A 54-year-old man was found by paramedics in his home face-down at his computer desk with a substantially reduced level of consciousness. He had not contacted his family for more than 50 hours. The patient lived alone and was a heavy smoker with a history of alcohol abuse. His medical history was otherwise unremarkable, and there was no history of cancer, psoriasis, or rheumatoid arthritis, nor was there a history of methotrexate administration. On presentation to the emergency department, he was mildly hypotensive and was experiencing hypercapnic respiratory failure and acute renal failure with rhabdomyolysis. His toxicology screen was mildly positive for opiates. He received naloxone (Narcan; Emergent) with minimal effect. An unenhanced CT scan of the head was obtained (Fig 1A). Of note, this patient’s presentation predated the COVID-19 pandemic. He was admitted to the intensive care unit for decreased level of consciousness and respiratory failure. The decreased level of consciousness was thought to be secondary to seizure, as he developed seizurelike movements prior to intubation, probably in the context of intoxication or alcohol withdrawal. Electroencephalography revealed moderate bilateral cerebral dysfunction and encephalopathy, with no evidence of nonconvulsive seizures. He had a short course of intermittent hemodialysis and was discharged home 8 days later with an appointment for neurology follow-up. At discharge, he was at his cognitive and functional baseline. Approximately 3 weeks later, the patient was brought back to the emergency department for progressive confusion and decrease in balance. He became apathetic with reduced psychomotor activity and was no longer able to perform basic daily activities, such as cooking or bathing. He displayed bizarre behavior, such as staring at a wall for hours, and was somnolent, irritable, and inattentive. He eventually became incontinent of urine and stool. Results of a neurologic examination of the cranial nerves, motor function, sensation, and reflexes were normal. The results of blood work-up were grossly normal, and the results of an extensive toxicology work-up were negative. Repeat head CT was performed (Fig 1B). MRI was ordered to further investigate the patient’s encephalopathic presentation (Figs 2, 3).Head CT performed at initial presentation revealed symmetric hypoattenuation in both globi pallidi (Fig 1A). Followup CT performed during the subsequent hospitalization 3 weeks later revealed an interval decrease in the globi pallidi hypoattenuation. There was no convincing new imaging finding; in particular, there was no acute infarct, intracranial hemorrhage, or mass effect (Fig 1B). T2-weighted and fluidattenuated inversion recovery (FLAIR) MRI scans (Fig 2) showed diffuse confluent abnormal signal intensity of the white matter in both cerebral hemispheres, with subcortical sparing. Focal involvement of the globi pallidi was again identified. Diffusion-weighted images and apparent diffusion coefficient maps (Fig 3) showed diffusion restriction of the involved white matter, predominantly in the corona radiata and centrum semiovale. No associated contrast enhancement was seen (not shown). What is your diagnosis?