However, if you have a history of substance use disorder or chronic alcoholics, you may be suggested to use alternatives to regular pain medications, like massage or acupuncture. Chronic heavy drinkers may be at risk for several different alcohol-related neurological issues. The most effective way to treat alcoholic polyneuropathy is to seek professional help from a medical doctor.

Conditions That May Mimic Alcoholic Neuropathy

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].

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The journal further reports that alcoholic polyneuropathy is likely caused by nutritional deficiencies and the depletion of thiamine that is caused by heavy and long-term drinking. It is most likely that drinking a lot of alcohol over several years causes direct damage to nerve cells and can also contribute to nutritional deficiencies in the body; these may both be factors in the onset of alcoholic polyneuropathy. Medical News Today publishes that medical procedures and therapies, medications, and adjunctive and alternative therapies are commonly used to treat alcoholic polyneuropathy. To diagnose alcoholic neuropathy, medical professionals will generally perform a few tests or exams to determine the severity of the disorder and what can be done to treat and manage the symptoms.

Relationship between alcoholic neuropathy and thiamine deficient neuropathy

But be sure you talk to your healthcare team before beginning a new exercise regimen because neuropathy can affect how you respond (or don’t respond) to injury or activities that risk injury. Before one of his patients begins exercising, Williams typically assesses the patient’s feet, degree of neuropathy, blood flow to the extremities, and their risk for deformities and foot ulcers. A demyelinating neuropathy in patients who present with symptoms summarized in clinical pattern #3 or #4 is highly suggestive for an immune-mediated neuropathy.

Miyoshi et al. [15] found that a significant decrease in the mechanical nociceptive threshold was observed after 5 weeks of chronic ethanol consumption in rats. Injection of (S)-2,6-diamino-N-[[1-(oxotridecyl)-2-piperidinyl]methyl] hexanamide dihydrochloride (NPC15437), a selective PKC inhibitor, once a day for a week after 4 weeks of ethanol treatment. Moreover, phosphorylated PKC was significantly increased in the spinal cord following chronic ethanol consumption.

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In addition to thiamine deficiency, recent studies indicate a direct neurotoxic effect of ethanol or its metabolites. Axonal degeneration has been documented in rats receiving ethanol while maintaining normal thiamine status [5]. Human studies have also suggested a direct toxic effect, since a dose-dependent relationship has been observed between severity of neuropathy and total life time dose of ethanol [6, 13].

• Increased nerve cross-sectional areas can be found in most patients with immune-mediated neuropathy, especially in an asymmetrical distribution in arm nerves and roots.
• Burning pain in the feet expending proximally in a stocking-glove distribution is often the most bothersome and typical symptom.
• The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies.
• The peripheral nerves transmit signals between the body, the spinal cord, and the brain.
• These functions are achieved by PKC mediated phosphorylation of other proteins [16].

Nutritional factors responsible for alcoholic neuropathy (indirect toxicity)

It is defined by axonal degeneration in neurons of both the sensory and motor systems and initially occurs at the distal ends of the longest axons in the body. This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally. Alcoholic polyneuropathy is caused primarily by chronic alcoholism; however, vitamin deficiencies are also known to contribute to its development.

Causes and Risk Factors of Neuropathy

However, in long-lasting neuropathies, distinguishing these two fundamentally different injury patterns is sometimes problematic, since also demyelinating neuropathies invariably go along with some (secondary) axonal degeneration. On the other hand, amplitude-dependent slowing of nerve conduction studies may lead to the false assumption of a primarily demyelinating disorder. Therefore, consented rules for diagnosing demyelination alcohol neuropathy are usually very strict [15]. The diagnosis of peripheral neuropathy necessitates a thorough workup of possible etiologies in order to identify treatable causes of this disease spectrum as early as possible. For instance, almost every 10th patient suffers from a polyneuropathy of autoimmune origin [1], which is amenable to causal (immunosuppressive or immunomodulatory) therapies and, therefore, must not be overlooked.