the direct toxic effects of alcohol as opposed to thiamine deficiency that has been attributed as the underlying cause of wernicke-korsakoff syndrome. the amnesia that is associated with this syndrome is a result of the atrophy in the structures of the diencephalon (the thalamus, hypothalamus and mammillary bodies), and is similar to amnesia that is presented as a result of other cases of damage to the medial temporal lobe. it has been argued that the memory impairments can occur as a result of damage along any part of the mammillo-thalamic tract, which explains how wks can develop in patients with damage exclusively to either the thalamus or the mammillary bodies. diagnosis diagnosis of wernicke–korsakoff syndrome is by clinical impression and can sometimes be confirmed by a formal neuropsychological assessment. wernicke encephalopathy typically presents with ataxia and nystagmus, and korsakoff's psychosis with anterograde and retrograde amnesia and confabulation upon relevant lines of questioning. frequently, secondary to thiamine deficiency and subsequent cytotoxic edema in wernicke encephalopathy, patients will have marked degeneration of the mammillary bodies. 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. axial mri flair image showing hyperintense signal in the mesial dorsal thalami, a common finding in wernicke encephalopathy. this patient was nearly in coma when iv thiamine was started, he responded moderately well but was left with some korsakoff type deficits. axial mri b=1000 dwi image showing hyperintense signal indicative of restricted diffusion in the mesial dorsal thalami axial mri flair image showing hyperintense signal in the periaqueductal gray matter and tectum of the dorsal midbrain 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. a healthy diet is imperative for proper nutrition which, in combination with thiamine supplements, may reduce the chance of developing wks. this prevention method may specifically help heavy drinkers who refuse to or are unable to quit. a number of proposals have been put forth to fortify alcoholic beverages with thiamine to reduce the incidence of wks among those heavily abusing alcohol. to date, no such proposals have been enacted. daily recommendations of thiamine requirements are 0.66 mg per 8,400 kilojoules (2,000 kilocalories) of food energy intake – approximately equivalent to 1.2 mg for men and 1.1 mg for women. treatment the onset of wernicke encephalopathy is considered a medical emergency, and thus thiamine administration should be initiated immediately when the disease is suspected. prompt administration of thiamine to patients with wernicke encephalopathy can prevent the disorder from developing into wernicke–korsakoff syndrome, or reduce its severity. treatment can also reduce the progression of the deficits caused by wks, but will not completely reverse existing deficits. wks will continue to be present, at least partially, in 80% of patients. patients with we should be given a minimum dose of 500 mg of thiamine hydrochloride, delivered by infusion over a 30-minute period for two to three days. if no response is seen then treatment should be discontinued but for those patients that do respond, treatment should be continued with a 250 mg dose delivered intravenously or intramuscularly for three to five days unless the patient stops improving. such prompt administration of thiamine may be a life-saving measure. banana bags, a bag of intravenous fluids containing vitamins and minerals, is one means of treatment. epidemiology wks occurs more frequently in men than women and has the highest prevalence in the ages 55–65. approximately 71% are unmarried. internationally, the prevalence rates of wks are relatively standard, being anywhere between zero and two percent. despite this, specific sub-populations seem to have higher prevalence rates including people who are homeless, older individuals (especially those living alone or in isolation), and psychiatric inpatients. additionally, studies show that prevalence is not connected to alcohol consumption per capita. for example, in france, a country that is well known for its consumption and production of wine, prevalence was only 0.4% in 1994, while australia had a prevalence of 2.8%. history wernicke encephalopathy carl wernicke discovered wernicke encephalopathy in 1881. his first diagnosis noted symptoms including paralyzed eye movements, ataxia, and mental confusion. also noticed were hemorrhages in the gray matter around the third and fourth ventricles and the cerebral aqueduct. brain atrophy was only found upon post-mortem autopsy. wernicke believed these hemorrhages were due to inflammation and thus the disease was named polioencephalitis haemorrhagica superior. later, it was found that wernicke encephalopathy and alcoholic korsakoff syndrome are products of the same cause. korsakoff syndrome sergei korsakoff was a russian physician after whom the disease "korsakoff's syndrome" was named. in the late 1800s korsakoff was studying long-term alcoholic patients and began to notice a decline in their memory function. at the 13th international medical congress in moscow in 1897, korsakoff presented a report called: "on a special form of mental illness combined with degenerative polyneuritis". after the presentation of this report the term "korsakoff's syndrome" was coined. although we and aks were discovered separately, these two syndromes are usually referred to under one name, wernicke–korsakoff syndrome, due to the fact that they are part of the same cause and because the onset of aks usually follows we if left untreated. society and culture the british neurologist oliver sacks describes case histories of some of his patients with the syndrome in the book the man who mistook his wife for a hat (1985). frontman and lead vocalist of the hard rock band breaking benjamin, benjamin burnley, is well known to be living with wernicke–korsakoff syndrome due to his past alcoholism. he has written multiple songs about addiction and his experiences with alcohol, with many of such songs being found on the band's 2009 album dear agony as it was the first album burnley had written and recorded completely sober.