spinal cord infarction caused by malignant intramedullary glioma: the traps of epidemiology and...

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NEUROSURGICAL IMAGE Spinal cord infarction caused by malignant intramedullary glioma: the traps of epidemiology and travel history M. LAWSON-SMITH 1 , G. SAMANDOURAS 1 , T. HINKS 2 , P. L. TAN 3 , G. QUAGHEBEUR 3 , P. MATHEWS 2 , O. ANOSGORE 4 & T. Z. AZIZ 1 Departments of 1 Neurosurgery, 2 Neurology, 3 Neuroradiology and 4 Neuropathology, Radcliffe Infirmary, Oxford, UK A 19-year-old patient of Pakistani origin presented with paraplegia and a sensory level at T4. The patient was well until 3 weeks prior to his admission when he developed back and left leg pain. One week later he developed paraparesis that over the next 10 days progressed to paraplegia and loss of sphincter function. On examination he was drowsy. He had power 0 MRC in his lower extremities and loss of all sensory modalities below T4. His symptoms started whilst he was on holiday in Pakistan where he spent 6 weeks. Routine labora- tory investigations were unremarkable and CSF studies obtained after a lumbar puncture were negative for infectious disease including TB, viruses, brucella, amoebic and Lyme disease. Imaging demonstrated normal chest radiographs. MRI of his brain was normal, while MRI of his spine revealed an intramedullary spinal lesion extending from T7 – T10 (Fig. 1). At the centre of the lesion a necrotic core was evident, while the spinal cord rostrally demonstrated extensive asso- ciated oedema (Fig. 1). FIG. 1. (A) Sagittal T2-W demonstrating an intramedullary heterogeneous lesion extending from T7 to T10 (right arrows). Observe the cord oedema rostral to the lesion (left arrows) and the preservation of the disc spaces. (B) Axial, T1-W MRI through the T9 level following administration of gadolinium. Observe the central, necrotic core of the intramedullary compartment (arrows) leaving at the periphery a rim of perfused spinal cord tissue (large arrow). Received for publication 6 January 2004. Accepted 27 January 2004. Correspondence: Mr G. Samandouras, Department of Neurosurgery, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, UK. Tel: + 44(0) 1865 311188. Fax: + 44(0) 1865 224898. E-mail: [email protected] British Journal of Neurosurgery, April 2004; 18(2): 199 – 200 ISSN 0268-8697 print/ISSN 1360-046X online/04/020199–02 # The Neurosurgical Foundation DOI: 10.1080/02688690410001681127 Br J Neurosurg Downloaded from informahealthcare.com by SUNY State University of New York at Stony Brook on 10/26/14 For personal use only.

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NEUROSURGICAL IMAGE

Spinal cord infarction caused by malignant intramedullary glioma: thetraps of epidemiology and travel history

M. LAWSON-SMITH1, G. SAMANDOURAS

1, T. HINKS

2, P. L. TAN

3, G. QUAGHEBEUR

3,

P. MATHEWS2, O. ANOSGORE

4& T. Z. AZIZ

1

Departments of 1Neurosurgery, 2Neurology, 3Neuroradiology and 4Neuropathology, Radcliffe Infirmary, Oxford, UK

A 19-year-old patient of Pakistani origin presented

with paraplegia and a sensory level at T4. The patient

was well until 3 weeks prior to his admission when he

developed back and left leg pain. One week later he

developed paraparesis that over the next 10 days

progressed to paraplegia and loss of sphincter

function. On examination he was drowsy. He had

power 0 MRC in his lower extremities and loss of all

sensory modalities below T4.

His symptoms started whilst he was on holiday in

Pakistan where he spent 6 weeks. Routine labora-

tory investigations were unremarkable and CSF

studies obtained after a lumbar puncture were

negative for infectious disease including TB,

viruses, brucella, amoebic and Lyme disease.

Imaging demonstrated normal chest radiographs.

