Escobar BE, Bazan C 3rd et al: MRI of cervical fa-cet dislocation. Neuroradiology, 39(8):583-588, 1997.

13. Mace SE: Emergency evaluation of cervical spine injuries:CT versus plain radiographs. Ann Emerg Med, 14(10):973-975, 1985.

14. Monti C, Malaguti MC, Bettini N et al: La TC nei traumiacuti del rachide. Da: La diagnostica per immagini nelle

“urgenze”, a cura di Romagnoli e Del Vecchio, Idelson, Na-poli: 191-198, 1991.

15. Murphey MD, Batnitzky S, Bramble JM: Diagnostic ima-ging of spinal trauma. Radiol Clin North Am, 27:855-873,1989.

16. Narayan RK: Emergency room management of the head-injured patient. Da: Textbook of head injury. Edited by DPBeker and SK Gaudeman, W.B. Saunders: 23-66, 1989.

17. Nuñez DB Jr, Quencer RM: The role of helical CT in theassessment of cervical spine injuries. AJR, 171:951-957,1998.

18. Olsen WL, Chakeres DW, Berry I et al: Traumatismes durachis et de la moelle. Da: Imagerie du rachis et de la moel-le, Scanner, IRM, Ultrasons. Edited by C Manelfe, Vi-got:387-426, 1989.

19. Pistolesi GF, Bergamo Andreis IA: L’imaging diagnosticodel rachide. Edizione Libreria Cortina, Verona: 637-706,1987.

20. Schmieder K, Hentsch A, Engelhardt M et al: Results ofspiral CT in patients with fractures of the craniocervicaljunction suspected on conventional radiographs. Eur Ra-diol, 9(5):1008, 1999.

21. Tan E, Schweitzer ME, Vaccaro L et al: Is computed tomo-graphy of nonvisualized C7-T1 cost-effective?. J Spinal Di-sord, 12(6):472-476, 1999.

22. Tehranzadeh J, Bonk RT, Ansari A et al: Efficacy of limitedCT for nonvisualized lower cervical spine in patients withblunt trauma. Skeletal Radiol, 23(5):349-352, 1994.


321

INTRODUCTION

Spinal trauma is a frequent cause of perma-nent disability which can often be severe. Thesocial and financial costs involved in treatmentand rehabilitation are substantial, especiallywhen one considers the young age of many ofthose affected. The typical causes of such spinaltrauma include motor vehicle accidents, falls,acts of violence and sports.

Spine traumas warrant early diagnosis in or-der to prevent or restrict spinal marrow dam-age. Conventional radiography, computed to-mography and magnetic resonance imaging areall useful diagnostic instruments and are oftencomplementary in trauma emergencies.

Conventional x-rays, which generally consti-tute the initial diagnostic modality utilized, mayshow the presence of vertebral fractures and/orsubluxations, thereby identifying specific levelsof abnormality allowing a more focused subse-quent analysis. CT enables a particularly de-tailed evaluation of the bony structures underexamination. MRI, however, plays a fundamen-tal diagnostic role as it is the only investigationthat is able to detect spinal cord injury and pro-vide information on the osteoarticular struc-tures, while covering large spinal segments oreven the entire spine. One restriction of MRI,

in addition to the usual contraindications (e.g.,metal clips, pacemakers, etc.), are life supportand vital function monitoring devices used intrauma patients.

PATHOGENESIS

Osteoarticular trauma

The occurrence of vertebral trauma derivesfrom the sum of both internal and external fac-tors. On the one hand, traumatic forces are ap-plied, and on the other there is resistance tothese forces by the bony, muscular and ligamen-tous tissues of the spinal column. Internal vari-ables include the individual’s anatomy, the pres-ence of underlying pathology that reduces os-teoarticular resistance to trauma (e.g., osteo-porosis, spondyloarthrosis, malformations, etc.)and the relative stance of the vertebral columnat the moment of the trauma.

The frequency of vertebral trauma variesconsiderably depending upon the segment ofthe spine in question, this in turn being de-pendent in part on the biomechanical charac-teristics of that level. The more mobile seg-ments of the spine (lumbar, cervical) are morefrequently the sites of trauma, especially in the

5.3

MRI IN EMERGENCY SPINAL TRAUMA CASES

A. Carella, A. Tarantino, P. D’Aprile

transition levels between spinal segments withdiffering mobility (e.g., thoraco-lumbar, cervi-co-thoracic, and cranio-cervical junctions). Thethoracic spine is affected to a lesser degree, be-ing more rigid and supported by the rib cage(2, 11).

Once the above factors have been taken intoaccount, the type of vertebral trauma dependsprincipally on the manner in which the trau-matic force is applied (11, 37). On the basis ofthe vectors of the traumatic force, four mainmechanisms of trauma can be recognized,which are usually seen in combination: com-pression, flexion, extension, rotation. Spinalcolumn trauma can then affect any or all of thebony, articular, ligamentous and muscular tis-sues of the spine.

On an anatomical and pathological basis,vertebral fractures can be categorised as fol-lows (11, 37):

Fractures of the upper (craniad) cervical spine:– fracture of the posterior arch of C1, often

along the sulcus of the vertebral artery– fractures of the anterior and posterior arch-

es of C1 (i.e., Jefferson’s fracture)– fracture of the odontoid process– bilateral fractures of the pedicles of C2 (i.e.,

hangman fracture)

Fractures of the lower (caudal) cervical spine:– anterior compression fractures– fractures of the posterior bony elements– burst fractures

Fractures of the thoracic and lumbar spinal segments:– anterior compression fractures– fractures of the posterior bony elements– burst fractures

These bony fractures can also be associatedwith trauma to the spinal and perispinal soft tis-sues (e.g., spinal ligaments, articular capsules ofthe posterior spinal facet joints, intervertebraldisks, intrinsic spinal muscles). Spinal liga-ments can be subject to rupture, avulsions orstretching. The intervertebral disks can rup-ture, resulting in protrusions, herniations and

extrusions with disk fragment migration, theposterior spinal facet joints can rupture theircapsules and the intrinsic spinal muscles canundergo rupture or avulsion.

Intersegmental subluxation can be ob-served with only very minor underlying bonyinjury and in some cases without bony trauma.The most common mechanism of such dislo-cations is “whiplash”, consisting of two parts:rapid hyperextension followed by rapid hy-perflexion. Types of subluxation include at-lanto-axial rotary dislocation, anterior/poste-rior/lateral spondylolisthesis, and completevertebral dislocation.

Trauma of the central spinal canal contents

Posttraumatic lesions of the contents of thecentral spinal canal can affect the spinal cord,spinal nerves/roots, thecal sac and epi- in-tradural arteries and veins. Spinal cord injuriesrepresent the most severe form of spinal trau-ma. Cord damage may be from direct or sec-ondary effects of the trauma (16). Direct trau-matic lesions are derived from the sudden im-pact of the bone or protruded/extruded inter-vertebral disk material against the spinal cord.In the acute phase, secondary effects such asoedema, lympho-granulocytic infiltration, is-chaemic alterations, formation and accumula-tion of free radicals, extracellular calcium,amino acids, arachidonic acid derivatives willhave damaging effects upon the underlyingcord tissue (17, 19, 23, 25, 34).

Within the first minutes following the trau-matic incident it is possible to observe dramat-ic neuronal alterations and even frank necrosisof neural tissue, and micro- macrohaemor-rhages. Although rare, gross haematomyeliamay develop (21).

Posttraumatic repair processes include thereabsorption of necrotic tissue and haemoglo-bin breakdown products, reactive gliosis andresidual cavity formation, processes that cantake 2-3 years or more (13). Terminal eventstypically are spinal cord atrophy and cysticmyelomalacia (12), a type of focal cavity thatcan evolve into extensive syringomyelia for-


mation (5, 13). In the case of particularly ex-tensive trauma, intramedullary gliosis and ex-tramedullary fibrous scarring may develop,with the formation of subarachnoid adhe-sions (13).

In addition, the spinal nerves and roots canbecome traumatized. The most common occur-rence is radicular compression, which may re-sult from bone or intervertebral disk material.Radicular avulsions are usually caused by theviolent hyperextension of a limb. Most avul-sions involve the cervical nerve roots, usually asa consequence of the forced adduction of theshoulder and arm in motorcycle accidents (2,18). Pseudo-meningocele formation is associat-ed with such avulsions as the meninges are torntogether with the neural tissue.

Finally, epidural haematomas result from thetraumatic rupture of the epidural venous plexi.Because the spinal dura mater is not firmly ad-herent to the vertebral surface, extensivehaematomas traversing multiple levels can de-velop.

SEMEIOTICS

MR investigations in cases of spinal traumabegin with the acquisition of sagittal imagesthat yield an overview with which to select andorient subsequent axial imaging sequences fo-cused on the areas of abnormality. A coronalplane study may also prove to be useful.

A combination of sequences must then beacquired directed toward critically examiningall of the spinal tissues. These include the ac-quisition of sagittal T1-weighted spin-echo(SE) images that provide accurate anatomical-morphological information. This acquisition isfollowed by T2-weighted fast spin echo (FSE)sequences providing good detail and MR signalcharacteristics of the spinal cord and nerveroots (14, 20, 27, 31, 33). One limitation of T2-FSE sequences is the relative absence of fattytissue suppression with persistence of thebright bone marrow fat signal, which can con-ceal the presence of oedema. This limitationcan be overcome by using fat signal suppres-sion techniques (35). Finally, it is imperative to

acquire T2*-weighted gradient recalled echo(GRE) images that are sensitive to the effects ofmagnetic susceptibility and which thereby re-veal the presence of certain haemorrhagicproducts (3, 13, 31). Specifically the GRE se-quences are sensitive to small areas of acutehaemorrhage (e.g., deoxyhaemoglobin), and inthe chronic phase in detecting haemosiderin.

Imaging of the container of the central spinal canal

To some degree, MRI makes it possible to visualize gross bony fractures, disk hernia-tions/extrusions, intersegmental subluxationand certain ligamentous injuries (Figs. 5.8, 5.9).However, subtle fractures, especially those thatare not distracted and those of the posteriorbony elements of the spine, are poorly seen onMRI (3, 4, 13, 24, 32) (Fig. 5.10). Thin fracturelines are better visualized with T2/T2*- weight-ed sequences (Fig. 5.11). In addition, the de-tection of small bony fragments has also beenpartly overcome by the use of T2*-weightedGRE sequences.

It should be pointed out that MRI is uniquein its ability to identify compression fractures ofthe vertebral bodies without gross evidence offracture on conventional radiography. In suchcases, the detection of MRI signal hyperintensi-ty on T2-weighted images and consonant hy-pointensity on T1-weighted sequences indi-cates oedema of the marrow and microfracturesof the trabecular structure of the vertebrae(Fig. 5.12).

One frequently encountered problem is thatof the differentiation between benign posttrau-matic fractures and pathological fractures re-sulting from underlying metastatic neoplasticdisease. Unfortunately, it must be stated thatthere are no absolute differential diagnostic cri-teria that unquestionably confirm metastaticneoplasia on a first imaging study in an individ-ual patient. Sequential follow-up imaging stud-ies may be the only recourse in such cases.

Posttraumatic herniations are similar oridentical to non-traumatic forms (Fig. 5.13). Infact it is usually impossible to distinguish the

5.3 MRI IN EMERGENCY SPINAL TRAUMA CASES 323

posttraumatic degenerative disk herniations.Generally speaking, the presence of other asso-ciated posttraumatic injuries at the same levelsuggests the diagnosis of traumatic disk hernia-tion (7, 13, 15).

Ligamentous trauma can be detected direct-ly or indirectly on medical imaging studies.However, while MRI is capable of visualizingthe spinal ligaments, it may not be able to dif-ferentiate between ruptured ligaments and ad-jacent tissue injury, all of which may be hy-pointense.

Serious vertebral trauma demands an eval-uation of the stability of the spine. This typeof assessment is aimed at recognizing thoseconditions that may require surgical stabiliza-tion in order to prevent secondary damage tothe neural structures. Of the various methodsemployed to evaluate spinal stability, the sim-plest is that of Denis which identifies threefunctional columns of the spine (9, 10): the an-terior column (the anterior longitudinal liga-ment and the anterior 2/3 of the vertebralbody); the middle column (the posterior 1/3of the vertebral body and the posterior longi-tudinal ligament); and the posterior column(the bony and ligamentous structures behindthe posterior longitudinal ligament). Accord-ing to this model, vertebral instability occurswith the loss of integrity of at least two con-tiguous columns.

A more recent method identifies five sepa-rate signs of spinal instability (6): intersegmen-tal vertebral subluxation of more than 2mm;increase in the interlaminar space of more than


Fig. 5.8 - Acute thoracic spine trauma. The MRI images show aburst fracture of the T12 vertebral body, with posterior dis-placement of bony fragments into the central spinal canal andresulting stenosis. There are no visible signal alterations of thespinal cord. [a) Sagittal T1-weighted MRI; b, sagittal T2-weighted MRI; c) axial T2-weighted MRI].

a

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2 mm in relation to the adjacent levels; widen-ing of the joint space of one or more posteriorspinal facet joints; interruption of the posteriorcortical margin of a vertebral body; and in-crease in the interpedicular distance of morethan 2 mm between adjacent vertebrae.


Fig. 5.9 - Acute lumbar spine trauma. The MRI reveals an L2burst fracture with posterior displacement of the upper portionof the vertebral body into the central spinal canal and conse-quent canal stenosis. [a) sagittal T1-weighted MRI; b) sagittalT2-weighted MRI].

Fig. 5.10 - Acute lumbar spine trauma. The MRI images showa burst fracture of the L1 vertebral body with anterior epidur-al tissue within the central spinal canal. The vertebral bonemarrow of L1 is hypointense on T1-weighted acquisitions andhyperintense on T2-weighted images indicating posttraumaticoedema/haemorrhage. The axial MRI T1-weighted imageshows compression of the thecal sac by indeterminate tissue.The supplemental CT examination better demonstrates an in-terruption of the bony cortex of the right posterolateral surfaceof the L1 vertebral body and better characterises the bone frag-ment that is displaced into the central spinal canal. [a, d) sagit-tal T1-weighted MRI; b, c) sagittal, coronal T2-weighted MRI;e) axial CT].

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Imaging of the spinal cord

Unquestionably, MRI is the imaging exami-nation technique of choice in the evaluation ofspinal cord injury (1, 2). In the acute phase, thisfacilitates the identification of those conditionsthat may benefit from emergency surgical treat-ment, while also enabling an immediate prog-nostic judgement to be made. MR examina-tions should aim in particular to detect oedema,

contusions, intramedullary haemorrhage, andspinal cord transection, in addition to deter-mining if cord compression is present (Figs.5.14, 5.15, 5.16).

The study involves the acquisition of sagittalT1-weighted SE and T2-weighted FSE or T2*-GRE images; the acquisition of axial images,preferably utilizing T2*-GRE. FLAIR (fluid at-tenuated inversion recovery) sequences can al-so provide useful information regarding spinalcord injury, due to the high contrast definitionbetween the lesion, normal tissue and CSF (26).

In the acute phase, the spinal cord may ap-pear swollen due to the presence of oedemaand haemorrhage. Spinal cord swelling is easi-ly shown on T1-weighted sequences. Thisswelling is hyperintense on T2-weighted se-quences in relation to the normal cord tissue,an expression of intramedullary oedema (1, 3,4, 6) (Fig. 5.17).

This is defined by several authors asmedullary contusion (16, 22) (Fig. 5.18). Thepresence of haemorrhagic products in thespinal cord injury is termed haemorrhagic con-tusion (Fig. 5.19). As mentioned above, frankintramedullary haemorrhage (i.e., haemato-myelia) may be encountered. In any case, theMR appearance of haemorrhagic productsvaries depending upon the time that haselapsed since the traumatic event, the modifica-tions undergone by the haemoglobin molecules


ce

Fig. 5.10 (cont.).

d


Fig. 5.11 - Acute cervical spine trauma. MRI in a patient withbilateral C2 pedicle fractures (Hangman fracture). a), b) Sagit-tal, axial T2-weighted MRI.

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Fig. 5.12 - Acute thoracic spine hyperflexion trauma. The MRIstudy shows a fracture of the T9-10 vertebrae with anteriorwedging of the vertebral bodies. There is also evidence of oede-ma of the involved vertebral bone marrow. The spinal cord, al-though deflected by posterior displacement of the T9 vertebra,does not show intrinsic signs of MRI signal alteration. [a) sagit-tal T1-weighted MRI; b) c) sagittal, axial T2-weighted MRI].

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present, and the strength of the magnetic field.In the acute phase, deoxyhaemoglobin yields ahypointense signal on T2-, and even morestrongly, on T2*-GRE sequences. A week ormore after the trauma, the transformation of

the deoxyhaemoglobin into methaemoglobinchanges the signal to hyperintense on T1- andT2-weighted acquisitions. It should be notedthat the evolution times of the various speciesof the haemoglobin molecule are slower than in


Fig. 5.13 - Acute cervical spine trauma. The images show aposttraumatic C4-C5 disk herniation and anterior subluxationof C4 on C5, with minor impingement upon the anterior sur-face of the cervical spinal cord. A minor C4 compression frac-ture is also noted. a) Sagittal T1-weighted MRI; b) sagittal T2-weighted MRI.

Fig. 5.14 - Acute cervical spine trauma. Identified is a burstfracture of C6 and with associated narrowing of the centralspinal canal and cervical spinal cord compression. Note the hy-perintensity of the spinal cord on the T2-weighted images indi-cating contusion. [a) sagittal T1-weighted MRI; b) sagittal T2-weighted MRI].

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Fig. 5.15 - Acute thoracic spine trauma. The MRI imagesdemonstrate a T11-12 fracture-subluxation. In addition, thecentral spinal canal is narrowed, and there is an anteriorepidural haematoma at the T11 level. The thoracic spinal cordis hyperintense on T2-weighted imaging at the T11-12 levelscompatible with oedema/contusion. The MRI re-evaluationfollowing surgical fixation and stabilisation shows good inter-vertebral realignment and a reduction of the spinal cord de-flection-compression (note the metallic artefact). [a) Sagittalproton density (PD)-weighted MRI; b) sagittal T2-weightedMRI; c) sagittal T1-weighted MRI; d) postoperative sagittalT1weighted MRI; e) postoperative sagittal T2*-weighted MRI].

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Fig. 5.16 - Acute cervical spine flexion trauma. The MRI ex-amination shows anterior dislocation of C6-C7 associated withmarked stenosis of the central spinal canal. The spinal cord isseverely compressed at this level, revealing oedema andswelling of the cord above and below the compression. [a)sagittal T1-weighted MRI; b) sagittal T2-weighted MRI].

Fig. 5.17 - Acute cervical spine trauma. The MRI images revealstraightening of the physiologic cervical lordotic sagittal spinalcurvature. In addition, there is a compression fracture of the C6vertebral body. The spinal cord is swollen and is hyperintenseon T2*-weighted MRI due to oedema associated with cord con-tusion, but no evidence of acute haemorrhage can be identified.[a) sagittal T1-weighted MRI; b) Sagittal T2*-weighted MRI].

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Fig. 5.18 - Acute cervical spine trauma. The MRI examinationshows a loss of the physiologic cervical lordotic sagittal spinalcurvature and pre-existent central spinal canal stenosis. A focalarea of spinal cord contusion (i.e., oedema and swelling) can beseen on the right side at the C4 level as well as a presumed trau-matic posterior disk herniation associated with underlyingspinal cord compression. [a, sagittal T2-weighted MRI; b) axi-al T2-weighted MRI].

Fig. 5.19 - Acute thoracic spine trauma. The MRI acquisitionsreveal a compression fracture of the body of T12 associatedwith T12-L1 anterior subluxation and central spinal canal nar-rowing. In addition, there is a small anterior epiduralhaematoma at T11. MRI signal hypointensity is present withinthe spinal cord on the T2* acquisition due to acute haemor-rhagic contusion (deoxyhaemoglobin). a) [sagittal T1-weightedMRI; b) sagittal T2*-weighted MRI].

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the brain due to the reduced oxygen tension inthe spinal cord (16). In the chronic phase, thepresence of haemosiderin in the macrophagescauses a marked signal hypointensity on T2-/T2*-weighted sequences.

