alcoholic polyneuropathy

There is still controversy about the reasons for the development of alcoholic polyneuropathy.

For unknown reasons, alcoholic polyneuropathy has a high incidence in women.

In most cases, individuals with alcoholic polyneuropathy have some degree of nutritional deficiency.

The clinical title of alcoholic polyneuropathy was widely recognized by the late nineteenth century.

The pathophysiology of alcoholic polyneuropathy is an area of current research.

Alcoholic polyneuropathy is not life threatening but may significantly affect one's quality of life.

If electrodiagnostic criteria is used, alcoholic polyneuropathy may be found in up to 90% of individuals being assessed.

This suggests that there is a possibility ethanol (or its metabolites) may cause alcoholic polyneuropathy.

This debate is ongoing and research is continuing in an effort to discover the real cause of alcoholic polyneuropathy.

Alcoholism is normally associated with nutritional deficiencies, which may contribute to the development of alcoholic polyneuropathy.

Alcoholic polyneuropathy is caused primarily by chronic alcoholism; however, vitamin deficiencies are also known to contribute to its development.

Although there is no known cure for alcoholic polyneuropathy, there are a number of treatments that can control symptoms and promote independence.

Alcoholic polyneuropathy is a neurological disorder in which multiple peripheral nerves throughout the body malfunction simultaneously.

The metabolic effects of liver damage associated with alcoholism may also contribute to the development of alcoholic polyneuropathy.

Alcoholic polyneuropathy is very similar to other axonal degenerative polyneuropathies and therefore can be difficult to diagnose.

Alcoholic polyneuropathy usually has a gradual onset over months or even years although axonal degeneration often begins before an individual experiences any symptoms.

The combination of all of them may result in a nutritional deficiency that is linked to the development of alcoholic polyneuropathy.

Thiamine deficiency alone could explain the impaired nerve conduction in those with alcoholic polyneuropathy, but other factors likely play a part.

Large studies have been conducted and show that alcoholic polyneuropathy severity and incidence correlates best with the total lifetime consumption of alcohol.

The mechanism of axonal degeneration has not been clarified and is an area of continuing research on alcoholic polyneuropathy.

Further research is looking at the effect an alcoholics' consumption and choice of alcoholic beverage on their development of alcoholic polyneuropathy.

The neurotoxicity resulting from the accumulation of acetaldehyde may play a role in the pathogenesis of alcoholic polyneuropathy.

Korsakoff studied the effects of alcoholism on the nervous system and drew attention to several cases of alcoholic polyneuropathy with distinctive mental symptoms.

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.

When alcoholics have sensorimotor polyneuropathy as well as a nutritional deficiency, a diagnosis of alcoholic polyneuropathy is often reached.