Neurologic disorders can include fetal alcohol syndrome, dementia, and alcoholic neuropathy. 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 aim of this systematic review is to characterise the presentation of alcohol-related peripheral neuropathy, to determine the typical ancillary test results, to establish the importance of various risk factors and to explore the likely pathogenetic mechanisms. Due to the breadth of the literature surrounding this topic, this review shall focus exclusively upon peripheral neuropathy, without discussing autonomic neuropathy. Antiepileptic drugs, such as the gamma aminobutyric acid (GABA) analogue (gabapentin), have proven helpful in some cases of neuropathic pain.

Our program will not only address the alcoholism that resulted in neuropathy, but also the underlying reasons for the alcohol abuse such as co-occurring mental health disorders. Contact us to learn more about our alcohol addiction treatment programs and begin your journey to recover today. One of the main mechanisms behind alcohol-induced nerve damage is the depletion of essential nutrients, particularly vitamin B1 (thiamine) and B12. Thiamine deficiency, coupled with the toxic effects of alcohol on nerve tissue, leads to the deterioration of nerve health and function. Alcohol also contributes to liver damage, impairing the body’s ability to absorb and utilize vital nutrients.

Methylcobalamin for the treatment of peripheral neuropathy

Avoiding alcohol and improving your diet can sometimes lead to a moderate to full recovery. While peripheral neuropathy generally cannot be cured, there are several medical treatments that can be used to manage the pain of alcoholic neuropathy, aiding in your recovery. Treating the alcohol use disorder, along with the health problems caused by chronic, heavy drinking, may be possible.

These abnormal proteins influence other cell populations especially the hepatocytes where the damage to hepatic mitochondria results in hepatic cirrhosis with reduction of energetic substrates in the liver. The action of these abnormal proteins is explained by competition with normal proteins causing the damage to function and metabolism of the cell [22]. The role thiamine plays in the pathogenesis and treatment alcohol neuropathy stages 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 problem (Fig. 1).

Treatment

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]. Alcohol-induced peripheral neuropathy (PN) is a chronic and painful condition in which the neurotoxic effects of alcohol and nutritional deficiencies cause a pathologic response in nerve function. This article presents the pathophysiology, signs and symptoms, diagnostic approaches, treatment options, and nursing care of patients with alcohol-induced PN.

Moreover, WE and KS can lead to sudden unexpected death due to injury in cardiorespiratory centers of the brainstem. Regarding the parasympathetic division of ANS, most of the studies are focused on the assessment of nerve conduction mainly in oculomotor and vagus nerves; these include pupil cycle time (PCT) and cardiovascular reflex tests correspondingly [160]. Further, ECG changes and functions of the digestive tract (dyspeptic symptoms, stomach and gallbladder motility, orocecal transit time) can also be assessed [162, 165]. PCT seems to be valuable due to the correlation between prolongation of pupil oscillation and exacerbations of cardiovascular symptoms which presents the colinear involvement of parasympathetic division of ANS. ALN can manifest differently, and patients might experience one, two, or even more clinical manifestations of ALN. Patients who have ALN might present such symptoms as cramps, impaired movement of the limbs, muscle atrophy, muscle weakness, spasms, or contractions, loss of sensation, or feeling of tingling.