The spinal cord is often more easily assessedin the sagittal plane due to the simplicity of de-termining an alteration in the continuity anduniformity of the medullary MR signal alongthe longitudinal axis of the cord. Axial and


Fig. 5.20 - Chronic spinal cord trauma. MRI images in a case oflate follow up of a burst fracture of L1 revealing diffuse spinalcord atrophy and a focal area of myelomalacia within the conusmedullaris. [a) sagittal T1-weighted MRI; b) sagittal T2-weighted MRI].

Fig. 5.21 - Chronic spinal cord trauma. MRI in the chronicphase following spinal cord trauma reveals a posttraumatic sy-ringomyelia cavity extending from C6-T1. [a) sagittal T1-weighted MRI; b) sagittal T2-weighted MRI, c) axial T2-weighted MRI].

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coronal images will help to clarify the complextraumatic changes. Multiplanar imaging is alsooften helpful in cases of spinal cord lacerations.

Sequelae of spinal cord trauma include cordatrophy, localized non-cystic and cystic myelo-

malacia and frank syringomyelia formation, thelatter of which may be progressive. Spinal cordatrophy appears as a reduction in the calibre ofthe cord both at the level of trauma as well ascaudally. Non-cystic/cystic myelomalacia ap-pears as an area that is hyperintense on T2-weighted images in the chronic phase followingtrauma. This alteration is often poorly visual-ized if at all on T1-weighted sequences, and isassociated with cord atrophy (Fig. 5.20). Sy-ringomyelia is easily demonstrated on both T1-and T2-weighted sequences, may be well de-


Fig. 5.21 (cont).

Fig. 5.22 - Chronic spinal cord trauma. MRI examination sev-eral years following flexion injury and spinal cord contusionshows postsurgical changes and a multisegmental syringohy-dromyelia cavity of the lower thoracic spinal cord. [a) sagittalT1-weighted MRI; b sagittal T2-weighted MRI, c) axial T2-weighted MRI].

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marcated and is associated with expansion ofthe spinal cord (Figs. 5.21, 5.22).

It is important to point out that in some pa-tients with posttraumatic neurological deficitsrelated to the spinal cord MRI of the spinalcord can be completely negative in the acutephase. These are usually transitory clinicaldeficits usually encountered in adult subjects,which regress completely in the first few hoursafter the injury. This syndrome, sometimesknown as SCIWORA (spinal cord injurieswithout radiological abnormalities) originatedduring the conventional radiographic era; cur-rently, with the advent of MRI the acronym hasbecome known by some as SCIWMRA (spinalcord injuries without magnetic resonance ab-normalities) (2, 7, 30). The transient syndromecan be explained by the mechanisms of stretch-ing or temporary compression of the spinalcord during the traumatic event, resulting in atype of spinal cord “concussion”, analogous tocerebral concussion. An association between

this clinical syndrome and severe degrees ofpreexisting cervical spondylosis and thereforecentral spinal canal stenosis has been estab-lished (30).

In cases of posttraumatic epidural haematoma,as mentioed above, the MR signal varies accord-ing to the oxidation state of the haemoglobinmolecules and the strength of the magnetic fieldof the MR unit (Figs. 5.15, 5.23). In the acutephase, extradural collections are isointense ascompared to the spinal cord on T1-weighted im-ages and isointense with regard to CSF on T2-weighted sequences. The IV administration ofgadolinium can be useful in some cases for bet-ter demarcating the enhancing peripheral rim ofthe haematoma (26).

Root avulsions are traditionally diagnosedusing myelography and CT myelography. Atthe levels of the avulsion, the associated pseu-do-meningocele is filled by the intrathecalcontrast medium used for the myelogram.However MRI is also able to identify thepseudo-meningocele, demonstrating hyperin-tensity of the intra- perispinal cavity on T2-weighted sequences. In some cases MRI withgadolinium can also document the interrupt-ed nerve roots, in particular at the pointwhere the root is partially-completely avulsed,an expression of blood-nerve barrier disrup-tion (18). Although not universally approved,the most recent myelographic MR techniquesare potentially capable of replacing conven-tional invasive myelography in many or all ofits applications (8).

REFERENCES

1. Beers GJ, Raque GH, Wagner GG et al: MRI imaging inacute cervical spine trauma. J CAT 12(5):755-761, 1988.

2. Beltramello A, Piovan E, Alessandrini F et al: Diagnosi neu-roradiologica dei traumi spinali. In Dal Pozzo G, SyllabusXV congresso nazionale AINR. Centauro, Bologna: 11-18,1998.

3. Carella A, D’Aprile P, Farchi G: Reperti RM nei traumivertebro-midollari. Studio con tecniche di acquisizionecon eco di gradiente. Rivista di Neuroradiologia 3:45-55,1990.

4. Chakeres DW, Flickinger F, Bresnahan JC et al: MRI Ima-ging of acute spinal cord trauma. AJNR 8(1):5-10, 1987

5. Curati WL, Kingsley DPE, Kendall BE et al: MRI in chro-nic spinal cord trauma. Neuroradiology 35:30-35, 1992.


Fig. 5.23 - Acute spinal trauma. Sagittal T1-weighted MRI re-veals anterior C4-C5 subluxation associated with a multilevelanterior epidural haematoma deflecting the spinal cord poste-riorly.

6. Daffner RH, Deeb ZL, Goldeberg AL et al: The radiologi-cal assessment of post-traumatic vertebral stability. SkeletalRadiology 19:103-108, 1990.

7. Davis SJ, Teresi LM, Bradley WG et al: Cervical spine hy-perextension injuries: MRI findings. Radiology 180(1):245-251, 1991.

8. Demaerel P, Van Hover P, Broeders A et al: Rapid lumbarspine MR mielography: imaging findings using a single-shottechnique. Rivista di Neuroradiologia 10:181-187, 1997.

9. Denis F: The three column spine and its significance in theclassification of acute thoraco-lumbar spinal injuries. Spine8:817-831, 1983.

10. Denis F: Spinal instability as defined by the three-columnspine concept in acute spinal trauma. Clin Orthop 189:65-76, 1984.

11. Faccioli F: La biomeccanica del trauma vertebro-midollare.In: Dal Pozzo G, Syllabus XV congresso nazionale AINR.Centauro, Bologna: 7-10, 1998.

12. Falcone S, Quencer RM, Green BA et al.: Progressive post-traumatic myelomalacic myelopathy. AJNR 15:747-754,1994.

13. Flanders AE, Croul SE: Spinal trauma. In: Atlas SW: Ma-gnetic resonance imaging of the brain and spine. 2° edition.Lippincott-Raven: 1161-1206, 1996.

14. Flanders AE, Tartaglino LM, Friedman DP et al: Applica-tion of fast spin-echo MRI imaging in acute cervical spineinjury. Radiology 185(P):220,1992.

15. Goldberg AL, Rothfus WE, Deeb ZL et al: The impact ofmagnetic resonance on the diagnostic evaluation of acutecervico-thoracic spinal trauma. Skeletal Radiol 17(2):89-95,1988.

16. Hackney DB, Asato LR, Joseph P et al: Hemorrhage andedema in acute spinal cord compression: demonstration byMRI imaging. Radiology 161:387-390, 1986.

17. Hall ED, Braughler JM: Central nervous system trauma andstroke. II. Physiological and pharmacological evidence forinvolvement of oxygen radicals and lipid peroxidation.Free Radical Biol Med 6:303-313, 1989.

18. Hayashi N, Yamamoto S, Okubo T et al: Avulsion injury ofcervical nerve roots: enhanced intradural nerve roots at MRImaging. Radiology 206:817-822, 1998.

19. Janssen L, Hansebout RR: Pathogenesis of spinal cordinjury and newer treatments. A review Spine 14:23-32,1989.

20. Jones KM, Mulkern RV, Schwartz RB et al: Fast spin-echoMR Imaging of the brain and spine: current concepts. AJR158:1313-1320, 1992.

21. Kakulas BA: Pathology of spinal injuries. CNS Trauma1:117-129, 1984.

22. Kalfas I, Wilberger J, Goldberg A et al: Magnetic resonan-ce imaging in acute spinal cord trauma. Neurosurgery23(3):295-299, 1988.

23. Kwo S, Young W, De Crescito V: Spinal cord sodium, po-tassium, calcium and water concentration changes in ratsafter graded contusion injury. J Neurotrauma 6:13-24,1989.

24. Levitt MA, Flanders AE: Diagnostic capabilities of magne-tic resonance and computed tomography in acute cervicalspinal column injury. Am J Emerg Med 9(2):131-135, 1991.

25. Meldrum B: Possible therapeutic applications of anthago-nists of excitatory aminoacid neurotransmitters. Clin Sci68:113-122, 1985.

26. Pellicanò G, Cellerini M, Del Seppia I: Spinal trauma. Rivi-sta di Neuroradiologia 11:329-335, 1998.

27. Posse S, Aue WP: Susceptibility artifacts in spin-echo andgradient-echo imaging. J Magn Reson 88:473-492, 1990

28. Quencer RM, Sheldon JJ, MJD et al: MRI of the chronical-ly injured cervical spinal cord. AJR 147:125-132, 1986.

29. Ramon S, Dominguez R, Ramirez L et al: Clinical and ma-gnetic resonance imaging correlation in acute spinal cordinjury. Spinal Cord 35:664-673, 1997.

30. Rogenbogen VS, Rogers LF, Atlas SW et al: Cervical spinalcord injuries in patients with cervical spondylosis. Am J Ra-diol 146:277-284, 1986.

31. Scarabino T, Polonara G, Perfetto F et al: Studio RM FastSpin-Echo dei traumi vertebro-midollari acuti. Rivista diNeuroradiologia 9:565-571, 1996.

32. Tarr RW, Drolshagen LF, Kerner TC et al: MRI Imaging ofrecent spinal trauma. J CAT 11(3):412-417, 1987.

33. Tartaglino LM, Flanders AE, Vinitski S et al: Metallic arti-facts on MRI images of the postoperative spine: reductionwith fast spin echo techniques. Radiology 190:565-569,1994.

34. Tator CH, Fehlindgs MJ: Review of the secondary injurytheory of acute spinal cord trauma with emphasis on va-scular mechanisms. J Neurosurg 75:15-26, 1991.

35. Tien RD: Fat suppression MR imaging in neuroradiology:techniques and clinical application. Am J Roentgenol158:369-379, 1992.

36. Weirich SD, Cotler HB, Narayana PA et al: Histopatholo-gic correlation of magnetic resonance signal patterns in aspinal cord injury model. Spine 15(7):630-638, 1990.

37. White AA, Panjabi MM: Clinical biomechanics of the spi-ne. PA JB Lippincott, Philadelphia: 169-275, 1990.


337

INTRODUCTION

Non-traumatic spinal emergencies includeall those clinical situations that present withacute and/or rapidly progressive signs andsymptoms of spinal cord-spinal nerve/rootcompromise. These can be a result of extrinsicspinal radiculomedullary compression or of in-trinsic pathology.

All of these conditions require rapid diag-nostic analysis: the recognition of a compres-sive or expanding spinal cord-canal lesionmakes it possible to determine a surgical solu-tion, whereas its exclusion guides diagnosis andtreatment in other directions. The main causesof non-traumatic acute and subacute myelo-pathic and/or radiculopathic syndromes aregiven in Table 1.

IMAGING TECHNIQUES

Worsening acute and/or subacute radicu-lomedullary compression constitutes the mostfrequent cause of non-traumatic spinal emer-gency. In the case of rapid onset of a severe neu-rological syndrome (e.g., sudden paraplegia),diagnostic imaging must be conducted as rapid-

ly as possible in order to proceed swiftly withsurgical decompression if deemed appropriate.

Conventional radiography makes it possibleto analyse the entire spine in a very short inter-

5.4

EMERGENCY IMAGING OF THE SPINE IN THE NON-TRAUMA PATIENT

G. Polonara, M.G. Bonetti, T. Scarabino, U. Salvolini

EXTRADURAL PATHOLOGYVertebrodiscal pathology: – vertebral metastases

– disk herniation– severe spondylosis and arthrosis– haemolymphopathies– benign tumours– primitive malignant tumours– spondylodiskitis

Epidural pathology: – lymphoma– metastasis– haematoma– arachnoid cyst

INTRADURAL PATHOLOGYExtramedullary intradural tumoursSpinal cord tumoursMultiple sclerosisSpinal cord infarctsSpinal cord arteriovenous malformationsSpinal arteriovenous fistulaeDural arteriovenous fistulaeCavernous angiomaMyelitis and spinal cord abscessesAcute disseminated encephalomyelitisRadiation myelopathy

Tab. 5.1 - Causative factors of emergency non-traumatic clini-cal spinal syndromes.

val of time, highlighting abnormalities in thephysiological curvature, bony spinal canalstenoses, vertebral collapse and other structur-al alterations. A negative x-ray examination,however, does not exclude the presence ofbony, intervertebral disk or ligamentouspathology and in any case it does not provideinformation, except very rarely, on the presenceof the pathology affecting the contents of thecentral spinal canal.

Today, almost all patients with acute syn-dromes of neurological radiculomedullary im-pairment can be rapidly sent to a diagnostic cen-tre where MRI equipment is available even with-out the delay entailed in an initial conventionalx-ray examination. MRI is currently the mostsensitive and specific technique available forstudying the spine. This methodology makes itpossible to acquire images in various spatialplanes without having to move the patient. Itclearly enables the visualization of the spinal col-umn (vertebrae, disks, ligaments and paraverte-bral soft tissues) and its contents (epidural space,thecal sac, spinal cord and roots/nerves) in a di-rect, thorough and panoramic way. In additionto establishing the focus of the lesion and the ex-tent of the process, the nature of the conditioncan often be surmised.

Although the cortical bone is best studiedusing x-rays and computed tomography, MRI isthe method of choice in studying vertebralbone marrow. In selected cases, a CT examina-tion focused on a precise location identified us-ing MRI can be a useful complement in non-traumatic radiculomedullary syndromes due tothe greater contrast resolution of bone achievedwith CT.

Myelography is rarely used in those caseswhere the usual exclusions of MRI exist (e.g.,pacemakers, MRI-incompatible metal surgicalcerebral aneurysm clips). In such cases it isused to search for indirect signs of non-osseouscauses of compression of the thecal sac and underlying spinal cord/cauda equina. Bonescintigraphy can be useful for a non-specificanalysis of possible active lesions in the skele-ton as a whole. In selected cases it can also beuseful in studying pathology limited to thespinal column.

CAUSES

In this section, the most frequent causes ofnon-traumatic spinal emergencies will be con-sidered, making a distinction between extradur-al (pathology affecting the vertebrae, interverte-bral disks, spinal ligaments and epidural space)and thecal sac, intradural-extramedullary andneural pathology (disease of the meninges, sub-arachnoid space, spinal cord and/or spinalnerves/roots).

EXTRADURAL PATHOLOGY

Back pain is the most frequent symptom ofepidural pathology. Signs and symptoms ofspinal cord and/or radicular involvement areprecipitated by pathological conditions thatprimarily affect the bony structures of thespinal column, with or without the collapse ofthe vertebrae at the site of the pathology. Thisis in turn followed by extraosseous involvementof the central spinal canal and neural foraminaand the subsequent onset of myelopathic andradiculopathic compression syndromes.

The pathogenesis of vertebral collapse canbe benign (e.g., osteoporosis, vertebral hae-mangiomas, spondylodiskitis) or malignant(e.g., primary or metastatic neoplastic dis-ease). Symptomatic vertebral collapse is mostoften caused by neoplastic metastases, haema-tological/lymphatic neoplastic conditions (i.e.,haemolymphopathies) and spondylodiskitis.All of these can be responsible for radicu-lomedullary compression even without verte-bral collapse due to extraosseous neoplastic orinflammatory mass-forming collections.

In some instances MRI makes it possible todistinguish between benign and malignantspinal column collapse, and it is also the mostsensitive method of identifying the overlyingspinal cord involvement in cases of extraduralpathology.

Spinal neoplasia and haemolymphopathies

Spinal neoplasia can be primary (benign 10%,malignant 10%), or secondary (metastases 80%).


Up to 5% of patients with known neoplasticconditions have symptomatic spinal metastases.

The most common type of primary “tumour”of a vascular nature affecting the spine is verte-bral haemangioma (Fig. 5.24), benign lesionsthat are usually discovered incidentally. They canaffect any part of the spine, however the thora-columbar spine is the most frequent site. Hae-mangiomas usually only affect the vertebralbody, but can also involve the posterior bonyarch and spread into the perivertebral soft tis-sues, thereby potentially causing neural com-pression syndromes (Fig. 5.25).

CT typically reveals a diminution in numberbut thickening of the individual trabeculae

within the affected vertebral marrow space.However, in certain cases it can be difficult todifferentiate these benign vascular lesions fromtrue neoplasia on the basis on CT alone.

On MR examinations using T1-weighted se-quences, haemangiomas have an irregular ap-pearance due to the simultaneous presence ofhyperintense areas (adipose tissue) and hy-pointense areas (thickened bony trabeculae).On T2-weighted images they appear generallyhyperintense due to their high cellularity andperhaps the collection of blood within the hae-mangioma itself.

Some rarer forms of benign tumour includeosteochondromas, osteoid osteomas, osteoblas-

5.4 EMERGENCY IMAGING OF THE SPINE IN THE NON-TRAUMA PATIENT 339

Fig. 5.24 - Vertebral haemangioma. The lateral radiographic examination shows the typical vertical striations consistent with a bonemarrow haemangioma at the L3 level. The T1-weighted MRI reveals bone marrow hyperintensity typical of vertebral haemangioma.[a) Lateral radiograph of lumbar spine; b) sagittal T-1 weighted MRI].

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Fig. 5.25 - Metameric haemangioma. The MRI examination shows a haemangioma involving of the T3 vertebral body, the peduncles,the articular processes, the posterior arch and the posterior epidural space with minor compression of the thecal sack and spinal cord.The internal vascular component of the haemangioma is observed to enhance following IV gadolinium (Gd) administration. [a), b)sagittal T2-weighted MRI; c) unenhanced sagittal T2-weighted MRI; d) sagittal T1-weighted MRI following IV Gd; e) axial T1-weighted MRI following IV Gd].

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tomas (Fig. 5.26) and aneurysmal bone cysts, allof which are clearly visualized on both radi-ographs and CT (7).

Rare malignant primary tumours include os-teosarcomas (including those presenting as amalignant degeneration of Paget’s disease ofthe spine), chondrosarcomas, Ewing’s sarco-mas, and fibrosarcomas. Chordomas, having anintermediate histological status between benignand malignant, originate from elements of thenotochord and are particularly common in thesphenoid bone, the clivus and the sacrum. Inthese cases MR is the best imaging techniquefor defining the extent of the tumour within thespine as well as determining the involvement ofthe perispinal soft tissues.

Undoubtedly the most frequent type of neo-plastic spinal involvement is haematogenouslyborne metastatic disease, which replaces thebone marrow tissue and destroys the bony cor-tex of the vertebrae. Statistically, 10% of casesof metastatic neoplastic disease affect the cervi-cal spine, 77% the thoracic and upper lumbarlevels and 13% involve the lumbar and sacralsegments. The vertebral body is more frequent-ly involved than are the posterior bony ele-ments, with the exception of the vertebral pedi-

cles which are often affected. Epidural metasta-tic disease is often present, either secondary toprimary disease, or in some cases as the solespinal location.

In most cases bony spinal metastatic diseasehas an osteolytic appearance on x-ray and CTimaging, however depending upon the histo-logical type, it may be sclerotic or mixed lytic-sclerotic.

Metastatic replacement of the bone marrowis clearly visible on MRI. Destructive lesionsdemonstrate areas of relative hypointensity onT1-weighted imaging and comparative hyperin-tensity on T2* STIR/chemical saturation fat-suppressed and T2-weighted sequences (Fig.5.27). The presence and extent of the tumourin the spinal canal and the perivertebral tissuesis well documented after the administration ofIV gadolinium contrast medium on T1-weight-ed images, especially when combined with fat-suppression techniques.

On MRI, an appearance similar to that de-scribed for metastases can be observed in cas-es of vertebral lymphoma, multiple myelomaand plasmocytoma affecting the spine (Fig.5.28). Lymphomas, like metastatic neoplasticdisease, can also have a solely epidural local-ization.

