Alcoholic neuropathy: possible mechanisms and future treatment possibilities

Electromyography and nerve conduction tests are performed in order to reveal signs of ALN. Sensory functions and reflexes can be tested during a neurological examination. Changes in muscle strength or sensation usually occur on both sides of the body and are more common in the legs than in the arms. Even though alcoholic neuropathy may not go away, there are things you can do to cope with this condition. Symptoms include tingling or numbness in the extremities, muscle weakness, changes in gait, heightened sensitivity to touch, chronic pain, and in advanced cases, muscle atrophy and gastrointestinal disturbances. The bladder, stomach, and intestines are among the organs in the body whose activities are regulated by autonomic nerves.

Symptoms & Signs

Alcoholic neuropathy is a condition in which drinking too much alcohol causes damage to nerve tissue. You may need to try many therapies and options before you and your medical team work out what is best to manage your side effects, restore nerve function where possible, and prevent further damage. If you are experiencing weakness, reduced muscle function, or control, you may be given orthopedic appliances to improve your stability. You’ll likely also be asked to participate in physical therapy to help regain and maintain your strength. Certain vitamin supplements, including folic acid and thiamine, will likely be provided to you during treatment since people with ALN tend to be deficient in these areas.

Electromyography (EMG) and nerve conduction studies (NCV):

Symptoms of AAN are non-specific; in the sympathetic division, these include impairments in perspiration, orthostatic hypotension, whereas in parasympathetic hoarseness, swallowing difficulties, or cardiac arrhythmias 111, 166. Gastrointestinal symptoms include delayed stomach emptying and intestinal transit, dyspepsia, and faster emptying of the gallbladder 165. Besides, approximately 55% of men with AAN develop erectile dysfunctions 167. 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 mechanism of direct damage of nerve fibers due to alcohol intoxication remains unclear. Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis appear to be implicated in this process 92,93,94,95,96,97.

Outlook of alcoholic neuropathy

• It also damages myelin, the fatty coating that surrounds and protects the nerves.
• This dual strategy is essential to manage the condition effectively and improve our quality of life.
• 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.
• The morphological basis of post-alcoholic damage of neural tissue includes primary axonopathy and secondary demyelination of motor and sensory (especially small) fibers 105.
• Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol.

Treatment will depend on the type, location, and severity of your symptoms. Research suggests that up to 66% of people with AUD have some type of alcohol-related neuropathy. Physical therapy and orthopedic appliances (such as splints) may be needed to maintain muscle function and limb position. Motor nerves are the nerves responsible for all voluntary skeletal and somatic movement such as moving the leg or arm.

Treatment / Management

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. Thus, in alcoholics with the mutated dehydrogenase enzyme, acetaldehyde concentrations may reach values about 20 times higher than in individuals without the mutation.

How to prevent alcoholic neuropathy

• When speaking with a doctor, a person should be honest about how much alcohol they consume.
• This phenomenon may be responsible for the induction of the neuropathic pain like behaviour following chronic ethanol consumption.
• The psychological impact of chronic conditions such as alcoholic neuropathy should not be underestimated.
• Giving up alcohol is the most crucial step in treating alcohol-related neuropathy.

There are many studies suggesting the role of MEK/ERK signaling in inflammatory pain in male 60–63 and female rats 64. It is important to stop drinking if you suffer from alcoholic polyneuropathy in order to stop the disease from getting worse and to correct the nutritional imbalance that is damaging the nerves and interfering with the nervous system. A medical detox program followed by a comprehensive alcohol rehab program can manage alcoholism and help a person to get sober and stay that way. Many alcohol rehab programs help to manage co-occurring disorders, such as alcoholic polyneuropathy.

One of the most irritating symptoms of alcoholic neuropathy is persistent pain in the hands or feet. The severity of the pain may fluctuate as the disease worsens, occasionally going away for months before getting worse again. According to experts, the best course of treatment should be to stop the peripheral nerves’ deterioration and concentrate on getting them back to normal. A well-balanced diet, vitamin B supplements, and correct and total abstinence from alcohol are the best ways to achieve that. Antidepressant drugs are frequently used to assist manage the pain of alcoholic neuropathy, even though they are not licensed expressly for this condition. Supplementing with vitamin B12, folate, vitamin E, and thiamine may be advised to address these deficits.

Sometimes alcohol Twelve-step program causes such severe damage to the body that a liver transplant may be necessary. In this case, there may be some improvement in the symptoms of alcoholic neuropathy after the liver transplant, but the neuropathy may also be so advanced that there may be little, if any, improvement, even after a transplant. There are no medications that can help improve loss of sensation, strengthen muscle weakness, or assist with the coordination and balance problems caused by alcoholic neuropathy. However, some people notice an improvement in symptoms a few months after discontinuing alcohol intake.

However, vulnerability to neuropathy and its severity and speed of progression varies. Women, continuous drinkers more so than episodic drinkers, and people with a family history of the disorder appear to be more vulnerable to alcoholic neuropathy and may develop more severe presentations. The medical community has recognized that addiction is a disease and some people are predisposed to it. As a result, it is usually necessary to get medical help to manage alcohol use disorder. While not specifically approved for the treatment of alcoholic neuropathy, antidepressant medications are often prescribed to help control the pain. Understanding that recovery from alcoholic neuropathy is a long-term, often variable process, allows us to work towards the best possible outcomes.

Can alcohol cause pain in your feet?

The most common findings are sensory-related and vary, including pain, numbness, and paresthesias. Pain seems consistent in the literature as 1 of the most common complaints and can be the first clinical indication of the disease. Keeping this disease process high on the differential with the right history is essential.