Wernicke's encephalopathy and cranial nerve VII palsy in a 24-year-old patient with COVID-19

Many documented secondary neurologic manifestations are associated with COVID-19, including mild peripheral and central nervous system disorders (such as hypo/anosmia, hypo/ageusia, and cranial nerve VII palsy) and severe problems (such as ischemic stroke, Guillain-Barré syndrome, and encephalitis). The list is growing. A new addition is non-alcohol Wernicke's encephalopathy.

We present the case of a 24-year-old male with no past medical history who developed stroke-like symptoms two days after testing positive for COVID-19. MRI of his brain showed T2 FLAIR hyperintensity in the splenium of the corpus collosum, mamillary bodies, periaqueductal gray matter, tectum, and ventral and dorsal medulla, an MRI signal concerning for non-alcohol Wernicke's encephalopathy. Our patient had no risk factors for Wernicke's encephalopathy. He was admitted and started on thiamine for Wernicke's encephalopathy and steroids for his cranial VII nerve palsy. Both his symptoms and imaging improved. He was discharged on oral thiamine. Follow-up in the Neurology Clinic has confirmed his continued stable state.

This case is one of three documented cases of Wernicke's encephalopathy believed to be caused by COVID-19 in patients without risk factors or chronic alcohol use. Ours is also the first case in which Wernicke's encephalopathy presents with a concomitant cranial nerve VII palsy. While Emergency Medicine doctors must maintain a high index of suspicion for stroke in younger patients with COVID-19, our patient's case augments the correlation between COVID-19 and Wernicke's encephalopathy in patients without other risk factors for developing the syndrome.