Infectious processes involving the spine

The early diagnosis of vertebral osteomyelitis,diskitis or epidural abscess formation bymeans of medical imaging (Fig. 5.29) facili-tates suitable treatment to be instituted rapid-ly, even though the clinical signs, symptomsand laboratory tests are frequently not specif-ic (10). In cases of spondylodiskitis, 2-8 weekscan elapse from the onset of clinical symptomsuntil visible signs are present on conventionalradiographic studies. These findings can in-clude a reduction in the height of the interver-tebral disk space, alterations in the vertebralend plates (e.g., erosion, blurring of margins,reactive bony sclerosis) and the presence of anextraosseous paravertebral soft tissue mass.The vertebral bodies can variably be de-stroyed, however the pedicles are rarely in-


Fig. 5.25 (cont.).

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volved in cases of infection, with the excep-tion of spinal tuberculosis.

CT, preferably performed after the IV ad-ministration of iodinated contrast medium, typ-ically reveals the existence of a mass in theperivertebral soft tissues and epidural space,and the fragmentation and destruction of verte-brae.

On MRI, spondylodiskitis has a character-istic appearance that includes the involve-ment of the two contiguous vertebrae (hy-pointense marrow signal on T1-weighted im-ages; hyperintense marrow signal on T2-weighted sequences) and the intervening in-tervertebral disk (reduction of height of disk

space; hyperintense signal on T2-weightedimages) (Fig. 5.30). In addition, MRI demon-strates bony erosions of the vertebral endplates, inflammatory epidural and periverte-bral soft tissue masses and semifluid abscesscollections (Fig. 5.31). Postcontrast imagesacquired with fat suppression are most sensi-tive in defining the extent of the complex in-flammatory processes.

It should be noted that while spinal metasta-tic neoplasia reveals signal alteration of the ver-tebrae similar to those described for spondy-lodiskitis, involvement of the adjacent interver-tebral disk and adjacent vertebral end plates isnot present.


Fig. 5.26 - Osteoblastoma of the posterior arch of C5. The MRIexamination reveals a hypointense lesion within the posteriorarch of C5 on the right. The CT study shows a sclerotic masslesion of the posterior arch of C5. [a) oblique-sagittal T1-weighted MRI; b) axial T1-weighted MRI; c) axial CT].

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OTHER TYPES

Extradural pathology

The differential diagnosis of acute clinicalradiculomedullary syndromes must also takeinto consideration other types of pathology (10,12), including: posterior spinal facet joint andinterspinous spondylosis (Fig. 5.32); disk hernia-tions-protrusions; osteopenic-osteoporotic verte-


Fig. 5.27 - Multiple vertebral neoplastic metastases from primarycolon cancer. The MRI examination shows partial collapse and ex-pansion of the L1 vertebral body and the presence of an epiduralsoft tissue mass that compresses the thecal sac, the conusmedullaris and the roots of the cauda equina. In addition, there isneoplastic involvement of T11, L5 and the adjacent perispinal softtissues. [a) sagittal T2-weighted MRI; b), c) sagittal T1-weightedMRI; d), e) axial T1-weighted MRI; f) coronal T2-weighted MRI].

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bral collapse; osteonecrosis; and developmentalspinal malformations especially at the cervico-occipital junction (Fig. 5.33).

The high contrast resolution of MRI regard-ing soft tissues enables a straightforward evalu-ation of degenerative/protrusive intervertebraldisk pathology. T2-weighted images acquired inthe sagittal plane characterize such degenerative


Fig. 5.27 (cont.).

Fig. 5.28 - Vertebral plasmocytoma. The MRI examination thesagittal picture clearly shows the expansion and partial collapseof the T9 vertebral body with associated invasion of the par-avertebral and epidural soft tissues. [a) sagittal T1-weightedMRI; b) axial T1-weighted].

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alterations thanks partly to the “myelographiceffect” of the high CSF signal. Spinal cord com-pression, with or without parenchymal oedema,

is also well visualised on sagittal T2-weighted se-quences; these alterations are generally less eas-ily visible on axial T2-weighted images. T1-


Fig. 5.29 - Iatrogenic epidural abscess. The MRI study shows a mass forming posterior epidural lesion that displaces the nerve roots of thecauda equina forwards. There is inhomogeneous enhancement of this process following IV Gd administration. [a) sagittal T2-weighted MRI;b) unenhanced sagittal T1-weighted MRI; c) sagittal T1-weighted MRI following IV Gd; d) coronal T1-weighted MRI following IV Gd].

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weighted acquisitions, that provide greater visi-bility of epidural and neural foramen fat, furtherassist in the diagnostic evaluation in the thoracicand lumbar regions. Finally, MR myelographyutilizing T2-wieghted sequences can facilitateevaluating the presence or absence of a radicu-lar compression.

Of the causes of compression emanating di-rectly from the epidural space, spontaneoushaematomas (Fig. 5.34), and extradural arachnoidcysts should be considered. Epidural haematomaswill typically demonstrate no other related find-ings on imaging studies; the MRI characteristicswill be the same as those previously described foracute-subacute spinal haematomas. CT and MRexaminations in cases of arachnoid cyst revealsmooth bony erosion, including: widening of thecentral spinal canal, pedicle erosion, widening ofthe affected neural foramen and erosion of the ad-jacent surfaces of the vertebral body. MRI showsan expanding lesion having signal similar or iden-tical to that of CSF. Signs indicating an extradur-al nature of the cyst are cranial and caudal dis-placement of the adjacent epidural fat, anteriordisplacement of the subarachnoid space and thespinal cord and extension into the neural foramen(8, 10) (Fig. 5.35).

Intradural pathology

In cases of extramedullary masses, radicularsymptoms usually precede medullary ones, theyare segmental and can be sensory and/or motor.Intramedullary masses most often present withnon-specific, gradual, progressive signs andsymptoms; pain may be the first symptom. Sen-sory deficits vary according to the location ofthe lesion. Bladder and bowel dysfunction andimpotence are rare and appear late in the clini-cal course (1).


Fig. 5.30 - Spondylodiskitis. The MRI examination demon-strates a pathologic process effecting simultaneous involvementof multiple thoracic vertebrae together with the intervening in-tervertebral disks. In addition, there is associated disk and ver-tebral collapse, perivertebral and epidural soft tissue mass for-mation and spinal cord compression. These findings are con-sistent with nonspecific spondylodiskitis. [a) coronal T1-weighted MRI; coronal T2-weighted MRI; unenhanced sagittalT1-weighted MRI; sagittal T1-weighted MRI following IV Gd].

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In the cases of intradural masses, x-rays mayshow a straightening of the physiological curva-ture of the spine or even progressive scoliosis.Especially in children with congenital in-tramedullary tumours, widening of the centralspinal canal and thinning of the pedicles maybe observed.

Myelography is rarely indicated, except insubjects where MRI is contraindicated or un-available, or when MRI is not diagnostic, aswhen small neurinomas, vascular malforma-tions and arachnoid lesions are suspected.

CT is not particularly helpful in these situa-tions and should principally be reserved for os-teoarticular pathology of the spinal column andfollowing myelography.

Spinal angiography is indicated in the exam-ination of vascular malformations and neopla-sia as a preliminary stage for interventional ra-diology procedures and in preoperative evalua-tion.

MR is the examination technique of choicefor imaging the subarachnoid space and thespinal cord, and should be the first study to beperformed where available. The examinationshould include T1- and T2-weighted images,and T1-weighted images after the IV adminis-tration of gadolinium. The entire spine can beexamined using dedicated phased-array surfacecoils. The images must be acquired in at leasttwo different scan planes in order to clearly define the lesion in three planes and to assist inthe differentiation between intra- and ex-tramedullary masses.

Neoplasia and non-neoplastic mass forming processes

The most frequent types of intradural ex-tramedullary neoplasia are meningiomas andneurinomas (1). Meningiomas are benign tu-mours that originate in the arachnoid mater, oc-cur more frequently in females in the fifthdecade of life and exert effects via mass effect.They are most often encountered in the tho-


Fig. 5.30 (cont.).

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racic spine. Only rarely are they multiple in thespine, and very seldom have large extraduralcomponents.

From a diagnostic imaging point of view,on x-rays it is only rarely possible to observecalcifications or signs of vertebral remodel-ling. Myelographic signs are indirect, typi-cally appearing as an obstruction of flow ofthe subarachnoid contrast medium, typical ofextramedullary intradural lesions, with asso-ciated displacement and compression of thespinal cord. On CT, meningiomas can be dis-tinguished from the surrounding anatomicalstructures by their intrinsic hyperdensity rel-ative to the spinal cord, calcifications whenpresent and dense enhancement followingthe IV administration of iodinated contrastmedium.

On MRI, meningiomas may have a similarintensity to spinal cord. Their identification isfacilitated by the use of heavily T2-weighted se-quences, and the administration of IV gadolin-ium contrast medium. Meningiomas typicallyreveal an intense, homogeneous pattern of en-hancement after the gadolinium injection (Fig.5.36).


Fig. 5.31 - Subacute spondylodiskitis caused by brucella species.The MRI study shows a simultaneous pathologic involvement oftwo adjacent vertebrae and the intervening intervertebral disk.There is irregular contrast enhancement in all involved struc-tures following IV Gd administration. The perivertebral soft tis-sues demonstrate limited involvement. [a) unenhanced sagittalT1-weighted MRI; b) sagittal T1-weighted MRI following IVGd; c) coronal T1-weighted MRI following IV Gd].

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Neurinomas originate from Schwann cellsand favour the posterior spinal nerve rootsas sites of origin. They are more frequentlyobserved at cervical and thoracic spinal lo-cations, but can involve the roots of the cauda equina. These neoplasms can be mul-tiple in Recklinghausen’s disease (Fig. 5.37).Neurinomas present in an intradural-ex-tramedullary location, can extend into theneural foramen and even grow outside thespinal canal (i.e., hourglass-shaped mass). Insuch cases on x-rays it is possible to observewidening of the neural foramen and, if suf-ficiently large, the presence of a paraverte-bral mass. If voluminous, neurinomas can al-

so cause scalloping of the posterior wall ofthe vertebral body(ies).

Concerning the intradural component ofthe neurinoma, myelography provides typicalfindings of spinal cord displacement andcompression, and cup-shaped blockage ofthe contrast medium by the neoplasm; myel-ography provides no information on the ex-tradural component of the lesion. CT fol-lowing the myelogram, however, reveals theentire extent of the tumour together with thebony remodelling when present. Neurinomasgenerally show heterogeneous enhancementon CT after IV iodinated contrast mediumadministration.


Fig. 5.32 - Spondylotic myelopathy. Multilevel degenerative discovertebral alterations result in central spinal canal stenosis and asso-ciated cervical spinal cord compression. In addition, a focal area of hyperintense MRI signal is observed on the T2-weighted image atthe C5 level consistent with myelomalacia. [a) sagittal T1-weighted MRI; (b) sagittal T2-weighted MRI].

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Fig. 5.33 - Os odontoideum. The MRI images show anterior subluxation of the C1 vertebral body and adjacent odontoid process inrelationship to the vertebral body of C2. In addition, the spinal cord is compressed between the posterior bony arch of C1 and thevertebral body of C2, and the intervening spinal cord is hyperintense indicating underlying myelomalacia. Note the partial reductionof the dislocation in extension. [a): neutral T1- and T2-weighted sagittal MRI; b): flexion T1- and T2-weighted sagittal MRI; c): ex-tension T1- and T2-weighted sagittal MRI].

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Unenhanced MRI provides all the diagnosticinformation outlined above.

The rarer mass-forming lesions of the sub-arachnoid space include (in decreasing order of

frequency) lipomas (most often associated withcongenital dysraphic conditions), teratomas,and subarachnoid metastases (Fig. 5.38) thatare typically multiple and widespread, fre-


Fig. 5.34 - Spontaneous subacute epidural haemorrhage in patient with plasmacytopenia. The MRI examination shows mass formingposterior epidural haematoma. IV Gd enhanced MRI shows minor peripheral enhancement around the haematoma. The remainingMRI study reveals hypointensity of the margins of the haematoma consistent with early haemosiderin evolution and anterior spinalcord deflection-compression. [a) unenhanced sagittal T1-weighted MRI; b) T1-weighted MRI following IV Gd; c) T2-weighted MRI;d) sagittal T2-weighted MRI with fat suppression; e) axial T1-weighted MRI; (f) axial T2-weighted MRI].

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quently covering the leptomeningeal surfacesof the spinal subarachnoid space (Fig. 5.39). Allthese pathological conditions are well docu-mented using MRI. CT is excellent in docu-menting adipose tissue and, unlike MRI, is ableto demonstrate tumour calcifications present insome neoplasms (e.g., teratomas).

MRI is also the best non-invasive technique fordocumenting non-neoplastic expanding processes,


Fig. 5.34 (cont.).

Fig. 5.35 - Extradural arachnoid cysts. The MRI images show aposterolateral intraspinal mass lesion that has an MRI signalthat is slightly higher than that of CSF. There is associated cra-nial and caudal displacement of the supra- and subjacentepidural fat surrounding the mass indicating its epidural loca-tion. There is also minor mass effect upon the thecal sac and ex-tension of the cyst into the contiguous, expanded spinal neuralforamen. [a) midline sagittal T2-weighted MRI; b) parasagittalT2-weighted MRI; c) midline T1-weighted MRI; d) coronal T1-weighted MRI; e) midlesion axial T2-weighted MRI; f) subja-cent axial T2-weighted MRI].

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including intradural arachnoid cysts and lateralspinal meningoceles (associated with von Reck-linghausen’s disease).

The most frequently encountered in-tramedullary neoplasms are astrocytomas, epen-

dymomas and haemangioblastomas. Astrocy-tomas represent 25-30% of all intramedullarytumours presenting in adults and more than90% of all spinal cord tumours in children. Typ-ical astrocytomas cause a fusiform expansion ofthe spinal cord. If a cystic component is present,it is typically intratumoral, although satellitecysts and secondary syringomyelia are observed.Astrocytomas reveal moderate, irregular en-hancement after IV contrast medium adminis-tration. The boundaries of the astrocytoma areusually poorly defined. The evolution of such le-sions into glioblastoma multiforme is occasional-ly seen (Fig. 5.40).

Ependymomas are typically located in thecervical region and are often associated with


Fig. 5.35 (cont.).

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a large satellite cyst(s). Although not alwaysseen, a low signal intensity area on T2-weight-ed MR typically surrounds the cranial andcaudal boundaries of the lesion, representing

repeated intralesional microhaemorrhages(Fig. 5.41). Ependymomas generally revealwell-defined boundaries and, with the excep-tion of the often associated cystic component,


Fig. 5.36 - Spinal meningioma. The MRI images reveal a spinal canal mass having MRI signal that is very similar to that of the spinalcord. The heavily T2-weighted images demonstrate the intradural-extramedullary location of the tumour. The lesion shows intense,homogeneous contrast enhancement following IV Gd administration. [a) sagittal T1-weighted MRI; b) sagittal T2-weighted MRI; c),d), e) sagittal, axial and coronal T1-weighted MRI following IV Gd].

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demonstrate intense, rather homogeneous en-hancement after IV gadolinium contrastmedium administration. Originating fromependymal cells, they occupy a less eccentriclocation that astrocytomas. They are mostcommonly encountered in adolescents andyoung adults. Not uncommonly they may belocated in the cauda equina because of em-bryonic rests of ependymal cells in the filumterminale (Fig. 5.42).

Haemangioblastomas represent 5% of allspinal cord neoplasia. This kind of tumour canbe isolated or multicentric. In the latter case,they are associated with von Hippel-Lindau’sdisease. Tumour nodes are typically small, rich-ly vascularized, generally located eccentricallyin the cord and often associated with extensivesyringomyelia formation and/or marked spinalcord oedema.

Rare tumours of the spinal cord include lym-phomas (usually a spinal cord deposit of a sys-temic lymphoma), congenital lipomas, neoplas-tic metastases, gangliogliomas and oligoden-drogliomas.

MRI is the examination of choice forstudying spinal cord tumours, especially as itis able to identify the extent of the neopla-sia and visualize various components of the

mass. The solid components of the tumourmay or may not have well-defined bound-aries. Generally speaking, low grade tumourssuch as ependymomas or haemangioblas-tomas have well-defined margins whereas in-filtrating or more aggressive tumours havepoorly limited confines. After IV contrastmedium administration ependymomas typi-cally reveal an intense, homogeneous en-hancement pattern; astrocytomas on the oth-er hand show a modest, inhomogeneous pat-tern of enhancement.

Intratumoral haemorrhages, often observedin spinal cord neoplasia, show increased signalon T1-weighted MRI images in the subacutephase (i.e., methaemoglobin) and reduced signalon T2-weighted sequences. In the late phases, ifgradient-echo sequences are used, haemosiderindeposits will demonstrate marked areas of hy-pointensity.

Parenchymal oedema can be seem in upto 60% of cases of ependymoma, 23% of astrocytoma and almost always in haeman-gioblastomas, in which case it is usually ex-tensive.

Intratumoral cystic components are usuallylocated within the boundaries of the neoplasticlesion itself. The MR signal of this type of cystis generally higher on T2-weighted images thanthat of the CSF due to the high protein contentof the fluid; the walls of these intrinsic tumourcysts show enhancement after IV contrastmedium administration. On the contrary, satel-lite cysts, which resolve spontaneously aftersurgical resection of the neoplasm, are foundcranially and caudally in relationship to the sol-id tumour mass. They demonstrate MR signalcharacteristics similar to those of the CSF andthe walls do not enhance after IV gadoliniumadministration.

Syringohydromyelia, which can be associat-ed with spinal cord neoplasia, also disappearsspontaneously after the total surgical removalof the neoplasm.

Spinal angiography may occasionally be use-ful in order to complete the diagnostic imagingexamination in the presence of clinical clues orMR findings that suggest the presence of hae-mangioblastoma.


Fig. 5.36 (cont.).

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Non-mass forming spinal cord pathology

MRI is also useful for the diagnosis of acutespinal cord involvement in multiple sclerosis

and sudden onset ischaemic medullary disease.Multiple sclerosis (MS) (6, 9) is a demyelinatingdisease that most frequently affects females,and which presents with variable neurological


Fig. 5.37 - Multiple spinal schwannomas in a subject with von Recklinghausen’s disease. The MRI imaging study demonstrates multi-ple intramedullary and intradural-extramedullary masses in the cervicothoracic region, which appear hyperintense on T2-weightedMRI, and show contrast enhancement following IV Gd administration. Also note the multiple perimedullary masses and the numer-ous masses within the nerve roots of the cauda equina. [a) sagittal cervicothoracic T2-weighted MRI; b) sagittal cervicothoracic T1-weighted MRI following IV Gd; c) axial cervical T1-weighted MRI following IV Gd; d) sagittal midthoracic T1-weighted MRI follow-ing IV Gd; e) axial upper thoracic T1-weighted MRI following IV Gd; f): sagittal lumbosacral T1-weighted MRI following IV Gd].

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signs and symptoms often in a relapsing-remit-ting pattern. Spinal cord involvement typicallyaffects the dorsolateral regions of the cervicalcord. Although isolated medullary involvement(i.e., in the absence of cerebral disease) can beobserved in up to 10% of cases, nevertheless,when a spinal cord lesion of a probable de-myelinating nature is identified using MRI, a

supplemental brain scan is required to com-plete the investigation. MRI generally underes-timates the number and presence of spinal corddemyelinative lesions, especially at a thoraciclevel, where fine detail can be reduced by arte-facts caused by CSF pulsation, chest wall move-ment and motion of the cardiovascular system.

On T2-weighted MRI, MS lesions appear assingle or more frequently multiple hyperintenseareas of the spinal cord that generally extendfor less than two spinal segments, located in theaxial plane in the white matter of the lateral andposterior columns. Areas of acute demyelina-tion can cause swelling of the spinal cord andenhancement after IV contrast medium admin-istration (Fig. 5.43).

The combination of retrobulbar optic neuri-tis and a spinal cord lesion is termed Devic’sdisease. The question of whether this patholo-gy is a variant of multiple sclerosis or a separateentity is still controversial. In Devic’s disease,MRI shows widespread spinal cord lesions withcord swelling and inhomogeneous enhance-ment after IV contrast medium injection.

Spinal cord infarcts (3, 5, 11) are rarely iso-lated events, but instead are more often associ-ated with spinal column trauma, inadvertentligation of the afferent radiculomedullary arter-ies, spinal arteriovenous malformations, hy-potension, vasculitis and neoplasia. The major-ity of spinal cord infarcts take place in the ter-ritory of the anterior spinal artery and have apropensity for the thoracolumbar region, wherethe normal blood supply to the spinal cord ismost sparse. MRI using axial T2-weighted se-quences demonstrates the ischaemic area as hy-perintensity affecting the entire volume of thespinal cord over multiple segments associatedwith moderate swelling (Fig. 5.44). Spinal cordinfarcts in the subacute phase (i.e., 2-6th day)may demonstrate contrast enhancement afterIV gadolinium administration; chronic phaseinfarcts evolve to spinal cord atrophy.

