It is not surprising that ethanol abuse significantly contributes to damage in a variety of tissues including liver, the central and peripheral nervous systems, and skeletal and cardiac muscle. After ingestion, alcohol distributes throughout body tissues and rapidly crosses the blood-brain barrier. The present review is focused around the multiple pathways involved in the development of peripheral neuropathy associated with chronic alcohol intake and the different therapeutic agents which may find a place in the therapeutic armamentarium for both prevention and management of alcoholic neuropathy.Īlcohol is one of the most commonly used substances in the world. However, in the setting of ongoing alcohol use, vitamin supplementation alone has not been convincingly shown to be sufficient for improvement in most patients. This can be achieved by alcohol abstinence and a nutritionally balanced diet supplemented by all B vitamins.
Treatment is directed towards halting further damage to the peripheral nerves and restoring their normal functioning. Nutritional deficiency (especially thiamine deficiency) and/or the direct toxic effect of alcohol or both have also been implicated in alcohol-induced neuropathic pain.
#Pins and needles after drinking alcohol free
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. The mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. 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. Chronic alcohol consumption produces painful peripheral neuropathy for which there is no reliable successful therapy, mainly due to lack of understanding of its pathobiology.
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