What is Alcoholic Neuropathy? Causes, symptoms, & treatment

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). Thus, these vitamin deficiencies were not considered to be major causal factors of neuropathy [26]. Similarly to acupuncture, an electric stimulus delivered to acupuncture points activates nerve fibers and produces analgesic effects [66]. A systematic review pointed out that acupuncture-E effectively decreased CIPN pain compared to Vitamin B [21].

ALN Pathophysiology

The treatment rests on abstinence from alcohol and the replacement of key nutrients. Unfortunately, patient compliance is poor, and the condition often progresses, leading alcohol neuropathy stages to poor quality of life. Behse & Buchthal [31] compared 37 Danish patients with alcoholic neuropathy with six patients with nonalcoholic post gastrectomy polyneuropathy.

• 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.
• Excessive, long-term consumption of alcohol can lead to malnutrition as well as nerve damage, and both contribute to the development of alcoholic neuropathy.
• The pathophysiology of ALN involves underlying mechanisms that include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters [52,53,54].
• What is crucial during ALN treatment is the alleviation of the major causation of ALN which is alcohol abuse.
• A recent global alcohol abuse report indicated that approximately 3 billion people consume alcohol worldwide (Global Status Report on Alcohol and Health, 2016).
• 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.

Motor symptoms

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Types and symptoms of alcohol-related neurologic disease

However, if caught early enough, you can minimize the damage from alcoholic neuropathy. Avoiding alcohol and improving your diet can sometimes lead to a moderate to full recovery. Fortunately, after receiving a diagnosis, people with alcoholic neuropathy can make healthy changes to minimize symptoms and receive help for chronic alcohol use. 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).

Antidepressants for the alleviation of neuropathic pain symptoms

Among patients with chronic alcohol use disorder, neuropathy is the most common harmful sequelae. It is estimated that in the United States, 25% to 66% of chronic alcohol users experience some form of neuropathy; however, the true incidence in the general population is unknown. The majority of patients were middle-class, working men, and continuous drinkers were more affected than episodic drinkers.

Oxidative-nitrosative stress and alcoholic neuropathy

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. According to a 2017 review, muscle myopathy is common in alcohol use disorder. In addition, about 40 to 60 percent of people who experience chronic alcohol misuse also experience alcohol-related myopathy. Researchers have not determined if this is caused by the effects of alcohol on the brain or is the result of thiamine deficiency.

• One patient with grade III neuropathy responded with the correction of low circulating vitamin B6.
• Chronic alcohol consumption leads to malnutrition with dysfunctions in protein and lipid metabolism which affect the metabolic pathways and progression of ALN symptoms within the central and peripheral nervous systems [89].
• Avoiding alcohol is the best way to treat these conditions and relieve symptoms.

Perfusion and Nerve Dissection

• 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.
• Alcohol misuse can lead to neurological damage that can affect multiple areas of a person’s health and well-being.
• Alcoholic neuropathy can result in hypersensitivity to touch and even resting pain.
• Accumulating evidence suggests a pivotal role for metabotropic glutamate receptors (mGluRs) in nociceptive processing, inflammatory pain and hyperalgesia [74, 75].

Use of this website and any information contained herein is governed by the Healthgrades User Agreement. © Copyright 2024 Healthgrades Marketplace, LLC, Patent US Nos. 7,752,060 and 8,719,052. The diagnostic process may https://ecosoberhouse.com/ involve neurological examination, blood tests, and electromyography. She has over a decade of direct patient care experience working as a registered nurse specializing in neurotrauma, stroke, and the emergency room.

• Nevertheless, heavy alcohol drinkers are usually significantly malnourished because of the improperly balanced diet and impaired absorption of the essential nutrients and elements [58, 59].
• Acupuncture-E effectively reduced CIPN symptoms in a study in which they improved motor and sensory disorders, especially by contributing to increased sensory nerve conduction velocity [20, 21].
• However, it is known to be directly related to heavy and long-term alcohol consumption.
• You may also benefit from a support group to help you reduce your drinking or completely quit drinking alcohol.
• Patients were admitted and treated with a diet containing thiamine, nicotinic acid, pantothenic acid, pyridoxine, folic acid, and vitamin B12.
• Alcohol administration protocols that induce nervous tissue damage vary from a four-day acute intoxication (Crews et al., 2004) to 40 weeks of chronic consumption (Dlugos, 2006).