Academic journal article Alcohol Health & Research World

Alcohol-Related Thiamine Deficiency

Academic journal article Alcohol Health & Research World

Alcohol-Related Thiamine Deficiency

Article excerpt

Alcohol abuse can be associated with structural brain damage and disturbed cognition, memory, intellect, and personality. The clinical features of alcohol's effects on the brain are heterogeneous and include mild to moderate cognitive impairment, amnesia, and dementia. The most commonly identified neurological disorder associated with chronic alcohol abuse is Wernicke-Korsakoff syndrome (WKS).(1) Its most characteristic symptoms are anterograde amnesia, (i.e., the inability to learn and form new memories), retrograde amnesia (i.e., the loss of memories formed prior to the onset of WKS), and impairment of several cognitive processes. For more information on the cognitive deficits of patients with WKS, see sidebar, pp. 116-117.) These cognitive and memory deficits are accompanied by characteristic pathological damage to several brain structures.

WKS is a relatively frequent complication of alcohol abuse and, consequently, is not uncommon in the general population. Among 8.735 post mortem analyses conducted by Torvik and colleagues (1982), brain damage characteristic of WKS was detected in 12.5 percent of all alcoholics and in 0.8 percent of all brains examined. These data are consistent with an Australian study that found brain pathology indicative of WKS in 2.1 percent of a sample from the general population (Harper et al. 1989).

The diagnosis of WKS combines the acute neurological symptoms of Wernicke's encephalopathy and the chronic amnesia of the Korsakoff state. Wernicke's encephalopathy is an acute disorder, characterized by confusion, incoordinated gait, and abnormal eye movements. Anatomically, the brains of patients with Wernicke's encephalopathy consistently show lesions in the diencephalon (i.e., the brain region encompassing the thalamus and the mammillary bodies), the cerebellum, and the brain stem (for the location of these and other brain structures, see figure 1 as well as the central brain figure and glossary on pp. 136-137).(Figure 1 omitted) Other structures, such as the hippocampus and basal forebrain, also may be damaged (Mayes et al. 1988; Jernigan et al. 1991). The disorder is thought to be caused primarily by a deficiency of thiamine (vitamin B) in the body, and a wide variety of mammalian species, including man, can develop it (Victor et al. 1989; Witt 1985). In developed countries, thiamine deficiency most commonly is a consequence of alcoholism. as described below. However, other conditions also can cause thiamine deficiency and Wernicke's encephalopathy,

The acute neurological features of Wernicke's encephalopathy often can be partially or completely reversed by thiamine administration. After treatment, however, approximately 50 to 65 percent of patients with Wernicke's encephalopathy retain "an abnormality of mentation. in which learning and memory are affected out of proportion to other cognitive functions in an otherwise alert and responsive patient" (Victor et al. 1989, p. 11). This chronic amnesic stage is known as Korsakoff's state. With prolonged thiamine treatment and abstention from alcohol, the amnesia also can improve in many patients. Victor and colleagues (1989) found that among their patients, almost all of whom were alcoholic. equal proportions either fully recovered their memory functions within 3 to 5 years, experienced significant but incomplete recovery, experienced slight recovery, or showed no measurable improvement of learning and memory functions.

This article reviews the roles of alcohol and thiamine deficiency in WKS development. Animal models of WKS suggesting that thiamine deficiency alone may be sufficient to produce learning and pathological changes similar to those observed in WKS also will be discussed. These findings suggest that it may not be alcohol's neurotoxicity but rather thiamine deficiency--which may be caused or augmented by chronic alcohol consumption--that may be responsible for the cognitive deficits and anatomic changes seen in WKS patients. …

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