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8/11/2019 Clinical Neurosurgical Vignettes for the Oral Board and Recertification Examinations First 2 Chapters.pdf

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i

Clinical Neurosurgical Vignettes for the

Oral Board and Recertification

Examinations:

A Self Assessment Guide


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iii iii

Clinical Neurosurgical Vignettes for the

Oral Board and Recertification

Examinations:

A Self Assessment Guide

Thomas G. Psarros, MD

Spine and Brain Neurosurgery Center

Reading Hospital and Medical Center

West Reading, Pennsylvania

Jonathan A. White, MD

Assistant Professor and Residency Program Director

Department of Neurological Surgery

Birsner Family Professorship in Neurological SurgeryUniversity of Texas Southwestern School of Medicine

Dallas, Texas

Howard Morgan, MD, MA., MS., FACS

Professor

Department of Neurological Surgery

Trammell Crow Professorship in Neurological Surgery

University of Texas Southwestern School of Medicine

Dallas, Texas

Anotatos Publishing 2008


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iv

Anotatos Publishing, LLC.Allentown, Pennsylvania 18104

2008 by Anotatos Publishing, LLC.

Typeset in Times New Roman

Printed in the United States

All rights including that of translation reserved. No part ofthis publication may be reproduced, stored in a retrieval

system or transmitted in any form or by any means,

including photocopying, electronic, mechanical, recording,

or otherwise, without the prior written permission of thepublisher.

The publisher and/or authors are not responsible (as a matter

of product liability, negligence, or otherwise) for any injury

resulting from any material contained herein. Thispublication contains information relating to general

principles of medical care that should not be construed as

specific instructions for individual patients. Manufacturersproduct information and package inserts should be reviewed

for current information including contraindications, dosages,

and precautions.

Library of Congress Control Number: 2007943015

Psarros, Thomas G., January 2008

Clinical Neurosurgical Vignettes for the Oral

Board and Recertification Examinations: A SelfAssessment Guide.

Thomas G. Psarros, Jonathan A. White, Howard

Morganp. 310

Includes index and bibliographical references.

ISBN-13: 978-0-9802096-0-0 ISBN-10: 0-9802096-0-9

for Library of Congress

The publishers and authors have made every effort to tracecopyright holders for borrowed material and reference all material

in this book in a just manner when appropriate. If they have inadvertently

overlooked any, they will be pleased to make any necessary arrangements

at the first opportunity.


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v v

Dedication

To my young son George for making me the proudest father in the world

To my lovely wife, Sandy, for her unconditional support


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vii vii

Table of Contents

Case 1: Anterior interosseous nerve syndrome............................................ 1-6

Case 2: Posterior communicating artery aneurysm ................................... 7-18

Case 3: Parkinsons disease ..................................................................... 19-28Case 4: Perimesencephalic subarachnoid hemorrhage ............................ 29-36

Case 5: Middle cerebral artery aneurysm ................................................ 37-46

Case 6: Normal pressure hydrocephalus.................................................. 47-52Case 7: Trigeminal neuralgia................................................................... 53-58

Case 8: Carotid-cavernous fistula............................................................ 59-62Case 9: Carotid stenosis........................................................................... 63-72

Case 10: Carpel tunnel syndrome .............................................................. 73-78

Case 11: Basilar apex aneurysm ................................................................ 79-88Case 12: Odontoid fracture........................................................................ 89-98

Case 13: Colloid cyst ............................................................................... 99-104

Case 14: Anterior communicating artery aneurysm .............................. 105-112Case 15: Posterior inferior cerebellar artery aneurysm ......................... 113-118

Case16: Mycotic aneurysm................................................................... 119-122

Case 17: Cerebral venous thrombosis.................................................... 123-128

Case 18: Middle cerebral artery infarct ................................................. 129-138Case 19: Vein of Galen malformation ................................................... 139-142

Case 20: Cerebral arterial venous malformation ................................... 143-150

Case 21: Cerebral amyloid angiopathy.................................................. 151-152Case 22: Far lateral lumbar disc herniation ........................................... 153-156

Case 23: Central nervous system germinoma........................................ 157-166

Case 24: Pituitary adenoma/Cushings disease ..................................... 167-178

Case 25: Vestibular schwannoma.......................................................... 179-186Case 26: Neurocysticercosis .................................................................. 187-192

Case 27: Myelomeningocele.................................................................. 193-198Case 28: Lipomyelomeningocele........................................................... 199-204

Case 29: Upper brachial plexopathy...................................................... 205-210

Case 30: Closed head injury .................................................................. 211-220

Case 31: Cubital tunnel syndrome......................................................... 221-228Case 32: Cervical spine fracture/ligamentous injury............................. 229-236

Case 33: Posterior interosseous nerve entrapment ................................ 237-240

Case 34: Isolated brain metastases......................................................... 241-248Case 35: Thoracic spinal cord tumor ..................................................... 249-254

Case 36: Carotid artery dissection ......................................................... 255-259Case 37: Spinal cord stimulation and failed back surgery syndrome ... 261-270Index: .................................................................................................... 271-282

Bibliography: ......................................................................................... 283-298


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ix

Preface

The thought of preparing a series of books for the written neurosurgery board

examination seemed to be an excellent one, but the task seemed daunting because the

fund of knowledge required to pass the test was felt to be as extensive as the field ofneurosurgery itself. Our first two books entitled The Definitive Neurological Surgery

Board Review andIntensive Neurosurgery Board Review: Neurological Surgery Q & A

primarily focused on the basic science aspects of the field in the form of a textbook and aQ & A book, respectively. This book is primarily intended for neurosurgeons preparing

for the oral board and recertification examinations, although should prove useful toneurosurgical residents studying for the written examination due to the growing number

of clinical-based questions popping up on this exam. It is certainly not meant to be a

comprehensive or authoritative narrative on the plethora of neurosurgical topics tested,but simply a compilation of case studies that I put together while studying for the Oral

Boards that may prove useful during your preparatory efforts. I primarily relied on two

board-certified neurosurgeons from The University of Texas Southwestern MedicalCenter while compiling these case studies, but have benefited tremendously from the

collective experience of many others during my residency in Dallas. This book is a

tribute to all of them because without their mentorship, guidance, and unselfish

dedication to neurosurgical education this book would not be in your hands today.

