Symptoms & Treatment for Alcoholic Neuropathy

Treatment with vitamin E was found to be beneficial in the treatment of patients with diabetic peripheral neuropathy 104 and neuropathic pain in streptozotocin-induced diabetic rats 105. 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. We found more potent effects with tocotrienol as compared with α-tocopherol 55. Izumi et al. 73 also demonstrated that a single day of ethanol exposure in rats on post natal day 7 results in significant apoptotic neuronal damage throughout the forebrain after 24 h of ethanol administration. Thus, it is quite possible that chronic alcohol consumption is responsible for inducing neuropathy by activation of the caspase cascade drug addiction and may be an important target for the treatment of alcoholic neuropathy.

Increased Pain and Hypersensitivity

In addition, patients with chronic alcoholism tend to consume smaller amounts of essential nutrients and vitamins and/or exhibit impaired gastrointestinal absorption of these nutrients secondary to the direct effects of alcohol. These relationships make chronic alcoholism a risk factor for thiamine deficiency. 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.

Progressed disease

• Epidermal nerve fibre density was assessed in two studies, both of which supported decremental nerve fibre density distally in the lower limb, anecdotally supportive of a length-dependent pattern 53, 63.
• It has been demonstrated that incubation of neural cells with advanced glycation end products of acetaldehyde (AA-AGE) induced dose-dependent degradation of neuronal cells while the addition of AA-AGE antibodies reduced neurotoxicity 51, 90.
• In addition, they may order blood tests to check for vitamin and nutrient deficiencies.
• Intensive research has been done on medications like alpha-lipoic acid, benfotiamine, acetyl-l-carnitine, and methylcobalamin.
• A review of the human literature implicates nutritional deficiencies, most often thiamine deficiency, that are common in alcoholic patients, as commonly accompanying complicating factors in the development of this neuropathy.

Thus, ALN might be induced by the combination of the effects of the direct activity of alcohol metabolites on the nerve fibers along with nutritional deficiencies primarily in a form of thiamine deficiency. In one clinical study, aimed at studying distinct clinicopathologic features of alcoholic neuropathy, 64 patients were assessed. In 47 of these patients sural nerve alcholic neuropathy biopsy was performed, with discrimination in terms of their thiamine status 3. The ethanol consumption of these patients was more than 100 g day–1 for more than 10 years. The subgroup without thiamine deficiency consisted of 36 patients, while the subgroup with thiamine deficiency consisted of 28 patients. In addition, 32 patients with nonalcoholic thiamine deficiency neuropathy were also evaluated for comparison.

Signs Of Alcohol Use Disorder

Valproate demonstrated varying effects in different studies of https://ecosoberhouse.com/ neuropathic pain, with three studies from one group reporting high efficacy 125–127 and others failing to find an effect 128, 129. N-acetylcysteine, an amino acid, is a potent antioxidant and helps to enhance glutathione concentrations. N-acetylcysteine may have application in the prevention or treatment of neuropathy.

Synthesis of results

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. Progression of the disease leads to symmetrical ascending motor and sensory deficits.

The only way to prevent alcoholic neuropathy is not to drink excessive amounts of alcohol. Thus, further preclinical and clinical studies are required to assess of this molecule in alcoholic neuropathy. Treatment for alcoholic neuropathy first focuses on stopping or significantly reducing alcohol intake. Early treatment and abstinence from alcohol are the most important elements for treating alcoholic neuropathy effectively.

Symptoms of Alcoholic Neuropathy

• 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.
• However, there is poor compliance on the part of patients, resulting in the progression of the condition and ultimately, poor quality of life.
• Constant pain in the hands or feet is one of the most bothersome aspects of alcoholic neuropathy.
• Other vitamin deficiencies seen with alcohol abuse include but are not limited to, B vitamins, folic acid, and vitamin E.
• Long-term heavy alcohol use, particularly when accompanied by nutritional deficiencies, can damage the body’s nerves, leading to a host of painful and debilitating symptoms.
• There are many studies suggesting the role of MEK/ERK signaling in inflammatory pain in male 60–63 and female rats 64.

There are several studies suggesting the involvement of protein kinases in alcoholic neuropathy. Dina et al. 16 maintained rats on a diet to simulate chronic alcohol consumption in humans and found mechanical hyperalgesia by the fourth week which was maximal at 10 weeks. Thermal hyperalgesia and mechanical allodynia were also present with decreased mechanical threshold of C-fibres.