Alcoholic Neuropathy: Symptoms, Causes, and Treatment

Supplementation with benfotiamine significantly increased concentrations of TDP and total thiamine compared with supplementation with thiamine HCl 96. An 8 week, randomized, multicentre, placebo-controlled, double-blind study compared the effect of benfotiamine alone with a benfotiamine complex (Milgamma-N) or placebo in 84 alcoholic patients. 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.

• Clinical features of alcoholic peripheral neuropathy develop slowly, extending over a period of months and include abnormalities in sensory, motor, autonomic and gait functions.
• Alcohol-related neuropathy can go away if you stop consuming alcohol and follow your treatment plan.
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Neurological Effects of Alcohol

The evidence points toward alcohol-related peripheral neuropathy being a form of toxic neuropathy, rather than nutritional neuropathy. They get worse with more alcohol consumption, so if you stop drinking and seek professional medical attention, you can manage the symptoms of the disorder and potentially keep the nerve damage from worsening. Alcoholic polyneuropathy is progressive and gets worse over time, as the damage to the nerves increases with continued alcohol abuse. The problems that alcoholic neuropathy causes with muscle weakness, balance, and coordination can make a person more at risk for falling down and getting injured. Not being able to tell when things are too hot because of the way the nerve damage interferes with the ability to sense temperature changes can make one more susceptible to alcohol neuropathy stages burns.

Can alcohol cause pain in your feet?

This causes a snowball effect within the body, all the way to the molecular level. According to the National Institutes of Health (NIH), it is estimated that about half of those who have heavy alcohol intake will develop alcoholic polyneuropathy at some point in their life. 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. Oxidative stress also leads to the indirect damage of nerve fibers via the release of free radicals and proinflammatory cytokines with protein kinase C and ERK kinase phosphorylation 98,99,100,101. Besides, ALN is characterized by insulin and insulin-like growth factor (IGF) resistance, which results in impaired trophic factor signaling 102, 103.

Progressive & Permanent Side Effects

Miyoshi et al. found that 5 weeks after ethanol treatment, the mechanical nociceptive threshold was significantly decreased and is further reduced up to 10 weeks 80. As supported by immunostaining, the membrane fraction showed that spinal mGluR5 concentrations in ethanol-treated rats were significantly increased compared with those in the control diet group. These findings support the idea that the increased number of membrane-bound mGluR5 following chronic ethanol consumption may lead to a long lasting activation of neuronal protein kinase C in the dorsal horn of the spinal cord. This phenomenon may be responsible for the induction of the neuropathic pain like behaviour following chronic ethanol consumption.

Oxidative-nitrosative stress and alcoholic neuropathy

The US National Library of Medicine (NLM) warns that around 50 percent of long-term heavy drinkers will suffer from alcoholic neuropathy. The chronic effects of alcohol abuse are myriad and include neurologic complications through both direct and indirect effects on the central and peripheral nervous systems. These disorders include several encephalopathic https://ecosoberhouse.com/ states related to alcohol intoxication, withdrawal, and related nutritional deficiencies; acute and chronic toxic and nutritional peripheral neuropathies; and myopathy.

• If liver damage is evident, appropriate consultation with a transplantation service is recommended.
• The journal further reports that alcoholic polyneuropathy is likely caused by nutritional deficiencies and the depletion of thiamine that is caused by heavy and long-term drinking.
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• A treatment protocol for alcohol withdrawal, including a titrating schedule of benzodiazepines, was implemented, and over the next 4 days he had close cardiac and neurologic ICU monitoring.