Spinal cord arteriovenous malformations arecongenital vascular abnormalities. They typical-ly present in the young and are most frequentlyencountered in the thoracic or cervical region.The lesion is generally principally supplied bythe anterior spinal artery. Patients present with


Fig. 5.37 (cont.).

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signs and symptoms of progressive myelopathy(venous congestion or arterial steal) or with theonset of an acute neurological deficit secondaryto spontaneous intramedullary and/or sub-arachnoid haemorrhage. In such cases MRIdemonstrates serpentine flow voids within ab-normal coiled vessels, focal spinal cordswelling, haemorrhage in various stages, andhyperintensity on T2-weighted images adjacentto the nidus of the malformation, representingoedema, ischaemia and/or gliosis. After IV con-trast medium administration, depending uponflow velocity and intravascular turbulence, en-hancement is seen in some of the vascular com-ponent and occasionally within the surround-ing parenchymal component if the latter hasundergone insult from spontaneous adjacentparenchymal haemorrhage of the vascular mal-formation or if related cord infarction has oc-curred.

Spinal dural arteriovenous fistulae are ac-quired lesions, most frequently encountered inelderly subjects in the thoracic spinal region. Inmost cases the fistula is supplied by the posteri-or spinal artery and represents a direct commu-nication between a dural branch of a radicu-lomedullary artery and a perimedullary in-tradural vein.

Dural arteriovenous fistulae represent ap-proximately 80% of all spinal vascular malfor-


Fig. 5.38 - Intradural spinal metastasis in a patient with primaryintracranial pinealoblastoma. The MRI examination shows thatthe spinal cord is compressed posterolaterally by an enhancingintradural-extramedullary mass consistent with subarachnoiddissemination of the pinealoblastoma. [a) sagittal T2-weightedMRI; b) sagittal T1-weighted MRI; c) axial T1-weighted MRIfollowing IV Gd].

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mations. They do not typically cause haemor-rhage, but instead patients present with eitherchronic signs and symptoms of progressivemyelopathy secondary to spinal cord ischaemiathat is generated by venous congestion, oracute clinical findings consistent with sudden


Fig. 5.39 - Metastatic neoplastic leptomeningeal spread in acase primary pineal region neoplasm. Sagittal T1-weightedMRI following IV Gd administration shows diffuse lep-tomeningeal contrast enhancement consistent with subarach-noid dissemination of the primary intracranial neoplasm.

Fig. 5.40 - Primary thoracic spine intramedullary glioblastomawith subarachnoid dissemination. The MRI imaging studyshows diffuse spinal cord swelling associated with inhomoge-neous MRI signal. Irregular contrast enhancement is presentfollowing IV Gd administration. Extramedullary masses are al-so present on the surface of the spinal cord as well as associat-ed with the roots of the cauda equina and the posterior fossadue to leptomeningeal spread of the primary spinal cord neo-plasm. [a) sagittal T2-weighted MRI; b) sagittal T1-weightedMRI; c), d) midline sagittal and parasagittal T1-weighted MRIfollowing IV Gd].

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Fig. 5.40 (cont.).

Fig. 5.41 - Thoracic spine intramedullary ependymoma. Theimages reveal a thoracic intramedullary mass having peripherallow signal intensity on T2-weighted images at the cranial andcaudal margins of the lesion, indicating repeated intratumouralmicrohaemorrhages. Note the extensive peritumoural hyperin-tense oedema on the T2-weighted images. [a) sagittal T2-weighted MRI b) sagittal T2*-weighted MRI; c), d) axial T2-weighted MRI].

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spinal cord infarction. T2-weighted MRI showsan indentation of the posterior surface of thespinal cord by dilated intradural-perimedullaryveins (Fig. 5.45), a finding that can often bemore clearly visible after IV gadolinium admin-istration; multilevel intramedullary spinal cordhyperintensity is also observed in acutely pre-senting cases as a result of the evolving infarct


Fig. 5.41 (cont.).

Fig. 5.42 - Ependymoma of the conus medullaris. The MRIstudy shows a septated partially cystic mass with a mural nodu-lar area of contrast enhancement. [a) sagittal T2-weighted MRI,b) sagittal T1-weighted MRI following IV Gd].

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which may also show homogenous multiseg-mental contrast enhancement (2). It has beenshown that on occasion MRI can be equivocalor even falsely negative in instances that subse-quently were proven to have spinal dural fistu-


Fig. 5.43 - Thoracic intramedullary multiple sclerosis. T2weighted MRI shows an area of intramedullary high signal in-tensity at the T8-9 level associated with minor focal swelling ofthe spinal cord. Contrast enhancement is seen within the areaof MRI signal abnormality following IV Gd administration. [a)sagittal T2-weighted MRI; a) sagittal T-1 weighted MRI follow-ing IV Gd].

Fig. 5.44 - Ischaemia of the thoracic spinal cord associated withspinal dural arteriovenous fistula. T-2 weighted MRI demon-strates high signal intensity within the central region of theconus medullaris associated with central medullary hyperinten-sity and vascular flow voids over the posterior surface of thethoracic spinal cord. [a) sagittal T1-weighted MRI; b) axial T2-weighted MRI; c) axial T-weighted MRI].

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Fig. 5.45 - Thoracic spinal dural arteriovenous fistula. The MRI study reveals subarachnoid space MRI signal irregularity posterior tothe spinal cord, which becomes much more evident on the T2-weighted images due to the presence of serpentine vascular flow voids.[a) sagittal T1-weighted MRI; b) sagittal T2-weighted MRI, c) coronal T2-weighted MRI].

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Fig. 5.44 (cont.).

lae. In such clinically suspected but MRI-nega-tive cases, myelography and spinal angiographymay be indicated, and when positive will defin-itively reveal the site of the dural fistula, thefeeding arteries and the dilated draining veins.In any case, angiography is a prerequisite fortherapeutic dural fistula embolization, thetreatment of choice in these patents.

Cavernous angiomas are usually indolentvascular malformations that are neverthelessprone to haemorrhage and intrinsic thrombo-sis. T1- and T2-weighted MRI typically showsa central hyperintense core with a peripheralmargin or margins of hyper- and hypointensitydue to the presence of mixed subacute andchronic haemoglobin metabolites (Fig. 5.46).Some cases demonstrate central enhancementafter IV contrast medium administration, rep-resenting the residual patent vascular compo-nent of the angioma. Cavernous angiomas canpresent acutely with signs and symptoms relat-ed to intramedullary haemorrhage (Fig. 5.47).

Acute spinal cord syndromes can also becaused by viral or granulomatous infections. In


Fig. 5.47 - Acute haemorrhage within intramedullary cavernousangioma. The spinal T1-weighted spinal MRI images demon-strate an extensive acute-subacute (deoxyhaemoglobin andmethaemoglobin) thoracic intramedullary haemorrhage associ-ated with an intramedullary cavernous angioma showing intrin-sic hypointensity on T2-weighted acquisitions consistent chron-ic peripheral microhaemorrhages (haemosiderin). The MRI ofthe brain showed several cavernous angiomas demonstrating themulticentric potential of this pathologic process. [a) sagittal T2-weighted spinal MRI b) sagittal T1-weighted weighted spinalMRI; c) sagittal T2*-weighted spinal MRI; d) axial T1-weightedspinal MRI; e) axial T2*-weighted cranial MRI].

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Fig. 5.46 - Chronic haemorrhage within thoracic intramedullarycavernous angioma. T2*-weighted sagittal MRI reveals hy-pointensity within the upper thoracic spinal cord as a conse-quence of deposition of haemosiderin associated with thrombo-sis-haemorrhage within an intramedullary cavernous angioma.

cases of infectious myelitis, MRI demonstratesmultisegmental non-specific intramedullaryhyperintensity on T2-weighted sequences, witha variable enhancement after contrast mediumadministration.

Spinal cord abscess formation is rare and isusually caused by the direct extension of in-

fections from adjacent perispinal tissues orfrom penetrating trauma. T2-weighted MRIdemonstrates an intramedullary mass that ishyperintense on T2-weighted sequences andreveals rim enhancement after IV gadoliniumadministration. Distinguishing this patternfrom other spinal cord lesions such as neopla-sia is not always possible on the basis of theimages alone.

Acute transverse myelitis is an acute in-flammatory process with a poor prognosis.The aetiology is unknown, however it is prob-ably autoimmune in nature. Acute transversemyelitis can be associated with various con-ditions such as multiple sclerosis, paraneo-plastic syndromes, prior vaccinations, vas-culitis or known autoimmune disorders. Clin-ically there is an acute onset of a profoundspinal cord neurological deficit in the absenceof other findings. It is for this reason thattransverse myelitis is always a diagnosis of ex-clusion. On MRI, acute transverse myelitisdemonstrates areas of hyperintensity on T2-weighted imaging associated with spinal cordswelling and irregular contrast enhancementfollowing gadolinium administration due toan associated breakdown in the blood-cordbarrier. In the chronic phase, the spinal cord


Fig. 5.47 (cont.).

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can appear atrophic, and areas of high signalon T2-weighted images may persist due togliosis.

Acute disseminated encephalomyelitis is amonophasic autoimmune disease that followswithin days or weeks of an antiviral vaccinationor viral infection. As the name indicates, it in-volves the brain but also concomitantly affectsthe spinal cord. Pathologically the lesions aresimilar to those of MS. The prognosis is typi-cally good and the majority of patients respondrapidly to steroid treatment. MRI shows hyper-intense areas on T2-weighted sequences withinthe parenchyma of the brain and spinal cordthat enhance after IV gadolinium; the spinalcord may be swollen.

The development of radiation myelopathyin part depends on the dose of radiation andthe time period over which it was adminis-tered. In the acute milder forms, typically pre-senting approximately three months after ra-diation is applied to the spinal cord, the pa-tient experiences sensations similar to electricshocks in the lower limbs; MRI may show noabnormality. However in severe cases the pa-tient reveals a severe, rapidly progressivemyelopathy; in such cases, the spinal cord isswollen, hyperintense on T2-weighted imagesand enhances following IV contrast injection.Evolution of spinal cord atrophy will occurover time (Fig. 5.48).


c

Fig. 5.48 - Radiation induced thoracic myelitis/spondylitisthree years following radiotherapy. T2-weighted MRI with fatsuppression shows hyperintense MRI signal within the thoracicspinal cord and within the bone marrow of several contiguousvertebral bodies, both of which are caused in this case by thepreceding radiation therapy. Axial T2*-weighted imagesdemonstrate again the intramedullary location of the patholog-ic process. No contrast enhancement of the intramedullaryprocess can be identified. Note the postsurgical alterations. [a)sagittal T2-weighted MRI; b) sagittal T1-weighted MRI follow-ing IV Gd; c) axial T2*-weighted MRI].

a

b

REFERENCES

1. Baleriaux DL: Spinal cord tumours. Eur Radiol 9 (7):1252-1258, 1999.

2. Chen CJ, Chen CM, Lin TK: Enhanced cervical MRI inidentifying intracranial dural arteriovenous fistulae withspinal perimedullary venous drainage. Neuroradiology 40:393-407, 1998.

3. Fortuna A, Ferrante L, Acqui M et al: Spinal cord ischemiadiagnosed by MRI. J Neuroradiol 22:115-122, 1995.

4. Karampekios S: Inflammatory, vascular and demyelinatingdiseases of the spine and spinal cord. Eur Radiol (S1)10:36,2000.

5. Liou RJ, Chen CY, Chou TY et al: Hypoxic - ischaemicinjury of the spinal cord in systemic shock: MRI. Neurora-diology 38:S 181-183, 1996

6. Lyclama à Nijeholt GJ, Uitdehaag BMJ et al: Spinal cordmagnetic resonance imaging in suspected multiple sclero-sis. Eur Radiol 10:368-376, 2000.

7. Obenberg J, Seidi Z, Plas J: Osteoblastoma in lumbar ver-tebral body. Neuroradiology 41:279-282, 1999.

8. Rimmelin A, Clouet PL, Salatino S et al: Imaging of thora-cic and lumbar spinal extradural arachnoid cysts: report oftwo cases. Neuroradiology 39:203-206, 1997.

9. Rocca MA, Mastronardo G, Horsfield MA et al: Comparisonof three MR sequences for detection of cervical cord lesions inpatients with multiple sclerosis. AJNR 20:1710-1716, 1999.

10. Silbergleit R Brunberg JA, Patel SC et al: Imaging of spinalintradural arachnoid cysts: MRI, myelography and CT.Neuroradiology 40:664-668, 1998.

11. Suzuki K, Meguro K, Wada M et al: Anterior spinal ar-tery syndrome associated with severe stenosis of the ver-tebral artery. AJNR 19:1353-1355, 1998.

12. Wilmink JT: MR imaging of the spine: trauma and degene-rative disease. Eur Radiol 9 (7):1259-1266, 1999.

13. Yamada K, Shrier DA, Tanaka H et al: A case of subacutecombined degeneration: MRI finding. Neuroradiology 40:398-400, 1998.


VI

NEUROPAEDIATRIC EMERGENCIES

371

INTRODUCTION

This chapter covers the most common emer-gency situations encountered in neuropaedi-atrics, including cerebrovascular disease, headinjuries, infections of the central nervous sys-tem (CNS) and intracranial hypertension.

CEREBROVASCULAR DISEASE

Cerebrovascular disease (15, 32) is rare in in-fants and newborns and when encountered doesnot have the same aetiological factors as in adults:the most common causes in the young age groupare congenital vascular abnormalities and thosesecondary to systemic illnesses. Various areas ofthe brain show significant differences in their sus-ceptibility to cerebral vasculopathy. In addition,there are also important physiological differencesin the blood vessels of different areas of the brain.The pathological conditions of cerebrovasculardisease are haemorrhage and ischaemia.

HAEMORRHAGE

NEWBORNS AT TERM AND YOUNG INFANTS

In newborns at term, a large number of possi-ble pathological events may result in intracranial

haemorrhage: a) trauma: subdural haematoma,epidural haematoma. subarachnoid haemor-rhage, intracerebral haemorrhage, intracerebellarhaemorrhage, b) clotting disorders: clotting de-fects, thrombocytopenia, c) vascular disorders:aneurysms, arteriovenous malformations, d)metabolic disorders, and e) idiopathic intra-parenchymal haemorrhage.

The clinical signs of an intracranial haemor-rhage lesion in a newborn are often modest andnon-specific: apathy or irritability/hyperex-citability without focal neurological signs,seizure, tremors, breathing disorders. Fre-quently acidosis, hypoglycaemia and hypoten-sion are associated with such haemorrhages.

a) Labour trauma is the most frequent causeof bleeding in newborns.

Subdural haematomas and subarachnoidhaemorrhage are the most common types ofhaemorrhagic lesion. The most frequent site ofsubdural bleeding is over the cerebral convexi-ty and within the temporal fossa, howeverhaemorrhages can also be encountered adja-cent to the falx cerebri, tentorium cerebelli andin the posterior cranial fossa.

Intraparenchymal haemorrhages are less fre-quent and can be associated with subarachnoidand subdural haemorrhage, should the bleed-ing extend into the ventricles. The prognosis of

6

NEUROPAEDIATRIC EMERGENCIES

N. Zamponi, B. Rossi, G. Polonara, U. Salvolini

small lesions is good, however serious sequelaeare typically observed following larger haemor-rhages.

Diagnostic imaging should first include CT,which demonstrates the presence, site and ex-tent of the cerebral bleed at an early stage; onthe other hand, haemorrhages associated withcerebral infarcts will only become evident somedays after the ischaemic event.

Ultrasound may not show epidural or sub-dural haemorrhages localized to the cranialconvexity or in the posterior fossa, whereaslarger haemorrhages are clearly visible on ultra-sound images as hyperechoic areas, and laterhypo- anechoic regions.

Both ultrasound and CT are capable of doc-umenting and sequentially monitoring the mostimportant sequelae: porencephalic cysts andhydrocephalus.

Porencephalic cysts usually form off of thebodies of the lateral ventricles. They typicallydevelop from a haemorrhage that ruptures intothe lateral ventricle or the subarachnoid space.Associated posthaemorrhagic hydrocephalusdevelops in 10-15% of patients with intraven-tricular haemorrhage. The hydrocephalus haltsor improves in most cases; more rarely it pro-gresses and can require surgical ventricular-peritoneal shunt placement.

b) Various clotting and platelet disorders canresult in intracranial haemorrhage in newborns.The most frequent causes of thrombocytopeniaare the use of medicines during pregnancy, ma-ternal infections, immunological disorders anddisseminated intravascular coagulation.

c) Vascular malformations and intracranialaneurysms may present with intracranial haem-orrhages in newborns in rare occasions.

Ultrasound may prove useful in diagnosis,especially in infants with aneurysmal dilatationof the vein of Galen. This is a rare congenitaldisorder wherein abnormal arteriovenous for-mations drain into the deep, dilated vessels ofthe galenic system. These direct connectionswith the vein of Galen can be by large fistulaeor by multiple smaller arteriovenous connec-tions. The pathogenesis would seem to involveintrauterine vascular thrombosis or absence offormation of the superior sagittal venous sinus.

In 90% of cases, signs and symptoms of vas-culopathy arise in early infancy: intracranialhaemorrhage (intraparenchymal or subarach-noid) and rapidly progressive hydrocephalusare the most frequent presentations. In new-borns these complications are frequently asso-ciated with cardiac insufficiency, the finalpathophysiological result of a preexistent con-genital haemodynamic anomaly (e.g., increasein blood flow across an arteriovenous fistula,increase in blood return to the right atrium,right-to-left blood flow through cardiac de-fects). In addition, the large blood flow throughthe fistula can create a secondary state of cere-bral ischaemia.

In newborns, the aneurysmal dilatation ofthe vein of Galen can be simply diagnosed us-ing ultrasound. On colour Doppler images,turbulent flow can usually be seen.

On CT without IV contrast medium, thevein of Galen appears as a rounded mass in theregion of the tentorial incisura and straight ve-nous sinus; aqueduct compression may causeobstructive hydrocephalus. After IV contrastmedium administration, intense enhancementis typically seen within the aneurysmally dilatedvessel which is smooth and well defined. In thepresence of thrombosis of this structure, vari-able degrees of non-enhancement will be ob-served.

On MRI the vascular malformation appearshypointense on both T1- and T2-weighted se-quences due to the rapid blood flow within theabnormal vessels. The arteries that supply themalformation can be reasonably well shownwith MRA. Conventional selective angiographywill still better define the arterial feeding ves-sels and the draining venous structures andmay assist in presurgical planning (27, 32, 37).

PREMATURE NEWBORNS

Subependymal and intraventricular haemor-rhages are more frequently encountered in pre-mature newborns than in those born at term (3,5, 11). Babies with a gestational age of less than35 weeks or a birth weight of less than 1.5 kghave a higher risk of such haemorrhages, which

372 VI. NEUROPAEDIATRIC EMERGENCIES

commonly present during the second or thirdday of life. The haemorrhage originates fromthe germinal matrix that surrounds the lateralcerebral ventricles. Small haemorrhages remainconfined to the subependymal regions, howev-er, when the bleeding is larger it can extensive-ly involve the cerebral parenchyma or ruptureinto the ventricular system. Certain factorsmake haemorrhage in this area more likely. Thevessels of the germinal matrix are fragile andcontain little connective tissue. This germinalmatrix begins to involute at approximately the35th week of gestation. Until that time it has ahigh arterial perfusion with consonantly elevat-ed venous and capillary pressure.

Two clinical syndromes have been describedin association with subependymal and intraven-tricular haemorrhage. The catastrophic syn-drome has an acute onset and a rapid evolutiontowards coma; the mortality rate is high. Thesalt losing syndrome is a disorder of conscious-ness, accompanied with a reduction in sponta-neous movements, hypotonia and oculomotorabnormalities; these signs evolve slowly and areoften followed by a period of stabilization fol-lowed by a second phase of deterioration. Themortality rate is lower for this syndrome thanfor the catastrophic syndrome.

