Alcohol-induced persisting amnestic disorder constitutes a continuum involving Wernicke's acute encephalopathy, the amnestic disorder per se (commonly known as Korsakoff's psychosis), and cerebellar degeneration. Alcohol-induced persisting amnestic disorder typically follows an acute episode of Wernicke's encephalopathy. The latter consists of ataxia, sixth cranial nerve (abducens) paralysis, nystagmus, and confusion. Wernicke's often clears with vigorous thia-
mine treatment, but 50-65% of patients show persistent signs of amnesia. If untreated, the mortality rate is about 15%.
The amnesia is characterized by anterograde amnesia (inability to form new memories due to failure of information acquisition), retrograde amnesia (loss of previously formed memories), and cognitive deficits, such as loss of concentration and distractibility.
The etiology is based on nutritional factors, specifically, the thiamin deficiency present with chronic alcohol use, either through intestinal malabsorption or poor dietary intake associated with alcohol. Other factors, such as familial transketolase deficiency may be important in the pathogenesis of this syndrome in a subgroup of individuals.
The disorder in memory that persists is correlated with microhemorrhages in the dorsomedial nucleus of the thalamus, in the mammillary bodies, and in the periventricular gray matter.
In contrast to other dementias, intellectual function is typically preserved. In a review of Wernicke-Korsakoff syndrome, McEvoy (1982) points out that 20% of patients show complete recovery over a period of months to years, 60% show some improvement, and 20% show minimal improvement. Previously believed to be a distinct clinical entity, alcoholic cerebellar degeneration may be indistinguishable clinically and pathophysiologically from the cerebellar dysfunction seen with Wernicke-Korsakoff syndrome.
Alcoholic amnestic disorder should not be confused with "blackouts," which are periods of retrograde amnesia during periods of intoxication. Blackouts, caused by high blood alcohol levels, may occur in nonalcoholics, as well as at any time in the course of alcoholism.
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