Treating alcoholic polyneuropathy must begin with treating a person’s alcohol use. If a person is still drinking, the first recommended course of treatment is to enter a medical detox program, followed by an intensive inpatient rehab program. However, it is not simply a lack of nutrition that causes nerve damage. The alcohol use itself is the most significant player in alcoholic polyneuropathy.
- The serotonin/norepinephrine re-uptake inhibitors (SNRIs), duloxetine and venlafaxine, have a well-documented efficacy in painful polyneuropathy [117, 118].
- The psychological impact of chronic conditions such as alcoholic neuropathy should not be underestimated.
What is alcohol-related neurologic disease?
Deficiencies in these nutrients can harm overall health and prevent nerves from functioning correctly. Some of the most common symptoms are numbness or tingling sensation of the extremities, pain or a burning sensation in the extremities, difficulty walking, difficulty urinating, and alcohol neuropathy difficulty talking or swallowing. However, experts still do not have a full understanding of how alcoholic neuropathy happens, which can make treatment challenging. In a 2019 article, researchers explain that breaking down alcohol in the body produces a chemical that damages axons.
ALN Pathophysiology
SSRIs have been studied in a few trials which have demonstrated a weak analgesic effect but the clinical relevance of these compounds is questionable [119]. Medication can help reduce some of the symptoms of alcoholic neuropathy. The most important strategy against alcoholic neuropathy lies in preventing the symptoms from getting worse by decreasing alcohol consumption as soon as possible.
Nutritional factors responsible for alcoholic neuropathy (indirect toxicity)
This condition is not just a result of the amount of alcohol consumed; it also hinges on the duration and consistency of consumption. The alcohol’s toxic effects on our nerves disrupt the intricate communication network between the brain, muscles, skin, and internal organs. Thirteen studies provided data from the biopsy of the sural nerve or the skin in patients with alcohol-related peripheral neuropathy. Alcohol-related peripheral neuropathy appears to be characterised by severe loss of myelinated fibres; and although profound small fibre loss can also be present, this appears to occur more variably [3, 51, 53, 59, 85]. The data indicates that there is both small and large fibre loss in alcohol-related neuropathy, but that small fibre loss is generally predominant [3, 51, 53, 56, 59, 63, 86].
Symptoms of alcohol-related nerve damage develop gradually over time, and can become worse without treatment. Until symptoms become serious, many people may ignore or neglect their neuropathy. What’s known is that symptoms of alcoholic neuropathy can affect various systems throughout the body.
Each case of alcoholic neuropathy is different and may require targeted treatments based on the patient’s medical needs. Once a person has stopped drinking, they can receive continued care for their nerve damage in addition to treatment for alcohol addiction. For the most part this review consists of non-interventional studies for which generally accepted tools to evaluate risk of bias are not available.
What Are the Causes of This Type of Nerve Damage?
Do not sell my personal information Privacy Policy and Terms of Use
- The subgroup without thiamine deficiency consisted of 36 patients, while the subgroup with thiamine deficiency consisted of 28 patients.
- Recently findings from our laboratory also suggest the benefecial effects of both α-tocopherol and tocotrienol, isoforms of vitamin E, in the prevention of hyperalgesia and allodynia in rats administered ethanol for 10 weeks [55].
- When you consume alcohol, it’s absorbed into your bloodstream from the stomach and the small intestine.
- 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.
- ALN can manifest differently, and patients might experience one, two, or even more clinical manifestations of ALN.