ataxia. This ataxia may be caused by cerebellar degeneration, sensory ataxia, or distal muscle weakness. Over time, alcoholic polyneuropathy may also cause difficulty swallowing (dysphagia), speech impairment (disarthria), muscle spasms, and muscle atrophy. In addition to alcoholic polyneuropathy, the individual may also show other related disorders such as Wernicke–Korsakoff syndrome and cerebellar degeneration that result from alcoholism-related nutritional disorders. Severity Polyneuropathy spans a large range of severity. Some cases are seemingly asymptomatic and may only be recognized on careful examination. The most severe cases may cause profound physical disability. Causes The general cause of this disease appears to be prolonged and heavy consumption of alcohol accompanied by a nutritional deficiency. However, there is ongoing debate over the active mechanisms, including whether the main cause is the direct toxic effect of alcohol itself or whether the disease is a result of alcoholism-related malnutrition. A 2019 metastudy found that the relationship between ethanol toxicity and neuropathy remained unproven. Effects due to nutritional deficiency Frequently alcoholics have disrupted social links in their lives and have an irregular lifestyle. This may cause an alcoholic to change their eating habits including more missed meals and a poor dietary balance. Alcoholism may also result in loss of appetite, alcoholic gastritis, and vomiting, which decrease food intake. Alcohol abuse damages the lining of the gastrointestinal system and reduces absorption of nutrients that are taken in. The combination of all of them may result in a nutritional deficiency that is linked to the development of alcoholic polyneuropathy. There is evidence that providing individuals with adequate vitamins improves symptoms despite continued alcohol intake, indicating that vitamin deficiency may be a major factor in the development and progression of alcoholic polyneuropathy. In experimental models of alcoholic polyneuropathy utilizing rats and monkeys no convincing evidence was found that proper nutritional intake along with alcohol results in polyneuropathy. In most cases, individuals with alcoholic polyneuropathy have some degree of nutritional deficiency. Alcohol, a carbohydrate, increases the metabolic demand for thiamine (vitamin B1) because of its role in the metabolism of glucose. Thiamine levels are usually low in alcoholics due to their decreased nutritional intake. In addition, alcohol interferes with intestinal absorption of thiamine, thereby further decreasing thiamine levels in the body. Thiamine is important in three reactions in the metabolism of glucose: the decarboxylation of pyruvic acid, d-ketoglutaric acid, and transketolase. A lack of thiamine in the cells may therefore prevent neurons