There are no conclusive statistical studies, all figures are based on partial studies, and because of the ethical problems in conducting controlled trials are unlikely to be obtained in the future.

Wernicke´s lesions were observed in 0.8 to 2.8% of the general population autopsies, and 12.5% of alcoholics. This figure increases to 35% of alcoholics if including cerebellar damage due to lack of thiamine.

Most autopsy cases were from alcoholics. 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's 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 had alcoholic habits, 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).

In this statistic fetal and infant damage with upcoming intellectual limitations should be included. WE is more likely to occur in males than females. Among the minority who are diagnosed, mortality can reach 17%. The main factors triggering death are thought to be infections and liver dysfunctions.

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. Some experts advise parenteral thiamine should be given to all at-risk patients in the emergency room.

In the clinical diagnosis should be remembered that early symptoms are nonspecific, and it has been stated that WE may present nonspecific findings. There is consensus to provide water-soluble vitamins and minerals after gastric operations.

In some countries certain foods have been supplemented with thiamine, and have reduced WE cases. Improvement is difficult to quantify because they applied several different actions. Avoiding alcohol and having adequate nutrition reduces one of the main risk factors in developing Wernicke-Korsakoff syndrome.

Chemotherapy medication, for example, fludarabine can cause a

permanent severe global encephalopathy. Ifosfamide can cause

a severe encephalopathy (but it can be reversible with stop using the drug and the use of methylene blue). Bevacizumab and other anti–vascular endothelial growth factor medication can cause posterior reversible encephalopathy syndrome.

There are many types of encephalopathy. Some examples include:

- Mitochondrial encephalopathy: Metabolic disorder caused by dysfunction of mitochondrial DNA. Can affect many body systems, particularly the brain and nervous system.

- Glycine encephalopathy: A genetic metabolic disorder involving excess production of glycine.

- Hepatic encephalopathy: Arising from advanced cirrhosis of the liver.

- Hypoxic ischemic encephalopathy: Permanent or transitory encephalopathy arising from severely reduced oxygen delivery to the brain.

- Static encephalopathy: Unchanging, or permanent, brain damage.

- Uremic encephalopathy: Arising from high levels of toxins normally cleared by the kidneys—rare where dialysis is readily available.

- Wernicke's encephalopathy: Arising from thiamine (B) deficiency, usually in the setting of alcoholism.

- Hashimoto's encephalopathy: Arising from an auto-immune disorder.

- Hypertensive encephalopathy: Arising from acutely increased blood pressure.

- Chronic traumatic encephalopathy: Progressive degenerative disease associated with multiple concussions and other forms of brain injury.

- Lyme encephalopathy: Arising from Lyme disease bacteria, including "Borrelia burgdorferi".

- Toxic encephalopathy: A form of encephalopathy caused by chemicals, often resulting in permanent brain damage.

- Toxic-Metabolic encephalopathy: A catch-all for brain dysfunction caused by infection, organ failure, or intoxication.

- Transmissible spongiform encephalopathy: A collection of diseases all caused by prions, and characterized by "spongy" brain tissue (riddled with holes), impaired locomotion or coordination, and a 100% mortality rate. Includes bovine spongiform encephalopathy (mad cow disease), scrapie, and kuru among others.

- Neonatal encephalopathy (hypoxic-ischemic encephalopathy): An obstetric form, often occurring due to lack of oxygen in bloodflow to brain-tissue of the fetus during labour or delivery.

- Salmonella encephalopathy: A form of encephalopathy caused by food poisoning (especially out of peanuts and rotten meat) often resulting in permanent brain damage and nervous system disorders.

- Encephalomyopathy: A combination of encephalopathy and myopathy. Causes may include mitochondrial disease (particularly MELAS) or chronic hypophosphatemia, as may occur in cystinosis.

- Creutzfeldt–Jakob disease (CJD; transmissible spongiform encephalopathy).

- HIV encephalopathy (encephalopathy associated with HIV infection and AIDS, characterized by atrophy and ill-defined white matter hyperintensity).

- Sepsis-associated encephalopathy (this type can occur in the setting of apparent sepsis, trauma, severe burns, or trauma, even without clear identification of an infection).

- Epileptic encephalopathies:

- Early infantile epileptic encephalopathy (acquired or congenital abnormal cortical development).

- Early myoclonic epileptic encephalopathy (possibly due to metabolic disorders).

