In particular, studies have demonstrated that clinical signs of the neurological problems that result from thiamine deficiency develop faster in rats that have received alcohol and were also deficient in thiamine than rats who did not receive alcohol. In another study, it was found that rats that were chronically fed alcohol had significantly lower liver thiamine stores than control rats. This provides an explanation for why alcoholics with liver cirrhosis have a higher incidence of both thiamine deficiency and WKS. Pathophysiology
The vitamin thiamine also referred to as Vitamin B1, is required by three different enzymes to allow for conversion of ingested nutrients into energy. Thiamine can not be produced in the body and must be obtained through diet and supplementation. The duodenum is responsible for absorbing thiamine. The liver can store thiamine for 18 days. Prolonged and frequent consumption of alcohol causes a decreased ability to absorb thiamine in the duodenum. Thiamine deficiency is also related to malnutrition from poor diet, impaired use of thiamine by the cells and impaired storage in the liver. Without thiamine the Krebs Cycle enzymes pyruvate dehydrogenase complex (PDH) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) are impaired. The impaired functioning of the Krebs Cycle results in inadequate production of adenosine triphosphate (ATP) or energy for the cells functioning. Energy is required by the brain for proper functioning and use of its neurotransmitters.
Thiamine (vitamin B1) is an essential coenzyme in carbohydrate metabolism and is also a regulator of osmotic gradient. Its deficiency may cause swelling of the intracellular space and local disruption of the blood-brain barrier. Brain tissue is very sensitive to changes in electrolytes and pressure and edema can be cytotoxic. In Wernicke this occurs specifically in the mammillary bodies, medial thalami, tectal plate, and periaqueductal areas. People with the condition may also exhibit a dislike for sunlight and so may wish to stay indoors with the lights off. The mechanism of this degeneration is unknown, but it supports the current neurological theory that the mammillary bodies play a role in various "memory circuits" within the brain. An example of a memory circuit is the Papez circuit. Prevention
As described, Korsakoff syndrome usually follows or accompanies Wernicke encephalopathy. If treated quickly, it may be possible to prevent the development of WKS with thiamine treatments. This treatment is not guaranteed to be effective and the thiamine needs to be administered adequately in both dose and duration. A study on Wernicke–Korsakoff syndrome showed that with consistent thiamine treatment there were noticeable improvements in mental status after only 2–3 weeks of therapy. Thus, there is hope that with treatment Wernicke encephalopathy will not necessarily progress to WKS.In order to reduce the risk of developing WKS it is important to limit the intake of alcohol in order to ensure that proper nutrition needs are met.