Neuro_MR_Brain: 64 M, AMS

CLINICAL HISTORY: 64-year-old male with 2 months of progressive cognitive changes, right hemiparesthesias and seizures.
Parenchyma: There is progressive
encephalomalacia in the posterior right temporal lobe and right parietal lobe. Gradient signal abnormality within the cortex is again seen representing petechial hemorrhage. There is redemonstration of gyral enhancement in this area.
Continued interval progression of T2 signal abnormality within the left occipital, parietal, and frontal lobes, minimally increased since the most recent comparison, however markedly increased compared to more remote exams. There is involvement of the splenium of corpus callosum without involvement of the contralateral white matter at this time. There are innumerable punctate foci of gradient signal abnormality as well as prominent linear structures seen within the area, representing multiple petechial hemorrhages with prominent medullary venous structures. There is increasing, somewhat heterogeneous gyral cortical as well as coarse subcortical enhancement in this area.
Ventricles and extra-axial spaces: Overall stable, ex vacuo dilatation of the atrium of the right lateral ventricle is noted.
There is a small cyst within the pituitary.
Orbits: Apparent T2 signal abnormality within the superior orbits bilaterally is noted, and may be artifactual.
Visualized paranasal sinuses: Clear.
Mastoid air cells: There are small bilateral mastoid effusions.
Bones: Normal.
1. Evolution of wedge-shaped injury in the right temporal and parietal lobe with progressive encephalomalacia, cortical petechial hemorrhage, and gyral enhancement compatible with evolving subacute posterior division MCA infarct.
2. Slightly increased extent of T2/FLAIR signal abnormality in the subcortical white matter in the left occipital, parietal, and frontal lobes with associated mass effect. Again seen are multiple foci of 
cortical petechial hemorrhage and multifocal parenchymal foci of GRE 
susceptibility some of which extends along the medullary veins. Interval increase in postcontrast enhancement. Overall findings are favored to represent inflammatory response to beta-amyloidosis. Other differential considerations include vasculitis, posterior reversible encephalopathy syndrome, and reversible cerebral vasoconstrictive syndrome syndrome but are felt to be less likely given the lack of abnormal vessel wall enhancement and the degree of GRE signal abnormality.

(Inflammatory amyloidosis)

Accession: CL27388341

Study description: MR BRAIN REFERENCE ONLY