Patient presenting with left eye visual loss, evaluate for ischemic stroke. Multiple sequences are degraded by motion. There is no evidence of intracranial hemorrhage, mass, or acute infarct. There are apparent foci of diffusion hyperintensity in the left pons and the right pontomedullary junction without associated T2 signal changes, most likely artifactual in etiology. The ventricles and basal cisterns are normal in size and configuration. There is no midline shift or herniation. There are patchy foci of T2/FLAIR hyperintensity in the subcortical and deep periventricular white matter, which are nonspecific but compatible with mild chronic microvascular ischemic disease. Small foci of T2 hyperintensity in the cerebellum with associated volume loss are suggestive of chronic infarcts. Additional small foci of T2 hyperintensity in the right posterior subinsular region and left thalamus may represent chronic lacunar infarcts. Incidentally seen is a partially empty sella. Motion degraded SWAN sequences do not demonstrate any gross evidence of intracranial hemorrhage. The major cerebral flow voids are intact. The orbits and paranasal sinuses are grossly unremarkable. Small right frontal scalp fluid collection/hematoma is noted.
1.No definite evidence of acute infarct. Subtle foci of diffusion hyperintensity in the left pons and right pontomedullary junction without associated T2 signal abnormality are favored to be artifactual in etiology.2.Scattered foci of T2/FLAIR hyperintensity in the subcortical and periventricular deep white matter, which are nonspecific, but compatible with mild chronic microvascular ischemic disease.3.Evidence of chronic lacunar infarcts, as described above.