From the standpoint of medical imaging,germinal matrix haemorrhages can be brokendown into 4 stages: stage I is characterized by asmall germinal matrix haemorrhages togetherwith a small intraventricular haemorrhage;stage II is characterized by germinal matrixhaemorrhage accompanied by a large intraven-tricular haemorrhage; stage III is characterizedby a subependymal haemorrhage, intraventric-ular haemorrhage, and hydrocephalus; and,stage IV indicates the spread of the parenchy-mal haemorrhage into one or both cerebralhemispheres.

The use of ultrasound, which can be per-formed safely at the bedside, has lead to an in-crease in the identification and characterizationof neonatal subependymal and intraventricularhaemorrhages. On ultrasound, stage I germinalmatrix subependymal haemorrhage appears asa hyperechoic mass lesion, which is either uni-or bilateral and is primarily located in the head

of the caudate nucleus. Generally speaking, inorder to be visualized, it must measure 4-5 mmin diameter. A Stage II haemorrhage appears ashyperechoic material within the lateral ventri-cle(s). A stage III haemorrhage is representedby a dilatation of the ventricular system and thepresence of intraventricular hyperechoic blood.The intraparenchymal component of a stage IVhaemorrhage appears on ultrasound as an in-tensely hyperechoic lesion located in the deepwhite matter of the centrum semiovale.

Subsequent ultrasound scans will show pro-gressive stages of resolution of the subependy-mal-intraventricular haemorrhage. An exten-sive haemorrhage can evolve over 2-3 monthstowards the formation of porencephalic cystsor the development of cystic encephalomalacia.

On CT, acute germinal matrix haemorrhagesappear as hyperdense foci, usually adjacent tothe lateral ventricle near the head of the cau-date nucleus. MRI is also fairly sensitive andspecific in demonstrating acute germinal ma-trix haemorrhage.

In premature neonates with the hypoxic-is-chaemic syndrome white matter alterations arealso frequently detected: periventricular leuko-malacia appears on ultrasound as widespread,poorly defined hyperechoic periventricular re-gions. These are especially prominent in theventricular trigone regions and adjacent to theforamina of Monroe. The hyperecho findingsare due to oedema and petechial haemorrhage.The abnormality is generally bilateral, but is of-ten asymmetric. After 2-3 weeks, small cystsform within the hyperechoic region that coa-lesce to form a multicystic lesion, before col-lapsing, fusing and being replaced by glialscars. In this late phase of glial scarring the ul-trasound findings are usually unremarkable.

During the acute phase of ischemia, CT canbe normal or can show a minor attenuation in theparenchyma of the periventricular regions; dur-ing the subacute phase it is only possible to iden-tify medium-sized cysts, whereas chronic glialscarring is not usually visible on CT (Fig. 6.1).

MRI is rarely used in the acute phase, how-ever it is the best technique for highlightingchronic periventricular leukomalacia. On T2-weighted scans the residual glial scars localized

NEUROPAEDIATRIC EMERGENCIES 373

to the periventricular areas appear hyperin-tense. These areas generally border the ventri-cles and typically spread into the adjacent whitematter in a flame-shaped configuration. A thin-

ning of the posterior body and splenium of thecorpus callosum are seen in the chronic phaseas a result of degeneration of the transcallosalfibres, ventricular dilatation and atrophy of thehemispheric white matter (Fig. 6.2).

INFANTS

Vascular malformations are the most com-mon cause of haemorrhage in infants (15, 32)and can be broken down into four maintypes: arteriovenous malformations, venousangiomas, capillary telangiectasias and cav-ernous angiomas. The most common clinicalmanifestations are headache and seizuresrather than haemorrhage; however, if the lat-ter do occur, they may be subarachnoid, in-traparenchymal or combined.

Arteriovenous malformations (AVM’s) con-sist of an aggregate of abnormal vessels withthin walls (i.e., nidus) in which there is directcontinuity between dilated arteries and veinswithout the interposition of capillaries. Ap-proximately 90% are superficial and are locat-ed within the cerebral hemispheres. AVM’s areresponsible for up to 40% of spontaneous in-tracranial haemorrhages in infants. The mortal-ity rate associated with the rupture of an AVMis approximately 10%.

On unenhanced CT, a typical AVM appearsas a heterogeneous area with slightly increaseddensity compared to the normal surroundingparenchyma. After IV contrast medium admin-istration, intense enhancement of the malfor-mation and its afferent and efferent vessels isobserved.

On MRI the fast blood flow within AVM’screates flow voids on spin echo sequences. Thenidus appears as a tangle of tubular shapedblack vessels. However, in order to obtain anaccurate anatomical map of the vascular mal-formation, an angiographic examination is re-quired. Typically a tangle of small, irregularblood vessels supplied by dilated and twistedarteries and drained by dilated veins that fillrapidly.

In the case of haemorrhage, unenhanced CTdetails the haemorrhagic spread into the sub-


Fig. 6.1 - Hypoxic-ischaemic injury in newborn. a, b) Unenhan-ced CT shows widespread hypodensity of the subcortical andperiventricular white matter and enlargement of the cerebralventricular system.

a

b

arachnoid space, cerebral parenchyma andcerebral ventricles. In severe cases haemor-rhage can obscure the underlying vascular mal-formation. In the acute phase the haematomaappears hyperdense and relatively homoge-neous (Fig. 6.3); in the chronic phase, en-cephalomalacia, rarely accompanied by calcifi-cations, may result.

Cavernous vascular malformations consist ofa tangle of dilated vessels that do not possessthe characteristics of normal arteries or ofveins. With the exception that thrombi can bepresent, the draining veins and arteries usuallyhave a normal calibre. The malformation maycontain small intrinsic areas of neural tissue.Most of these lesions are located in the cerebralparenchyma, and although they are usually iso-lated they can also be multiple and have a fa-milial pattern of expression. The clinical pres-entation is typically seizures, but more rarely itcan be cerebral haemorrhage. In fact, subclini-cal haemorrhages often occur. The diagnosis iscurrently based on MRI due to the characteris-tic imaging findings, including a mixed signalcore surrounded by a hypodense haemosiderinring on T2-weighted sequences.

Venous malformations are often incidentallydetected on MR or CT scans. The risk ofbleeds is generally low. MRI, which is moresensitive than CT, shows a branching networkof small draining veins that unite to form a sin-gle, large terminal vein. In the venous phase,conventional angiography shows a collectionof abnormal veins (i.e., “Medusa head”) thatdrain into a single large collecting vein beforeemptying into a superficial cortical vein or dur-al venous sinus.

Aneurysms are rare in children under the ageof ten years; males are more frequently affectedthan are females. The clinical presentation istypically a subarachnoid haemorrhage, howev-er, some patients present with seizures.Aneurysms in children under 2 years usuallyoriginate from the anterior cerebral or the in-ternal carotid arteries. Such aneurysms are usu-ally larger than 1 cm in diameter.

CT at presentation shows an acute sub-arachnoid haemorrhage. If the aneurysm is suf-ficiently large it will demonstrate intense en-


Fig.6.2 - Periventricular leukomalacia. A, b) Axial FLAIR MRIshows an increase in the subependymal and periventricular whi-te matter MR signal with sickle shape of the cerebral ventricles.

a

b

hancement with a smooth, round or oval con-figuration after IV contrast medium adminis-tration. Internal thrombosis may be observed.While MR and angio-MR better define theaneurysm, conventional angiography defini-tively visualizes the lumen and neck of theaneurysm, and its relationship to the vessel oforigin.

ISCHAEMIA

Cerebrovascular occlusions may occur in ar-teries, veins or capillaries, as a single acuteevent, a recurrence or a progressive phenome-non. They can be associated with a number ofpathological conditions including inflamma-tion, infection, cardiac disease, neoplasia, trau-ma, primary arterial dysplasia, vascular malfor-mations and metabolic disease (26, 32).

The clinical symptoms vary according to theage of the infant and the vascular territory in-volved. The most common sign of internalcarotid occlusion is acute hemiplegia. A vascu-lar occlusion in the vertebrobasilar circulationcan result in pyramidal and cerebellar signs,hemiparesis, paralysis of the cranial nerves, lat-eral conjugate deviation of the eyes, dizziness,nausea and vomiting.

Acute phase CT is typically normal. After24-48 hours the infarction appears as a hypo-dense area with poorly defined margins and isaccompanied by varying mass effect. After thesecond to third week, enhancement is usuallyobserved after IV contrast medium administra-tion. In the later stages encephalomalacia,porencephalic cyst formation and focal atrophyare typical terminal sequelae.

MRI is more sensitive in detecting acute/sub-acute postinfarction oedema, which appears hyperintense relative to the normal cerebralparenchyma on T2-weighted sequences. MRA(Fig. 6.4) may reveal vascular thrombosis of thecranial circulation (Fig. 6.5).

Despite the fact that it is the most sensitivetechnique for examining the cranial vascular sys-tem, in infants angiography is reserved for se-lected cases where it will clearly influence futuretherapy or when the diagnosis is in doubt (12).


Fig.6.3 - Intraparenchymal haematoma caused by AVM hae-morrhage. a, b) Unenhanced CT demonstrates inhomogeneousright frontoparietal intraparenchymal haemorrhage associatedwith compression of the right lateral ventricle and contralateralshift of the midline structures.

a

b

THE MOYA-MOYA PHENOMENON

The moya-moya phenomenon (6, 32) is adisorder that characteristically affects childrenand adolescents. Approximately 70% of casesare diagnosed within the first 20 years of life.The disorder consists of an idiopathic pro-gressive stenosis of the supraclinoid internalcarotid arteries. A prominent collateral circu-lation is formed by small branches of therubrothalamic arteries and the lenticulostriatearteries, resulting in an MRA and convention-al angiographic appearance similar to that of apuff or cloud of smoke (moya-moya meansfoggy in Japanese).

The aetiology and pathogenesis are unknown,although there are many pathological condi-tions that are sometimes associated with moya-moya type angiographic patterns (e.g., neurofi-bromatosis, tuberculosis, Down’s syndrome,tuberous sclerosis, prior radiation therapy,etc.). Nevertheless, in certain cases the diseasepresents as an isolated phenomenon. In infants,moya-moya phenomenon clinically revealstransient-relapsing ischaemic episodes, with theappearance of neurological deficits and convul-sions. In adolescents, headaches and cerebralhaemorrhages are the most common clinicalpresentations.

Unenhanced CT typically reveals the pres-ence of multiple cerebral infarcts in differentstages of evolution. In certain cases, enhancedCT may demonstrate absence of visualizationof the proximal internal carotid vessels and thevessels of the circle of Willis. These findings aremore clearly visible on MRI and MRA. Suffi-ciently large collateral vessels are seen at thebase of the brain in the region of the basal gan-glia (Fig. 6.6). In time regional cerebral en-cephalomalacia and intracranial calcificationsmay develop.

The definitive diagnosis is angiographic: thesupraclinoid sections of the internal carotid ar-teries are stenotic or completely occluded asmay be the proximal segments of the anteriorand middle cerebral arteries. Distal to the oc-clusion the collateral vessels appear as a tangleof dilated, twisted vessels. The marked, denseblood flow within these small collateral vessels


Fig.6.4 - Ischaemia of the basal ganglia. a) Unenhanced CTshows hypodensity in the head of the caudate nucleus and thefrontal aspect of the putamen on the right side, with involve-ment of the anterior limb of the internal capsule. b) Corre-sponding MRI.

a

b


Fig.6.5 - Left cerebellar ischaemia. a) Unenhanced CT scan shows minor cortical-subcortical hypodensity. b, c) Unenhanced T2-wei-ghted MRI demonstrates areas of increased signal in the left cerebellar hemisphere and midbrain-pontine junction. d) Enhanced T1-weighted MRI reveals breakdown in the blood-brain barrier following IV gadolinium administration.

b

a c

d

can produce the typical cloud of smoke ap-pearance.

FIBROMUSCULAR DYSPLASIA

This is a rare progressive idiopathic condi-tion typically encountered in children and ado-lescents and adult women. The most common


Fig. 6.5 (cont.).

Fig.6.6 - Moya-Moya syndrome. a) coronal MR angiogram shows that the flow signal of the internal carotid arteries is not visible inan intracranial vessels above the supraclinoid segments of the internal carotid artery siphons. b) MR angiogram reveals absence offlow signal in the arterial vessels of the circle of Willis, which have been replaced by a number of small, irregular vessels at the baseof the brain. c) T2-weighted MRI demonstrates poor visualisation of the anterior and middle cerebral arteries and the presence of nu-merous irregular vascular structures.

e

a

b

c

form consists of concentric rings of mural fi-brous proliferation and smooth muscle hyper-plasia resulting in thickening of the media asso-ciated with destruction of the elastic lamina. Inaddition to the cervical and intracranial arter-ies, this disease process can also affect the renalarteries. The findings are frequently bilateral al-though asymmetric. The diagnosis is an angio-graphic one, having the appearance of a typicalstring of beads pattern as a result of a series ofmultiple constrictions alternating with dilata-tions along the course of the artery involved.Signs and symptoms may result from either dis-section of the diseased vessel and/or thrombo-sis as well as spontaneous intracranial haemor-rhage. Intracranial aneurysms also may be asso-ciated with this condition, and may themselveslead to haemorrhage upon rupture.

CEREBROVASCULAR OCCLUSIONS SECONDARYTO SYSTEMIC ILLNESSES

Venous thromboses, venous sinus throm-boses and arterial embolic disease are not in-frequent consequences of cyanogenic congen-ital heart malformations, in particular tetralo-gy of Fallot and the transposition of the greatvessels. The initial signs/symptoms are typi-fied by the sudden onset of focal neurologicaldeficits and/or intracranial hypertension. Ve-nous thrombosis is the most commonly en-countered complication, often related to thepolycythaemia typically present in such pa-tients.

Arterial embolism usually occurs as a conse-quence of right-to-left vascular/cardiac shuntsor the presence of septic endocarditis. Falci-form cell anaemia results in stroke in up to 8%of cases, especially in the 5-10 year age group.A condition of homozygous protein C deficit,one of the components of the antithromboticsystem, may present in newborns with a purpu-ra fulminans and cerebral venous/venous sinusthrombosis.

The MELAS syndrome (i.e., mitochondrialencephalomyopathy, lactic acidosis and stroke-like episodes) presents with repeated migraine-like events, with vomiting at onset and repeat-

ed stroke-like episodes later in the evolution ofthe disease. Children may be short in stature,with multisystem involvement. MR shows mul-tifocal hyperintense areas on T2-weighted se-quences that involve the cerebral cortex andthe subcortical white matter. MR spectroscopymay demonstrate characteristic patterns with acertain degree of specificity (25, 43, 45).

HEAD INJURIES

Head injuries (9, 18, 30, 33) are a not un-common cause of disability and death in the in-fant population. Approximately one in ten chil-dren experiences posttraumatic loss of con-sciousness during childhood. However, mosttraumatic incidents are minor and do not re-quire hospitalization or any specific treatment.Falls are the most common cause of head in-juries in children under ten and road traffic ac-cidents are the most frequent cause in adoles-cents.

Head injuries can be classified in variousways: according to the general type of trauma(e.g., closed or open), the location and extent ofthe traumatic lesion (e.g., skull fracture, focalintracranial lesion, widespread intracranial le-sion) and the severity of the traumatic lesion(e.g., minor, moderate, severe). The severity ofhead injuries is clinically defined using theGlasgow Coma Scale (GCS) score, modified tosuit children with the Paediatric Coma Scale.Severe head injuries are associated with a GCSscore lower than or equal to 8, moderate headinjuries with a GCS between 9 and 13 and mi-nor head injuries with a GCS score between 13and 15.

MINOR/MODERATE DEGREE HEAD INJURIES

Patients with minor or no external signs oftrauma, who are awake and cooperative with anormal orthopaedic and neurological examina-tion, and who have no symptoms with the ex-ception of slight headache and/or nausea-vom-iting, do not necessarily require emergencymedical imaging examinations (e.g., skull x-ray,


CT), but they should be hospitalized for an ob-servation period of 24 hours. Should they re-quire general anaesthesia in order to operate ontrauma to other body parts, cranial CT shouldbe performed prior to the surgery.

Brief immediate posttraumatic loss of con-sciousness and/or confusion and disorientationare not necessarily indicators of cerebral struc-tural damage, however, CT should be consid-ered in such cases.

In general, the indications for CT in cases ofminor/moderate head trauma include: the on-set/progression of neurological signs; progres-sive reduction of the level of consciousness; andpatients whose mental status is difficult to eval-uate.

Currently, certain practitioners recommendabandonment of the use of standing-order skullradiography in favour of CT. However, certaincases of minor/moderate head injury, and spe-cific situations such as x-ray evidence of frac-tures (e.g., depressed fracture, skull base frac-ture, etc.), can mandate the need for hospital-ization for clinical observation as well as foremergency CT.

SEVERE DEGREE HEAD INJURIES

Children with severe head injuries have aGCS of less than 9 and are incapable of fulfill-

ing simple commands due to their impairedstate of consciousness. The disability and mor-tality associated to this type of trauma can bedramatically reduced by the rapid initiation ofspecific treatment (e.g., stabilization of the vitalfunctions, respiratory control, reduction of in-tracranial hypertension) in order to curb theconsequences of the primary traumatic lesionas well as the sequelae resulting from hypoten-sion, hypoxia, hypercapnia, ischaemia andoedema.

The initial imaging examination of choice incases of severe head trauma is unenhanced CT,using 5 mm thick slices for the base of the skulland posterior fossa, and 10 mm thick slices forthe remainder of the brain. Cervical spine CTshould also be included in the protocol. Dia-gram 6.1 illustrates a recommended diagnosticpathway (21).

Extracranial traumatic lesions

In newborns, the presence of a cephalo-haematoma (i.e., subperiosteal scalp haematoma)is most frequently a consequence of the applica-tion of the forceps during delivery, but can also occur in 1% of unassisted vaginal births.Cephalohaematomas appear on ultrasound, CTand MRI as a crescent-shaped extracranial softtissue mass directly adjacent to the outer table of


HEAD INJURY

slight moderate severe

no x-ray in the absence of CT: skull x-ray + observation

no worsening worsening

observation hospitalisationat home for brief period CT + NeurosurgeryDiagram 6.1

the skull, limited by the cranial sutures (Fig. 6.7).On CT in the acute phase, cephalohaematomasare hyperdense, becoming progressively hypo-dense in the chronic phase. Calcification may oc-cur late in the evolutionary process.

Another common post-partum posttraumat-ic lesion is so-called caput succedaneum charac-terized by haemorrhagic oedema of the scalpsecondary to a trauma occurring in the vaginaat the time of labour and delivery. They can be


Fig.6.7 - Cerebral haematoma. a) T1-, b) T2-, c) T2*-, d) T1-weighted MRI shows a large extracranial haemorrhage in the right pa-rietal region.

a

b

c

d

distinguished from cephalohaematomas bytheir superficial site and the fact that they tra-verse the cranial suture lines.

The third type of extracranial posttraumaticlesion encountered in newborns is the subgalealhaematoma, which consists of a haematoma de-lineated externally by the calvarial aponeurosisthat covers the scalp beneath the frontal andoccipital scalp muscles.

Traumatic bony lesions

Fractures of the vertex and the base of theskull can be linear or stellate, depressed or non-depressed. Subgaleal haematomas are often as-sociated with skull fractures of the calvaria.Therefore the detection of such haematomas ina child would indicate the performance of askull x-ray.

A “ping-pong ball” type depressed fracturein newborns may be a consequence of the useof the forceps during labour or due to fallsfrom a height. In most cases, cerebral pulsation

re-establishes the normal bone contour withinweeks of the initial injury.

The so-called “growing fracture” or lepto-meningeal cyst on the other hand occurs whenthe leptomeninges are entrapped between theedges of a skull fracture. Vascular and CSF pul-sations result in the progressive enlargement ofthe fracture site.


Fig.6.8 - Acute extradural haematoma. CT shows a biconvexextradural haemorrhage in the right frontoparietal region.Marked mass effect upon the underlying cerebral structures ispresent.

a

c

b

Depressed skull fractures are a consequenceof major traumatic impact and are often associ-ated with serious underlying cerebral injury.Therefore, CT must always be performed evenwhen there are no clinical neurological signs orsymptoms. This being said, most depressed

fractures smaller than 1 cm in diameter do notrequire surgical elevation. Fractures of the skullbase must be suspected in cases of periorbitalor retroauricular ecchymoses. They can some-times be associated with oto- or rhinorrhea andmandate the performance of a CT scan.


