Alcoholic Neuropathy: Symptoms, Causes, and Treatment

Fortunately, after receiving a diagnosis, people with alcoholic neuropathy can make healthy changes to minimize symptoms and receive help for chronic alcohol use. In a study by Mellion et al. (2013) with three different strains of rats, they investigated the effects of alcohol exposure on nerves and muscles. This phenomenon varied according to different susceptibility of genetic patterns, suggesting that nerve injury is influenced by individual genetic characteristics, in addition to chronicity and ingested volume of alcohol (Goldman et al., 2005, Mellion et al., 2013). It includes more than 30 independent observation parameters, which are grouped into domains. The domains are neurological, autonomic, and behavioral; each one with its measurement and evaluation parameters (Boucard et al., 2010). This test is commonly used in studies of neuropathic disorders, and it is easily replicable.

• The peripheral nerves also send sensory information to the central nervous system through sensory nerves.
• This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally.
• Current postulation holds that dysfunctions within the central and peripheral nervous system are due to both direct and indirect toxic effects of alcohol [31, 85,86,87].
• Neuropathic syndromes may develop from diabetes mellitus, vasculitis secondary to immune-mediated diseases, genetic disorders, malignancies, infections, vitamin deficiencies, medications, toxins, trauma, compression, and chronic heavy alcohol consumption.
• Taking these medications at bedtime may be indicated because of their sedative effects.

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. Not only mGluRs but ionotropic glutamate (NMDA) receptors are also involved in alcoholic-induced neuropathic pain. Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy. Chronic alcoholism can alter the intake, absorption and utilization of various nutrients (nicotinic acid, vitamin B2, vitamin B6, vitamin B12, folate or vitamin E). Deficiencies of B vitamins other than thiamine also may contribute to variation in clinical features, but characteristic symptoms of multiple vitamin deficiency were not seen in patients with thiamine deficiency neuropathies due to gastrectomy and dietary imbalance [26].

Alcohol addiction treatment

Thiamine deficiency resulted in the progression of sensory dysfunctions; further, histological examination of the sural nerves revealed the loss of small nerve fibers and segmental demyelination. Patients with non-alcoholic thiamine deficiency neuropathy showed more abrupt onset of symptoms, mainly in a form of motor dysfunctions; biopsy showed damage to greater fibers with subperineurial edema. ALN with thiamine deficiency was manifested as a variable mixture of these symptoms. It was proposed that ALN pathogenesis, besides thiamine deficiency itself, could be due to its inappropriate use in the organism or transketolase deficiency [150]. Further, alcohol impairs vitamin B1 absorption and its storage in the liver [151,152,153]. Alcohol abuse affects the peripheral and the central nervous system adversely.

There are several possible causes of neuropathy, and knowing about a person’s alcohol intake can help the doctor to make an accurate diagnosis. Some researchers estimate that 65 percent of people in the United States who have been diagnosed with alcohol use disorder also have alcoholic neuropathy. The medical community has recognized that addiction is a disease and that some people are predisposed to it. As a result, it is usually necessary to get medical help to manage alcohol use disorder. While not specifically approved for the treatment of alcoholic neuropathy, antidepressants are often prescribed to help control the pain. Constant pain in the hands or feet is one of the most bothersome aspects of alcoholic neuropathy.

Other areas of the body

Vitamin B9 (folic acid) levels tend to be decreased, reducing the density of small and large nerve fibers. Important in carbohydrate metabolism and neuron function, vitamin B3 (niacin) may also be decreased. Early alcoholic neuropathy, usually presenting as sensory symptoms in the extremities, is reversible if the patient stops drinking and establishes proper nutrition. However, more severe cases may be intractable, even with abstinence, and lead to lifelong impairment. Thus, treatment with TCAs may provide symptomatic relief in patients with alcoholic neuropathy.

CDT is an indirect metabolite of ethanol and constitutes either a marker of prolonged, heavy alcohol consumption or a marker of relapse. Peth on the other hand is a direct alcohol metabolite that can be measured to monitor alcohol consumption as well as for the identification of early signs of alcohol-related clinical manifestations. Other non-specific biomarkers useful in the diagnosis of alcohol use disorder are gamma-glutamyl transferase (GGT), mean corpuscular volume (MCV) of the red blood cells, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Generally symmetrical, peripheral nerve damage may be focal, multifocal, or diffuse. A variety of sensory, motor, and autonomic symptoms develop over months to years and worsen with time.