Although every attempt has been made to ensure the clarity and accuracy of the questions

and answers, the reader is referred to the multiple referenced textbooks and journalarticles for further clarification should the need arise. Each vignette is generally

formulated with a differential diagnosis, most likely diagnosis, treatment

recommendations, and surgical approaches and techniques. This volume will serve as an

eye-opening refresher for busy neurosurgeons studying for the oral board andrecertification examinations, and should prove to be a valuable vehicle for rapid and

systematic pre-test review for neurosurgery residents preparing for the written boards.We wish you luck during your preparatory efforts.

Thomas G. Psarros, MD


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Anterior interosseous nerve syndrome 1

Case 1

A 17-year-old female fractured her

right forearm during a high schoolvolleyball game and required casting.

Two-months after removal of the cast

she complained of a painful right hand.

Her neurologic examination was

normal except that she was unable to

perform the maneuver depicted below

with the right hand.

_______________________________

_______________________________

1. What is the most likelydiagnosis?

Anterior interosseous nerve (AIN)

injury or compression (also known as

Kiloh-Nevin syndrome) causesweakness of the long flexors of the

thumb (flexor pollicis longus), index

and middle fingers (flexor digitorumprofundus I and II), and the pronator

quadratus muscle. When one tries to

pinch the index finger and thumb, theend of the fingers extend and instead of

the tips of the fingers, the pulps touch

producing the classic pinch sign, as

depicted above. (Brazis, et al., 1996, p14-15 )

[19]; (Greenberg, 2001, p

540)[51]

.

2. Describe the course of the AIN?

The AIN originates from theposterolateral surface of the median

nerve (between the two heads of thepronator teres muscle) approximately 5

to 8 cm distal to the medial epicondyle.Typically, the AIN branches just distal

to the proximal border of the

superficial head of the pronator teresmuscle, and accompanies the median

nerve through the fibrous arch of the

flexor digitorum superficialis (FDS)muscle. The AIN then comes to lie in

front of the interosseous membrane,

coursing distally with the anteriorinterosseous artery (branch of the ulnarartery) to the level of the wrist. The

AIN supplies motor branches to the

flexor pollicis longus (FPL) muscle,flexor digitorum profundus (FDP)

muscles of the index and long fingers,

and pronator quadratus (PQ) muscle.The branches to the FPL and FDP

muscles arise near the tendinous origin

of the FDS muscle approximately 4 cm

distal to AIN origin. The AINterminates in the PQ muscle (Wilkinsand Rengachary, 1996, p 3081)

[161].

3. What is the etiology of a painfulhand with this syndrome?

The AIN has no cutaneous innervationand is most often considered a purely

motor nerve. The AIN, however, does

have terminal sensory branches fromthe wrist radiocarpal, radioulnar,

intercarpal, and carpometacarpal joints.

Damage to the terminal sensory

branches can cause chronic, naggingvolar wrist and forearm pain (Brazis, et

al., 1996, p 14-15)[19]

; (Wilkins and

Rengachary, 1996, p 3081)[161]

.


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2 Clinical Neurosurgical Vignettes

4. What are some causes of AINsyndrome?

Trauma including supracondylar

humeral fracture, forearm fracture(as in this case), dislocation of the

elbow, penetrating missile injury,stab wounds, and crush injuries

Compression of the AIN bymusculotendinous bands or other

anomalous structures within the

forearm (from pronator teresmuscle, flexor digitorum

superficialis arch)

Iatrogenic injury

Arterial or venous access(cutdowns, catheterization,venipuncture)

Anomalous AIN course deep topronator teres muscle

Accessory muscles: Gantzersmuscle, aberrant head of flexor

carpi radialis muscle

Forearm mass

Enlarged bicipital bursa

Aberrant radial artery

Thrombosed ulnar collateral artery

Inflammation

The AIN may be involved as partof neuralgic amyotrophy

Infection (cytomegalovirus)

Arteritis (polyarteritis nodosa)(Brazis, et al., 1996, p 14)

[19]

5. What are typical features of acomplete AIN syndrome?

There is a history of spontaneous pain

in the proximal volar wrist and

forearm. Symptoms tend to increasewith activity, especially repetitive

forearm motion. Weakness is usually

preceded by pain, with the pain oftensubsiding partially or completely over

weeks to months. There is classically

weakness of the FPL, FDP of the index

and long fingers, and PQ muscles. Thisoften leaves patients complaining of

difficulty with writing or picking up

small objects. On clinical examination,

the most prominent feature is weaknessof the thumb FPL and index and long

finger FDP muscles causing the

"classic attitude" of the weak pinch(Wilkins and Rengachary, 1996, p

3081)[161]

.

6. What are the typical features ofan incomplete AIN syndrome

and how is it usually caused?

There are reports of various"incomplete AIN syndromes, alsoreferred to as pseudo-anterior

interosseous nerve syndromes. These

atypical presentations may be causedby anatomic variations including:

A. The ulnar nerve may innervate thelong finger (partial or complete in half

the population), which will preserve

the long finger FDP muscle strength.

B. The Martin-Gruber anastomosis,present in approximately 17% of the

population has a connection between

the median and ulnar nerves. One

common variant has a connectionbetween the anterior interosseous to

ulnar nerve. In this situation, many of

the ulnar-mediated hand intrinsicmuscles will be affected as well.

C. The AIN may innervate the entireFDP muscle, which would result inweakness of all fingers.

D. The AIN may also supply part ofthe FDS muscle (30% of people)

(Brazis, et al., 1996, p 15)[19]

.


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7. What is the differential diagnosisof AIN syndrome?

The most commonly misdiagnosed

problem is a tendon rupture, usually ofthe FPL muscle, but also of the FDP

muscle. Hill reported that 10 of 33patients with AIN syndrome were

initially diagnosed as having a tendon

rupture (three had FPL explorationunnecessarily) (Hill, et al., 1985, p 4-

16)[59]

. Electrical stimulation of the

FPL or FDP muscle can help identifythe presence of an intact tendon

(Howard, 1986, p 737-785)[62]

. Other

common conditions in the differentialinclude acute brachial plexusneuropathy, partial proximal median

nerve injury, thoracic outlet syndrome,

and cervical radiculopathy (especiallyC8, although relatively uncommon).