Fig. 6.9 - Posterior fossa extradural haematoma. a) CT shows a fracture of the base of the skull involving the occipital bone on theleft with anterior extension into the left petrous bone. b, c and d) CT reveals a posterior fossa extradural haemorrhage with signs ofcompression on the left cerebellar hemisphere and the 4th ventricle.

a

b

c

d

Meningeal lesions

Epi- or extradural haematomas usually occurfollowing arterial laceration in the space be-tween the inner and outer layers of the cranial

dura mater. The haematoma can potentially ex-tend to the margins of the dura mater, only be-ing delimited by the cranial sutures. Thesehaematomas appear as a sickle-shaped or bi-convex/lens-shaped lesion in cross section onCT (Figs 6.8, 6.9). Approximately 75% ofthese haematomas are associated with overly-ing skull fractures. If there are no other craniallesions, the patient may remain conscious anddevoid of neurological deficits until the in-tracranial structures are significantly compro-mised (i.e., the clinically lucid interval); if thehaematoma continues to enlarge, this earlyphase if followed by a rapid deterioration inconsciousness and the onset of focal neurolog-ical symptoms. At this point, surgical drainagebecomes imperative, and if performed swiftlytypically results in a good outcome. In infants,the lucid interval may be longer and the clini-cal signs less rapidly progressive. This is due, atleast in part, to the open state of the sutures ininfancy which allows for a limited expansion ofthe cranial case in the presence of a growinghaematoma. About half of infants do not loseconsciousness. Another complication, anaemiaand hypovolemic shock, may be observed insmaller babies.

Subdural haematomas are usually a conse-quence of the rupture of the bridging veins be-tween the brain and the dura mater. On CTacute subdural haematomas appear as a cres-cent-shaped extraaxial hyperdense collection(Fig. 6.10). There may be associated lesions ofthe underlying cerebral parenchyma. In pa-tients under one year of age, peripheral sub-dural haematomas, parenchymal haematomasand/or parafalcian haematomas are typical ofthe battered child syndrome. These findingsare in turn frequently associated with extracra-nial soft tissue ecchymoses and cranial fractureswhich are often star-shaped or depressed. Oth-er bony structures may also be fractured in bat-tered children, especially the ribs and limbs(Fig. 6.11).

Shaking trauma is a common cause of in-tracranial traumatic lesions. When babies aregrasped by the chest and shaken violently thehead is subject to intense whiplash and rotationforces due in part to the relative weakness of


a

b

Fig.6.10 - Acute subdural haematoma. Unenhanced CT showsa) a left occipital skull fracture and b) an acute right frontalsubdural haematoma.

the muscles of the neck and to the dispropor-tionate size of the head as compared to thebody at this age. This type of movement cancause the rupture of the bridging veins. Inter-hemispheric or convexity haematomas canevolve into the chronic stage. In such cases CTreveals low density blood collections, whereasMRI shows low signal on T1-weighted scansand high signal on T2-weighted sequences.

Neuroradiological investigations may revealthe simultaneous presence of acute and chron-ic haematomas, the consequences of repeatedtraumatic abuse. Subarachnoid haemorrhageand extradural haematomas are less frequentlyencountered, being more typically an expres-sion of direct, nonshaking trauma. Physicallyabused children may also show a variety ofparenchymal lesions, including: oedema, non-haemorrhagic contusions, and intraparenchy-mal haematomas.

In subjects who have suffered severe rota-tional forces, there may be a sudden rapid com-pression of the cervical spinal cord with a con-sequent contusion with or without haemor-

rhage, typically observed first at the grey-whitematter junction (10, 16, 24, 29).

Subarachnoid haemorrhage. In the more se-vere cranial injuries, there may be a widespreadhaemorrhage into the subarachnoid space,which exposes the patient to the risk of subse-quent development hydrocephalus due to ab-normalities in CSF reabsorption. CT revealshyperdensity within the basal subarachnoid cis-terns, the parietal subarachnoid spaces or theinterhemispheric fissure.

Posttraumatic parenchymal lesions

On CT oedema appears as a focal hypodenselesion that is sometimes on the opposite side ofthat of the traumatic impact. Alternatively, wide-spread swelling associated with small ventriclesand flattening of the cerebral sulci against theoverlying inner table of the skull. Oedema canalso typically be detected on the periphery ofacute/subacute haemorrhagic lesions after thefirst few hours following the event.

The malignant cerebral oedema syndrome isencountered exclusively in children, with an av-erage age at presentation of 6 years. The patho-genesis is not clear, however it is probably re-lated in part to a loss of cerebrovascular au-toregulation with resultant uncontrolled hyper-aemia. CT shows collapsed cerebral ventriclesand an obliteration of the cranial subarachnoidspaces. Frank oedema is more clearly visible inthe peripheral regions of the cerebral hemi-spheres; it is usual to observe relative sparing ofthe basal ganglia, thalami and structures of theposterior cranial fossa.

Cerebral contusion. Parenchymal contusionis the manifestation of direct trauma to thebrain tissue. Its macroscopic appearance de-rives from oedema, haemorrhage and necrosis.On CT, the appearance of brain contusion de-pends upon the components of the haemor-rhage: in most cases haemorrhage appears as aheterogeneous hyper- hypodense, mixed signallesion with indistinct margins. Multiple contu-sions are the sign of widespread cerebral dam-age. These extensive injuries are particularlywell shown on MRI.


Fig.6.11 - Chronic subdural haematoma resulting from shakinginjury in child. Unenhanced CT demonstrates a chronic left he-misphere subdural haematoma with a fluid-fluid level due tothe sedimentation of the haemorrhagic content. Also note thesigns of compression of the left lateral ventricle and shift of themidline cerebral structures.

Diffuse axonal injury (DAI) is caused by ac-celeration-deceleration phenomena that affectdifferent areas of the brain as the diffusion ofthe forces are applied on impact. The appear-ance of DAI on CT can vary from minor de-grees having a reduction in the differentiationbetween white and grey matter, small cerebralventricles and small quantities of intraventricu-lar blood, to more severe situations with multi-ple brain contusions, diffuse brain swelling,disappearance of the basilar subarachnoid cis-terns and involvement of the brainstem. Theinitial CT appearance may lead to an underesti-mation of the severity of the lesion, however thepatient’s clinical condition rapidly worsens.DAI may progress over the first 48-76 hours ofthe traumatic incident, making serial CT re-evaluations necessary. A system for classifyingthe severity of DAI has recently been proposed,based on the obliteration of the basal subarach-noid cisterns and on the degree of midline shiftwhen present (Tab. 6.1) (28, 42).

MRI is presently assuming a more importantrole in the evaluation of paediatric patientswith acute head injuries. The advantages of thetechnique include safety, multiplanar imagingcapability, excellent anatomical definition, ma-jor blood vessel identification without usingcontrast agents and critical posterior fossaanalysis absent of artefacts typically present onCT. The technique’s main disadvantages are therelatively long acquisition times and the unsuit-ability of the method in critical patients requir-ing continuous extracorporeal monitoring andlife support devices.

Therefore, with the exception of certain sit-uations (e.g., very small extraaxial haematomasover the cranial convexity or the posterior cra-

nial fossa, small contusions, DAI), the tech-nique of choice in the acute phase of cranialtrauma remains CT. MRI is of greater diagnos-tic utility in the subacute phase (e.g., suba-cute/chronic haematomas that may be isodenseon CT, posttraumatic white matter lesions suchas DAI) and in the evaluation of late sequelae(e.g., hydrocephalus, atrophy, monofocal/mul-tifocal encephalomalacia) (46).

CNS INFECTIONS

CNS infections are a rather varied group ofdisorders. Acute meningitis is an inflammationof the meninges and the CSF spaces. En-cephalitis is an inflammation of the cerebralparenchyma. Encephalitis may result as an ex-tension of a meningitic process or as a de novoisolated event.

The associated clinical symptoms vary inpart with age: in children the onset is abrupt,with fever, headache, vomiting, neck stiffnessand gait abnormality that may or may not be as-sociated with disorders of consciousness. Innewborns and infants the clinical signs andsymptoms are dominated by alterations of be-haviour and the sleep-wake pattern, digestivedisorders, hypotonia and tension/protrusion ofthe cranial fontanels.

Meningitis

In the absence of complications, neuroradio-logical investigations may not be useful in viralmeningitis (4, 35, 40). If performed, CT andMRI may be entirely normal or may show evi-


DEGREE OF CT APPEARANCE DEATH RATEDIFFUSE LESION

I Normal 9.6%II Cisterns present/Shift < 5mm 13.5%III Cisterns compressed/Shift < 5mm 34%IV Shift > 5mm 56.2%

Tab. 6.1.

dence of minor extraaxial fluid accumulationsurrounding the cerebral hemispheres (2). Inbacterial meningitis CT and MRI can be normal,show an increase in the density of the CSF orvariable, diffuse enhancement of the meningesafter IV contrast medium administration.

During the course of the illness, the persist-ence of fever and the appearance of seizures,focal neurological signs and/or signs of in-tracranial hypertension suggest the presence ofcomplications and indicate the need for the ex-ecution of diagnostic imaging examinations. Inyoung infants with purulent meningitis (esp.Haemophilus influenzae) it is possible to ob-serve the formation of extraaxial subdural fluidcollections that may be either uni- or bilateral.The pathophysiologic mechanism that leads tothe formation of such collections has not beenclarified. The fluid is serous-haematic, rich inpolymorphonucleocytes, and is usually sterile.On CT, such collections show increased densi-ty as compared to the normal CSF and follow-ing IV contrast medium injection, enhance-ment of the overlying meninges is typically ob-served (Fig. 6.12). In most cases spontaneousresolution of the extraaxial collections occurs;more rarely, these collections become chronic,may progressively increase and can undergofibrinous organization.

Approximately 90% of newborns with bac-terial meningitis present with concomitant ven-triculitis, an occurrence that is more rarely en-countered in older children. On CT or MRI di-latation of the cerebral ventricles is observed,often associated with intense contrast enhance-ment of the ventricular ependyma. Cerebralparenchymal alterations can also be seen in cas-es of purulent meningitis. Typically these alter-ations are small superficial infarctions due toseptic microemboli. On CT these infarcts ap-pear as hypodense, oedematous areas near thegrey-white matter junction. On occasion theremay be enhancement after IV contrast mediumadministration. More widespread cerebral in-farctions caused by septic thrombosis or spasmof the major cerebral arteries are rare.

Thromboses of the cranial venous sinuses,especially the sagittal sinus, are only rarely en-countered. Early in the process, CT demon-

strates hyperdensity of the venous sinus in-volved. Subsequently, the thrombus becomesisodense in relation to the cerebral parenchy-ma; at this point the IV administration of con-trast media shows an absence of enhancement


Fig. 6.12 - Subdural hygroma associated with haemophilus me-ningitis. CT shows a left hemispheric subdural hygroma with si-gns of mass effect upon the midline structures.

a

b

of the intraluminal thrombus (i.e., delta sign)and marked enhancement of the collateral dur-al venous draining structures. On MRI, throm-bosis of a venous sinus appears as a hyperin-tense signal on T1-weighted scans associatedwith partial/complete loss of the normal flowvoid within the sinus itself.

A possible complication of bacterial menin-gitis and septic embolization is the formation ofa cerebral abscess. A parenchymal abscess ap-pears as a heterogeneous mass resulting in thedisplacement of adjacent structures. On CTfollowing IV contrast medium administrationthere is typically peripheral enhancement in theform of a thin, regular thickness ring surround-ing a hypodense round-oval center. In more ad-vanced stages, the abscess may be multilocular,and adjacent secondary satellite abscesses maybe identified. The abscesses are typically locat-ed at the grey-white matter junction.

On MRI, during the initial phases of abscessformation, the wall of the lesion appears hyper-intense on both T1- and T2-weighted sequences,whereas the centre appears hypointense on T1-and hyperintense on T2-weighted images. Inmature abscesses, the wall is isointense on T1-weighted scans and markedly hypointense in T2-eighted acquisitions; the necrotic central portionis slightly hypointense on T1-weighted and hy-perintense on T2-weighted scans. The enhance-ment pattern after IV contrast medium injectionis the same as that described for CT.

Tuberculous (TB) meningitis is today a rela-tively rarely encountered disease process in in-dustrialized countries, although with the AIDSepidemic, the infection is once again on the risein incidence. TB meningitis has a bimodal dis-tribution, affecting young infants and the elder-ly. The involvement of the central nervous sys-tem results from haematogenous disseminationof the bacilli, usually from a site in the lung; TBmeningitis in infants almost always coincideswith primary pulmonary TB. The clinical pres-entation in this young age group often differsfrom that of classic bacterial meningitis (e.g.,inconsistent fever, stiff neck, headache, non-spe-cific prodromal signs, greater incidence of focalneurological deficit, involvement of the cranialnerves, disorders of consciousness including

coma). The involvement of the meninges can besecondary to the rupture of a small tuberculo-ma of the adjacent cerebral cortex or spinalcord, or to direct haematogenous disseminationto the meninges. A gelatinous exudate fills thebasal subarachnoid cisterns; vasculitis andthrombosis of the lenticulostriate and thalam-operforating arteries frequently result from thisexudate and communicating hydrocephalus iscommon (i.e., 50-75% of cases).

The typical CT finding in TB meningitis ishomogeneous hypodensity within the basal sub-arachnoid cisterns, with marked enhancementafter IV contrast medium administration. MRIshows a hyperintensity of the basal cisterns onT1-weighted sequences. Septic emboli leadingto the formation of tuberculomas localized at thegrey-white matter junction may be isolated ormultiple and supra- and/or infratentorial. OnCT tuberculomas appear hypodense with indis-tinct margins with mass effect and intense en-hancement after IV contrast medium injection.

The differential diagnosis in such cases in-cludes other forms of granulomatous/neoplas-tic meningitis, such as cryptococcosis, coccid-ioidomycosis, sarcoidosis and diffuse carcino-matosis.

Encephalitis

Viral encephalitis (23, 34, 36, 44) caused byHSV1 (herpes virus 1) is one of the most com-mon forms of cytotoxic encephalitis encoun-tered in infancy and childhood. The clinical syn-drome in infants is characterized by the pres-ence of fever, seizures that are often unilateral,disorders of consciousness including coma andfocal neurological signs. In newborns, patientsmay be asymptomatic, but the ultimate mortali-ty is higher than in the older age groups. The di-agnosis is based on CSF data (e.g., the presenceof specific IgM antibodies, the demonstration ofviral replication through PCR), EEG recordings(e.g., temporal, periodic, slow wave abnormali-ties) and medical imaging findings.

CT is the first diagnostic imaging examina-tion performed in emergency situations in thesecases. The initial findings may be negative, in


part due to the relatively poor resolution of thetemporal fossae as a result of bone-related arte-facts. A negative CT examination must not ex-clude immediate, specific antiviral treatment.

Some days later, CT may show hypo- hyper-density of one or both temporal lobes, oede-ma/mass effect and sometimes contrast en-hancement.


Fig. 6.13 - Herpes encephalitis. a, b) CT shows cortical and subcortical temporal-insular hypodensity with signs of associated cere-bral swelling. Corresponding c) coronal T2-weighted and d) sagittal T2-weighted MRI in the subacute phase.

c

d

a

b

MRI is far more sensitive in detecting theseparenchymal alterations, even within the first24-48 hours from onset of the event. In theacute phase after contrast medium administra-tion selective enhancement of the hippocampusmay be observed, demonstrating the affinity ofthe virus for the hippocampal, parahippocam-pal and insular cortex. In the case of wide-spread infection, MRI may reveal lesions in thecentral/anterior temporal cortex, the insula andthe grey matter nuclei of the cerebral hemi-spheres (Fig. 6.13). At a later stage, MRI showsatrophy in one or both of the two amygdaloidnuclei (70-80% of cases) associated with hip-pocampal atrophy. Overall, CT shows a sensi-tivity of 73% and a specificity of 89% duringthe first 5 days of the illness and 90% and 92%respectively from the 6th day onwards. Howev-er, there are many other pathological condi-tions that can simulate herpesvirus encephalitisincluding cerebritis, early abscess formation,TB meningoencephalitis, cryptococcosis andeven some brain tumours.

In newborns, the most frequently encoun-tered form of herpesvirus encephalitis is HSVtype 2. This viral particle is transmitted to theinfant during delivery via an infected birthcanal. The risk of such infection is greater dur-ing delivery, whereas intrauterine infection israre. The typical clinical manifestation is rep-resented by a mucocutaneous vesicular erup-tion; without treatment, 75% of cases evolveinto encephalitis. The disease usually presentsduring the second week of life. Common clin-ical signs and symptoms include poor ap-petite, lethargy, seizures, fever and signs ofsepsis.

On CT and MRI the most frequent findingof herpes encephalomyelitis is focal oedema lo-calized in most cases in the temporal lobes.However, these patients may also present withinvolvement of the frontal or parietal lobes oreven the entirety of one or both hemispheres.In the later phases, widespread cortical atrophywith areas of porencephalic cyst formation isthe most common finding; calcifications bothin the cortex and the white matter are also fre-quently observed. There is cerebellar involve-ment in 50% of cases.

Acute Disseminated Encephalomyelitis

Acute disseminated encephalomyelitis (ADEM)is a demyelinating disorder associated with a pre-vious viral infection or antiviral immunization thatacts through an autoimmune mechanism (17, 31).Many viral infections can precede ADEM, includ-ing measles, mumps, chickenpox, influenza, viralhepatitis and also infections from Campylobacter,mycoplasm, and rarely streptococci.

The clinical onset is characterized by thesudden appearance of signs and symptoms in-volving scattered areas of the CNS associatedto headache and dizziness and, more uncom-monly, minor fever. MRI shows multifocal de-myelinating lesions, sometimes of considerablesize, which can pose problems of differentialdiagnosis with MS (Fig. 6.14). However, theclinical pattern is monophasic; there is a ten-dency towards slow resolution over time. Typi-cally there are residual chronic areas of gliosison imaging studies.

INTRACRANIAL HYPERTENSION

Normal intracranial pressure is the result ofthe pressures exerted by the cerebral parenchy-ma, blood vessels and CSF; on average, thecerebral tissue and the support structures occu-py 70% of the intracranial volume, whereas thevascular component, CSF and interstitial waterportion account for 10% each of the remain-der. Intracranial hypertension in children is de-fined as a condition in which intracerebralpressure is higher than 15 torr in babies ormore than 7 torr in newborns (1, 20, 39).

As in adults, regarding pathophysiology thereare three different potential sources of intracra-nial hypertension: abnormalities of the cerebralparenchyma, the CSF compartment and the vas-cular tissue. The previous chapter should beconsulted for parenchymal and vascular causes;attention will be paid here to the CSF compart-ment, and in particular, hydrocephalus.

The clinical characteristics with which in-tracranial hypertension presents are variable,depending on the compensating mechanismsand the age of the patient.


Compensated intracranial hypertension

The signs and symptoms of intracranial hy-pertension include headache, vomiting and vi-sual problems as well as other less specific con-ditions such as tinnitus, dizziness, behavioural

alterations, irritability, mood swings, and sys-temic vasomotor abnormalities that are mani-fested by paleness or intense flush.

The headache may present in a frontoorbitalor occipital location, often has an intermittentcharacter, and it tends to worsen with the evo-


Fig. 6.14 - Acute disseminated encephalomyelitis (ADEM). a,b) CT demonstrates areas of hypodensity of the subcorticalwhite matter. c-e) axial T2-weighted and d) coronal T2-weigh-ted MRI reveals regions of signal alteration in the subcorticalwhite matter with associated mass effect.

a

d

b

c

lution of the illness. In cases where there is amobile intraventricular mass lesion, theheadache has a positional character wherebyhead movements can alter its intensity. Theseheadaches are refractory to even the most pow-erful analgesics. The vomiting is sudden and“projectile” in character, and is not precededby nausea; it is often the first sign of illness.

Visual involvement is represented by hori-zontal diplopia caused by a uni- or bilateralparalysis of the 4th cranial nerves; the 3rd cranialnerves are less frequently affected. On occasionthere may be a frank reduction in vision, al-though this suggests an unfavourable coursethat can lead to ischaemia of the optic nerveand permanent loss of sight. Ophthalmoscopicexaminations may detect papillary oedemawhen intracranial hypertension has been pres-ent for some days; whitish exudates along thecourse of the peripapillary vessels may be ob-served together with flame-shaped haemor-rhages of a venous origin, both of which arenegative prognostic factors relative to irre-versible visual loss.

