Clinicians are often taught to diagnose WE on the basis of the presence of the classic clinical triad of ocular motor abnormalities, cerebellar dysfunction, and altered mental state. Ocular motor abnormalities occur in ≈30% of patients with WE and may include nystagmus or ophthalmo plegia, while cerebellar dysfunction can be found in ≈25% of patients with this disorder and may manifest as loss of equilibrium, incoordination of gait, trunk ataxia, dysdiadochokinesia and, occasionally, limb ataxia or dysarthria. Approximately 80% of patients with WE exhibit an altered mental state, which may comprise mental sluggishness, apathy, impaired awareness of an immediate situation, an inability to concentrate, confusion or agitation, hallucinations, behavioral disturbances mimicking an acute psychotic disorder, or coma.3,10,21 A retrospective analysis of the clinical signs and symptoms of patients diagnosed at autopsy as having WE revealed that only 20% of patients with this disorder presented with the full triad of clinical features and ≈30% of such indivi duals exhibited only cognitive impairment.21 Thus, through the requirement of the full triad for a positive diagnosis, WE is missed by routine clinical examination
