 Exam is mildly degraded by motion artifact.BRAIN: There is cortical and subcortical T2 hyperintensity and mainly cortical diffusion restriction that is most prominent within the right occipital lobe, but also involves the right frontal, parietal, and temporal lobes. There is mild enhancement in these regions. There is an additional focus of diffusion restriction within the midline dorsal pons with associated susceptibility effect and T2 hyperintensity. There is also additional confluent T2 hyperintensity mainly within the bilateral occipital subcortical white matter but also within the bilateral parietal and left frontal subcortical white matter. There is a punctate focus of susceptibility effect within the right occipital lobe. The ventricles are somewhat slit like. The basal cisterns are normal in size and configuration. There is dilatation of the bilateral optic nerve sheaths, and mild flattening of the optic discs. There is no midline shift or herniation. The major cerebral flow voids are intact. The skull, paranasal sinuses, and scalp soft tissues are unremarkable. There is fluid within the bilateral mastoid air cells, right greater than left.MRA HEAD: The intracranial internal carotid arteries are normal in course and caliber. The middle and anterior cerebral arteries are unremarkable. The vertebral arteries, basilar artery, and posterior cerebral arteries are normal in course and caliber. There is no evidence of flow-limiting stenosis or aneurysm.MRV HEAD: There is no evidence of venous sinus thrombosis.MRA NECK: There is a separate origin of the left subclavian artery, left common carotid artery, and brachiocephalic artery from the arch. The common carotid arteries and cervical internal carotid arteries are normal in course and caliber. Both vertebral artery origins are patent. There is no evidence of flow-limiting stenosis or occlusion.
1.Findings as detailed above are most compatible with posterior reversible encephalopathy syndrome with superimposed progression to right occipital cortical infarction and pontine infarction.2.Findings suggestive of increased intracranial pressure, likely secondary to the above process. 3.No evidence of venous sinus thrombosis.4.No evidence of intracranial aneurysm or significant steno-occlusive lesion within the head or neck.