Alcohol-related peripheral neuropathy: a systematic review and meta-analysis PMC

It also appears that the addition of NCS may improve the identification of alcohol-related peripheral neuropathy. Peripheral neuropathy happens when the nerves that are located outside of the brain and spinal cord (peripheral nerves) are damaged. This condition often causes weakness, numbness and pain, usually in the hands and feet. It also can affect other areas and body functions including digestion and urination.

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. 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. The authors hypothesized that vitamins B6 and B12 might have competed with the effects of vitamin B1 in the Milgamma-N group [97]. In another small Russian study, 14 chronic alcoholic men with polyneuropathy were given 450 mg benfotiamine daily for 2 weeks, followed by 300 mg daily for an additional 4 weeks. During the treatment the regression of neuropathy symptoms, other sensor and movement disorders were observed.

Enhancing Healthcare Team Outcomes

Hawley et al. followed up 11 patients with alcohol-related neuropathy who were abstinent from alcohol and who had begun to consume a normal diet [67]. This identified improvement in sensory symptoms within a few days and a clinical improvement in strength over a period of weeks to months, but in up to 2 years in the most severe cases. There was not however, alcohol neuropathy complete resolution of symmetric neuropathy with persistent mild loss of vibration sense or pinprick sensation in the feet or loss of ankle tendon reflexes. Four studies addressed the management of patients with alcohol-related peripheral neuropathy. These studies addressed abstinence from alcohol consumption and administration of vitamins.

The role thiamine plays in the pathogenesis and treatment of ALN is still unclear. The possibility that thiamine may be a cofactor or modulating factor, but not the main etiologic factor causing ALN, has to be entertained. This possibility opens the door to consideration of other possible causes, including problems with thiamine utilization unique to alcohol abuse or alcohol as a direct neurotoxin in which thiamine deficiency may be a superadded https://ecosoberhouse.com/article/relation-between-alcohol-and-dementia/ problem (Fig. 1). As yet there is no effective therapeutic intervention available for relieving the neuropathic pain due to chronic alcohol consumption. Thus there is a need to understand the basic pathophysiological mechanisms involved in alcohol induced neuropathic pain so that new therapeutic modalities targeting disrupted molecular events can be developed for prevention as well as clinical management of alcoholic neuropathy.

Alcoholic neuropathy Menu

A longitudinal study of nerve conduction velocity in children who had prenatal exposure to greater than 2 oz. Of absolute alcohol per day also confirmed the neurotoxicity of alcohol to peripheral nerves.46 Seventeen exposed children were compared with 13 non-exposed children at birth and again at 12–14 months of age. The exposed children had significantly slowed velocities and reduced amplitudes in the ulnar and tibial motor nerves at birth.

Although the clinical and animal studies have focused on nutritional deficiency, biochemical studies provide evidence that alcohol may affect thiamine utilization rather than cause thiamine deficiency. Thiamine levels in the ALN group were comparable to those of normal subjects, whereas there was a significantly lower concentration among those in the Wernicke–Korsakoff group. The transketolase activity was lower in both groups as compared with controls.10 The investigators suggested that thiamine utilization rather than lack of thiamine itself was implicated in the development of ALN.

Food and water consumption; body mass variation; alcohol intake and its concentration in the blood

But there is always some amount of acetaldehyde that will not get metabolized and which will bound to proteins. The dissection of the sciatic nerves was performed at the origin of the nerve between L5 and S1 segments to tibiofibular bifurcation. Each slice was fixed in buffered 2.5% glutaraldehyde and stored in the same fixative for subsequent dehydration and embedding in Epon resin 812.

• The exact mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed.
• If liver damage is evident, appropriate consultation with a transplantation service is recommended.
• The abnormalities were usually of reduced amplitude, in keeping with axonal loss [2, 3, 5, 11, 12, 16, 21, 27, 37–39, 47, 51, 53, 54, 56, 63–68].
• The disease manifests itself through a tingling sensation in the limbs, caused by nerve and brain damage from alcohol consumption.
• The mechanism of this is presently unclear, one possible explanation is that is resolves concomitant vitamin-dependent neuropathy which exacerbates alcohol-related neuropathy.