[2] The condition is part of a larger group of thiamine deficiency disorders that includes beriberi, in all its forms, and alcoholic Korsakoff syndrome.

[3][6] It is treated with thiamine supplementation, which can lead to improvement of the symptoms and often complete resolution, particularly in those where alcohol misuse is not the underlying cause.

Medical literature notes how managing the condition in a timely fashion can avoid worsening symptoms.

[6][8][9] Wernicke encephalopathy may be present in the general population with a prevalence of around 2%, and is considered underdiagnosed; probably, many cases are in patients who do not have commonly-associated symptoms.

[10] The classic triad of symptoms found in Wernicke encephalopathy is:[11] Other possible symptoms include: Although hypothermia is usually diagnosed with a body temperature of 35 °C (95 °F) or less, incipient cooling caused by deregulation in the central nervous system (CNS) needs to be monitored because it can promote the development of an infection.

There may be tachycardia, dyspnea, chest pain, orthostatic hypotension, changes in heart rate and blood pressure.

[34][35] In the last stage, other symptoms may occur: hyperthermia, increased muscle tone, spastic paralysis, choreic dyskinesias, and coma.

[citation needed] Because of the frequent involvement of the heart, eyes, and peripheral nervous system, several authors prefer to call it Wernicke disease rather than simply encephalopathy.

Korsakoff syndrome, characterised by memory impairment, confabulation, confusion, and personality changes, has a strong and recognised link with WE.

[2] Wernicke encephalopathy has classically been thought of as a disease solely of people who drink excessive amounts of alcohol, but it is also found in the chronically undernourished, and in recent years has been discovered post bariatric surgery.

The body only has 2–3 weeks of thiamine reserves, which are readily exhausted without intake, or if depletion occurs rapidly, such as in chronic inflammatory states or in diabetes.

[51] Focal lactic acidosis also causes secondary oedema, oxidative stress, inflammation and white matter damage.

[citation needed] Lesions are usually symmetrical in the periventricular region, diencephalon, the midbrain, hypothalamus, and cerebellar vermis.

[53] Large proteins passing into the brain can put neurological tissue at risk of toxic effects.

[6][57] Caine et al. in 1997 established criteria that Wernicke encephalopathy can be diagnosed in any patient with just two or more of the main symptoms noted above.

[5] Some British hospital protocols suspect WE with any one of these symptoms: confusion, decreased consciousness level (or unconsciousness, stupor or coma), memory loss, ataxia or unsteadiness, ophthalmoplegia or nystagmus, and unexplained hypotension with hypothermia.

There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent diarrhea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and others.

Avoiding or moderating alcohol consumption and having adequate nutrition reduces one of the main risk factors in developing Wernicke–Korsakoff syndrome.

[65] 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.

[39] The observation of edema in MR, and also the finding of inflation and macrophages in necropsied tissues,[54] has led to successful administration of antiinflammatories.

Considering the slight affectations, previous to the generation of observable lesions at necropsy, the percentage should be higher.

[73][75] 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.

[77] He also pointed to the possibility of conduction aphasia since he came to understand the arrangement of the brain's extrinsic and intrinsic connections.