Alcoholic Neuropathy: Symptoms, Causes, Treatments

Acetyl-L-carnitine has been tested in clinical 102 and animal studies 103 for the treatment of chemotherapy-induced peripheral neuropathy. The decreases in nerve conduction velocity were significantly less in groups supplemented with acetyl-L-carnitine. In addition, acetyl-L-carnitine did not interfere with the antitumour effects of the drugs.

What is alcoholic neuropathy muscle weakness?

Propensity score matching was applied to balance age, sex, race, ethnicity, comorbidities, and medication use. Further, ECG changes and functions of the digestive tract (dyspeptic symptoms, stomach and gallbladder motility, orocecal transit time) can also be assessed 162, 165. PCT seems to be valuable due to the correlation between prolongation of pupil oscillation and exacerbations of cardiovascular symptoms which presents the colinear involvement of parasympathetic division of ANS. ALN can manifest differently, and patients might experience one, two, or even more clinical manifestations of ALN. Patients who have ALN might present such symptoms as cramps, impaired movement of the limbs, muscle atrophy, muscle weakness, spasms, or contractions, loss of sensation, or feeling of tingling. Besides, the gastrointestinal and urinary systems are also affected and include the presence of diarrhea, constipation, nausea, swallowing difficulties, abdominal bloating, and urinary retention.

• PKC is involved in receptor desensitization, modulating membrane structure events, regulating transcription, mediating immune responses, regulating cell growth and in learning and memory.
• Moreover, phosphorylated PKC was significantly increased in the spinal cord following chronic ethanol consumption.
• Constant pain in the hands or feet is one of the most bothersome aspects of alcoholic neuropathy.
• After PSM, the SMD for all variables was less than 0.1, suggesting the achievement of balanced cohorts.
• To better understand the neurological effects of alcohol, it helps to explore some of the more well-known pathologies, disorders, and diseases.
• Doctors tailor specific treatments and alcohol abstinence programs to the individual.

Is alcoholic neuropathy fatal?

Tricyclic antidepressants (TCAs) are often the first line drugs to alleviate neuropathic pain symptoms. They have central effects on pain transmission and block the active re-uptake of norepinephrine and serotonin. TCAs have been shown to relieve various neuropathic pain conditions in many trials 115. In agreement with this, one recent study has confirmed the efficacy of TCAs in central pain 116. The serotonin/norepinephrine re-uptake inhibitors (SNRIs), duloxetine and venlafaxine, have a well-documented efficacy in painful polyneuropathy 117, 118. SSRIs have been studied in a few trials which have demonstrated a weak analgesic effect but the clinical relevance of these compounds is questionable 119.

Getting help for alcohol use disorder

Demyelination is probably the effect of axoplasmic transmission slowdown; such degeneration so-called dying back bears semblance to Wallerian degeneration is alcoholic neuropathy dangerous 64, 84. An animal study on axonal transport in vitro using dorsal roots of the sciatic nerve showed decreased axonal transmission after long-term ethanol consumption 106. In vivo study on rats showed impaired retrograde axonal transport 107, 108.

How can alcohol-related neurologic disease be prevented?

Female mouse with injected testosterone showed the decreased activity of cytosolic isoform of ALDH which implies that those enzymes are sensitive to estrogen and testosterone and alcohol metabolism is greater in females. Alcoholic neuropathy is nerve damage that results from the toxic effect of alcohol on nerves. Alcohol-induced peripheral neuropathy is a common complication of alcohol use disorder.Excess alcohol consumption can also result in malnutrition and vitamin deficiencies that have a damaging effect on nerves.

• In 47 of these patients sural nerve biopsy was performed, with discrimination in terms of their thiamine status 3.
• Cerebellar degeneration caused by alcohol occurs when neurons in the cerebellum deteriorate and die.
• In a similar study, SSR was used to assess the number of reactive sweat glands (SGN), which turned out to be decreased in alcohol-dependent patients 164.
• Limiting alcohol consumption and avoiding excessive alcohol use can help prevent or stop the progression of many alcohol-induced neurological diseases.
• 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.

What causes alcohol-related neurologic disease?

This type of degeneration, so called ‘dying-back’, resembles Wallerian degeneration. Ethanol and its toxic degradation metabolites affect neuronal metabolism including the metabolic pathways of nucleus, lysosomes, peroxisomes, endoplasmatic reticulum and cytoplasm 21. Alcohol enters the blood as early as 5 min after ingestion and its absorption peaks after 30–90 min. The key role in the degradation of ethanol is played by ethanol dehydrogenase and acetaldehyde dehydrogenase-two step enzymatic systems by which ethanol is converted to acetate which is further metabolized in humans. Acetaldehyde dehydrogenase is a mitochondrial enzyme which undergoes a single amino acid substitution (mutation) in about 50% of the Asian population in a way similar to the genetic changes in sickle cell anaemia 21.