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Besides, the gastrointestinal and urinary systems are also affected and include the presence of diarrhea, constipation, nausea, swallowing difficulties, abdominal bloating, and urinary retention. The most important strategy against alcoholic neuropathy lies in preventing the symptoms from getting worse by decreasing alcohol consumption as soon as possible. Detoxification is a crucial stage that tackles physical alcohol dependence and is the first step towards recovery from alcohol addiction and the neuropathy that goes along with it. To ensure that the person safely overcomes the acute physical symptoms of safely reducing alcohol intake alcohol, detox entails medically managed withdrawal. To rid the body of toxins and get ready for the longer-term rehabilitation process, this stage is essential. Alcoholic neuropathy is suggested by certain patterns, including slowing of nerve activity, reduced amplitude of nerve waves, and diminished function in the hands and feet.
Alcohol-Induced Neuropathy in Chronic Alcoholism: Causes, Pathophysiology, Diagnosis, and Treatment Options
Parameters measured included vibration perception in the great toe, ankle and tibia, neural pain intensity, motor function and paralysis, sensory function and overall neuropathy score and clinical assessment. Although benfotiamine therapy was superior to Milgamma-N or placebo for all parameters, results reached statistical significance only for motor function, paralysis and overall neuropathy score. The reason for better results in the benfotiamine alone group than in the Milgamma-N group, despite the fact that the benfotiamine dosage was equivalent, is not completely understood. The authors hypothesized that vitamins B6 and B12 might have competed with the effects of vitamin B1 in the Milgamma-N group 97. In another small Russian study, 14 chronic alcoholic men with polyneuropathy were given 450 mg benfotiamine daily for 2 weeks, followed by 300 mg daily for an additional 4 weeks.
Role of nutritional status other than thiamine deficiency
- Rats with experimentally-induced diabetes for 2 months had a 20% reduction in nerve conduction velocity and 48% reduction in endoneurial blood flow.
- Symptoms of AAN are due to impairments in both sympathetic and parasympathetic autonomic fibers of the cardiovascular, digestive, and urogenital systems.
- Home remedies like gentle exercise, warm baths, and maintaining a balanced diet can help manage alcoholic neuropathy symptoms.
- It is important to supplement the diet with vitamins, including thiamine and folic acid.
- The most important thing you can do to treat alcohol-related neuropathy is to stop consuming alcohol.
- In fact, a person who drinks heavily might not recognize that the symptoms they are experiencing are related to their alcohol consumption.
The reduction of internodal length contributes to the decreased speed of nerve conduction which may be implemented in impairments in perspiration, baroreceptor reflexes, and functions of internal organs. To determine the functions of the sympathetic division of the autonomic nervous system (ANS), sympathetic skin response (SSR) is used; the abnormal results of this test suggest subclinical transmission impairments 162. Navarro et al. (1993) showed that nearly half of the alcohol-dependent patients without AAN symptoms and any aberrations in electrophysiologic studies presented abnormal SSR results 163. 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. It is likely to get worse if the person continues to use alcohol or if nutritional problems are not corrected.
Muscle Weakness
This damage prevents the nerves from communicating information from one body area to another. Yes, long-term excessive alcohol consumption may lead to peripheral neuropathy, which can cause pain in your feet. Understanding neuropathy involves peeling back the layers to reveal the intricate web of risk factors and causes contributing to this nerve-damaging condition. From the duration and quantity of heavy alcohol use to genetic predispositions and nutritional deficiencies, below are some risk factors.
Methylcobalamin for the treatment of peripheral neuropathy
Alcohol-related peripheral neuropathy (ALN) can occur when someone drinks a lot of alcohol, which is often the case in individuals suffering from alcohol use disorder and high alcohol use. Medicines may be needed to treat pain or uncomfortable sensations due to nerve damage. They will be prescribed the smallest dose of medicine needed to reduce symptoms. This may help prevent drug dependence and other side effects of chronic use.
Counseling or therapy can help us cope with the emotional and mental challenges of a lengthy recovery process. Alcoholic liver disease is more likely to develop if a person has consumed more than 30 grams of alcohol daily for more than five years. People who consume more than 40 grams of alcohol per day over an extended period may develop cirrhosis, a form of alcoholic liver disease.
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- PKC is involved in receptor desensitization, modulating membrane structure events, regulating transcription, mediating immune responses, regulating cell growth and in learning and memory.
- Ethanol diminishes thiamine absorption in the intestine, reduces hepatic stores of thiamine and affects the phosphorylation of thiamine, which converts it to its active form 12.
- Some of the symptoms of alcoholic neuropathy can be lessened with medication.
- Alcoholic neuropathy is usually not life threatening, but it can severely affect quality of life.
- Heat sensitivity, unusual feelings like “pins and needles,” and numbness or painful sensations in the arms and legs are common signs of sensory problems.
- Densities of small myelinated fibres and unmyelinated fibres were more severely reduced than the density of large myelinated fibres, except in patients with a long history of neuropathic symptoms and marked axonal sprouting 2.
Unfortunately, patient compliance is poor, and the condition often progresses, leading to poor quality of life. It is still unclear what is the major determinant in the pathogenesis of ALN. Primarily, thiamine deficiency is the crucial risk factor of ALN since it induces the progression of Korsakoff’s syndrome and beriberi 144, 145. Due to similar histologic and electrophysiological symptoms, it Alcoholics Anonymous was believed that ALN may make up a subtype of beriberi 146.
Intensive research has been done on medications like alpha-lipoic acid, benfotiamine, acetyl-l-carnitine, and methylcobalamin. Other botanical or nutrient therapies include myo-inositol, vitamin E, topical capsaicin, and N-acetylcysteine. Chronic alcohol consumption can have deleterious effects on the central and peripheral nervous systems. One of the most common adverse effects seen in patients with chronic alcohol use disorder is alcohol neuropathy.