Wernicke Essay

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Wernicke-Korsakoff Introduction Carl Wernicke first described the syndrome in 1881. He referred to the disorder as acute superior hemorrhagic polioencephalitis. Some of the original patients he described included two male alcoholics and a women with esophageal stenosis. He described a clinic triad of encephalopathy, ophthalmoplegia, and ataxia. Unfortunately, most diagnoses are not made clinically but rather at autopsy. This suggests that the classic clinical triad is rare, or that clinicians do not properly recognize the symptoms. In some clinical studies, only one third of patients diagnosed with Wernicke’s encephalopathy (WE) presented with the classical triad. The majority of the patients presented encephalopathy (characterized by disorientation, indifference, and inattentiveness). Ocular motor abnormalities (nystagmus, lateral rectus palsy, and conjugate gaze palsies) occurred in 96%, resulting from oculomotor, abducens, and vestibular nuclei lesions. Gait ataxia presented in 87%, probably due to a combination of cerebellar and vestibular involvement as well as polyneuropathy. However, an autopsy-based study revealed that while 82% had mental status abnormalities only 23% had ataxia, 29% ocular motor abnormalities, and 11% polyneuropathy. The clinical triad was identified in only 17% of autopsy cases, and 19% showed none of the classic symptoms. This discrepancy between the clinical and autopsy-based studies is probably due to exclusion of atypical cases in the clinical series and the underestimation in the autopsy series of classic signs that were not properly elicited, recognized, or recorded (1). At autopsy the characteristic lesions of WK occur primarily in nuclei and structures surrounding the third and fourth ventricle and cerebral aqueduct. The mammillary bodies are affected in the vast majority of cases, usually showing atrophy (identified

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