The continuity hypothesis: the relationship of long-term alcoholism to the Wernicke-Korsakoff syndrome

Abstract

Although alcoholic Korsakoff's syndrome has traditionally been considered an acute disorder related to a nutritional deficiency, recent evidence demonstrating that ethanol may be neurotoxic has raised the possibility that the perceptual, problem-solving, and memory deficits associated with this chronic neurological disorder may develop slowly over decades of alcohol abuse. A review of the recent cognitive literature provides only limited support for this "continuity hypothesis." Long-term alcoholics, as with patients with alcoholic Korsakoff's syndrome, are impaired on numerous visuoconceptual and learning tasks, but there is little or no evidence that the information-processing deficits underlying the two patient groups' anterograde memory problems are similar. Furthermore, experimental and clinical studies of retrograde amnesia have noted only mild remote memory impairments in non-Korsakoff alcoholics as well as clear indications that alcoholic Korsakoff patients' severe loss or access to remote memories occurs acutely with the onset of Wernicke's encephalopathy. It is concluded that while the continuity hypothesis has heuristic value, there is still insufficient evidence to place the Korsakoff patient, the detoxified long-term alcoholic, and the heavy social drinker at different points on a single continuum of cognitive impairment.