There are several possible causes of neuropathy, and knowing about a person’s alcohol intake can help the doctor to make an accurate diagnosis. Other studies have shown a direct, negative effect from alcohol and its many metabolites on the nervous system. Axonal degeneration and demyelination of neurons were seen in both humans and lab mice receiving alcohol. The cause is a diverse multifactorial process caused from damage by free radicals, the release of inflammatory markers, and oxidative stress. The medical community has recognized that addiction is a disease and that some people are predisposed to it. As a result, it is usually necessary to get medical help to manage alcohol use disorder.
Like many other health conditions, peripheral neuropathy can get progressively worse. Even if your loved one seeks help, you may still need help and support to overcome the effects. Many people refer to alcoholism as a “family disease” because it can have a major impact on all members of the family whether they realize it or not. Chronic, long-term drinking can contribute to malnutrition by replacing foods needed for essential nutrients and by interfering with absorption, storage, or metabolism of the essential nutrients.
Alcohol Abuse and Nerve Damage
In addition to thiamine deficiency, recent studies indicate a direct neurotoxic effect of ethanol or its metabolites. Axonal degeneration has been documented in rats receiving ethanol while maintaining normal thiamine status [5]. Human studies have also suggested a direct toxic effect, since a dose-dependent relationship has been observed between severity of neuropathy and total life time dose alcohol neuropathy stages of ethanol [6, 13]. The exact mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. Some other studies have indicated that chronic alcohol intake can decrease the nociceptive threshold with increased oxidative-nitrosative stress and release of pro-inflammatory cytokines coupled with activation of protein kinase C (Figure 1) [10, 16].
- At present, it is unclear what the pathogenetic mechanisms for the development of neuropathy amongst those who chronically abuse alcohol are, and therefore, it is unknown whether it is attributed to the direct toxic effects of ethanol or another currently unidentified factor.
- These findings constitute direct evidence that spinal PKC plays a substantial role in the development and maintenance of an ethanol-dependent neuropathic pain-like state in rats.
- Dedicating her life to helping others, Midge continues to assist individuals in accessing their own power to create positive change in their lives, release emotional blocks, and encourage self-healing.
- Depending on the extent of the damage, symptoms may lessen or disappear when a person stops drinking alcohol; however, nerves have less self-healing ability than many other body components, and neuropathy harm is often permanent.
Lacosamide, a new anticonvulsant drug, had a small but significant pain relieving effect on painful diabetic neuropathy [130], while subsequent trials have failed to find an effect, except for the efficacy of a 400 mg dose in subgroup analyses [131, 132]. Alcoholic neuropathy damages the nerves due to prolonged and excessive alcohol consumption. This damage prevents the nerves from communicating information from one body area to another. Sometimes alcohol causes such severe damage to the body that a liver transplant may be necessary.
Motor
The first step will likely be a medically supervised detox, which will help rid your body of toxins and manage the symptoms of withdrawal. In general, most of the aforementioned diseases are the result of chronic excessive alcohol use. Limiting alcohol consumption and avoiding excessive alcohol use can help prevent or stop the progression of many alcohol-induced neurological diseases.
Current postulation holds that dysfunctions within the central and peripheral nervous system are due to both direct and indirect toxic effects of alcohol [31, 85,86,87]. Indirect effects are mainly induced by vitamin deficiencies (B1, B2, B3, B5, B6, B7, B9, and B12) [84, 88]. Thirteen studies provided data from the biopsy of the sural nerve or the skin in patients with alcohol-related peripheral neuropathy. Alcohol-related peripheral neuropathy appears to be characterised by severe loss of myelinated fibres; and although profound small fibre loss can also be present, this appears to occur more variably [3, 51, 53, 59, 85].