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Alcoholic polyneuropathy is a neurological disorder in which peripheral nerves throughout the body malfunction simultaneously. It is defined by axonal degeneration in neurons of both the sensory and motor systems and initially occurs at the distal ends of the longest axons in the body. This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally. Alcoholic polyneuropathy is caused primarily by chronic alcoholism ; however, vitamin deficiencies are also known to contribute to its development. This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol.
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Alcoholic neuropathy: possible mechanisms and future treatment possibilities
Understanding Alcoholic Neuropathy
Fortunately, there are means — and medications — to help ease the condition. Neuropathy is a disease of one or more peripheral nerves that causes numbness, pain and weakness. After headaches, it is the second most common neurological condition, affecting more than 20 million Americans. Diabetes is the most common culprit, causing about half of all neuropathy cases. Even prediabetes is of concern to physicians because it leads so often to diabetes. Treatment of diabetes can slow the progression of neuropathy and also help people with other health problems related to diabetes, including eyesight complications, kidney problems, strokes and heart attacks.
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Chronic alcohol consumption produces painful peripheral neuropathy for which there is no reliable successful therapy, mainly due to lack of understanding of its pathobiology. Alcoholic neuropathy involves coasting caused by damage to nerves that results from long term excessive drinking of alcohol and is characterized by spontaneous burning pain, hyperalgesia and allodynia. The mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. These include activation of spinal cord microglia after chronic alcohol consumption, oxidative stress leading to free radical damage to nerves, activation of mGlu5 receptors in the spinal cord and activation of the sympathoadrenal and hypothalamo-pituitary-adrenal HPA axis.