History, clinical examination, and

electrophysiologic studies can helpexclude these other entities (Brazis, et

al., 1996, p 15)[19]

.

8. What diagnostic studies may helpconfirm the diagnosis?

Electromyography can help confirm

the diagnoses of AIN syndrome byhelping to localize the muscles

affected. It may show evidence of

abnormal membrane irritability withloss of motor units in any or all of the

muscles supplied by the AIN. Needle

examination of these muscles mayprove difficult, however, due to their

fairly deep location (Hill, et al., 1985, p

4-16)[59]

.

9. What are some characteristics ofnormal and abnormal single-

motor-unit potentials on

electromyography (EMG)?

In order to understand abnormalities on

EMG, it is imperative that one have asound understanding of how a needle

EMG study is conducted and what the

expected norms should be. EMGinvolves placing a recording needle

into specific muscles and recording

action potentials from muscle fibers,which can be used to determine if any

pathology exists in motoneurons and/or

muscles. There are generally 2 aspectsof an EMG examination that meritdiscussion. They include: 1) assessing

whether there is spontaneous muscle

fiber action potentials, and 2)measuring motor unit action potential

(MUAP) duration, amplitude, and

phases.

Spontaneous muscle activity

When a patient is not moving andunder resting conditions, muscles areessentially silent with no significant

activity. If a motor neuron or muscle is

damaged, however, it is common to see

spontaneous muscle fiber activity onEMG due to hypersensitivity of

denervated muscles. The most common

spontaneous activities that have clinicalsignificance are fibrillation potentials,

positive sharp waves, and complex

repetitive discharges. Fibrillationpotentials are abnormal, spontaneous

contractions of single muscle fibers

that are not visible through the skin,but have a characteristic EMG

waveform. They usually occur

rhythmically and are thought to result

from oscillations of the restingmembrane potential in denervated

muscles. They have a characteristic


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biphasic or triphasic waveform that canoften be distinguished from normal end

plate potentials. Positive sharp waves

are similar to fibrillation potentials and

appear on EMG as a downward waveafter needle insertion, which is

indicative of needle irritation of

denervated muscle fibers. Denervationof muscle fibers results in fibrillation

potentials and positive sharp waves

within approximately two weeks, buttheir onset may take up to five weeks

in certain cases. These findings usually

persist until the muscle is reinnervated,typically within 3 to 4 months in mild

injuries, or until the injured muscleundergoes complete atrophy (may takeyears). Complex repetitive discharges

are generated from muscle fibers that

have been denervated for longer

periods of time (> 2 months) resultingin chronic muscle fiber necrosis. The

disorders causing complex repetitive

discharges are similar to the onescausing fibrillation potentials and

positive sharp waves, except that

complex repetitive discharges occurwith chronic disease states. Insertional

activity is the discharge of a singlemuscle fiber during insertion of the

EMG needle, and does not necessarily

indicate abnormality unlesssignificantly increased activity is seen

(Winn and Youmans, 2004, p 3856-

3857)[162]

.

MUAP amplitude, duration, and

phases

Muscle potentials appear normally as

waveforms with duration of 5-15 ms,

2-4 phases, and amplitude of 0.5-3 mV.The size of the MUAP is related to the

number of muscle fibers within the

recording range of the EMG needle. If

the MUAP is larger than normal

(increased amplitude and duration),there must be an increased number of

summated action potentials per motor

unit. An increased number of muscle

fibers per motor unit are usually theresult of reinnervation of a previously

injured nerve, suggesting that there was

some insult to the motor nerveapproximately 2 months earlier. If the

MUAP is smaller than normal

(decreased amplitude and duration),there is decreased number of muscle

fibers per motor unit, which generally

occurs with neuromuscular junctiondisorders or myopathies. Polyphasic

units (greater than 4 phases) areabnormal, and can be seen in bothneurogenic and myogenic disorders.

With neurogenic disorders, however,

motor units have a longer duration and

higher amplitude than normalpotentials, while with myopathic

potentials, they are just the opposite

(shorter durations and smalleramplitudes) (Rowland and Merritt,

2000, p 75-76)[136]

; (Winn and

Youmans, 2004, p 3856-3857)[162]

.

10.What are the treatment optionsfor AIN syndrome?

The treatment of patients with AINsyndrome depends primarily on the

cause of the injury. Closed crush

injuries or those related tomusculoskeletal trauma are usually

treated expectantly. Patients are

oftentimes followed closely with serialclinical examinations and diagnostic

studies (electromyograms), and, if,

after 3 to 4 months there is norecovery, surgery is considered. Most

insidious or spontaneous cases are

initially treated nonoperatively, as well.

Immediate exploration is usuallyindicated for penetrating trauma.


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Nonoperative treatment

The initial treatment is generally rest,

avoidance of aggravating factors,

splinting, and nonsteroidal anti-inflammatory medication. If

signs/symptoms persist, some have

advocated corticosteroid injections intothe region of the pronator teres muscle.

Controversy arises as to the duration of

conservative or nonsurgical treatment.The surgical literature generally still

supports nonoperative treatment for 2

to 3 months. If there is noimprovement, surgical exploration is

advocated. When the deficit is partialor slowly improving, the observationperiod can be extended.

In spontaneous or unexplained cases,

treatment depends upon whethercompression or inflammation is the

suspected cause. Features suggestive of

entrapment include slow development,mild pain (primarily volar

wrist/forearm pain), or neurological

deficits isolated to the AIN.Inflammation may be suspected if the

pain is severe, extends above the elbowinto the shoulder region, precedes the

neurological deficit by a matter of

days, and/or there is an associatedipsilateral or contralateral brachial

plexopathy.

If inflammation is suspected, somesuggest that nonsurgical treatment be

carried out for 6 months, while othersargue it may not be needed at all sincereports document improvement even

beyond 2.5 years (Hill, et al., 1985, p

4-16)[59]

. All patients in one reportexperienced full recovery when treated

without surgery (England and Sumner,

1987, p 60)[41]

. The surgical literature

suggests exploration at 3 months if

entrapment is the suspected cause aftera trial of nonsurgical therapy (Kaye

and Black, 2000, p 2092)[77]

.

