Beyond Ophthalmoplegia: Wernicke Encephalopathy with Anisocoria

A 69-year-old man with a history of heavy alcohol consumption and poor nutrition presented with disorientation and gait instability. The cognitive assessment was severely affected, with the Hasegawa Dementia Scale-Revised score was 4. Neurological examination revealed anisocoria (right 4.0 mm, left 2.0 mm) with sluggish light reflexes, gaze-evoked horizontal nystagmus, and vertical gaze restrictions. He exhibited disorientation and limb ataxia; deep tendon reflexes were normal. Brain MRI showed bilateral thalamic hyperintensities on diffusion-weighted imaging and periaqueductal high signal on T2 FLAIR. Laboratory testing confirmed a severely reduced serum thiamine level of 10.5 ng/mL, establishing Wernicke encephalopathy (WE) based on Caine’s criteria. Immediately upon admission (Day 1), high-dose thiamine therapy was initiated at 700 mg/day (300 mg/day intravenous drip plus 400 mg/day oral) for 7 days, followed by 400 mg/day oral. Despite prompt, high-dose thiamine administration, the 2.0 mm anisocoria persisted consistently throughout the 19-day hospitalization, whereas cognitive function and ataxia partially improved. The 2.0 mm interocular difference confirmed pathologic anisocoria, indicating asymmetric autonomic disruption involving descending sympathetic pathways in the periaqueductal gray matter. While neuro-ophthalmic signs in WE are typically reversible, this case demonstrates that autonomic deficits may persist despite comprehensive thiamine therapy, highlighting WE as a critical metabolic mimic of life-threatening structural brainstem disorders.