MRI of his brain was normal, while MRI of his

spine revealed an intramedullary spinal lesion

extending from T7 –T10 (Fig. 1). At the centre of

the lesion a necrotic core was evident, while the

spinal cord rostrally demonstrated extensive asso-

ciated oedema (Fig. 1).

FIG. 1. (A) Sagittal T2-W demonstrating an intramedullary heterogeneous lesion extending from T7 to T10 (right arrows). Observe the cord

oedema rostral to the lesion (left arrows) and the preservation of the disc spaces. (B) Axial, T1-W MRI through the T9 level following

administration of gadolinium. Observe the central, necrotic core of the intramedullary compartment (arrows) leaving at the periphery a rim of

perfused spinal cord tissue (large arrow).

Received for publication 6 January 2004. Accepted 27 January 2004.

Correspondence: Mr G. Samandouras, Department of Neurosurgery, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, UK. Tel: + 44(0) 1865 311188.

Fax: + 44(0) 1865 224898. E-mail: [email protected]

British Journal of Neurosurgery, April 2004; 18(2): 199 – 200

ISSN 0268-8697 print/ISSN 1360-046X online/04/020199–02 # The Neurosurgical Foundation

DOI: 10.1080/02688690410001681127

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Despite the absence of serological evidence, in

view of his travel history, infection including TB was

considered the most likely diagnosis, although the

differential also included bacterial abscess, schisto-

somiasis or intrinsic tumour. The patient was started

on anti-tuberculous treatment and a decision to

proceed to diagnostic biopsy was made. Following a

standard thoracic laminectomy the dura was incised

and tented laterally, revealing a dark, necrotic spinal

cord dorsally (Fig. 2A). A myelotomy was performed

and an intramedullary lesion was found to infiltrate

diffusely the spinal tissue (Fig. 2A). Several vessels

were seen to be thrombosed accounting for the

infarcted cord (Fig. 2B). Attempts to develop a plane

between the lesion and the spinal tissue using

microsurgical techniques were unsuccessful.

Histology demonstrated a pleomorphic astrocyto-

ma with vascular proliferation, mitoses and areas of

tumour necrosis (Fig. 3), diagnostic of a malignant

astrocytoma (WHO grade IV). The patient devel-

oped no further deficits during his hospital stay and

following palliative radiotherapy he was transferred

to a rehabilitation centre.

In the case reported, the diagnosis of intramedul-

lary malignant glioma was not considered mainly

because of its rarity, but also of the patients’ ethnic

background and his recent travel history. Also the

presence of infarcted spinal tissue was highly

atypical. To our knowledge, cord infarction caused

by malignant intramedullary glioma has not been

previously reported.

Intramedullary malignant gliomas are extremely

rare representing less than 1.5% of spinal cord

tumours.1 Owing to their rarity, they are not often

considered as a cause of spinal intramedullary

lesions.2 They have a poor prognosis; in a series of

36 patients the median survival time was 10 months

with younger patients having longer survival peri-

ods.2 The treatment remains controversial, as it

appears that debulking, radiotherapy or chemother-

apy do not significantly affect the outcome.

References

1 Ciappetta P, Salvati M, Capoccia G, Artico M, Raco A, Fortuna

A. spinal glioblastomas: report of seven cases and review of the

literature. Neurosurgery 1991;28:302 – 6.

2 Santi M, Mena H, Wong K, Koeller K, Olsen C, Rushing EJ.

Spinal cord malignant astrocytomas. Clinicopathological fea-

tures in 36 cases. Cancer 2003;98:554 – 61.

FIG. 2. (A) The dura is tented laterally to the paraspinal muscles exposing the dark, necrotic spinal cord caudally (left arrow) adjacent to the

swollen but still perfused spinal tissue rostrally (right arrow). (B) Following myelotomy several specimens were obtained from the

intramedullary mass (top arrow). Observe the thrombosed spinal vessels on the surface of the spinal cord (arrows).

FIG. 3. Malignant astrocytoma with vascular proliferation (arrow).

H&E, Magnification 630.

200 M. Lawson-Smith et al.

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