Operative Treatment

The operative treatment is generally

similar to the techniques used for thepronator syndrome. A curvilinear

incision can be made on the

anteromedial side of the armapproximately 8 cm above the elbow,

and carried across the flexor crease into

the midforearm. The median nervecan then be identified proximal to the

take-off of the AIN and followeddistally being sure it is decompressedat all potential sites of entrapment.

Approximately 4-5 cm above the

elbow, one needs to look for a fibrousband connecting the medial epicondyle

to a rare bony prominence of the

humerus called the ligament ofStruthers. It only occurs in about 2% of

the population, but if identified, needs

to be divided. The next commonentrapment site of the median nerve is

at the lacertus fibrosis, which arisesfrom the biceps tendon. The median

nerve generally runs under the lacertus

fibrosis, which may cause entrapmentif hypertrophic or fibrotic. The median

nerve then courses between the two

heads of the pronator teres muscle. At

the level of the pronator teres muscle,the AIN arises from the median nerve.

Together they may be entrapped by afibrotic pronator teres muscle,especially adjacent to the deep or ulnar

head of this muscle. The deep head of

the pronator teres muscle can bedivided to relieve the compression on

the nerve if the ulnar head is fibrotic or

hypertrophic. The dissection is then

carried distally to the level of the


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sublimis bridge, which is the fibrousarch of the flexor digitorum

superficialis muscle. The AIN travels

under the sublimis bridge, and needs to

be transected to relieve anycompression on the AIN. The AIN is

then followed further distally to ensure

there is no entrapment from anomalousmuscle origins (i.e. Gantzer's muscle,

flexor carpi radialis brevis muscle).

Dissection adjacent to the origin of theAIN may be difficult due to a

constellation of multiple small arteries

and veins that tend to congregate nearorigin of the FDS muscle, which need

to be preserved (Kaye and Black, 2000,p 2092-2093)

[77]; (Wilkins and

Rengachary, 1996, p 3081)[161]

; (Winn

and Youmans, 2004, p 3925)[162]

(Batjer and Loftus, 2003, p 1757)[13]

.

End of case


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Posterior communicating artery aneurysm 7

Case 2

A 62-year-old female with a history ofmalignant hypertension and aortic

valve insufficiency was brought to the

emergency room by paramedics

complaining of severe headache, neck

stiffness, and photophobia. There was

no history of trauma. On examination,

she was fully alert with no ocular gaze

restriction or neurological deficit. Her

noncontrast computed tomography

(CT) scan is depicted below.

1. As the consulting neurosurgeon,you inform the emergency room

physician that the next course of

action should include?

After making a diagnosis of

subarachnoid hemorrhage (SAH) by

CT scan (will demonstrate blood in85% of patients scanned within 48

hours), cerebral angiography should be

performed as soon as possible.Traditional catheter-based angiography

remains the gold standard for

diagnosing cerebral aneurysms,although other imaging modalities are

gaining widespread popularity

including computed tomographic

angiography (CTA) and magneticresonance angiography (MRA).

During cerebral angiography, it isimperative to identify the entire course

of blood vessels in two planes,

including the posterior inferiorcerebellar arteries and anterior

communicating artery complex. The

angiogram should demonstrate, ifpossible, the etiology of the SAH, the

aneurysmal neck and projection, thevessels arising next to the aneurysm,determine whether multiple aneurysms

exist (up to 20% of cases), and assess

the degree of concomitant vasospasm

that may be present (althoughvasospasm is extremely unlikely in the

hours immediately following a SAH)

(Hughes, 2003, p 253)[63]

.

The experience with MRA is rapidly

evolving as acquisition protocols andMRI technology improve. Earlier

studies suggest 86% sensitivity indetecting aneurysms greater than 3 mm

compared to digital subtraction

angiography (Ross, et al., 1990, p 449-456)

[135]; (Ronkainen, et al., 1997, p

380-384)[133]

, while other studies show

that MRA sensitivity approaches 95%

when compared to angiography (Atlas,1994, p 1-16)

[9]. The false positive rate

for MRA is approximately 16%(Ronkainen, et al., 1997, p 380-384)

[133]. There are a number of

variables that affect MRAs ability to

detect aneurysms including: aneurysmsize, rate and direction of blood flow in

the aneurysm in relation to the

magnetic field, thrombosis, and

calcification. Moreover, it has limited


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resolution in the setting of vasospasmand in detecting blood products in the

acute period following SAH. MRI,

however, has proven invaluable and

highly effective in the evaluation ofgiant intracranial aneurysms. Because

giant aneurysms are often partially

thrombosed, they often opacifyincompletely during angiography,

which can result in an underestimation

of their true size (Hackney, et al., 1986,p 878-880)

[53]; (Barboriak and

Provenzale, 1998, p 1469)[10]

;

(Greenberg, 2001, p 757)[51]

.

CTA is a more recent development,and its role is becoming better defined.Evidence suggests that it has similar

sensitivity to conventional angiography

in detecting aneurysms, and its use

among cerebrovascular surgeons forsurgical planning has steadily grown.

It has a reported sensitivity and

specificity of 95% and 83%,respectively, in detecting aneurysms as

small as 2.2 mm. Unlike conventional

angiography, however, CTA has theadvantage of showing a 3-dimensional

image and demonstrating theaneurysms relationship to adjacent

structures. Bone artifact may hinder

adequate visualization of certainaneurysms adjacent to the skull base

(Anderson, et al., 1997, p 522-528)[6]

;

(Zouaoui, et al., 1997, p 125-130)[170]

;

(Greenberg, 2001, p 758)[51]

; (Korogi,et al., 1999, p 497)

[85]; (Liang, et al.,

1995, p 1497)[90]

.

Lumbar puncture (LP) after SAH is

risky, and should not be performed in

the patient presented here. In onestudy, 13% of patients undergoing

lumbar puncture after SAH

deteriorated neurologically. Whether or

not clinical deterioration was related to

the LP is unclear, but since it carries arisk of brain herniation or aneurysmal

rebleeding, this procedure should

generally be reserved for patients

where the diagnosis remains uncertainfollowing CT scanning.

