Long before individuals with alcohol misuse or dependence develop Wernicke's Encephalopathy the neurons and other cells of the body are functioning sub-optimally because of the inadequate supply of thiamine and the neurotoxic effect of alcohol. Some individuals are probably genetically predisposed to develop Wernicke's. The accumulated damage is likely to render the use of oral thiamine therapeutically inadequate since the body is unable to produce high enough concentrations of thiamine in the blood to traverse the blood-brain barrier. The damage caused by the combination of thiamine deficiency and alcohol metabolism probably interferes with adequate thiamine transport at a number of sites in the body, including the blood-brain barrier, as well as causing damage to the apoenzymes which then require higher concentrations of thiamine to work normally. Thiamine deficiency leads to a reduction in the activity of these enzymes, and this leads to alterations in mitochondrial activity, impairment of oxidative metabolism, decreased energy status and eventually selective neuronal death. Thiamine diphosphate acts as a co-factor for a number of thiamine-dependent enzymes. The reasons for this difference in treatment will be discussed. On the other hand, thiamine deficiency associated with alcohol misuse/dependence may require up to 1 gram of thiamine IV in the first 24 hours to be treated successfully. Wernicke's Encephalopathy can result from dietary deficiency alone and this form is usually successfully treated, with little chance of Korsakoff's Syndrome supervening. If undiagnosed or inadequately treated, it is likely to proceed to Korsakoff's Syndrome. Wernicke's Encephalopathy is an acute neuro-psychiatric condition caused by an insufficient supply of thiamine (Vitamin B1) to the brain.
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