64-year-old male with altered mental status and weakness Redemonstrated are multiple small foci of hyperintensity on diffusion weighted images in the anterior right paramedian medulla, right middle cerebellar peduncle, left mid and posterior temporal white matter, right cerebral peduncle, midline splenium of corpus callosum, splenium of corpus callosum and several larger lesions in bilateral subcortical and periventricular white matter of the cerebral hemispheres, unchanged in appearance. Several demonstrate tiny internal signal void suggestive of vasculature. As before, a tiny right anterior medullary lesion demonstrates restricted diffusion and consistent with acute ischemia. The remaining lesions lesions are well visualized on FLAIR and T2-weighted images as well-demarcated foci of hyperintensity. Several also demonstrate T1 hypointensity. Also redemonstrated are multiple ill-defined foci of FLAIR hyperintensity in bilateral middle cerebral peduncles, diffusely in the pons and a focus of hemorrhagic encephalomalacia in the right cerebellum. Many of these lesions are highly suggestive of chronic ischemic changes however possibility of overlapping chronic demyelinating disease cannot be entirely excluded. None demonstrate abnormal contrast enhancement.As before there is slight prominence of cortical sulci and supratentorial ventricular system for patient's stated age. No evidence of midline shift.Flow voids within bilateral internal carotid arteries , bilateral anterior and middle cerebral arteries are identified. Small caliber bilateral vertebrals and basilar artery is noted. As noted before, there is abnormal signal intensity of the left intracranial vertebral artery which could be artifactual or as a result of vascular lumen compromise.Unremarkable barium and orbits. Left maxillary sinusitis is unchanged and unremarkable other paranasal sinuses are noted.
1.Diffusion-weighted images demonstrate a single tiny focus of restricted diffusion in the right anterior paramedian medulla of acute ischemia, unchanged. As noted before, there is abnormal signal intensity of the left intracranial vertebral artery which could be artifactual or as a result of vascular lumen compromise.2.None of the many additional supratentorial and infratentorial foci of diffusion/T2 hyperintensity, without restricted diffusion, demonstrate abnormal contrast enhancement. These findings remain concerning for demyelinating disease given lesional morphology and locations. Other differential considerations remain possible, but are more rare and less likely, such as ADEM, Susac syndrome, vasculitides, or other etiologies if the patient is HIV positive.3.Additionally patchy foci of FLAIR hyperintensity is noted in the periventricular and sub-cortical white matter, pons, bilateral middle cerebellar peduncles, corpus callosum and right cerebellum as detailed above which may represent superimposed chronic small vessel ischemic disease, although findings of the aforementioned processes mentioned in number two may also represent a primary source for these findings.