Xanthochromia develops only after redblood cells lyse, and is usually

detectable after 4 hours, is maximal at

1 week, and is typically undetectableby 3 weeks. If cerebrospinal fluid is

bloody due to SAH, the blood will

usually not clot if left to stand (Duffy,1982, p 1163-1164)

[35].

2. What is the clinical Hunt andHess grade of this patient?

Once a diagnosis of SAH has beenestablished, patients are given a clinical

grade based on one of the accepted

grading schemes. Although numerousgrading scales have been devised since

the 1930s, one of the most universally

accepted grading scales is that of Hunt

and Hess, described originally in 1968(see Table 2.2a).

Table 2.2a Hunt and Hess clinical grading scale afterSAH

Grade Clinical symptomatology

Grade I Awake, mild headache, + nuchal rigidity

Grade II Awake, moderate- to- severeheadaches, nuchal rigidity

Grade III Drowsy or confused + focal deficits

Grade IV Stuporous, mild- to- moderatehemiparesis, and signs of increasedintracranial pressure

Grade V Comatose, severe disability, severeincreased intracranial pressure


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Of note, the Hunt and Hess gradingscale places the patient into the next

worse grade if serious systemic disease

or vasospasm is present (Hunt and

Hess, 1968, p 14-20)[64]

. This gradingscale was later revised by Hunt in 1974

to include two additional grades. Grade

0 was added to include patients withunruptured aneurysms without

symptoms, and grade 1a to include

patients with no acute meningealreaction, but a fixed neurological

deficit (Hunt and Kosnik, 1974, p 79-

84)[65]

. The patient in this casepresented with a severe headache,

photophobia, nuchal rigidity, and nodecline in her level of consciousness;all characteristic of a Hunt and Hess

grade II category. Her comorbid

conditions (malignant hypertension and

aortic valve insufficiency), however,drop her one grade into a grade III

category (Hughes, 2003, p 255-256)[63]

.

Although the Hunt and Hess grading

system remains the most widely used

grading scale for patient assessmentfollowing SAH, some have proposed

using other scales to improvepredictive value. For example, Oshiro,

et al., developed a grading scale

(World Federation of NeurologicalSurgeons, WFNS) based on the

Glasgow Coma Scale (GCS). In the

WFNS grading scheme, GCS scores of

15, 12-14, 9-11, 6-8, and 3-5 replacedthe Hunt and Hess scores of 1-5,

respectively (see Table 2.2b). Theauthors of this scale (WFNS) felt thattheir grading scheme was better than

the Hunt and Hess system at predicting

overall patient outcomes while at thesame time being more reproducible

across observers (Hughes, 2003, p 255-

256)[63]

; (Oshiro, et al., 1997, p 140-

148)[115]

.

Table 2.2b World Federation of NeurologicalSurgeons Scale

3. What is the Fisher grade of thispatient?

Fisher (1980) developed a four-tieredgrading scale for the appearance of

SAH on CT scanning dependent upon

the severity and location of the bloodpattern. Grade I patients had noevidence of blood detectable on CT

scanning, while grade II patients had a

thin layer of blood (< 1 mm thick)diffusely spread throughout the

subarachnoid space. Grade III patients

had a thicker amount of cisternalsubarachnoid blood (>1mm thickness

as depicted in this case), while grade

IV patients had intraventricular or

intraparenchymal blood with orwithout a significant subarachnoid

component. The Fisher grading system

can help predict the probability ofdeveloping vasospasm by the amount

of blood detected on CT scan . Patients

with Grade I, II, and IV bleeds had noor minimal incidence of clinically

significant vasospasm, while grade III

patients had a 95.8% incidence in

Grade Clinical findings

Grade I Glasgow coma score 15, no motordeficit

Grade II Glasgow coma score 13 14, nomotor deficit

Grade III Glasgow coma score 13 14, motordeficit

Grade IV Glasgow coma score 7 12, with orwithout motor deficit

Grade V Glasgow coma score 3 6, with orwithout motor deficit


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Fishers original paper (Fisher, et al.,1977, p 1-9)

[44]. These findings suggest

that blood breakdown products are an

important factor in the genesis of

cerebral vasospasm, with largerquantities of blood increasing the

likelihood that vasospasm will occur

(Hughes, 2003, p 252)[63]

.

4. The cerebral angiogram for thispatient is depicted below. What is

the diagnosis?

This angiogram of the left internal

carotid artery (ICA) depicts a bilobedposterior communicating artery

(PcomA) aneurysm originating at the

level of a fetal PcomA (Wilkins andRengachary, 1996, p 2306)

[161].

5. Describe two angiographic

findings in this patient that areimportant for surgical planning?

Care needs to be taken when evaluating

angiograms of patients with a PComA

aneurysm, SAH, and no third nervedeficit because the aneurysms often

project laterally onto the medial edge

of the temporal lobe rather than inmore common posterolateral or

downward directions. This is important

during surgical planning sincepremature retraction of the temporallobe may result in aneurysm rupture.

Additionally, the integrity of a fetal

PComA needs to be preserved duringsurgery and aneurysm clip placement.

If the area supplied by the PComA is

small, inadvertently placing this vesselinto the clip construct may not cause

any adverse sequelae, however, if the

PComA is fetal or there is a

hypoplastic P1, it may result in aclinically significant PCA infarct(Wilkins and Rengachary, 1996, p

2306)[161]

; (Psarros, 2006, p 199)[124]

.

6. The emergency room physicianreviews the CT scan with you and

wants to begin an infusion of

epsilon-aminocaproic acid

(AMICAR). What are some

important factors to consider

about this medication?