Methylcobalamin for the treatment of peripheral neuropathy

FOB was performed immediately after last session of alcohol and before perfusion by two independent observers, who examined the reactivity of each animal to manipulation and stimuli, such as behavioral changes, motor activity, coordination, and sensory-motor reflex responses. During the initial stages of ALN, the disease may appear asymptomatic and demonstrable only on electroneurographic investigation [71, 111, 112]. Because ALN is a length-dependent axonopathy, it manifests mainly in a “stocking-glove” https://ecosoberhouse.com/ form, affecting the lower extremities at the beginning [28, 113]. The main symptoms of ALN include dysesthesia, paresthesia, numbness, and pain in the lower extremities which progressively reach higher parts of the body [114,115,116,117]. The pain is described as burning, cramp-like, or itching; also, a common symptom is a subjective feeling of cold in both feet [118,119,120,121,122,123]. The symptoms deteriorate through touch and pressure which intensify pain while standing or walking [124].

It may also be that comorbid hepatic dysfunction is a risk factor for alcohol-related peripheral neuropathy. Further studies are required to develop a greater understanding of the interaction these entities. Regarding the autonomic domain, our findings were just significant for piloerection.

Thus, from the above discussion it is clear that stress hormones, catecholamines and glucocorticoids, from the sympatho-adrenal and HPA neuroendocrine stress axes, respectively, play a very important role in initation and maintenance of alcoholic neuropathy. The combined actions of catecholamines and glucocorticoids, via their receptors on sensory neurones, demonstrate a novel mechanism by which painful alcoholic neuropathy is induced and maintained. The most important strategy against alcoholic neuropathy lies in preventing the symptoms from getting worse by decreasing alcohol consumption as soon as possible.

• This phenomenon varied according to different susceptibility of genetic patterns, suggesting that nerve injury is influenced by individual genetic characteristics, in addition to chronicity and ingested volume of alcohol (Goldman et al., 2005, Mellion et al., 2013).
• During a 72-hour period of alcohol withdrawal, the dependent group developed allodynia.
• The sural nerve was the most commonly reported nerve [2, 3, 5, 11, 27, 37,38,39, 51, 53, 59, 63, 68].
• Dr. Roberto and her team are continuing to investigate how the inflammatory proteins identified in this study might be used to diagnose or treat alcohol-related chronic pain conditions.
• Other studies have shown a direct, negative effect from alcohol and its many metabolites on the nervous system.

This activity describes the evaluation and management of alcoholic neuropathy and reviews the role of the interprofessional team in improving care for patients with this condition. Clinical features of alcoholic peripheral neuropathy develop slowly, extending over a period of months and include abnormalities in sensory, motor, autonomic and gait functions. Painful sensations with or without burning quality represent the initial and major symptom of alcoholic neuropathy [2, 4]. Later on, weakness appears in the extremities, involving mainly the distal parts. Progressively, the sensory and motor symptoms and signs extend proximally into the arms and legs and finally the gait may become impaired [11].

Workup in alcoholic neuropathy

The Foundation for Peripheral Neuropathy and the US Food and Drug Administration estimate that 20 million people in the US experience PN. Neuropathic syndromes may develop from diabetes mellitus, vasculitis secondary to immune-mediated diseases, genetic disorders, malignancies, infections, vitamin deficiencies, medications, toxins, trauma, compression, and chronic heavy alcohol consumption. In general, the nerves in lower limbs were more affected than the upper limbs [3, 37,38,39].

By Heidi Moawad, MD

Heidi Moawad is a neurologist and expert in the field of brain health and neurological disorders. Dr. Moawad regularly writes and edits health and career content for medical books and publications. Heidi Moawad is a neurologist and expert in the field of brain health and neurological disorders. Some of the most common symptoms are numbness or tingling sensation of the extremities, pain or a burning sensation in the extremities, difficulty walking, difficulty urinating, and difficulty talking or swallowing. Once alcohol use has been addressed, your doctor can focus on the neuropathy itself.