If you drink alcohol, it’s important to understand how much alcohol can cause neuropathy and how to deal with this issue if you begin experiencing its symptoms. Benfotiamine, a synthetic derivative of vitamin B1, improves neuropathic pain and motor movement by increasing nerve conduction velocity. A nutritious diet; vitamin supplements, especially vitamins B1 and B12; and reduction of or abstinence from alcohol use is the only way to improve the patient’s PN by allowing nerves to slowly regenerate. The prevalence of alcohol-induced PN varies depending on demographics and the diagnostic criteria used in individual research studies. According to studies by the CDC, nearly 30% of adults in the US consume alcohol excessively.
- This often means the nerves, especially those farther away from the heart, become deficient.
- 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.
- Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy.
Alcoholic neuropathy has many of the same symptoms as peripheral neuropathy. For most, this includes a tingling, burning, or painful feeling in their legs, feet, arms, and hands. They may not feel strong sensations in these areas, either, due to the damage to the nerves. They may notice a weakness in their hands or that they have lost some of their coordination. Their balance can be affected due to the nerve damage in the legs and feet. Most patients with alcohol neuropathy initially present with symmetrical polyneuropathies in the lower distal extremities, however; heavier abuse can progress to distal upper extremity symptoms.
Biochemical Studies: Thiamine Deficiency vs. Utilization
The most common findings are sensory related and are varied to include pain, numbness, and paresthesias. Pain seems to be consistent through the literature to be one 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. Our muscles need to receive a message from nearby nerves in order to function. When this message is interrupted due to damaged nerves, the muscles cannot function as they normally would.
With fewer of these nutrients to go around, the body has to prioritize where the existing nutrients go. This often means the nerves, especially alcoholic neuropathy recovery time those farther away from the heart, become deficient. Needle EMG usually involves an evaluation of a proximal and distal muscle.
Harvard Health Publishing
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. In an animal study, it has been found that chronic alcohol consumption in rats resulted in a significant depletion in thiamine diphosphate (TDP), the active coenzyme form of thiamine. 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.
- However, recognizing the symptoms and seeking medical attention early can minimize the impact of the condition.
- Motor function of the tibial nerve was the next common [3, 11, 51, 54, 59, 63].
- Clinical correlation of signs and symptoms and close patient surveillance are essential.
- In agreement with this, one recent study has confirmed the efficacy of TCAs in central pain [116].
- The clinical presentation of alcohol-induced PN is similar to other etiologies of PN.
- Brian Obinna Obodeze is a professional health-niche content developer for AlcoRehab.org with six years of experience as a research writer.