Amnesia, especially anterograde amnesia, or memory loss for recent events, is an intriguing but serious disorder. When amnesia occurs as a consequence of long-term alcoholism, it is referred to as alcoholic Korsakoff's syndrome. Patients with Korsakoff's syndrome are permanently unable to remember new information for more than a few seconds. However, memories that were formed prior to the onset of alcohol-related brain damage are relatively well preserved. Because new events are forgotten a few seconds after they occur, virtually nothing new is learned, and the patient with Korsakoff's syndrome lives in the past.
The critical brain lesions of alcoholic Korsakoff's syndrome are thought to include the mammillary bodies of the hypothalamus and/or medial thalamic nuclei (Oscar-Berman & Evert, 1997). Damage to these or to other regions of the brain (hippocampus, fornix, anterior thalamus) has long been associated with memory impairments (Mesulam, 2000). The impairments include severe anterograde amnesia for recent events, and some retrograde amnesia (i.e., loss of memory for events that happened prior to the appearance of obvious symptomatology). Damage to basal forebrain structures (important in the production of neuro-transmitters, which are needed for normal memory functions) may also be involved.
Although anterograde amnesia is the most obvious presenting symptom in Korsakoff patients, these individuals have other cognitive impairments as well. Like patients with bilateral prefrontal cortical lesions, Korsakoff patients are abnormally sensitive to distractions (proactive interference). This sensitivity may be due to alcoholism-related prefrontal dysfunction, which impairs the ability to counteract the effects of cognitive interruptions. In addition to their memory problems and their sensitivity to interference, Korsakoff patients also tend to repeat unnecessary behaviors (perseverative responding) and have restricted attention, retarded perceptual processing abilities, and decreased sensitivity to reward contingencies (Oscar-Berman & Evert, 1997). These additional abnormalities reflect widespread cerebral atrophy accompanying sustained alcohol abuse. Thus, consideration should be given to sensory and cognitive deficits that may be integral to the disease process caused by chronic alcoholism.
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