Alcoholic Neuropathy StatPearls NCBI Bookshelf

Chronic consumption of alcohol has been implicated in end-organ damage to multiple systems. Patients with multisystem damage as a result https://ecosoberhouse.com/ of alcohol consumption often die of cardiac or liver failure. The best way to prevent alcoholic neuropathy is to avoid excessive alcohol consumption and to seek treatment for alcoholism if you have difficulty doing so. Acetyl-L-carnitine has been tested in clinical 102 and animal studies 103 for the treatment of chemotherapy-induced peripheral neuropathy.

• This suggests that these pathways are potential targets for novel pharmacological agents for the treatment of inflammatory as well as neuropathic pain 71.
• Treatment for alcoholism may include counseling, social support such as Alcoholics Anonymous (AA), or medicines.
• The primary risk factor for alcoholic neuropathy is chronic consumption of large amounts of alcohol.
• Poor absorption and low intake of these vitamins have clinical features of dermatitis, neuropathy, and anorexia.
• However, impairments of autonomic functions are scarcer and less intensified, and, usually, clinical symptoms are delayed 156.

Vitamins

An ankle-foot orthosis (AFO) may be needed to assist patients with weak ankle dorsiflexion, eversion, and/or plantar flexion. This device also can help with ankle proprioception and can improve neuropathy and alcohol gait and prevent ankle sprains. Vigilant foot care and the use of shoes with an enlarged toe box are useful in preventing foot ulcers.

Vitamin B1 (Thiamine)

The symptoms of alcoholic neuropathy are caused by the toxic effects of alcohol leading to degeneration of nerve cell axons, the long fibers that transmit electrical signs from nerve to nerve, and a loss of myelin, the fatty coating that protects nerves. Long-term heavy alcohol use, particularly when accompanied by nutritional deficiencies, can damage the body’s nerves, leading to a host of painful and debilitating symptoms. Alcoholic neuropathy can affect both sensory and motor nerves, causing pain, hypersensitivity, numbness, muscle weakness, and lack of coordination and fine motor controls, largely in the extremities.

The role of oxidative stress

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. In general, the nerves in lower limbs were more affected than the upper limbs 3, 37,38,39. Four studies reported abnormalities only in sensory nerves 33, 47, 63, 64, while ten reported abnormalities in both sensory and motor nerves 2,3,4, 16, 38, 54, 56, 58, 59, 65. This may be a reflection of the severity of the neuropathy in which motor nerve function is affected at a later stage. The abnormalities were usually of reduced amplitude, in keeping with axonal loss 2, 3, 5, 11, 12, 16, 21, 27, 37,38,39, 47, 51, 53, 54, 56, 63,64,65,66,67,68. H and F wave latencies Drug rehabilitation were not routinely reported but were found to be prolonged in those with alcohol-related peripheral neuropathy in studies that did 4, 67.

• The prevalence of alcoholic cardiomyopathy appears to be similar among males and females; however, males present a higher disease burden 132, 133.
• What is crucial during ALN treatment is the alleviation of the major causation of ALN which is alcohol abuse.
• The sural nerve was the most commonly reported nerve 2, 3, 5, 11, 27, 37,38,39, 51, 53, 59, 63, 68.
• 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.
• Twenty-four-hour urine heavy metals showed detectable levels of arsenic, but were within normal limits.
• The study was interpreted as consistent with an axonal sensorimotor peripheral neuropathy.

Although the study provided control for nutritional deficiencies, the female group with chronic alcoholism had a significantly lower sural SNAP amplitude compared with the male group with similar total lifetime dose of ethanol consumption (TLDEC). This study suggested that females may demonstrate increased sensitivity to the toxic effects of alcohol on peripheral nerves. Protein kinase C (PKC) is a family of protein kinases consisting of approximately 10 isozymes.

Conditions That May Mimic Alcoholic Neuropathy

• Cardiac arrhythmias in patients with AAN might increase the probability of sudden cardiac death, which is probably due to toxic effects of alcohol on a cardiac muscle that is also observed in alcoholic cardiomyopathy 168, 169.
• The histologic features of sural nerve biopsy specimens demonstrated small fibre predominant axonal loss as characteristic of the pure form of alcoholic neuropathy.
• The sometimes-conflicting findings between biopsy findings may be representative of the complex interplay of pathological factors in alcohol-related peripheral neuropathy and is indicative of the need for further research in this area.
• Learn more about this condition, including its symptoms, how it’s treated, and ways to cope.

The main symptoms of ALN include dysesthesia, paresthesia, numbness, and pain in the lower extremities which progressively reach higher parts of the body 114,115,116,117. The pain is described as burning, cramp-like, or itching; also, a common symptom is a subjective feeling of cold in both feet 118,119,120,121,122,123. The symptoms deteriorate through touch and pressure which intensify pain while standing or walking 124. Further progression of ALN leads to the weakening of tendon reflexes or total areflexia and disturbed proprioception, which additionally impair the ability to walk 28, 113. ALN further manifests as weakness and atrophy of muscles due to the damage of greater motor fibers and impaired neuromuscular transmission.