Toxic encephalopathy is often irreversible. If the source of the problem is treated by removing the toxic chemical from the system, further damage can be prevented, but prolonged exposure to toxic chemicals can quickly destroy the brain. Long term studies have demonstrated residual cognitive impairment (primarily attention and information-processing impairment resulting in dysfunction in working memory) up to 10 years following cessation of exposure. Severe cases of toxic encephalopathy can be life-threatening.

In those with cirrhosis, the risk of developing hepatic encephalopathy is 20% per year, and at any time about 30–45% of people with cirrhosis exhibit evidence of overt encephalopathy. The prevalence of minimal hepatic encephalopathy detectable on formal neuropsychological testing is 60–80%; this increases the likelihood of developing overt encephalopathy in the future. Once hepatic encephalopathy has developed, the prognosis is determined largely by other markers of liver failure, such as the levels of albumin (a protein produced by the liver), the prothrombin time (a test of coagulation, which relies on proteins produced in the liver), the presence of ascites and the level of bilirubin (a breakdown product of hemoglobin which is conjugated and excreted by the liver). Together with the severity of encephalopathy, these markers have been incorporated into the Child-Pugh score; this score determines the one- and two-year survival and may assist in a decision to offer liver transplantation.

In acute liver failure, the development of severe encephalopathy strongly predicts short-term mortality, and is almost as important as the nature of the underlying cause of the liver failure in determining the prognosis. Historically, widely used criteria for offering liver transplantation, such as King's College Criteria, are of limited use and recent guidelines discourage excessive reliance on these criteria. The occurrence of hepatic encephalopathy in people with Wilson's disease (hereditary copper accumulation) and mushroom poisoning indicates an urgent need for a liver transplant.

Research is being done by organizations such as NINDS (National Institute of Neurological Disorders and Stroke) on what substances can cause encephalopathy, why they do this, and eventually how to protect, treat, and cure the brain from this condition.

Strong evidence suggests that ethanol interferes directly with thiamine uptake in the gastrointestinal tract. Ethanol also disrupts thiamine storage in the liver and the transformation of thiamine into its active form. The role of alcohol consumption in the development of WKS has been experimentally confirmed through studies in which rats were subjected to alcohol exposure and lower levels thiamine through a low-thiamine diet. 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.

The fact that gastrointestinal surgery can lead to the development of WKS was demonstrated in a study that was completed on three patients who recently undergone a gastrectomy. These patients had developed WKS but were not alcoholics and had never suffered from dietary deprivation. WKS developed between 2 and 20 years after the surgery. There were small dietary changes that contributed to the development of WKS but overall the lack of absorption of thiamine from the gastrointestinal tract was the cause. Therefore, it must be ensured that patients who have undergone gastrectomy have a proper education on dietary habits, and carefully monitor their thiamine intake. Additionally, an early diagnosis of WKS, should it develop, is very important.

The rate of incidence of alcoholic polyneuropathy involving sensory and motor polyneuropathy varies from 10% to 50% of alcoholics depending on the subject selection and diagnostic criteria. If electrodiagnostic criteria is used, alcoholic polyneuropathy may be found in up to 90% of individuals being assessed. The distribution and severity the disease depends on regional dietary habits, individual drinking habits, as well as an individual’s genetics. Large studies have been conducted and show that alcoholic polyneuropathy severity and incidence correlates best with the total lifetime consumption of alcohol. Factors such as nutritional intake, age, or other medical conditions are correlate in lesser degrees. For unknown reasons, alcoholic polyneuropathy has a high incidence in women.

Certain alcoholic beverages can also contain congeners that may also be bioactive; therefore, the consumption of varying alcoholic beverages may result in different health consequences. An individual’s nutritional intake also plays a role in the development of this disease. Depending on the specific dietary habits, they may have a deficiency of one or more of the following: thiamine (vitamin B1), pyridoxine (vitamin B6), pantothenic acid and biotin, vitamin B12, folic acid, niacin (vitamin B3), and vitamin A.

The onset of alcohol dementia can occur as early as age thirty, although it is far more common that the dementia will reveal itself anywhere from age fifty to age seventy. The onset and the severity of this type of dementia is directly correlated to the amount of alcohol that a person consumes over his or her lifetime.

