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Cortney
Hedman
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University
of North Carolina, Charlotte
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Undergraduate
Journal of Psychology, Volume 13, 2000. University of North Carolina At
Charlotte.
Department of Psychology. |
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| © The articles contained in this journal remain the property of the author(s). No part may be reproduced without express permission from the author(s), except in the case of brief quotations in critical reviews or articles. | ||
| Korsakoff’s syndrome is an amnesic disorder affecting approximately 2.5% of chronic alcoholics. It is related to decreased thiamine intake and absorption resulting in lesions in cortical and subcortical structures important for memory and higher cognitive functions. This paper discusses the characteristics, physiological aspects and theoretical explanations of Korsakoff’s syndrome. | ||
| Korsakoff’s syndrome, or Wernicke-Korsakoff syndrome, is named for S.S. Korsakoff, a Russian physician in the 19th century who worked with alcohol-induced brain-damaged patients. This neurological disorder is associated with chronic alcohol abuse, characterized by tolerance, physical and psychological dependence on alcohol. Julien (1998) discusses the withdrawal period experienced by chronic alcoholics during periods of abstinence from alcohol. The withdrawal period is characterized by rebound hyperexitability, tremulousness, hallucinations, confusion and psychomotor agitation (Julien 1998). In many cases, chronic alcoholism leads to Korsakoff’s syndrome, which is marked by anterograde amnesia, retrograde amnesia and widespread cognitive impairment (Berman, 1990). This paper discusses the manifestation, physiological aspects, and theoretical explanations of Korsakoff’s syndrome. | |
| Characteristics | |
| Korsakoff’s syndrome occurs in 1.7 to 2.8 percent of chronic alcoholics (Arria, 1992), and is the “most commonly identified neurological disorder associated with chronic alcohol abuse” (Langlais, 1995, p. 113). The specific manifestations of the cognitive and memory deficits associated with Korsakoff’s syndrome are attention deficits, visual and verbal memory loss, difficulty with abstract thinking, and decreased motor coordination. When compared with normal subjects, “patients with Korsakoff’s syndrome have more difficulty completing fragmented pictures or determining whether two odors, colors, or short musical passages are the same or different” (Langlais 1995, p. 125). Executive functions such as the ability to plan, organize and regulate behavior are also impaired (Arria, 1992). | |
| Physiological Aspects | |
| Theories suggest that Korsakoff’s syndrome is the result of an alcohol-related thiamine (B1) deficiency. In many cases, chronic alcoholism leads to a poor diet, resulting in less thiamine intake and poor thiamine absorption. Thiamine plays an important role in “maintenance of enzymatic function, maintenance of cell membrane structure, excitability of nerve cells, and conduction of nerve impulses” (Langlais, 1995, p. 114). One of the enzymes which requires the availability of thiamine, transketolase, is necessary for myelin synthesis. When myelin begins to break down, the result is motor impairment, which is one of the first signs of Wernicke’s encephalopathy, the condition preceding Korsakoff’s amnesia. When the brain suffers from a deficit in thiamine, the result is Wernicke’s encephalopathy, “an acute disorder, characterized by confusion, uncoordinated gait, and abnormal eye movements” (Langlais, 1995, p. 113). These patients typically have lesions in the diencephalon, (more specifically cell death in the thalamus and hemorrhaging in the mammillary body), the cerebellum and the brain stem. | |
| The exact molecular mechanisms causing changes in the brains of chronic alcoholics are unknown. One theory suggests that in states of thiamine deficiency, excess amounts of excitatory neurotransmitters are released, and in combination with reduced energy production, lead to nerve cell death. This theory is supported by experimental treatment with drugs that suppress the release of such excitatory neurotransmitters preventing diencephalic damage and behavioral deficits (Langlais, 1995). | |
| The idea that thiamine deficiency is the primary causal factor in the development of Korsakoff’s syndrome is also supported by research from Reinhart et al (1949) in which thiamine deficiency was produced in rhesus monkeys. At autopsy, lesions of the thalamus, mammillary body, brain stem, cerebellum and basal ganglia were found. A similar study of thiamine deficient monkeys showed that they displayed the typical signs of Wernicke’s encephalopathy, such as abnormal eye movements, uncoordinated gate, and confusion (Langlais, 1995). | |
| Treatment for Wernicke’s encephalopathy includes abstinence from alcohol and thiamine replacement therapy, and is usually successful in stopping the progression of the disease. However, when left untreated, Wernicke’s encephalopathy will result in Korsakoff’s amnesia in 25% of affected patients. | |
| Theoretical approaches | |
| Cermak (1990) presents three theories with which to explain cognitive decline in patients with Korsakoff’s syndrome. These are the continuum theory, the premature aging theory, and the right hemisphere theory. These theories could prove very insightful in discovering the brain structures damaged as shown by specific types of cognitive decline and eventually developing a systematic schema of this decline and how to prevent it. | |
| The continuum theory posits that the area involved in damage resulting from alcohol abuse, mainly the diencephalic structures, is the part of the brain most sensitive to the toxicity of alcohol. Thus, the cognitive changes in alcoholics without Korsakoff’s syndrome will begin to emulate the cognitive deficits found in patients with Korsakoff’s syndrome. The theory suggests that alcohol abuse lies along a continuum between occasional drinkers and those with Korsakoff’s syndrome (Cermak 1990). Ryan and Butters (1980) reported that alcoholics without Korsakoff’s syndrome failed the same memory tasks as alcoholics with Korsakoff’s syndrome. Control subjects performed considerably better than either the alcoholics with Korsakoff’s or the alcoholics without Korsakoff’s (Ryan 1980). This study supports the theory that damage resulting from alcohol abuse lies along a continuum. | |