The role of antifibrinolytics for the

purpose of preventing or decreasingclot breakdown following SAH is

controversial (Kassell, et al., 1984, p

225-230)[74]

; (Adams, 1982, p 256-259)

[2]; (Mizoi, et al., 1991, p 807-

813)[99]

; (Findlay, et al., 1988, p 723-

735)[43]

. During normal fibrinolysis,


21/27


plasminogen is converted to plasmin,which facilitates the digestion of fibrin

and aids in clot lysis. AMICAR

inhibits the conversion of plasminogen

to plasmin, and reduces the extent offibrinolysis and clot breakdown after

SAH. Intravenous injection of

AMICAR generally peaks in thebloodstream in about 20 minutes. It

crosses the blood-brain barrier and

achieves maximal antifibrinolyticactivity within the cerebrospinal fluid

approximately 48 hours later (Findlay,

et al., 1988, p 723-735)[43]

. A typicalregimen includes infusing 2 g/ hour

intravenously for 48 hours, and then1.5 g/ hour until surgery is performed.Review of the results of one study

found a reduction in rehemorrhage and

death at 14 days from 21% to 10% with

its use (Burchiel, et al., 1984, p 57-63)

[21]. Although it halved the

rebleeding rate the first 14 days

following SAH, there was an increasedrisk in associated medical morbidity,

the most frequent being diarrhea in

approximately 24% of patients.Additionally, communicating

hydrocephalus was 25% more likelywith antifibrinolytic therapy (Burchiel,

et al., 1984, p 57-63)[21]

. The greatest

concern over its use, however, was theincreased risk of vasospasm that

negated its benefits in some studies

(Kassell, et al., 1984, p 225-230)[74]

.

The general consensus about the role ofantifibrinolytics is that they have little

role in acute SAH, especially if surgeryis anticipated within a few hours ordays of admission (Hughes, 2003, p

267)[63]

.

7. What is the rate of rebleedingfollowing a SAH?

The frequency of rebleeding is in the

range of 4% within the first 24 to 48

hours, and approximately 1.5% eachday for the next 13 or 14 days. It

approaches 20% within the first 2

weeks, and approximately 50% at 6

months. Thereafter, the risk is believedto level off to approximately 3% per

year. The mortality rate from

aneurysmal rebleeding is between 44%and 78%. Early surgery or aneurysm

coiling offers the best protection

against rebleeding and its attendantcomplications (Hughes, 2003, p

267)[63]

; (Kassell, et al., 1982, p 337-

343)[73]

.


22/27


8. What are some advantages anddisadvantages of early versus

delayed surgery after SAH?

Table 2.8 Advantages and disadvantages of earlyversus delayed surgery after SAH

Despite the potential microsurgicalchallenges associated with operating on

a swollen brain, the majority of grade

I-III patients at various institutions stillundergo surgery early after SAH to

minimize the incidence of rebleeding.

Although early surgery can certainly betechnically more challenging,

experience has shown that patient

outcomes are not necessarily adversely

affected, as demonstrated by theInternational Cooperative Study on the

Timing of Aneurysm Surgery

(ICSTAS) (Kassell, et al., 1990, p 37-47)

[75]. Intraoperative ventriculostomy

placement and aggressive gravity

drainage of cerebrospinal fluid haveproven to be very useful in overcoming

an initially swollen brain soon after

SAH (Paine, et al., 1988, p 1107-1109)

[117].

9. The patient is taken to theoperating room for aneurysm

clipping. After elevating a

pterionally-centered bone flap

and modestly craniectomizing the

squamosal portion of the

temporal bone, attention is

directed toward the sphenoid

ridge. This bony wing is

typically removed from lateral

to medial to the level of origin ofwhat structure?

One of the most useful adjuncts to

avoid brain retraction for anterior

circulation aneurysms during initialexposure is to aggressively remove the

bony wing (or sphenoid ridge) of the

sphenoid bone. It is removed usingrongeurs and a power drill from

lateral to medial for a distance of

approximately 4 cm, to the level of theorbital meningeal artery. This

maneuver must include removing the

thin spine of the sphenoid ridge,which, oftentimes, is very adherent to

the underlying dura adjacent to the

horizontal portion of the Sylvian

fissure. If the spine is left intact, thedegree of initial frontal lobe elevation

necessary to expose the carotid cistern

Early approach Delayed approach

ADVANTAGES ADVANTAGES

Decreases rebleeding risk

Allows for aggressivemanagement ofvasospasm

Early removal ofsubarachnoid blood andpossible prevention of

hydrocephalus

Earlier patient ambulationand rehabilitation;perhaps reduced hospitalstay

Reduced medicalcomplications associatedwith bedrest

Evacuation of hematoma,if applicable

Brain less swollen

Easier microdissection

Stable patient

DISADVANTAGES DISADVANTAGES

Swollen brain may makesurgery more difficult

Unstable patient in someinstances

Scheduling problems,possibility ofinexperienced operativeteam

Higher rebleeding risk

Does not facilitate or allowfor aggressivemanagement ofvasospasm

Delayed ambulation,longer hospital stay

Increased risk of medicalcomplications whileawaiting surgery


23/27


is increased, and surgical access alongthe flattened ridge and frontal fossa

floor can be markedly hindered. After

the sphenoid ridge is removed and

bony and dural hemostasis is obtained,the dura can be opened in a routine

curvilinear fashion and held with

retention sutures flat against theinferior aspect of the craniectomy and

adjacent muscle (Samson and Batjer,

1990, p 57)[138]

.

10.Describe the pertinent stepsduring surgery for a PcomA

aneurysm?

Initial exposure after dura opened

InIntracranial Aneurysm Surgery:Techniques, Samson and Batjereloquently describe the steps for

clipping PcomA aneurysms (Samson

and Batjer, 1990, p 57-58)[138]

.Withthe aid of a microscope, a small self-

retaining brain retractor is used to

gently elevate the frontal lobe adjacent

to the horizontal portion of the Sylvianfissure. The retractor is then advancedin a step-by-step fashion as the

arachnoid opening is extended from the

horizontal portion of the Sylvian

fissure to its junction with the carotidcistern. As frontal lobe elevation brings

the optic nerve and internal carotid

artery (ICA) covered by arachnoid intoview, the arachnoid covering the

Sylvian fissure usually thickens.

Oftentimes, a small vein will be foundbridging the temporal to frontal lobe

immediately under this thicker

arachnoidal layer adjacent to theSylvian fissure. This vein usually lies

above the origin of the middle cerebral

artery (MCA), and can be coagulated

and cut to complete the opening of thehorizontal portion of the Sylvian

fissure. The retractor blade can then be

advanced to expose the arachnoid layerthat surrounds the optic nerve and ICA.