Epidemiological studies show an association between long-term alcohol intoxication and dementia. Alcohol can damage the brain directly as a neurotoxin, or it can damage it indirectly by causing malnutrition, primarily a loss of thiamine (vitamin B1). Alcohol abuse is common in older persons, and alcohol-related dementia is under-diagnosed. A discredited French study claimed that moderate alcohol consumption (up to four glasses of wine per week) protected against dementia, whereas higher rates of consumption have conclusively been shown to increase the chances of getting it.

It is also thought there is perhaps a genetic predisposition for some alcoholics that results in increased frequency of alcoholic polyneuropathy in certain ethnic groups. During the body’s processing of alcohol, ethanol is oxidized to acetaldehyde mainly by alcohol dehydrogenase; acetaldehyde is then oxidized to acetate mainly by aldehyde dehydrogenase (ALDH). ALDH2 is an isozyme of ALDH and ALDH2 has a polymorphism (ALDH2*2, Glu487Lys) that makes ADLH2 inactive; this allele is more prevalent among Southeast and East Asians and results in a failure to quickly metabolize acetaldehyde. The neurotoxicity resulting from the accumulation of acetaldehyde may play a role in the pathogenesis of alcoholic polyneuropathy.

In a small proportion of cases, the encephalopathy is caused directly by liver failure; this is more likely in acute liver failure. More commonly, especially in chronic liver disease, hepatic encephalopathy is triggered by an additional cause, and identifying these triggers can be important to treat the episode effectively.

Hepatic encephalopathy may also occur after the creation of a transjugular intrahepatic portosystemic shunt (TIPS). This is used in the treatment of refractory ascites, bleeding from oesophageal varices and hepatorenal syndrome. TIPS-related encephalopathy occurs in about 30% of cases, with the risk being higher in those with previous episodes of encephalopathy, higher age, female sex and liver disease due to causes other than alcohol.

A number of factors may increase a person's risk to develop Korsakoff’s syndrome. These factors are often related to patients’ general health and their food intake habits.

- Age

- Alcoholism

- Chemotherapy

- Dialysis

- Extreme dieting

- Genetic factors

The prevalence varies from country to country, but is estimated to be around 12.5% of heavy drinkers.

The most effective method of preventing Korsakoff's syndrome is to avoid B vitamin/thiamine deficiency. In Western nations, the most common causes of such a deficiency are alcoholism and eating disorders. Because these are behavioral-induced causes, Korsakoff's syndrome is essentially considered a preventable disease. Thus, fortifying foods with thiamine, or requiring companies that sell alcoholic beverages to supplement them with B vitamins in general or thiamine in particular, could avert many cases of Korsakoff's Syndrome.

The most common cause of is overly rapid correction of low blood sodium levels (hyponatremia). Apart from rapid correction of hyponatraemia, there are case reports of central pontine myelinolysis in association with hypokalaemia, anorexia nervosa when feeding is started, patients undergoing dialysis and burns victims. There is a case report of central pontine myelinolysis occurring in the context of re-feeding syndrome, in the absence of hyponatremia.

It has also been known to occur in patients suffering withdrawal symptoms of chronic alcoholism. In these instances, occurrence may be entirely unrelated to hyponatremia or rapid correction of hyponatremia. It could affect patients who take some prescription medicines that are able to cross the blood-brain barrier and cause abnormal thirst reception - in this scenario the CPM is caused by polydipsia leading to low blood sodium levels (hyponatremia).

In schizophrenic patients with psychogenic polydipsia, inadequate thirst reception leads to excessive water intake, severely diluting serum sodium. With this excessive thirst combined with psychotic symptoms, brain damage such as CPM may result from hyperosmolarity caused by excess intake of fluids, (primary polydipsia) although this is difficult to determine because such patients are often institutionalised and have a long history of mental health conditions.

It has been observed following hematopoietic stem cell transplantation.

CPM may also occur in patients prone to hyponatraemia affected by

- severe liver disease

- liver transplant

- alcoholism

- severe burns

- malnutrition

- anorexia

- severe electrolyte disorders

- AIDS

- hyperemesis gravidarum

- hyponatremia due to Peritoneal Dialysis

- Wernicke encephalopathy

In light of recent research, high concentrations of sulfur intake has also been deemed responsible for PEM. Sulfur is necessary for the synthesis of important sulfur-containing amino acids and their contribution to the synthesis of different hormones, enzymes, and structural proteins. The ruminant diet, especially that of cattle, can be overly concentrated with sulfur. In ruminants, the same rumen microbes that generate thiamine molecules reduce sulfur into toxic sulfides. Among the sulfide toxins is hydrogen sulfide, a gas compound that will compete with oxygen to bind with red blood cells and eventually enter the brain to disrupt neural activity.