| The premature aging theory states that all areas of the brain are subject to the same gradual attrition due to the toxicity of alcohol. The thought is that chronic alcohol abusers will behave on the same cognitive level as older persons who do not abuse alcohol. Also, those alcoholics who have severe cognitive impairments will be on the same cognitive level as patients with dementia due to general cerebral deterioration (Cermak, 1990). Brandt et al (1983) offered empirical support for this theory. They presented younger alcoholics, older alcoholics, and a control group with pairs of numbers and pairs of geometric shapes. After the subjects had time to study the pairs, they were given a non-related task and then asked to recall the paired items. The researchers found that alcoholics performed on a level below the controls of the same age, and older subjects scored lower than younger subjects. The conclusion was that alcoholics retrieve information similarly to non alcoholics ten years or more their senior (Brandt, 1983). | |
| The third theory presented by Cermak to explain cognitive decline in patients with Korsakoff’s syndrome is the right hemisphere theory. This theory suggests that the right hemisphere is more sensitive to alcohol toxicity than the left hemisphere. This is brought about by the thought that chronic alcohol abusers perform poorly on nonverbal cognitive tasks as compared to their performance on verbal cognitive tasks. This theory suggests that the cognitive decline displayed by chronic alcohol abusers is similar to that experienced by persons with right hemisphere damage. Cermak et al (1989) tested alcoholics and patients with right hemisphere damage on interpretation of emotion. Alcoholics tested the same as the controls whereas the right hemisphere damaged patients had difficulty with the task. They found that alcoholics performed normally on right hemisphere tasks and their performance was only compromised when the tasks were complex or numerous. Their conclusion from this evidence does not support the right hemisphere theory because Cermak et al observed that chronic alcohol abusers did not display the same type of cognitive decline as persons with right hemisphere damage (Cermak 1990). | |
| The continuum theory suggests that chronic alcohol abuse falls along a continuum between abstinence and Korsakoff’s syndrome. The implications of this theory are important in discovering the disease processes of chronic alcoholism as well as Korsakoff’s syndrome to develop a systematic and scientific way of diagnosing and treating chronic alcoholics based on what damage has been done to the brain and other parts of the body, such as the liver and digestive tract. The premature aging theory suggests that chronic alcohol consumption leads to rapid cognitive decline, which if implemented in preventative alcohol education could have positive ramifications in reducing the number of patients hospitalized with dementia by acting as a deterrent to making unhealthy lifestyle choices regarding alcohol abuse. The third theory shows that the ability for the right hemisphere to process complex or numerous tasks can be compromised by chronic alcohol abuse. This idea also has medical and social ramifications. If these theories can be integrated into alcohol prevention programs, they could act as incentives for abstinence from alcohol as well as helping those who are afflicted with chronic alcoholism and/or Korsakoff’s syndrome by discovering what the disease processes entail. | |
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CONCLUSION
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| Korsakoff’s syndrome is a neurological disorder associated with chronic alcohol abuse, marked by amnesia and widespread cognitive impairment. It is the result of the depletion and decreased absorption of thiamine (B1). Those afflicted with Korsakoff’s syndrome experience attention deficits, memory loss, and decreased motor coordination. The treatment for Korsakoff’s syndrome consists of abstinence from alcohol and thiamine supplements. If left untreated, patients with Korsakoff’s will eventually need to be institutionalized due to dementia. Unfortunately this can be very costly for both the individual and the taxpayer. The theoretical approaches to the cognitive decline experienced in Korsakoff’s could be used to develop a systematic and scientific way to approach this disorder as well as act as a deterrent to alcohol abuse in preventative education. Unfortunately Korsakoff’s syndrome is a chronic condition for which there is no cure. The damage to the brain from alcohol toxicity is irreversible. It is the goal of researchers to learn more about the physiological mechanisms of this disorder so that alcoholics can be educated about the danger of their abuse and how to modify their behavior so that they do not develop this disease. | |
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REFERENCES
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| Arria, AM, and Van Thiel, DH. (1992). The epidemiology of alcohol-related chronic disease. Alcohol Health & Research | |
| World, 16(3), 209-217. | |
| Berman, MO. (1990). Severe brain dysfunction. Alcohol Health & Research World, 14(2), 120-130. | |
| Brandt, J, Butters, N, Ryan, C, and Bayog, R. (1983). Cognitive loss and recovery in long-term alcohol abusers. Archives | |
| of General Psychiatry, 40(4), 435-442. | |
| Cermak, LS. (1990). Cognitive-processing deficits in chronic alcohol abuse. Alcohol Health & Research World, 14(2), | |
| 130-137. | |
| Langlais, PJ. (1995). Alcohol-related thiamine deficiency. Alcohol Health & Research World, 19(2), 113-122. | |
| Ryan, C and Bitters, N. (1980). Further evidence for a continuum of impairment encompassing male alcoholic Korsakoff | |
| patients and chronic alcoholic men. Alcoholism: Clinical and Experimental Research, 4, 190-198. | |
| © | This article remains the property of the author. No part may be reproduced without express permission from the author, except in the case of brief quotations in critical reviews or articles. |
| Additional information is available from the: Department of Psychology, UNC Charlotte, 9201 University City Blvd. Charlotte, NC 28223-0001. (704) 687- 4731. | |
| Journal Editors:
Jane Gaultney, Ph.D. & Paul Foos, Ph.D. Layout and Design: Jodi Hankins Web Layout: Sue Spaulding |
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