Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

88 III. SUBSTANCES OF ABUSEmine treatment, but 50–65% of patients show persistent signs of amnesia. Ifuntreated, the mortality rate is about 15%.The amnesia is characterized by anterograde amnesia (inability to formnew memories due to failure of information acquisition), retrograde amnesia(loss of previously formed memories), and cognitive deficits, such as loss of concentrationand distractibility.The etiology is based on nutritional factors, specifically, the thiamin deficiencypresent with chronic alcohol use, either through intestinal malabsorptionor poor dietary intake associated with alcohol. Other factors, such as familialtransketolase deficiency may be important in the pathogenesis of thissyndrome in a subgroup of individuals.The disorder in memory that persists is correlated with microhemorrhagesin the dorsomedial nucleus of the thalamus, in the mammillary bodies, and inthe periventricular gray matter.In contrast to other dementias, intellectual function is typically preserved.In a review of Wernicke–Korsakoff syndrome, McEvoy (1982) points out that20% of patients show complete recovery over a period of months to years, 60%show some improvement, and 20% show minimal improvement. Previouslybelieved to be a distinct clinical entity, alcoholic cerebellar degeneration maybe indistinguishable clinically and pathophysiologically from the cerebellar dysfunctionseen 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 asat any time in the course of alcoholism.Alcohol-Induced Persisting DementiaThis disorder develops in approximately 9% of alcoholics (Evert & Oscar-Berman, 1995) and consists of memory impairment combined with aphasia,apraxia, agnosia, and impairment in executive functions, such as planning,organizing, sequencing, and abstracting. These deficits are not part of a deliriumand persist beyond intoxication and withdrawal. The dementia is caused by thedirect effects of alcohol, as well as by vitamin deficiencies.Models of cognitive impairment in alcoholics include “premature aging,”which means that alcohol accelerates the aging process, and/or that vulnerabilityto alcohol-induced brain damage is magnified in people over the age of 50;the “right-hemisphere model,” which is derived from the evidence that nonverbalskills (reading maps, block design tests, etc.) are more profoundly impairedin alcoholics than left-hemisphere tasks (language functions); and the “diffusebrain dysfunction” model, which proposes that chronic alcoholism leads towidespread brain damage (Ellis & Oscar-Berman, 1989).Personality changes, irritability, and mild memory deficits in an abstinent