Alcoholic Neuropathy: Causes, Symptoms, & Treatments

These include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters. Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis also seem to be implicated in the pathophysiology of this alcoholic neuropathy. The goal of treatment is to impede further damage to the peripheral nerves while also restoring their normal physiology. Alcohol abstinence, intake of balanced diets, and treatment with medications are suggested including benfotiamine, alpha-lipoic acid, acetyl-l-carnitine, vitamin E, methylcobalamin, myo-inositol, N-acetylcysteine, capsaicin, tricyclic antidepressants, or antiepileptic drugs.

• Statistical calculation of pooled proportions was conducted in R language, using the default settings of the “meta” package and the “metaprop” function with a random effects model [8].
• These individuals draw the majority of calories from calorie rich alcoholic beverages with low nutritive value.
• Occupational therapy can help the patient with self-care activities and safely navigating the home environment.
• Biomarkers of alcohol abuse include carbohydrate-deficient transferrin (CDT) and phosphatidylethanol (PEth).
• Western immunoblot analysis indicated a higher level of PKCε in dorsal root ganglia from alcohol-fed rats, supporting a role for enhanced PKCε second messenger signalling in nociceptors contributing to alcohol-induced hyperalgesia [16].

Patients are likely to experience heat intolerance, excessive sweating, difficulty while swallowing, nausea, diarrhea, and constipation. Sexual drive and performance are diminished in both men and women, including https://ecosoberhouse.com/ erectile dysfunction in men. If you’re struggling to control your drinking and worried about alcoholic neuropathy, help is available. For a list of rehabs and treatment centers near you, visit our rehab directory.

Motor symptoms

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].

Sometimes symptoms get better, especially if caused by a condition that can be treated. Additionally, people with alcohol use disorder experience allodynia during alcohol withdrawal. Allodynia is a condition in which a nonpainful stimulus causes pain or discomfort. 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.

Data collection process

In this phase of our study we used male rats, but it is our intention to analyze this process with females as well, providing the oestrous cycle variable can be included. Furthermore, we intend to compare the toxic effect of alcohol on pain central processing to better understand the association between chronic alcohol intake and alcohol-induced neuropathy. Alcohol abuse contributes to peripheral neuropathy development involving both somatic and autonomic nerves [154, 155].

Excessive, long-term consumption of alcohol can lead to malnutrition as well as nerve damage, and both contribute to the development of alcoholic neuropathy. Our muscles need to receive a message from nearby nerves in order to function. When this message is interrupted due to damaged nerves, the muscles cannot function as they normally would. One of the first symptoms of AN is a slowly progressive sensory-dominant neuropathy, which affects motor and autonomic functions, being related to the amount and duration of alcohol consumption (Chopra and Twari, 2012). This is the first study to generate a preclinical model of alcohol withdrawal-related allodynia and alcohol-induced neuropathic pain in vivo. The chronic intermittent ethanol vapor-two bottle choice (CIE-2BC) mouse model used in this study paves the way for more research in this area.

Treatment options

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].

One of the other important issues in alcoholic individuals is the source of their calorie intake. These individuals draw the majority of calories from calorie rich alcoholic beverages with low nutritive value. Chronic abuse of alcohol depletes the pool of liver proteins which are consumed for energy production and insufficient intake of proteins only worsens this imbalance. 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. Based on these studies, it can be determined that there is a high rate of peripheral neuropathy amongst chronic alcohol abusers.

Benfotiamine, a synthetic derivative of vitamin B1, improves neuropathic pain and motor movement by increasing nerve conduction velocity. A nutritious diet; vitamin supplements, especially vitamins B1 and B12; and reduction of or abstinence from alcohol use is the only way to improve the patient’s PN by allowing nerves to slowly regenerate. The prevalence of alcohol-induced PN varies depending on demographics and the diagnostic criteria used in individual research studies. According to studies by the CDC, nearly 30% of adults in the US consume alcohol excessively. Excessive or heavy alcohol consumption is defined by the CDC when men have 15 or more drinks each week and women have 8 or more drinks each week. The National Institute on Alcohol Abuse and Alcoholism reports that 16 million people in the US have been diagnosed with alcohol use disorder (AUD).

Sensory functions and reflexes can be tested during a neurological examination. Capsaicin is a topical agent that modulates the inflammatory effects of the neurotransmitter neurokinin A to reduce neuropathic pain. Nonsteroidal anti-inflammatory agents, acetylsalicylic acid, and acetaminophen may be helpful in mild PN as a complement to other medication. Research indicates that the antioxidant alpha-lipoic acid may improve pain through nerve regeneration. Transcutaneous electrical nerve stimulation may increase conduction through neurons and improve neuropathic pain. Autonomic nerve damage may cause a fluctuation in heart rate and BP, leading to orthostatic hypotension.