To describe a case of post-infectious encephalopathy following COVID-19 with MRI brain changes suggestive of Wernicke’s encephalopathy and a transient presence of anti-GAD65 autoantibodies in the cerebrospinal fluid (CSF).

Chronic malnutrition and alcoholism are known risk factors for developing Wernicke’s encephalopathy. However, it is not typically associated with thiamine deficiency resulting from acute starvation as in this case of severe respiratory syndrome due to coronavirus-2 (SARS-CoV-2).

A 59 year-old female presented to the neurointensive care unit with subacute disorientation, decreased verbal fluency, memory deficits, gait dysfunction, confusion, and rapid weight loss that progressed to coma over two months following COVID-19 infection. Initial lumbar puncture (LP) one month following infection was notable for positive anti-GAD65 autoantibodies and elevated protein which was suggestive of post-infectious encephalitis. MRI brain at the time of initial evaluation was unremarkable for abnormalities and the patient’s symptoms continued to progress to include depressed mentation. Subsequent MRIs of the brain with and without contrast showed T2 FLAIR abnormalities in the periaqueductal grey, lateral walls of the third ventricle, splenium, and mammillary bodies. Repeat LP showed similar CSF profile and absence of anti-GAD65 autoantibodies. Electroencephalogram showed slowing with frequent generalized periodic discharges.

Patient’s treatment course included high dose thiamine, methylprednisolone, intravenous immunoglobulin, and plasmapheresis without clinical improvement. The patient did not show meaningful cognitive recovery and was transitioned to comfort care.

The patient's progression to coma was suspected to be due to development of COVID-19 encephalopathy precipitating Wernicke’s encephalopathy in the setting of severely diminished oral intake. Because Wernicke’s encephalopathy is potentially reversible with thiamine administration, we propose that early empiric treatment should be considered in all patients suffering from persistent encephalopathy following COVID‐19 infection.