Glioblastoma NOS presenting as stroke

Case contributed by Peter Mitchell
Diagnosis almost certain

Presentation

Acute onset dysphasia. Code stroke pathway activated.

Patient Data

Age: 70 years
Gender: Male

No definite abnormality on non-contrast CT. CT perfusion demonstrates a small area deep adjacent to the left trigone has subtle elevated CBV. No ischemic perfusion change. No large vessel occlusion. 

Stroke MRI (Quick DWI)

mri

There is a 14 x 13 mm region of abnormal signal lateral to the left lateral ventricle trigone, probably deep to the left supramarginal gyrus and posterior end of superior temporal gyrus, involving white matter but not clearly involving cortex. This lesion demonstrates mildly heterogeneous T2 hyperintensity that contains internal tiny foci of low T2 signal, and high signal on the DWI without corresponding high or low ADC values.

On the CT brain this region may have subtle increased density, while on the perfusion imaging performed at that time there is a corresponding focus of elevated cerebral blood volume (CBV). No definite enhancement within the lesion on the arterial phase images from the CT angiogram circle of Willis.

Conclusion: Although a subacute infarct is the most likely clinical diagnosis, on limited imaging sequences available there is a differential diagnosis of neoplasia.

Within the left posteromedial temporal lobe a lesion with dimensions of 16 mm x 15 mm x 14 mm ( CC x trans x AP ) demonstrates irregular nodular enhancement. The lesion has intrinsic low T1/high T2 signal. There is minimal surrounding FLAIR abnormal signal. This is probably contiguous with an abnormality within the posterior aspect of the left middle temporal gyrus that has cortical FLAIR hyperintense signal and gyral expansion, associated sulcal effacement and local nodular sulcal enhancement.

No susceptibility artefact to suggest recent or previous hemorrhage or calcification. DWI signal within the white matter lesion is hyperintense without low ADC value.

Perfusion studies demonstrate elevated cerebral blood volume. Spectroscopy reveals reversal of choline: creatine ratio with a slight decrease in NAA. Elevated choline extends beyond the FLAIR/enhancing abnormality. No elevated myoinositol. No definite bony remodeling.

Conclusion: Overall the findings within the left temporal lobe are most in keeping with tumor. Although slightly unusual, a glial series tumor, particularly a higher grade astrocytoma or oligodendroglioma with the elevated CBV, with local leptomeningeal involvement, is thought most likely.

3 months later

mri

The T2/FLAIR hyperintense lesion at the trigone of the left lateral ventricle has increased in size, now measuring 2.7 x 2.2cm. This is again seen to be contiguous with FLAIR hyperintensity more laterally within the left posterior temporal lobe that involves and expands the cortex. The white matter component demonstrates contrast enhancement and there is also irregular left posterior temporal lobe nodular sulcal enhancement.

Conclusion: Increase in size of the left temporal lobe lesion, which is favored to represent a high grade glial series tumor.

Case Discussion

The patient went on to have a biopsy which confirmed a high-grade glioma (GBM). 

Note: IDH mutation status is not provided in this case and according to the current (2016) WHO classification of CNS tumors, this tumor would, therefore, be designated as a glioblastoma NOS

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