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Year : 2010  |  Volume : 58  |  Issue : 5  |  Page : 808-810

Primary glioblastoma multiformis of cerebellum mimicking infarct

1 Department of Neurosurgery, Fortis Hospital, Mohali, Punjab, India
2 Department of Radiology, Fortis Hospital, Mohali, Punjab, India

Date of Acceptance23-Jul-2010
Date of Web Publication28-Oct-2010

Correspondence Address:
Tarun Sharma
Department of Neurosurgery, Fortis Hospital, Mohali, Punjab
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.72197

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How to cite this article:
Sharma T, Khosla V K, Brar R. Primary glioblastoma multiformis of cerebellum mimicking infarct. Neurol India 2010;58:808-10

How to cite this URL:
Sharma T, Khosla V K, Brar R. Primary glioblastoma multiformis of cerebellum mimicking infarct. Neurol India [serial online] 2010 [cited 2022 Oct 1];58:808-10. Available from: https://www.neurologyindia.com/text.asp?2010/58/5/808/72197


Glioblastoma multiformis (GBM) of the cerebellum is rare and the reported incidence is about 1%. [1] Cerebellar GBM presenting clinically as cerebellar infarct has not been reported till date. We describe a case of primary cerebellar GBM resembling as cerebellar infarct clinically and radiologically.

A 65-year-old, male presented with one week history of acute-onset vertigo, dizziness and imbalance while walking; this was followed by vomiting and mild headache of three days' duration. He was a known hypertensive and diabetic. On examination he was normotensive, conscious, alert and well oriented. He had right cerebellar signs. Routine hematological and biochemical tests were unremarkable. Echocardiography was normal and color Doppler of the neck vessels showed mild narrowing of both carotids without any significant limitation of flow. Magnetic resonance imaging (MRI) brain showed a focal area of altered signal intensity in the right cerebellar hemisphere, which was hyperintense on T2W and FLAIR and hypointense on T1W images. The lesion showed significant contrast enhancement on post-contrast T1W images and a clear-cut margin and wedge shape. Minimal mass effect was seen on the right lateral wall of the fourth ventricle [Figure 1]a and b. There was no diffusion restriction in the lesion [Figure 2]a. A possible diagnosis of right cerebellar subacute infarct was made, and the patient was put on aspirin 75 mg twice a day and atorvastatin 10 mg once a day. At follow-up after two weeks, the patient had deterioration in neurological status in the form of marked trunkal ataxia, bilateral cerebellar signs and slurred speech. Repeat MRI brain, showed no change in the size of the lesion as compared to first imaging, but mass effect over the fourth ventricle was increased leading to obstructive hydrocephalus with periventricular ooze [Figure 1]c-f. No evidence of restricted diffusion was seen in DW images. Single-voxel MR spectroscopy (MRS) of the lesion demonstrated decrease in N-acetyl aspartate (NAA) and creatine with mild increase in the choline level, along with increased choline-NAA ratio in the lesion [Figure 2]b.
Figure 1 :(a) Axial T1W image showing an isointense lesion in the right cerebellar hemisphere having a well-defined edge with some mass effect on the fourth ventricle. (b) T1W post-contrast axial image showing gyral contrast enhancement in the lesion. (c) Follow-up axial T1W image showing increased size of lesion. (d) Follow-up T1W post-contrast axial image showing heterogenous contrast enhancement in the lesion. (e and f) Follow-up T1W coronal and sagittal images showing obstructive hydrocephalus with periventricular ooze

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Figure 2 :(a) DWI and ADC maps showing no restriction of diffusion in the lesion. (b) Single-voxel MR spectroscopy (TE= 135 ms) showing significantly elevated choline-NAA ratio

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As the temporal course of lesion and the radiological findings on follow-up scan were not consistent with cerebellar infarct, ventriculo-peritoneal shunt followed by excision of the lesion was planned. Midline sub-occipital craniectomy was done. An abnormal bulge was seen over the right cerebellar hemisphere with widening of folia. A soft-to-firm cerebellar mass was found, which was moderately vascular. Near-total excision of the mass was done. Frozen sections of tissue revealed features of high-grade glial tumor, and final histopathological analysis of the section showed cerebellar tissue infiltrated by a poorly differentiated glial neoplasm with pleomorphism, mitosis, endothelial proliferation and small areas of necrosis [Figure 3]. The patient was subjected to whole posterior fossa craniospinal fractionated radiotherapy (56 Gy) starting four weeks after surgery, along with concomitant temazolamide in dose of 150 mg/m 2 body surface area. At the 3-month follow-up, the patient was conscious and alert. His headache and vomiting was relieved but cerebellar deficits were persistent.
Figure 3 :Microphotograph showing mitotically active highly cellular glial tumor (H and E, ×100). Inset: Necrotic area in tumor section

