Alcoholic neuropathy: possible mechanisms and future treatment possibilities PMC

The SDTC was normal compared to controls, but the rheobase was significantly different suggesting that APN may affect internodal channels other than nodal channels or the Na+ –K+ ATP pump. Accumulating evidence suggests a pivotal role for metabotropic glutamate receptors (mGluRs) in nociceptive processing, inflammatory alcohol neuropathy pain and hyperalgesia [74, 75]. Several mGluR subtypes have been identified in the superficial dorsal horn of the spinal cord [76, 77] and on primary afferent fibres [78]. Glutamate concentrations are elevated in the superficial dorsal horn of rats after chronic ligature of the sciatic nerve [79].

Resulting disturbances in protein and lipid metabolism lead to undernourishment which adversely influences other metabolic pathways, including those influencing the function of the nervous system. The available data addressing the role of hepatic dysfunction is presently inconclusive. It is possible that hepatic dysfunction and alcoholic toxicity each cause neuropathy independently, and that there is frequently overlap between the two. It may also be that comorbid hepatic dysfunction is a risk factor for alcohol-related peripheral neuropathy. Further studies are required to develop a greater understanding of the interaction these entities.

Enhancing Healthcare Team Outcomes

Biomarkers of alcohol abuse include carbohydrate-deficient transferrin (CDT) and phosphatidylethanol (PEth). CDT is an indirect metabolite of ethanol and constitutes either a marker of prolonged, heavy alcohol consumption or a marker of relapse. Peth on the other hand is a direct alcohol metabolite that can be measured to monitor alcohol consumption as well as for the identification of early signs of alcohol-related clinical manifestations. Other non-specific biomarkers useful in the diagnosis of alcohol use disorder are gamma-glutamyl transferase (GGT), mean corpuscular volume (MCV) of the red blood cells, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Alcohol abuse causes a wide range of disorders that affect the nervous system. These include confusion, cerebellar ataxia, peripheral neuropathy, and cognitive impairment.

In general, the nerves in lower limbs were more affected than the upper limbs [3, 37–39]. Four studies reported abnormalities only in sensory nerves [33, 47, 63, 64], while ten reported abnormalities in both sensory and motor nerves [2–4, 16, 38, 54, 56, 58, 59, 65]. The abnormalities were usually of reduced amplitude, in keeping with axonal loss [2, 3, 5, 11, 12, 16, 21, 27, 37–39, 47, 51, 53, 54, 56, 63–68].

Workup in alcoholic neuropathy

According to many studies, alcohol-induced autonomic neuropathy (AAN) not only leads to potential damage to internal organs but also increases the mortality rate of patients [157, 158]. It was observed that abstinence may lead to the regression of several symptoms of AAN [159]. Alcohol causes neuropathy via multifactorial processes, many of which are still under investigation.

Some of the most common symptoms are numbness or tingling sensation of the extremities, pain or a burning sensation in the extremities, difficulty walking, difficulty urinating, and difficulty talking or swallowing. These include vascular disorders (which affect your body’s blood vessels), kidney problems, cancer, benign tumors, and other diseases. Car accidents, sports injuries, broken bones, or even surgery can cause nerve damage. Recovered is not a medical, healthcare or therapeutic services provider and no medical, psychiatric, psychological or physical treatment or advice is being provided by Recovered.