Progression of ataxia, cerebellar atrophy. Revaluate left frontal and DWI lesion, and question of multiple possible cavernoma There is no restricted diffusion to suggest acute ischemia. There are multiple T2 hyperintense lesions throughout the periventricular and subcortical white matter. Relatively largest of these is seen in the left frontal lobe involving the posterior aspect of the left superior frontal gyrus. There are tiny foci of susceptibility within this lesion suggestive of microhemorrhages. There is diffusion hyperintensity with increased ADC. There is mild associated enhancement.There is a 9-mm intraparenchymal focus of susceptibility effect involving the right parietal lobe with additional susceptibility effect in the adjacent intraparietal sulcus indicative of prior subarachnoid component of the hemorrhage. There is mild enhancement associated with the intraparenchymal focus. Mild associated mineralization better seen on prior CT. Additional foci of susceptibility are also seen in the right parietal lobe involving the cuneus as well as along the cortex of the right temporo-parieto-occipital junction.There is severe volume loss involving the cerebellum including the cerebellar hemispheres and vermis as well as the pons, midbrain, and bilateral middle cerebellar peduncles.Sella and orbits are grossly within normal limits. Paranasal sinuses and mastoid cells are clear. Bone marrow signal and extracranial soft tissues are within normal limits.
1. No evidence of acute ischemia, intracranial mass, or mass effect.2. Multiple foci of chronic microhemorrhage in the right parietal and occipital lobes, as described above. Favored differential is amyloid angiopathy. Multiple cavernous malformations is also a possibility although appearance is not typical. Relatively largest of these lesions measures 9 mm in the right parietal lobe and associated with evidence of prior subarachnoid hemorrhage including hemosiderin deposition along the right intraparietal sulcus. There is mild associated enhancement as well. 3. Multiple foci of FLAIR hyperintensity in the subcortical and periventricular white matter. These may be related to chronic small vessel ischemic disease but are nonspecific. There are tiny foci of hemorrhage associate with the left frontal lesion with increased diffusivity and enhancement. Subacute ischemia remains a possibility although amyloid angiopathy, again can be considered, with possible inflammatory component. Other vasculitides can also be considered although the visualized vessels on recent CTA were normal in caliber. Patient age and presence of hemorrhage within the left frontal lesion makes demyelinating disease much less likely.4. Cerebellar and brainstem volume loss compatible with diagnosis of spinocerebellar ataxia.