Presentation
Unwitnessed fall.
Patient Data
There is extensive abnormal white matter hypoattenuation involving the bilateral posterior frontal and parietal lobes, more pronounced on the right side. Grey-white matter differentiation is overall preserved. No mass effect or brain herniation is evident.
Ventricular size and sulcal pattern are normal. No intracranial hemorrhage.
There is a large left parieto-occipital scalp hematoma. No calvarial or skull base fracture.
Multiple punctate foci of susceptibility artefact throughout the superficial supratentorial brain and cerebellar hemispheres at the grey-white interface without particular lobar predilection, consistent with prior microhemorrhage secondary to known cerebral amyloid angiopathy.
There is extensive confluent T2 FLAIR hyperintense signal associated throughout the white matter of the bilateral posterior frontal lobes, parietal, and occipital lobes with mild positive mass effect noted in the superior parietal regions with sulcal effacement. These appearances raise the possibility of the inflammatory sub-type of angiopathy.
Further scattered punctate foci of T2 FLAIR hyperintense signal are seen throughout the temporal and anterior frontal lobes bilaterally are non-specific.
No abnormal diffusion restriction. No abnormal enhancement on the post-contrast study.
Normal ventricles and basal cysterns.
Case Discussion
Innumerable superficial micro hemorrhages throughout the supra- and infratentorial brain consistent with cerebral amyloid angiopathy. Extensive white matter change with regions of positive mass effect raises the possibility of inflammatory subtype.
There has been significant imaging improvement of edema after corticosteroid therapy (not shown).
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