A 77-year-old right-handed woman with a history of peripheral artery disease and diabetes mellitus presented for routine aortic angiogram. Immediately after the procedure she reported complete vision loss. Examination was notable for left arm and leg weakness, right gaze deviation, visual confabulation, and disorientation. 

Initial CT head without contrast demonstrated hyperdensities in the right frontal cerebral convexities. MRI brain without contrast two hours after symptom onset showed no evidence of acute infarct or hemorrhage. CT head nine hours after onset showed edema in the right cerebral hemisphere. MRI brain performed ten hours after onset showed a punctate area of restricted diffusion in the right cerebellar hemisphere. Cerebral angiogram on day two showed no evidence of aneurysm. Electroencephalogram demonstrated generalized slowing with no epileptiform discharges.

The patient experienced mild visual improvement prior to cerebral angiogram but was noted to have worsening visual confabulation and encephalopathy after the procedure. Over the next 48 hours of close monitoring and supportive management, symptoms resolved.

This patient presented with visual anosognosia and a right hemispheric syndrome. CT head appeared consistent with contrast extravasation. Differential diagnosis included subarachnoid hemorrhage, ischemic stroke, posterior reversible encephalopathy syndrome, and seizures. Her clinical presentation with symptom onset immediately after aortography, recurrence after cerebral angiogram, and rapid resolution suggests a diagnosis of contrast-induced encephalopathy. Existing studies propose a mechanism of vasogenic edema involving the occipital lobes due to disruption of tight junctions, blood brain barrier permeability and autoregulation following high contrast doses. Further investigation is warranted to guide premedication and monitoring protocols to reduce complications associated with procedural contrast.