usually continued until clinical improvement ceases. considering the diversity of possible causes and several surprising symptomatologic presentations, and because there is low assumed risk of toxicity of thiamine, because the therapeutic response is often dramatic from the first day, some qualified authors indicate parenteral thiamine if we is suspected, both as a resource for diagnosis and treatment. the diagnosis is highly supported by the response to parenteral thiamine, but is not sufficient to be excluded by the lack of it. parenteral thiamine administration is associated with a very small risk of anaphylaxis. people who consume excessive amounts of alcohol may have poor dietary intakes of several vitamins, and impaired thiamine absorption, metabolism, and storage; they may thus require higher doses. if glucose is given, such as in people with an alcohol use disorder who are also hypoglycaemic, thiamine must be given concurrently. if this is not done, the glucose will rapidly consume the remaining thiamine reserves, exacerbating this condition. the observation of edema in mr, and also the finding of inflation and macrophages in necropsied tissues, has led to successful administration of antiinflammatories. other nutritional abnormalities should also be looked for, as they may be exacerbating the disease. in particular, magnesium, a cofactor of transketolase which may induce or aggravate the disease. other supplements may also be needed, including: cobalamin, ascorbic acid, folic acid, nicotinamide, zinc, phosphorus (dicalcium phosphate) and in some cases taurine, especially suitable when there cardiocirculatory impairment. patient-guided nutrition is suggested. in patients with wernicke–korsakoff syndrome, even higher doses of parenteral thiamine are recommended. concurrent toxic effects of alcohol should also be considered. epidemiology there are no conclusive statistical studies, all figures are based on partial studies. wernicke's lesions were observed in 0.8 to 2.8% of the general population autopsies, and 12.5% of people with an alcohol use disorder. this figure increases to 35% of such individuals if including cerebellar damage due to lack of thiamine. most autopsy cases were from people with an alcohol use disorder. autopsy series were performed in hospitals on the material available which is unlikely to be representative of the entire population. considering the slight affectations, previous to the generation of observable lesions at necropsy, the percentage should be higher. there is evidence to indicate that wernicke encephalopathy is underdiagnosed. for example, in one 1986 study, 80% of cases were diagnosed postmortem. is estimated that only 5–14% of patients with we are diagnosed in life. in a series of autopsy studies held in recife, brazil, it was found that only 7 out of 36 had consumed excessive amounts of alcohol, and only a small minority had malnutrition. in a reviewed of 53 published case reports from 2001 to 2011, the relationship with alcohol was also about 20% (10 out of 53 cases). we related to alcohol misuse is more common in males and is more common in females when not related to alcohol misuse. in alcohol-related cases, we patients average the age of 40, and non-alcohol-related cases typically occur in younger people. history we was first identified in 1881 by the german neurologist carl wernicke, although the link with thiamine was not identified until the 1930s. carl wernicke discovered the sensory center of speech. wernicke figured out that broca’s area was not the only center of speech, it was also able to distinguish motor aphasia from sensory aphasia. he also pointed to the possibility of conduction aphasia since he came to understand the arrangement of the brain’s extrinsic and intrinsic connections. he demonstrated that the sensory information reached its corresponding area in the cerebral cortex through projection fibers. from there, this information, following the association system, would be distributed to different regions of the cortex, integrating sensory processing. he reported three patients with we, including two men (aged 33 and 36) who were alcoholics and one woman (aged 20) who ingested sulfuric acid, leading to pyloric stenosis. all three had ocular motor abnormalities and he performed an autopsy on each, providing a clinical-pathological correlation. a similar presentation of this disease was described by the russian psychiatrist sergei korsakoff in a series of articles published 1887–1891; where the chronic version of we was described as korsakoff's syndrome, involving symptoms of amnesia.