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. This commonly presents with pain, paresthesias, and ataxia in the distal lower extremities. The exact number of people affected by this condition is not known, but studies have shown that up to 66% of patients with chronic alcohol use disorder may have some form of the disease. The cause is multifactorial, from both nutritional deficiencies and alcohol metabolism’s direct toxic effects on neurons.
Alcoholic neuropathy: possible mechanisms and future treatment possibilities
- If the sensation is decreased enough, you may feel actual numbness after drinking alcohol.
- A doctor may also want to test the functioning of the kidneys, liver, and thyroid.
- These individuals draw the majority of calories from calorie rich alcoholic beverages with low nutritive value.
- This phenomenon may be responsible for the induction of the neuropathic pain like behaviour following chronic ethanol consumption.
- This type of degeneration, so called ‘dying-back’, resembles Wallerian degeneration.
- Nerves don’t have a resilient ability to regenerate if they are severely damaged.
In addition to thiamine deficiency, recent studies indicate a direct neurotoxic effect of ethanol or its metabolites. Axonal degeneration has been documented in rats receiving ethanol while maintaining normal thiamine status [5]. Human studies have also suggested a direct toxic effect, since a dose-dependent relationship has been observed between severity of neuropathy and total life time dose of ethanol [6, 13]. The exact mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. Therefore, alcoholic neuropathy may occur by a combination of the direct toxic effects of ethanol or its metabolites and nutritional deficiencies, including thiamine deficiency.
Alcohol-Related Neurologic Disease
- Referral to a behavioral health addiction facility may be required to treat alcohol addiction.
- Lettsom has observed that paralysis and hypoesthesia related to ALN presented a higher prevalence rate in lower limbs compared to upper limbs [60].
- Alternative therapies like chiropractic care, body manipulation, acupuncture, meditation, and massage therapy can be helpful in managing pain and symptoms of alcoholic polyneuropathy.
- It is estimated that consumption of more than 100 ml of ethyl alcohol per day significantly increases the risk of ALN [56].
It has been recognized that spinal cord glial cells, astrocytes and microglia are activated by neuropathic pain or peripheral inflammation [42]. Many different stimuli, including growth factors, cytokines, viral infection, ligands for alcohol neuropathy stages heterotrimeric G protein-coupled receptors, transforming agents, and carcinogens, activate the ERK pathway. There are many studies suggesting the role of MEK/ERK signaling in inflammatory pain in male [60–63] and female rats [64].
Causes of Alcoholic Neuropathy
- Since your ability to engage in some of these may be affected by neuropathy and/or alcoholism, schedule an appointment with a doctor or therapist to create a detailed, individualized health plan.
- Other vitamin deficiencies seen with alcohol abuse include but are not limited to, B vitamins, folic acid, and vitamin E.
- Contact us to learn more about our alcohol addiction treatment programs and begin your journey to recover today.
- Pain seems consistent in the literature as 1 of the most common complaints and can be the first clinical indication of the disease.
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. Thus, treatment with TCAs may provide symptomatic relief in patients with alcoholic neuropathy. https://ecosoberhouse.com/ Therefore, topical application with capsaicin may provide symptomatic relief from neuropathic pain in patients suffering from alcoholic neuropathy. At Healthgrades, our Editorial Team works hard to develop complete, objective and meaningful health information to help people choose the right doctor, right hospital and right care.
- 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].
- Drinking too much can alter levels of these nutrients and affect the spread of alcoholic neuropathy.
- A deficiency of vitamin B1 in chronic alcoholics can be due to inadequate dietary intake, reduced capacity for hepatic storage, inhibition of intestinal transport and absorption or decreased formation of the active coenzyme form.
- 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].
- These drugs have central and peripheral anticholinergic effects, as well as sedative effects, and they block the active re-uptake of norepinephrine and serotonin.
- 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.
- However, some people notice an improvement in symptoms a few months after discontinuing alcohol intake.
Role of caspases in alcoholic neuropathy