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Occasionally brain tumors can present as stroke like symptoms. [2] Incidence of this type of presentation is between 3% and 5%; and reported in literature with supratentorial tumors. [2],[3],[4] The mechanism of acute "tumor attack" has been a subject of much speculation. Plausible explanations include post-seizure/Todd's paralysis, acute intracranial pressure changes and consequent reduced cerebral blood flow, vascular steal phenomenon, acute hemorrhage, vascular compression and resultant infarction and tumor embolus. [4]

The typical MR finding in cerebellar GBM is a heterogeneous mass, isointense to hypointense on T1W and hyperintense on T2W images. Lesion may contain foci of bleeding and necrosis. Heterogeneous contrast enhancement is present and ring enhancement due to thick irregular wall of the tumor is usually seen. [1] The imaging findings of an infarct is typical particularly the restricted diffusion on DWI. Pattern of contrast enhancement depends upon the different stages of evolving infarct. In the acute stage (first 5 to 7 days) a pattern of progressive intravascular enhancement is seen. This is attributed to slower blood flow in arteries surrounding the ischemic tissue, resulting in decreased-flow void effects and thus an increased signal from the contrast agent. During this period, parenchymal enhancement is usually absent or sparse. Radiologically, the subacute stage usually begins at the end of the first week and may persist for 6 to 8 weeks. Subacute stage is characterized by gyral parenchymal enhancement, irregular contrast uptake or even ring enhancement in some cases and little or no mass effect. [5] There may be overlap between the radiological features of ischemic and neoplastic lesions, particularly in the subacute stage of infarct. Confounding diagnostic features in a neoplastic lesion which may be mistaken for an infarct are atypical presentation, such as sudden onset of neurological symptoms, a well-defined lesion in a vascular territory and absence of significant mass effect. In our case, presence of heterogeneously enhancing lesion with clear-cut margins and wedge shape in the territory of medial branch of posterior inferior cerebellar artery, were the features that mislead us to diagnose the lesion as subacute cerebellar infarct. DWI and MR spectroscopy are the additional modalities which may be helpful in distinguishing between the two, particularly when the clinical history is obscure. In late subacute-to-chronic infarction, restricted diffusion may not be evident, thus making DWI less useful in making the distinction between a tumor and an infarct, as in our case.

MR spectroscopy of astrocytomas shows a significant reduction in NAA due to loss of neuronal elements, as well as elevation of choline peak which may reflect increased membrane synthesis. Presence of lactate correlates with higher degree of malignances commonly observed in GBM. [1],[3] MR spectroscopy in the present case pointed toward a neoplastic pathology; however, it is well known that in infarcts also, there is loss of NAA and increased lactate levels, especially in late subacute and chronic stages [6]

A close follow-up in such cases both clinically and radiologically is therefore necessary to avoid misdiagnosis. Failure of clinical improvement and atypical temporal profile of symptoms, along with increased mass effect seen on follow-up imaging, suggested that the lesion may be neoplastic rather than an infarct. A high index of clinical suspicion and repeat imaging are required in such cases.

  References Top

1.Dormann GJ, Dunsmore RH. Glioblastoma multiformis of cerebellum. Surg Neurol 1975;3:219-23.  Back to cited text no. 1
2.Elsberg CA, Globus JH. Tumors of brain with acute onset and rapidly progressive course. Arch Neurol Psych1926;21:1044-78.  Back to cited text no. 2
3.Weisberg LA, Nice CN. Intracranial tumors simulating the presentation of cerebral vascular syndromes. AMJ Med1977;63:517-24.  Back to cited text no. 3
4.The UK TIA study group: Intracranial tumors that mimic transient cerebral ischaemia: Lessons from a large multicentre trial. J Neurol Neurosurg Psych 1993;56:563-6.  Back to cited text no. 4
5.Marks MP. Cerebral ischemia and infarction. In: Atlas SW, editors. 3 rd ed. Magnetic resonance imaging of the brain and spine. Philadelphia: Lippincott-Raven; 2002. p. 919-79.  Back to cited text no. 5
6.Smith JK, Castilo M, Kwock L. MR spectroscopy of brain tumors. Magn Reson Imaging Clin N Am 2003;11:415-29.  Back to cited text no. 6


  [Figure 1], [Figure 2], [Figure 3]

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