Patients with elevated intracranial pressuremay present with anoxic-ischaemic attacks sec-

ondary to low cerebral perfusion pressure.These events have a limited duration and acomplete remission; clinically an intense asthe-nia can be observed, together with problems ofvigilance, changes in muscle tone and extremi-ty tremors. If intracranial pressure is higher, in-ternal herniation of the cerebral parenchymamay occur, which in turn can lead to seriousclinical consequences. According to the anatom-ical site, these internal herniations include: lat-eral herniation of the cingulate gyrus beneaththe free edge of the falx cerebri, lateral midlineshifts, downward herniation of the structures ofthe medial temporal lobe through the tentori-um cerebelli, downward herniation of the cere-bellar tonsils through the foramen magnum,downward herniation of the diencephalon andthe brainstem, and upward herniation of theposterior fossa contents through the tentoriumcerebelli.

The clinical presentations can be subdividedinto central, temporal or cerebellar involve-ment. In central involvement, the clinical signsinclude:– diencephalic: disorders of consciousness, al-

teration of muscle tone, absence of photo-motor reflex, myosis, Cheyne-Stokes respi-ration;

– mesencephalic: coma, decerebration, Cheyne-Stokes respiration or shallow hyperventila-tion, non-reactive pupils, altered ocular-vestibular reflex;

– pontine: rapid shallow breathing, non-reac-tive pupils in intermediate position, absenceof oculovestibular reflex;

– medullary: slowed breathing alternatingwith phases of apnoea and gasping, dilatednon-reactive pupils.

In temporal involvement, the clinical signsinclude:– ipsilateral/bilateral pupil dilation caused by

the compression of the 3rd cranial nerve(s);– contralateral hemiplegia or hemiparesis due

to the compression of the cerebral pedun-cles;

– cortical blindness due to haemorrhagic in-farction of the mid-inferior portion of theoccipital lobe secondary to the compression


Fig. 6.14 (cont.).

e

of the ipsilateral posterior cerebral arteryagainst the free edge of the tentorium cere-belli;

– bradycardia, disorders of consciousness, de-cerebrate posturing and hyperventilation inresponse to nociceptive stimuli secondary tocompression of the brainstem.

In cerebellar involvement, the clinical signsinclude:– opistotonus;– nystagmus.

The clinical picture will vary yet more if theintracranial hypertension occurs before closureof the cranial sutures. Tab. 6.2 shows the clini-cal difference between an acute increase of theintracranial pressure in children over and un-der the age of two.

Clinical presentation in children under two years of age

Intracranial hypertension presents physical-ly with a rapid increase in the skull circumfer-ence; repeated measurements are particularlyimportant as the rapidity of growth provides anestimate of the degree of severity.

Clinically, macrocephalia (defined as skullcircumference >98° percentile or >2 standarddeviation than average for that age) is manifest-ed by symmetric enlargement of the cranium.The anterior fontanel is tense or even outward-

ly bulging and pulsating. The cranial suturesare widened and palpable, the scalp appearsthin and the superficial veins are dilated.

Ocular examination may show a “settingsun” phenomenon, characterised by a con-joined deviation of the glance downwards sothat the iris is covered by the lower eyelid,whereas the sclera is exposed at the top; nys-tagmus, proptosis and a reduction in the pupil-lary reflex to light complete the clinical picture.

Clinical presentation in children over two years of age

Intracranial hypertension that arises later inchildhood presents with signs and symptomsthat include: headache on awaking that im-proves when in an erect position, vomiting, pa-pilloedema, strabismus, cerebellar signs andmotor spasticity. Moreover, the chronic com-pression of the hypothalamic-pituitary axiscaused by the dilatation of the inferior recessesof the 3rd ventricle can cause endocrine abnor-malities.

Hydrocephalus

Making a diagnosis of the precipitatingcause of hydrocephalus (1, 22, 39) is importantas the prognosis is in part connected to themechanism that caused the ventricular dilata-tion. Estimates in paediatric cases indicate that


Specific signs Common signs Specific signs

Child under 2 Child over 2

Papilloedema Mental alterations HeadacheMacrocrania StrabismusTense fontanelle Signs of cerebral herniation

«Setting sun» sign

Suture diastasis Alteration of vital parameters Papilloedema

Tab. 6.2.

38% of cases are caused by congenital cerebralmalformations, 20% by neoplasia or otherspace-occupying lesions, 15% by haemor-rhages, 7% by meningitis and the remainder byundetermined conditions.

From the standpoint of pathogenesis, thereare two types of hydrocephalus: that due to anexcessive production of CSF and that due to anobstruction of flow or insufficient absorptionof CSF (Fig. 6.15).

Congenital cerebral malformations

Congenital hydrocephalus may result from avariety of cerebral malformations:– Dandy-Walker malformation: enlargement

of the 4th ventricle accompanied by partial orcomplete agenesis of the cerebellar vermis;in many cases hydrocephalus is not presentat birth but develops during the first year oflife;

– Neural tube closure defects;– Cerebral aqueduct stenosis;– Arnold-Chiari malformations: especially

type II, in which in addition to the cere-bral malformation myelomenigocele is alsopresent;

– Malformation of the vein of Galen: com-pression of the aqueduct of Silvius resultingfrom aneurysmal dilation of the vein ofGalen;

– Premature craniosynostosis.

Neoplasia and space-occupying lesions

The manner in which a space-occupying le-sion within the cranium produces signs andsymptoms is partially linked to the position ofthe mass and its rapidity of growth.

Neoplasia is a relatively common cause ofhydrocephalus in infancy. The location ofbrain tumours during childhood is somewhatage-dependent: in the first six months of lifeneoplasia has a preferential supratentorial lo-calization; between the 7th and 12th months tu-mours have a balanced incidence of supra-subtentorial localization; and after the first

year of life, neoplasia is typically localised inthe posterior fossa.

The most common primary neoplasia in thisyoung age group includes medulloblastomas,ependymomas and those tumours recently de-fined as “scarcely differentiated embryonic tu-mours”. Papillomas of the choroid plexuses, al-though only representing 2-5% of intracranialtumours in childhood, often result in hydro-cephalus due to an excessive production ofCSF. Typically they are located in the lateralventricles and less frequently in the 3rd and 4th

ventricles.

Haemorrhages

Haemorrhage can cause hydrocephalus forvarious reasons. In the acute phase blood clotsmay cause an intraventricular obstruction; inthe chronic phase obstruction may be the resultof meningeal adhesions or granular ependymi-tis. Spontaneous haemorrhages arise most fre-quently in preterm newborns.

Infectious processes

Acute or chronic meningeal infections mayprecipitate hydrocephalus if adhesions andsubarachnoid pathway stenosis arise. The typesof meningitis most frequently responsible forhydrocephalus include toxoplasmosis, cyster-cercosis and tubercular meningitis.

Neuroimaging techniques (e.g., ultra-sound, CT and MR) are fundamental in de-termining the presence and aetiology of hy-drocephalus. In complex abnormalities, thesite of the obstruction can be documented us-ing a CT utilizing intrathecal contrast medi-um, administered via lumbar puncture. Auterine diagnosis of hydrocephalus using pre-natal ultrasound has potential therapeutic im-plications.

Dilated ventricles under normal pressurecan be associated with passive cerebral atrophy(i.e., ex vacuo ventricular dilatation), cerebralmalformations (e.g. developmental cerebralwhite matter hypoplasia such as lissencephaly


and culpocephaly) and arrested, non-progres-sive hydrocephalus. The radiological character-istics that suggest a high pressure hydro-

cephalus include compressed superficial sulciand periventricular oedema (i.e., transependy-mal CSF absorbtion/penetration).


Fig. 6.15 - Communicating hydrocephalus. a and b) CT shows marked dilatation of the entire cerebral ventricular system. c) axial PD-weighted MRI again demonstrates the marked ventricular dilatation. d) Sagittal T1-weighted, and d, e) sagittal T2-weighted MRI re-veals the patency of the aqueduct of Sylvius, ventricular dilatation, thinning and upward expansion of the corpus callosum, and ex-pansion of an “empty” the sella turcica. In the posterior fossa, note the enlargement of the extraventricular cranial subarachnoid spa-ces and a prominent cisterna magna.

a

b

c

d

Cerebral neoplasia in childhood

Generally speaking, intracranial neoplasia(7, 8, 13, 19, 22, 38, 41) in childhood representsthe most frequent group of neoplasia afterleukaemia. The diagnosis of neoplasia is con-firmed by neuroimaging techniques. The clini-cal signs and symptoms vary with age, thechild’s neuropsychiatric condition and tumourlocation. The most common clinical manifesta-tions are those that can be attributed to in-tracranial hypertension, although focal signsmay be present and suggest the site of the pri-mary lesion.

In most cases, MRI with or without IV con-trast agent administration or CT after IV con-trast medium injection can of course provideexcellent definition of space-occupying lesionsof the brain. MRI in particular is able to reveallesions that are situated in regions that may bedifficult to visualize using CT (e.g., posteriorfossa, spinal canal). T1-weighted images pro-vide an excellent definition of the anatomy andT2-weighted acquisitions clearly identify boththe tumour and the surrounding oedema whenpresent. Long image acquisition times and the

need for sedation represent limiting factors ofMRI in smaller children.

Other diagnostic techniques tend to be lessvaluable: angiography provides information re-garding the vascularization of the tumour andexcludes the possibility of a vascular malforma-tion; MRA replaces this examination in manycases of gross hypervascularization.

Analytical details concerning the variousforms of cranial neoplasia are provided in oth-er chapters; we will therefore presently discussthe neuroradiological characteristics of the tu-mours most frequently encountered in the pae-diatric population.

Medulloblastoma

This is the most frequent type of neoplasmencountered in the posterior fossa during in-fancy. Up to 40% of medulloblastomas are di-agnosed in children five years of age or under.The main signs and symptoms include nausea,vomiting, headache, ataxia and macrocephaly.On CT, medulloblastomas are typically well-de-fined mass lesions originating from the cerebel-lar vermis with or without extension into thecerebellar hemispheres. On unenhanced CT,these tumours are hyperdense lesions sur-rounded by a perilesional hypodense oedema.Contrast enhancement of the neoplasm may behomogeneous or irregular. In up to 20% of cas-es, medulloblastomas contain cystic or necroticareas and more rarely calcifications. In a highpercentage of patients the compression or inva-sion of the 4th ventricle results in obstructivehydrocephalus. On MRI the mass is typicallyhypointense on T1-weighted images and slight-ly hyperintense on T2-weighted sequences inrelation to the normal cerebellar parenchyma.Considerable enhancement of the tumour isusually observed after IV gadolinium injection(Fig. 6.16).

Cerebellar Astrocytomas

Astrocytomas can originate in any point ofthe cerebellum and spread to the cerebellar


Fig. 6.15 (cont.)

e

hemispheres in 30% of cases. They are general-ly quite large, of a primarily cystic nature (e.g.,pilocytic astrocytomas), but can also be solidwith or without an intrinsic necrotic area.

On CT or MRI cerebellar astrocytomas inthis age group typically present as a voluminous

mass with a vermian or hemispheric location.They are frequently cystic and slightly hypo-dense on unenhanced imaging studies. After IVcontrast medium administration, there is en-hancement in up to 50% of cases. On MRI thesolid components are typically hypointense onT1-weighted images and hyperintense on T2-weighted acquisitions. The signal characteris-tics of the cystic components depend on thecontent of the cavity. Uncomplicated, simplecysts yield an MR signal similar to that of CSF;intracystic necrotic material on the other handproduces a signal on T1-weighted images thatis slightly hyperintense in comparison to CSF,which becomes yet more hyperintense on T2-weighted sequences.

Papillomas of the choroid plexus

These tumours represent 5% of supratento-rial tumours and less that 1% of intracranialneoplasia in infants. This type of neoplasia orig-inates from the epithelium of the choroidplexus and has papillary and/or carcinomatouscharacteristics. Signs and symptoms can be sec-


Fig.6.16 - Obstructive hydrocephalus associated with posteriorfossa medulloblastoma. a) sagittal, b) axial and c) coronal T1-weighted MRI following IV gadolinium administration revealsinhomogeneous enhancement of a midline posterior fossa massassociated with poorly defined borders and with signs of com-pression of the 4th ventricle and brainstem. Note the early ob-structive hydrocephalus.

a

b

c

ondary to hydrocephalus as well as local cere-bral infiltration.

On CT choroid plexus papillomas appearas intraventricular masses with irregularboundaries and are generally isodense in rela-

tion to the cerebral parenchyma; they are onoccasion hyperdense and may show peritu-moural oedema. After IV contrast mediumadministration, one may observe a somewhathomogeneous enhancement of the lesion. Of-


Fig.6.17 - Papilloma of the choroid plexus. a) CT shows an intraventricular mass lesion associated with obstructive hydrocephalus.b) PD-weighted and c) T2-weighted MRI shows an intraventricular mass lesion with inhomogeneous signal on long TR sequences, inpart possibly due to intratumoural macroscopic neoplastic vasculature. Also noted is obstructive hydrocephalus and signs of transe-pendymal resorption of CSF. d) digital angiogram confirms the neovascularisation of the intraventricular neoplasm.

a

b

c

d

ten, the papillomatous forms are associatedwith severe hydrocephalus. On MRI, these tu-mours appear homogeneous or non-homoge-neous in intensity; the mass can be better vi-sualized on T1-weighted scans; on both con-trast enhanced studies and T2-weighted imag-ing the tumour and the CSF appear hyperin-tense and are therefore poorly differentiated(Fig. 6.17).

Pseudotumour cerebri (benign intracranial hypertension)

Pseudotumour cerebri (14) is a condition ofintracranial hypertension whose salient clinicalsigns and symptoms are represented byheadache, papilloedema, diplopia and progres-sive visual loss. The CSF reveals a high proteinbut a normal cellular composition.

Pseudotumour cerebri can be precipitatedby a number of factors including obesity, var-ious medicines (e.g., antibiotics, vitamin Aand indometacin), and endocrinopathy, al-though most frequently it remains a patholog-ical condition of unknown aetiology that ismost commonly encountered in infants andadult female.

Neuroimaging techniques represent the de-finitive diagnostic method of patient evalua-tion by enabling the exclusion of neoplasticcauses and cases resulting from thrombosis ofthe cranial dural venous sinuses. The diagno-sis is made by showing normal cranial imagingfindings; an ancillary imaging sign is disten-sion of the optic subarachnoid space withinthe sheaths of the optic nerves, and in 1/3 ofcases, an empty sella. In most cases, the treat-ment is medical (e.g., diuretics, steroids, andCSF drainage); patients usually recover, how-ever permanent visual loss or even blindnessmay ensue in untreated cases.

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42. Toutant S, Klauber MR, Marshall L et al.: Absent or com-pressed basal cysterns of the first CT scan: ominous pre-dictors of outcome in severe head injury. J Neurosurg 61:691-694, 1984.

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403

acquired hepatocellular degeneration (AHCD) 245

acute disseminated encephalomyelitis (ADEM) 366,391, 392

acute transverse myelitis 365ADC, see apparent diffusion coeffi-

cientADEM, see acute disseminated en-

cephalomyelitisAHCD, see acquired hepatocellular

degenerationalcoholic 32, 242– encephalopathy 241anaemia 34anaplastic choroid plexus

papilloma 222anastomosis 94aneurysm 112, 121– Charcot-Bouchard 42– in children 375– multiple 49– of the basilar artery 55– of the circle of Willis 49– of the distal vertebral

cerebellar artery 55– of the middle cerebral

artery bifurcation/trifurcation 55– of the pericallosal artery 56– of the posterior inferior cerebellar

artery 55– of the supraclinoid internal carotid

artery 55– rupture 28, 31, 52, 53, 89– – of the anterior communication ar-

tery 54aneurysmal bone cyst 341angiography 4– conventional 117– in infants 376angioplasty– internal carotid artery 126

– left subclavian artery 125– middle cerebral artery 127– percutaneous 122anoxia 269anterior communication artery 54aortic coarctation 112apparent diffusion coefficient (ADC)

66, 74aqueduct of Sylvius 149, 158, 204aqueductal stenosis 205arachnoid– cyst 352, 353– villi 198Arnold-Chiari malformation 206, 207,

395arterial– embolism 380– thrombosis 14arteriovascular malformation rupture

28arteriovenous– fistula 156– malformation (AVM) 25, 31, 53, 115– – in infants 374articular abnormality 300astrocytoma 218, 234, 353ataxia 243atlanto-occipital dislocation 303atrophy 32AVM, see arteriovenous malformationaxial– compression trauma 316– herniation 200axonal injury 167

back pain 338bacterial– encephalitis 25– meningitis 388BAEP, see brainstem auditory evoked

potentialbasilar artery 55

benign tumour 339bleeding 87blood– clot 36– – liquefaction 151– CSF 46– high pressure 29– proton 102blood–brain barrier breakdown 15B-mode echotomography 94bone scintigraphy 338bony spinal canal stenosis 338brachiocephalic vessel 103brain– contusion 148– death 177, 261, 263, 265, 275– haemorrhage 17– lesion 131, 137– perfusion 76– swelling 203, 257, 263, 264, 281– trauma 263– tumour 229, 391brainstem 255, 393– auditory evoked potential (BAEP)

268, 276– – determination 268– lesion 171– perfusion 271– traumatic lesions 146burst fracture 316

CAA, see cerebral amyloid angiopathycampylobacter 391capsulo-putaminal haematoma 37caput succedaneum 382carbon monoxide intoxication 250carotid ratio (CR) 96catastrophic syndrome 373cavernous– angioma 364– vascular malformation in children

375

SUBJECT INDEX

cavum septi pellucidi 55CBF, see cerebral blood flowcentral nervous system (CNS) 241– infection 387– toxin 241central spinal canal 323centrum semiovale 152cephalohaematoma in newborns 381cerebellar astrocytoma in childhood

397cerebellum diaschisis 269cerebral– abscess 389– amyloid angiopathy (CAA) 33– angiography 229, 277– aqueduct stenosis 395– blood flow (CBF) 255, 276– contusion 167, 386– haematoma 382– haemorrhage 33, 118, 119– herniation 200– infarction 58, 118– ischaemia 7, 58, 63, 117, 119, 260,

267, 269– metastases 236– microcirculation damage 66– neoplasia in childhood 397– oedema 155, 176, 201, 261, 267,

279, 286– perfusion 64– – pressure (CPP) 276– swelling 175cerebrospinal fluid (CSF) 18, 28, 90,

195, 275– fistula 288, 289– leakage 160, 291– production 198cerebrovascular disease in infants and

newborns 371cervical– disectomy 290– laminectomy 290– spine 288– – fracture 180– – trauma 308, 313– – flexion trauma 330Charcot-Bouchard aneurysm 42chemical– arachnoiditis 57– shift 80choline (Cho) 80chondrosarcoma 341choroid plexus papilloma 234chronic alcoholics 32circle of Willis 12, 52, 94, 105– aneurysm 49circulatory system shock 292cisternal hyperdensity 52clot– density 36– lyses 14clotting 91– and platelet disorder 372CNS, see central nervous systemcoiling 95, 98coma 179, 245, 253, 271– depassée 275– high grade 180

– irreversible 275– low grade 181– postanoxic 265, 269– posttraumatic 267comma-shaped haematoma 56commissural lesion 170communicating hydrocephalus 207,

209, 396complete ictus 3compression ischaemia 154computed tomography

(CT) 4– angiography 5, 53– coma 253– myelography 334– scanogram 312– semeiotics 8– spinal structures 302congenital hydrocephalus 395continuous wave (CW) 95contrast– enhancement (CE) 19, 103– medium 43, 57, 139, 277contusion 166– cerebral 167– cortical 142– haemorrhagic 166– haemorrhagic 173– non-haemorrhagic 166– of the brain 148contusion-shearing injury 168conventional angiography 117corpus callosum 142cortical– contusion 142– sulcus 50cortico-medullary junction 153CPP, see cerebral perfusion pressureCR, see carotid ratiocranial– injury 182– neoplasia 235– trauma 132– – closed 137– – contrast medium 139– – open 137craniectomy 284, 286craniopharyngiomas 213craniotomy 284, 287cranium 182cryptic angioma 35– rupture 31cryptococcosis 391CsA, see cyclosporin ACSF, see cerebrospinal fluidCT, see computed tomographyCW, see continuous wavecyclosporin A (CsA) intoxication 249cyst, leptomeningeal 25, 160cystic– formation 25– myelomalacia 322cytotoxic oedema 13, 66, 69, 202, 261DAI, see diffuse axonal injuryDandy-Walker malformation 395deep grey structure– traumatic lesions 146deoxyhaemoglobin 35, 165, 217, 328

depressed skull fracture 384Devic’s disease 357diabetes insidipus 160diencephalon 393diffuse axonal injury (DAI) 140, 145,