The arachnoid incision, which was

started over the horizontal portion of

the Sylvian fissure, is then extendedposteriorly and anteriorly for better

visualization of the ICA and optic

nerve. The release of cerebrospinalfluid from the subarachnoid Sylvian

and prechiasmatic cisterns will

generally help relax the brain tofacilitate further microdissection and

eventual aneurysm clipping (Samson

and Batjer, 1990, p 57-58)[138]

.

Microdissection after basal cisternsopen

After the basal cisterns open, the next

step should be to focus attention on

securing proximal arterial control priorto more definitive microdissection

distally. Because of the most common

location of PComA aneurysms(projecting posterior and laterally), it is

advantageous to accomplish this

control by beginning the exposure ofthe ICA on its anterior-medial aspect at

the apex of the opticocarotid triangleand then carrying the microdissection

laterally, across the ICA. This should

complete the establishment of proximalarterial control and simultaneously

establish initial exposure of the

proximal aneurysm complex in most

cases. Initial microdissection ofthickened arachnoid and clot in the

posterior carotid cistern should belimited to meticulous proximal-to-distal exposure of the ICA only, as the

surgeon defines in succession the

following vessels: the origin of theposterior communicating artery,

posterior communicating artery (PCA)-

proximal aneurysm junction, aneurysm

neck, the distal origin of the aneurysm


24/27


neck from the carotid wall, and finallythe anterior choroidal artery origin.

Extensive removal of subarachnoid clot

or identification of the distal posterior

communicating and anterior choroidalvessels or aneurysm fundus should be

postponed until satisfactory exposure

of the entire posterior carotid wall hasbeen exposed to permit safe and early

distal temporary arterial control, should

it be necessary. In most instances,distal control of the ICA is obtained, if

necessary, by placing a temporary clip

just proximal to the ICA bifurcation.After appropriate preparations have

been made for proximal and distalarterial control and with satisfactorypreliminary inspection of the posterior,

anterior and medial carotid walls, the

surgeon is nearly ready to begin

definitive dissection of the aneurysmneck in preparation for clip application

(Samson and Batjer, 1990, p 57-

65)[138]

.

It is first important to identify the distal

PComA for temporary clip placement,if possible, because obtaining proximal

and distal control of the ICA may notbe enough to stop back bleeding from

the PComA if intraoperative rupture

occurs. Sometimes, this cansignificantly hinder visualization and

make further microdissection and

aneurysm clipping difficult. Moreover,

if the PComA is not identified prior toclip placement, the surgeon runs the

risk of including this vessel into theclip construct, especially if vision isimpaired by intraoperative rupture

(Samson and Batjer, 1990, p 63)[138]

;

(Psarros, 2006, p 199)[124]

.

11.Postoperatively, the patient wasfound to have a homonymous

visual field defect of both upper

and lower quadrants. This was

most likely the result of intra-operative injury to what

structure/s?

Occlusion of the anterior choroidal

artery (AchA) may cause ahomonymous defect in the upper and

lower quadrants with sparing of the

horizontal sector (quadruplesectoranopia), which is diagnostic of a

lateral geniculate body infarct in the

AchA distribution. Injury or ligation ofthis vessel may also produce theclassically reported features of

contralateral hemiplegia,

hemianesthesia, and hemianopsia(Brazis, et al., 1996, p 132-140)

[19];

(Psarros, 2006, p 199)[124]

.

The AchA arises from the ICA in 75%

of patients, but can arise from either

the MCA or PcomA in up to 25% of

patients. The AchA supplies: 1) thetemporal lobe - uncus, pyriform cortex,and a portion of the amygdala; 2) the

visual system - optic tract, lateral

geniculate nucleus, and a portion of the

optic radiations; 3) the internal capsuleand basal ganglia - medial globus

pallidus, tail of caudate, genu and

posterior limb of internal capsule; 4)the diencephalon - lateral thalamus and

subthalamus; 5) the mesencephalon -

middle one-third of cerebral peduncleand substantia nigra.

Generally, the sites for temporary clipplacement chosen during surgery for

PComA aneurysms include the

proximal ICA near the anterior clinoid

process, on the distal ICA immediatelyproximal to the carotid bifurcation, and

on the PComA distal to the aneurysm


25/27


fundus. Obviously, the territorysupplied by the AchA will be rendered

ischemic during the period of

temporary occlusion, which can result

in a choroidal infarct shouldprolonged temporary occlusion time be

necessary.

Samson and Batjer describe the

following steps for clipping a PcomA

aneurysm after preparation of thevessels to receive temporary clips


58)[138]

. The arterial blood pressureshould be normalized, and either

etomidate (0.3 mg/kg) or a barbiturate(often pentobarbital) should be given toachieve burst suppression.

Subsequently, temporary clips are

applied from proximal to distal, and the

aneurysm fundus could be moreaggressively manipulated. If necessary,

a small gauge spinal needle could be

used to puncture the aneurysm dome(for larger aneurysms), well away from

the aneurysm neck for easier

manipulation. The suction can then beintermittently placed over the puncture

site and despite continued bleeding ofthe PcomA (if temporary clip

application not possible), suction will

transiently decompress the aneurysmadequately enough to allow dissection

to progress sufficiently to permit

permanent clip placement. Should

protracted microdissection be required,at intervals of approximately 10 to 15

minutes, a small cottonoid can beplaced over the puncture site and thetemporary clips removed to allow for

reperfusion of the carotid (and anterior

choroidal artery) territory, with thebleeding from the aneurysm being

controlled with suction and tamponade


64)[138]

.

12.What percent of patients withaneurysmal SAH develop

angiographic and clinical

vasospasm?

Vasospasm is one of the greatest

causes of morbidity in patientssurviving the initial SAH.