Thiamine availability is controlled by the direct dietary consumption of thiamine. Thiamine availability is also regulated by thiaminases, which are enzymes that readily cleave thiamine molecules and inhibit essential thiamine-regulated pathways such as the metabolism of glucose. Ruminants have working rumen microbes that synthetize thiamine molecules for the body; therefore ruminants do not need to ingest thiamine rich foods for thiamine. However, feed concentrates given to ruminants, specifically sheep and cattle, are often heavily stocked with thiaminases. The presence of thiaminases counter the production of thiamine by breaking them down, resulting in a futile cycle between rumen microbes and thiaminases. Eventually, when the rate of synthesis production can not exceed thiaminase intake, a state of thiamine deficiency will be reached. Thiaminase rich foods include different grains, fresh water fish, and ferns, all of which are often processed together to make feed concentrate.

The prognosis is very poor. Two studies reported typical age of deaths in infancy or early childhood, with the first reporting a median age of death of 2.6 for boys and less than 1 month for girls.

Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD).

Though traditionally, the prognosis is considered poor, a good functional recovery is possible. All patients at risk of developing refeeding syndrome should have their electrolytes closely monitored, including sodium, potassium, magnesium, glucose and phosphate.

Recent data indicate that the prognosis of critically ill patients may even be better than what is generally considered, despite severe initial clinical manifestations and a tendency by the intensivists to underestimate a possible favorable evolution.

While some patients die, most survive and of the survivors, approximately one-third recover; one-third are disabled but are able to live independently; one-third are severely disabled. Permanent disabilities range from minor tremors and ataxia to signs of severe brain damage, such as spastic quadriparesis and locked-in syndrome. Some improvements may be seen over the course of the first several months after the condition stabilizes.

The degree of recovery depends on the extent of the original axonal damage.

Different genetic causes and types of Leigh syndrome have different prognoses, though all are poor. The most severe forms of the disease, caused by a full deficiency in one of the affected proteins, cause death at a few years of age. If the deficiency is not complete, the prognosis is somewhat better and an affected child is expected to survive 6–7 years, and in rare cases, to their teenage years.

Beriberi may also be caused by shortcomings other than inadequate intake: diseases or operations on the digestive tract, alcoholism, dialysis, genetic deficiencies, etc. All these causes mainly affect the central nervous system, and provoke the development of what is known as Wernicke's disease or Wernicke's encephalopathy.

Wernicke's disease is one of the most prevalent neurological or neuropsychiatric diseases. In autopsy series, features of Wernicke lesions are observed in approximately 2% of general cases. Medical record research shows that about 85% had not been diagnosed, although only 19% would be asymptomatic. In children, only 58% were diagnosed. In alcohol abusers, autopsy series showed neurological damages at rates of 12.5% or more. Mortality caused by Wernicke's disease reaches 17% of diseases, which means 3.4/1000 or about 25 million contemporaries. The number of people with Wernicke's disease may be even higher, considering that early stages may have dysfunctions prior to the production of observable lesions at necropsy. In addition, uncounted numbers of people can experience fetal damage and subsequent diseases.

If the symptoms of alcohol dementia are caught early enough, the effects may be reversed. The person must stop drinking and start on a healthy diet, replacing the lost vitamins, including, but not limited to, thiamine. Recovery is more easily achievable for women than men, but in all cases it is necessary that they have the support of family and friends and abstain from alcohol.

Organic solvents that cause CSE are characterized as volatile, blood soluble, lipophilic compounds that are typically liquids at normal temperature. These can be compounds or mixtures used to extract, dissolve, or suspend non-water-soluble materials such as fats, oils, lipids, cellulose derivatives, waxes, plastics, and polymers. These solvents are often used industrially in the production of paints, glues, coatings, degreasing agents, dyes, polymers, pharmaceuticals, and printing inks.

Exposure to solvents can occur by inhalation, ingestion, or direct absorption through the skin. Of the three, inhalation is the most common form of exposure, with the solvent able to rapidly pass through lung membranes and then into fatty tissue or cell membranes. Once in the bloodstream, organic solvents, due to their lipophilic properties, easily cross the blood-brain barrier. The mechanism of effect that these solvents have on the brain that cause CSE, however, is not yet fully understood. Some common organic solvents known to cause CSE include formaldehyde, acetates, and alcohols.