259, 260, 387diffusible tracer 64diffusion weighted– factor 66– imaging (DWI) 5, 73, 79digital subtractive angiography (DSA)

101, 118diplopia 196, 393disk abnormality 300diskitis 341disorder of recent memory 196distal vertebral cerebellar artery 55Doppler-effect echotomography 95DSA, see digital subtractive angiogra-

phydura mater 140, 148Duret haemorrhage 158DWI, see diffusion weighted imagingdysfunction 255

ECD, see echo-colour-Dopplerecho planar imaging (EPI) 65, 59echo-colour-Doppler (ECD) 95echo-Doppler (Duplex) 95ectodermal tumour 230embolism 14, 70, 93embolus 64embryogenic tumour 230emergency surgery 134, 165empty delta sign 24encephalitis 387– bacterial 25– herpes 390– viral 25, 389encephalomalacia 144, 160encephalopathy– toxic 241– Wernicke 243endocrinological alteration 196endoluminal clot lyses 14ependymoma 211, 234, 353, 354, 360– gyral 24– intravascular 19– leptomeningeal 20– of the conus medullaris 361– parenchymal 20– vascular 19epiaortic vessel 106epidural– abscess 341– haematoma 147, 172, 254, 286, 385– haemorrhage 118, 146erythrocyte– alteration 90– lysis 86ethylene-glycol intoxication 246Ewing’s sarcoma 341extraaxial– haemorrhage 285– traumatic lesion 147, 171– arachnoid cyst 346– haematoma 172, 385extrapontine myelinolysis 242

404 SUBJECT INDEX

ex-vacuo ventricular enlargement 208eyesight impairment 196

facial– injury 182– skeleton 181, 182– trauma 179false localizing sign 160falx cerebri 158, 159, 200fast spin echo (FSE) 5, 88fibromuscular dysplasia 119, 379fibrosarcoma 341fistula 156– spinal dural arteriovenous 362– thoracic spinal dural arteriovenous

363– thoracic spinal region 358FLAIR, see fluid attenuation inversion

recoveryFLASH 65flexion trauma 319fluid attenuation inversion recovery

(FLAIR) 52focal– neurological deficit 182– oedema 142fogging effect 17, 20, 21foramina of Monro 204fracture– in newborns 383– of the bony orbit 187– of the lower (caudal) cervical spine

322– of the mandible 183– of the maxilla– – complex 188– – simple 183– of the nasal bone 183– of the nasal-ethmoid midface 189– of the occipital condyle 303– of the thoracic and lumbar spinal

segments 322– of the upper (cranial) cervical spine

322– of the zygomatic arch 183, 184– ping-pong ball type 383Froin’s syndrome 210FSE, see fast spin echo

gadolinium 65, 103, 108, 347GCD, see Guglielmi detachable coinGCS, see Glasgow Coma Scale German plane 138germinoma 214Glasgow Coma Scale (GCS) 133, 380glioblastoma 211, 233, 234, 359– multiforme 216, 353gliocarcinoma 31glioma 211, 233gliosis 323global– cerebral hypoxia 269– hypoperfusion 262globus pallidus 251glucose 85, 266gradient-recalled echo (GRE) 88growing fracture 383Guglielmi detachable coin (GDC)

124, 127gyral enhancement 24

haemangioblastoma 353, 355haemangioma 339– metameric 340– vertebral 339haematoma 29, 34, 145, 284– capsulo-putaminal 37– comma-shaped 56– epidural 146, 147, 286, 385– extradural 385– intraparenchymal (IPH) 51, 59– putaminal 28, 32– subdural 59, 146, 149, 151, 173,

371, 385– thalamic 31– traumatic intraparenchymal 144haematomyelia 291haemoglobin 34, 50, 84, 165, 250– alteration 90haemophilus influenzae 388haemorrhage 4, 18, 259, 326– arterial infarct 22– cerebral 33, 118, 119– contusion 166, 173– differential diagnosis 44– epidural 118– extraaxial 285– in childhood 395– in infants 374– in newborns 371– infarct 42, 46– infratentorial 88– intraaxial 83, 284– intracranial 83– intraparenchymal (IPH) 27, 371– intratumoral 355– intraventricular 46, 88, 146– lobar 41, 42, 88– mesencephalic 164– multiple 47– non-ischaemic 24– nucleo-capsular 87– parenchymal 118– petechial 23– pontine 43– putaminal 37, 39– stroke 4– subarachnoid 49, 118, 121, 123, 154,

155, 172, 371, 386– subcortical intraparenchymal 41– subdural 118– thalamic 39haemosiderin 84, 87, 217, 332Hangman’s fracture 304, 310head– injury 131, 137, 381– – in children 380– – open 140, 143– trauma 133headache 150, 195helical scan 139hemiplegia 96, 376hemispheric cerebral infarction 203heparinization 119herniation– axial 200

– internal cerebral 158, 199, 213, 220,223

– subfalcian 158, 200, 223, 255– temporal 200– tonsillar 158– transphenoid 158– transtentorial 158, 223herpes– encephalitis 390– virus 389Heubner’s artery 10hexamethyl propylene-amine-oxime

(HMPAO) 266hippocampus 391HMPAO, see hexamethyl propylene-

amine-oximeHorner’s syndrome 105hydrocephalus 43, 51, 58, 59, 160,

195, 203, 205, 206, 213, 287, 288,394

– communicating 206, 207, 209, 396– congenital 395– CSF sequestration 226– hyperfunction of the shunt 226– hypersecretory 208– infection 226– normotensive 207– obstructive 205– recurrence 226hygroma 156, 175hyperaesthesia 89hypercapnia 198hyperdensity 36– cisternal 52hyperextension 303– trauma 316, 319hyperflexion trauma 313hyperplasia of the Alzheimer type 246hypersecretory hydrocephalus 208hypodensity 36hypo-isodensity 260hyponatraemia 243hypophysis 288hypotonia 30hypoxia 269hypoxic-ischaemic injury in newborn

374

iatrogenic epidural abscess 345ICH, see intracranial hypertensionICP, see intracranial pressureinfarct, see infarctioninfarction 287– cerebral 58– – posttraumatic 159– differential diagnosis 24, 44– haemorrhagic 46– hemispheric cerebral 203– lacunar 23– venous haemorrhagic 23infection 33, 286– in childhood 395– myelitis 365– postsurgical 224, 289– spinal 289– spinal column 292infratentorial haemorrhage 88injury

SUBJECT INDEX 405

– axonal 167– contusion-shearing 168– cranial 182– diffuse axonal 140, 145– facial 182– of larger arteries and veins 159– of the head 131, 137, 140– shearing 170, 171internal– carotid artery 156– cerebral herniation 157, 176, 199,

213, 220, 223interstitial oedema 203intoxication 211– carbon monoxide 250– cyclosporin A (CsA) 249– ethylene-glycol 246– methanol 246– methotrexate 247intraarterial fibrinolysis 121, 124intraaxial– haemorrhage 83, 284– lesion 140– traumatic lesion 166intracerebral tumour 211intracranial– air collection 160– aneurysm 372– haemorrhage 83, 258– hypertension (ICH) 195, 391– – cerebral perfusion 199– neoplasia 213– pressure (ICP) 196, 255, 276– – cerebral function 201– – homeostasis 198– – waves 198– tumour in childhood 395– vessel 105intraparenchymal– haematoma 51, 59– haemorrhage (IPH) 27, 371– – contrast agent 43– – prodromic symptoms 30– – tumours 31intratumoral haemorrhage 355intravascular enhancement 19intraventricular haemorrhage (IVH)

46, 59, 88, 146ipsilateral hemisphere 11irreversible coma 275ischaemia 7, 257– cerebral 7, 58, 63, 117, 119– – posttraumatic 159– compression 154– in infants 376– lacunar 76– of the basal ganglia 377– of the thoracic spinal cord 362– temporal phases 13ischaemia-based brain damage 250ischaemic– infarction 257– oedema 201– penumbra 73, 74, 81, 269– stroke 4, 101– swelling 256IVH, see intraventricular haemorrhage

Jefferson’s fracture 304junctional lesion 169

Katzman’s lumbar infusion test 209kidney disease 112, 2445kinking 95, 98Korsakoff’s syndrome 244kyphosis 290

labour trauma 371laceration-contusion 166lactate 80, 81lactic acid accumulation 66lacunar– infarction 21– ischaemia 76laminoplasty 290last meadow infarct 8, 10Le Fort fracture 188lenticular nucleus 18leptomeningeal– cyst 25, 160, 383– enhancement 20leptomeninges 12, 57leukocyte adhesion 68leukoencephalopathy 247ligamentous trauma 324lipids 80lipoma 351liver cirrhosis 245lobar haemorrhage 41, 42, 88locked-in syndrome 171lumbar– hyperflexion trauma 317– spine trauma 325lumbosacral spine 292lymphoma 214

macrocephalia 394magnetic resonance (MR)– angiography (MRA) 101, 172– venography 108– imaging (MRI) 4– – angiography 5– – cranial trauma 132– – diffusion 79– – diffusion weighted imaging 5– – head injury 163– – in ischaemia 63– – intrinsic limits 163– – perfusion 75, 79– – semeiological limits 163– – spectroscopy 5, 80– – trauma 163magnetization transfer contrast (MTC)

102malar fracture 186malignant– cerebral oedema syndrome 386– gliomas 217Marchiafava-Bignami disease 244mass-forming lesion 351mean transit time (MTT) 78medulloblastoma 211, 234– in childhood 397MELAS syndrome 380meningeal sarcoma 232meningioma 211, 230–232, 237, 286,

347, 348– olfactory groove 232meningitis 51, 57, 288, 387– bacterial 388– purulent 388mental confusion 243mesencephalic– haemorrhage 164– tuberculoma 206mesodermal tumour 230metahaemoglobin 50metameric haemangioma 340metastases 217metastatic disease 341methaemoglobin 86, 217, 260, 328methanol intoxication 246methotrexate– intoxication 247– neurotoxicity 249methyl-ethylketone 246microhaemorrhage 216midbrain haemorrhage 281middle cerebral artery bifurcation/tri-

furcation 55Monro-Kellie doctrine 197MOTSA, see multiple overlapping thin

slab acquisitionmoya-moya syndrome 377, 379MTC, see magnetization transfer con-

trastMTT, see mean transit timemultiple– aneurysm 49– haemorrhage 47– overlapping thin slab acquisition

(MOTSA) 102– sclerosis 356, 357, 362multislice CT 301mycoplasm 391myelinolysis– extrapontine 242– osmotic 243– pontine 243myelocisternal-CT 208myelography 338, 347

Na+-K+ ion pump 65– dysfunction 65NAA, see N-acetyl-aspartateN-acetyl-aspartate (NAA) 80– depression 81nasal-ethmoid midface fracture 189necrotic brain tissue 35neoangiogenesis 17neoplasia 21, 24, 46, 87, 211, 347– cranial 235– in childhood 395– intracranial 213– spinal metastatic 342neoplasm 31, 349– of the cerebellar vermis 204neoplastic lesion 214neural tube closure defect 395neurinoma 349neuroectodermal tumour 229neurological– injury 299– syndrome 337

406 SUBJECT INDEX

neuroocular plane 181neuropaediatric 371neuroresuscitation 265non-haemorrhagic contusion 166non-ischaemic primary haemorrhage

24non-traumatic– bleeding 27– spinal emergency 337normotensive hydrocephalus 207nuclear medicine method 279nucleo-capsular haemorrhage 87

obstructive hydrocephalus 205occipital lobe 159occlusive venous pathology 108oedema 68, 326, 386– cerebral 155, 176, 201, 261, 267,

279, 286– – posttraumatic diffuse 158– cytotoxic 66, 69, 202, 261– focal 142– interstitial 203– ischaemic 201– parenchymal 355– perilesional 44, 213– vasogenic 17, 176, 201, 220, 260olfactory groove meningioma 232oligodendroglioma 234ophthalmoplegia 243orbital trauma 187os odontoideum 350osmotic myelinolysis 243osteoarticular trauma 321otorrhagia 138oxygen 266oxyhaemoglobin 50, 84, 165, 260

Pacchionian granulation 205Paget’s disease of the spine 341papilloma 235– of the choroid plexus 398, 399paralysis of the facial nerve 138paraplegia 337parenchymal– enhancement 20– haemorrhage 118– oedema 355PC, see phase contrastpCO2 94PD, see power-Dopplerpeak time (PT) 78percutaneous angioplasty 122perfusion– MRI 75, 79– pressure (PP) 255– – index (PPI) 96pericallosal artery 56perilesional– oedema 44– – vasogenic 213perimesencephalic cistern 50perivertebral soft tissue abnormality

300PET, see positron emission tomogra-

phypetechial haemorrhage 23phagocytosis of blood pigments 35

phase contrast (PC) 102phenomenon 394pilocytic astrocytoma 221, 398pineal region germinoma 215plasmacytopenia 351PNET, see primitive neuroectodermal

tumourpneumocephalus 155, 288pO2 90, 94polycystic kidney disease 112polycythaemia 380polytrauma 179, 298, 300– patient in a coma 302pontine– haemorrhage 43– myelinolysis 243porencephalic cyst 372, 391positron emission tomography (PET)

4postanoxic coma 265, 269posterior– fossa 29– inferior cerebellar artery 55postsurgical– cerebritis 225– craniospinal emergency 283– infection 224, 289posttraumatic– cerebral infarction 159– cerebral ischaemia 159– coma 267– diffuse cerebral oedema 138power-Doppler (PD) 95, 99PP, see perfusion pressurePPI, see perfusion pressure indexpremature– craniosynostosis 395– neonate 373– newborn 372pressure-volume ratio 197PRF, see pulse repetition frequencyprimitive neuroectodermal tumour

(PNET) 213proton MR spectroscopy 66, 80pseudoaneurysm 156, 289pseudo-bulbar paralysis 243pseudo-meningocele 289, 290, 323,

334pseudotumour cerebri 203, 400PT, see peak timepulse repetition frequency (PRF) 95pulsed wave (PW) 95purulent meningitis 388putaminal– haematoma 28, 32– haemorrhage 37, 39PW, see pulsed wave

Queckenstedt test 210

radiation myelopathy 366radiofrequency (RF) 77radionuclide 279radionuclide myelocisternography 208radiotherapy 232rCBF, see regional cerebral blood flowRecklinghausen’s disease 349, 353, 356recombinant tissue plasminogen activa-

tor (rt-PA) 16regional cerebral blood flow (rCBF)

78resistance index (RI) 95reversible ischaemic neurological

deficit (RIND) 3, 7RF, see radiofrequencyRI, see resistance indexRIND, see reversible ischaemic neuro-

logical deficitring enhancement 24rt-PA, see recombinant tissue plas-

minogen activatorrupture– of a cavernous angioma 30– of cryptic angiomas 42

SAH, see subarachnoid haemorrhagesalt losing syndrome 373scanogram 138, 301, 302Schwann cells 349SCIWMRA, see spinal cord injury

without magnetic resonance abnor-mality

SCIWORA, see spinal cord injurywithout radiological abnormality

scoliosis 291, 347SDH, see subdural haematomaSE, see spin echosetting sun 394shaken baby syndrome 150shaking trauma 385shearing injury 170, 171siderosis 91single photon emission computerized

tomography (SPECT) 78, 265skull– base fracture 160– fracture 134, 137, 139, 173– vertex fractures 138– x-rays 134slit ventricle syndrome 287SPECT, see single photon emission

computerized tomographyspin echo (SE) 5, 323– sequences 74spinal– angiography 347, 355– column infection 292– cord 299, 326– – abscess 365– – arteriovenous malformation 357– – atrophy 333– – compression 297– – infarct 357– – injury 302, 316, 322– – injury without magnetic resonance

abnormality 334– – injury without radiological abnor-

mality 334– – rare tumours 355– – swelling 326– – trauma 332– dural arteriovenous fistula 358, 362– emergency 288, 297– infection 289– instability 313, 324– meningioma 354

SUBJECT INDEX 407

– metastases 339– metastatic neoplasia 342– neoplasia 338– nerve 299– nerve root– – compression 297– schwannoma 356– segment 301– stenosis 291– trauma 180, 299, 321, 323, 334spiral CT 179, 301spondylodiskitis 338, 341, 342, 346,

348spontaneous haematoma 346stairstep artefact 139stenosis 93, 104, 107, 123stenotic-occlusive atheromatous

pathology 104, 107sterile inflammation 286streptococci 391stroke 3– haemorrhagic 4– ischaemic 4stupor 245subarachnoid– haemorrhage (SAH) 49, 89, 112,

118, 121, 123, 154, 155, 172, 371,386

– – after aneurysms 53– – cisternal hyperdensity 52– – contrast agent 57– – CT 49– – perimesencephalic 54– – rebleeding 58– – sine materia 52, 54– metastases 351subcortical intraparenchymal haemor-

rhage 41subdural– haematoma (SDH) 59, 149, 151,

172, 173, 198, 371, 385– haemorrhage 118, 146– hygroma 156, 175, 388subfalcian herniation 158, 200, 223,

255subluxation 322superficial siderosis 91supraaortic vessel 103supracellar cistern 50supraclinoid internal carotid artery 55Sylvian fissure 38, 42, 50syringohydromyelia 355syringomyelia 333

TB meningoencephalitis 39199TC 266TCD, see transcranial Dopplerteardrop fracture 313temporal herniation 200tentorium– cerebelli 159, 193, 200– incisura 158teratoma 351, 352thalamic– haematoma 31– haemorrhage 39– infarct 15– nucleus 37

thalamus 11thecal sack 292thiamine 243thoracic spine 291– compression trauma 314– dural arteriovenous fistula 363– trauma 324, 329thoracolumbar spinal trauma 318thrombolysis 63thrombophlebitis 210thrombosis 17, 23, 93, 118, 388– arterial 14thrombus 64TIA, see transient ischaemic attacktilted optimized non-saturation excita-

tion (TONE) 102time of flight (TOF) 102TOF, see time of flighttoluene 246TONE, see tilted optimized non-satu-

ration excitationtonsillar herniation 158torsion trauma 171, 319torticollis 307toxic encephalopathy 241transcranial Doppler (TCD) 98, 99,

276transient ischaemic attack (TIA) 3, 7,

117transphenoid herniation 158transtentorial herniation 158, 223trauma 131, 137, 268– axial compression 316– cervical spine 308, 313– – flexion 330– cranial 302– flexion 319– hyperextension 316, 319– hyperflexion 313– ligamentous 324– lumbar hyperflexion 317– lumbar spine 325– of the central spinal canal contents

322– osteoarticular 321– spinal 299, 321, 323– spinal cord 332– thoracic spine 324, 329– – compression 314– thoracolumbar spinal 318– torsion 319– vertebral 321, 324– vertical compression 319trauma-induced arterial spasm 148traumatic– intraparenchymal haematoma 144– vascular lesion 156tripod fracture 184–186tuberculous (TB) meningitis 389tumour 31, 213– brain 229– ectodermal 230– embryogenic 230– intracerebral 211– mesodermal 230– neovessel 233– neuroectodermal 229– tuberculous (TB) 389

ultrasound 4, 93

vascular– dissection 105– lesion 176– malformation 372– territories 9– tracer 64vasculopathy 7vasodilatation 211vasogenic oedema 17, 176, 201, 220,

260vasospasm 51, 59, 121, 257, 263vasular enhancement 19vein of Galen 372– malformation 395velocity 97venous– haemorrhagic infarction 23– malformation in children 375– stasis 257– thrombosis 108, 210, 380ventriculomegaly 210ventriculostomy 40vertebral– alignment abnormality 300– collapse 338– haemangioma 339– neoplastic metastases 343– osteomyelitis 341– plasmocytoma 344– trauma 321, 324vertex 140vertical compression trauma 319vessel– brachiocephalic 103– epiaortic 106– hyperdensity 14– intracranial 105– occlusion 64– rupture 145– supraaortic 103viral encephalitis 25, 211, 389vomiting 195

Wallerian degeneration 170watershed infarct 8, 10, 13Wernicke encephalopathy 243Wernicke-Korsakoff syndrome 244

X-ray 134

408 SUBJECT INDEX

emergency neuroradiology

Health & Medicine