Angiographic vasospasm has been

reported to occur in approximately70% of patients following SAH, with

approximately 20-30% having

clinically significant narrowing. It hasa peak incidence around the seventh

day following SAH, although it can

occur anytime up to approximately 13-14 days post-bleed, beyond of which itis fairly uncommon (Heros, et al.,

1983, p 599-608)[58]

; (Ropper and

Zervas, 1984, p 909-915)[134]

. Whenvasospasm develops, it may last for

several weeks (Heros, et al., 1983, p

599-608)[58]

; (Weir, 1982, p 39-43)[157]

.The most common indicator

predisposing to vasospasm is the

amount of subarachnoid blood on the

CT scan. Thick blood in the basalcisterns (Fisher grade III) carries ahigher vasospasm risk than focal

loculations (Fisher, et al., 1977, p 245-

248)[44]

. Lobar hematomas and

interhemispheric blood are associatedwith a low risk of vasospasm, while

subarachnoid blood in the Sylvian

fissure appears to carry an intermediatevasospasm risk (Pasqualin, et al., 1984,

p 344-353)[118]

; (Kistler, et al., 1983, p

424-436)

[81]

.


26/27


13.On postoperative day 9 thepatient developed new right arm

and leg weakness while

recovering in the ICU, but her

level of consciousness remainedunchanged. Her ventriculostomy

continued to function properly.

This neurologic change from

baseline was preceded by slight

fever and leukocytosis. What

should be the next course of

action in this patients care?

Clinical vasospasm usually develops

slowly over hours or days and may be

associated with a slow decline inneurologic status. Headache, fever, andleukocytosis may precede and herald

the onset of vasospasm prior to

neurological deterioration. Permanentneurological deficit or death has been

reported to occur in approximately

12% of patients who develop severeclinical vasospasm (Heros, et al., 1983,

p 599-608)[58]

; (Fisher, et al., 1977, p

245-248)[44]

. Although this clinical

history is highly suggestive ofvasospasm, obtaining an emergent CTscan in the face of a new neurologic

deficit is often the first step in

management. This is done to rule out

any structural abnormality(hemorrhage, hydrocephalus, etc.) that

may require alternative treatment

strategies.

14.What is the mainstay of

treatment of clinically significantcerebral vasospasm?

In the chapter on management of SAHinNeurological Emergencies,

Kopitnik, et al., give a thorough

discussion on the management ofcerebral vasospasm, which is

summarized below (Hughes, 2003, p

278-281)[63]

. Presently, the mainstay of

treatment for clinically significantcerebral vasospasm is the induction of

hypervolemia, systemic hypertension,

and hemodilution, commonly referred

to as triple-H therapy orhyperdynamic therapy. The

neurologic deficits seen with

vasospasm result from arterialnarrowing and increased

cerebrovascular resistance.

Autoregulation is often disruptedfollowing SAH, and any intervention/s

that increase cerebral perfusion

pressure can increase cerebral bloodflow in the hypoperfused regions of the

brain and potentially improveoutcomes (Symon, 1979, p 7-22)

[150];

(Pritz, et al., 1978, p 364-368)[123]

.

Patients undergoing Triple H therapy

are best treated in an intensive care unit

(ICU) environment with arterial andcentral venous lines, an indwelling

foley catheter, and pulse oximetry. An

arterial catheter or A-line assessesblood pressure continuously and lends

itself well to frequent blood draws for

blood gas measurements should theybe necessary. A SwanGanz catheter

monitors pulmonary capillary wedgepressure (or central venous pressure if

central venous line is used), a

transcutaneous pulse oximetermonitors oxygen saturation, and an

indwelling foley catheter can be a

useful adjunct to arterial and central

venous lines to gauge volume statusand certain urine electrolytes.

Desaturations may indicate earlypulmonary decompensation fromhypervolemic therapy. Fluid balance is

assessed hourly.

Specifically, the initial therapy for

symptomatic vasospasm consists of

volume expansion with crystalloid

and/or albumin to create a positive


27/27


fluid balance. Pulmonary artery wedgepressure is generally maintained

between 14 and 18 mm Hg and central

venous pressure is kept at

approximately 10 mm Hg. If clinicalimprovement is not seen soon after

volume expansion or blood pressure

can not adequately be raised withvolume expansion alone, arterial blood

pressure can be elevated with

dopamine, dobutamine, and/ornorepinephrine and systolic pressures

typically maintained between 180 and

220 mm Hg. Kassell reported goodresults in 58 patients treated for

cerebral vasospasm with volumeexpansion and induced arterialhypertension in which he demonstrated

reversal of neurological deficits in 75%

of patients. Neurological improvement

was permanent in 74% of patients(Kassell, et al., 1982, p 337-343)

[73]. As

intravascular volume is expanded,

patients, oftentimes, undergo asecondary diuresis, which can make

artificial elevation of the pulmonary

capillary wedge pressure difficult.Under these circumstances, the use of

low dose vasopressin can helpminimize the diuresis and maintain an

elevated intravascular fluid volume, if

necessary. Triple H therapy can becontinued until one of the following

conditions are met: neurologic

symptoms resolve, vasospasm clears as

demonstrated by arteriography orDoppler monitoring, or complications

from hyperdynamic therapy occur.Complications may include congestiveheart failure, brain edema, pulmonary

edema, hypertensive cerebral

hemorrhage, systemic complications ofprolonged vasopressor use, and

myocardial infarction (Shimoda, et al.,

1993, p 423-429)[145]

. Calcium channel

blockers may improve SAH patient

outcome (nimodipine 60 mg orallyevery four hours for 21 days) and are

now part of the overall management

algorithm at most institutions. Their

efficacy in reducing the detrimentaleffects of vasospasm has been shown

in controlled studies, (Allen, et al.,

1983, p 619-624)[5]

although the truemechanism of action remains

somewhat elusive (Kassell, et al., 1992,

p 848-852)[72]

.

When hyperdynamic therapy has

proven ineffective, other interventionsmay prove useful. Selective intra-

arterial infusion of papaverinehydrochloride or calcium channelblockers into the symptomatic vascular

territory may reverse angiographic

vasospasm in some patients. The

results of this therapy can be clinicallydramatic but, in a similar fashion, may

be extremely fleeting or completely

unsuccessful (Minami, et al., 2001, p169-179)

[98]. Additionally, transluminal

balloon angioplasty of the large

intracranial vessels (ICA, M1segmentof MCA, vertebral and basilar arteries)

may also prove beneficial. A numberof investigators have reported

encouraging results with the use of

these techniques (Zubkov, et al., 1984,p 65-79)

[171]; (Newell, et al., 1989, p

654-660)[106]

; (Hughes, 2003, p 278-

281)[63]

.

End of case

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