Presentation
Clinical history not available.
Patient Data
Post contrast imaging has been obtained for operative planning purposes.
Poorly defined areas of hyperdensity (presumably representing enhancement given preceding MRI study) involving the corona radiata and centrum semiovale of bilateral cerebral hemispheres is noted with subtle involvement of the corpus callosum in the midline.
There is confluent T2 / FLAIR hyperintense signal abnormality affecting the corona radiata and the centrum semiovale of the cerebral hemispheres with involvement of the corpus callosum, the right frontal operculum, the hippocampi, to lesser extent the thalami and the left cerebral peduncle. In the right frontal operculum there is involvement of grey and white matter, and the suggestion of gyral expansion.
Within the centrum semiovale, there are number of focal high T2 / FLAIR hyperintensities with predominantly peripheral irregular enhancement.
In addition, there is a 5 mm nodule of enhancement within the body of the corpus callosum and a 6 mm rather enhancing nodule in the chest cortical white matter of the right middle frontal gyrus.
There is diffusion restriction within the T2 hyperintense signal abnormality in the centrum semiovale bilaterally. There is no leptomeningeal enhancement. There is no pathological susceptibility artefact.
Conclusion:
Appearance could represent gliomatosis with foci of higher-grade glioma.
Tumefactive demyelination (monophasic acute disseminated encephalomyelitis) and atypical infection (particularly if the patient is immunocompromised) should also be considered.
Comparison with previous imaging and CSF analysis would be very useful.
The cerebral lesions seems to correspond a continuum that involves the corpus callosum and shows a straight alignment of enhancing lesions on axial planes.
Case Discussion
This case was pathologically proven to be a GBM and the imaging features illustrate a multifocal disease, where multiple areas of enhancement are connected to each other by abnormal white matter signal (T2/FLAIR), which represents microscopic spread to tumor cells. Furthermore, there is involvement of the corpus callosum (see also butterfly glioma).
Callosal lesions, are typically aggressive as the corpus callosum is composed of very dense white matter tracts which acts as a barrier to tumor spreading.
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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