Alcoholic Neuropathy: Symptoms, Causes, and Treatment

The H-reflex and F-wave are measures of peripheral nerve conduction, often delayed or absent in alcohol-induced PN. Abnormalities in the F-wave response are a sensitive and early indicator of alcohol-induced PN. In general, the nerves in lower limbs were more affected than the upper limbs [3, 37–39]. Four studies reported abnormalities only in sensory nerves [33, 47, 63, 64], while ten reported abnormalities in both sensory and motor nerves [2–4, 16, 38, 54, 56, 58, 59, 65].

• People who drink too much may start to feel pain and tingling in their limbs.
• Joseph & Levine [71] suggested that activity in signaling pathways that ultimately lead to apoptosis plays a critical role in the generation of neuropathic pain, before death of sensory neurones becomes apparent.
• She also holds certifications in Reiki, Hypnotherapy, Neurolinguistics and Cranio-Sacral Therapy.
• However, neuropathy is generally an exclusion criterion for transplantation.

Has been contributing to medical fields including mental health and addiction since she retired from medicine; with over 19 years of practicing clinical experience. However, vulnerability to neuropathy and its severity and speed of progression varies. Women, continuous as opposed to episodic drinkers, and people with a family history of the disorder appear to be more vulnerable to alcoholic neuropathy and more severe presentations. Patients may also have a deficiency in vitamin B12 (cobalamin), affecting the axon and causing muscle weakness, sensory disturbances, and anemia. Vitamin B9 (folic acid) levels tend to be decreased, reducing the density of small and large nerve fibers.

Outlook of Alcoholic Neuropathy

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]. Progression of symptoms is usually gradual, continuing over months or years [2, 4]. Electrophysiologic and pathologic findings mainly indicate axonal neuropathy with reduced nerve fibre densities.

• Progressively, the sensory and motor symptoms and signs extend proximally into the arms and legs and finally the gait may become impaired [11].
• This study found that the response to treatment depended upon the severity of neuropathy and whether there was severe cirrhosis.
• The most important strategy against alcoholic neuropathy lies in preventing the symptoms from getting worse by decreasing alcohol consumption as soon as possible.

Learn how to recognize the signs and symptoms so you can connect patients with the resources they need. The use of warm or hot footbaths is a potential hazard in alcoholic neuropathy, because such treatment may cause burns to a patient with an insensate extremity. Consultation with a nutritionist may be indicated to help formulate strategies for replacement of essential nutrients in malnourished alcoholic patients. The only way to prevent alcoholic neuropathy is not to drink excessive amounts of alcohol.

Treatment & Therapy

Lee et al. [36] suggested that reactive oxygen species are importantly involved in the development and maintenance of capsaicin-induced pain, particularly in the process of central sensitization in the spinal cord in rats. Naik et al. [38] suggested the involvement of oxidative stress in experimentally induced chronic constriction injury of the sciatic nerve model in rats. Endoneural oxidative stress leads to nerve dysfunction in rats with chronic constriction injury [39].

Alcoholic neuropathy can affect both sensory and motor nerves, causing pain, hypersensitivity, numbness, muscle weakness, and lack of coordination and fine motor controls, largely in the extremities. Vitamin E is used to refer to a group of fat-soluble compounds that include both tocopherols and tocotrienols. Treatment with vitamin E was found to be beneficial in the treatment of patients with diabetic peripheral neuropathy [104] and neuropathic pain in streptozotocin-induced diabetic rats [105].

Risk Factors For Alcohol Polyneuropathy

Take the following steps if you suspect you have neuropathy from overconsumption of alcohol. Other options include community-based support offered by various organizations such as Self-Management and Recovery Training or Alcoholics Anonymous. Once alcohol enters the bloodstream is starts to be degraded by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) into acetate to be further metabolized.

• Home evaluations can be ordered to assess the safety, appropriateness, and functionality of the patient in the home.
• Consultation with a nutritionist may be indicated to help formulate strategies for replacement of essential nutrients in malnourished alcoholic patients.
• Transcutaneous electrical nerve stimulation may increase conduction through neurons and improve neuropathic pain.
• But if you have developed neuropathy as a result of alcohol use, it’s important to stop drinking as soon as possible.
• Excessive or heavy alcohol consumption is defined by the CDC when men have 15 or more drinks each week and women have 8 or more drinks each week.
• There are several studies suggesting the involvement of protein kinases in alcoholic neuropathy.

These roles are essential for nerve cell division during nerve tissue repair and rapid growth. Besides alcohol consumption, other causes of neuropathy may include non-alcohol-related nutritional imbalances, metabolic issues, infections, traumatic injuries, inherited, and exposure to toxins. However, it is most common among people with a history of heavy, long-term alcohol use. Esther has been with Hemet Valley Recovery Center since 2008, having over 16 years of experience in the field of Chemical Dependency. Esther received a Certificate of Achievement in Addiction Studies at San Diego City College and has been a certified CADCII since 2002.

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There are several studies suggesting the involvement of protein kinases in alcoholic neuropathy. Dina et al. [16] maintained rats on a diet to simulate chronic alcohol consumption in humans and found mechanical hyperalgesia by the fourth week which was maximal at 10 weeks. Thermal hyperalgesia and mechanical allodynia were also present with decreased mechanical threshold of C-fibres. The hyperalgesia was acutely attenuated by intradermal injection of nonselective PKC or selective PKCε inhibitors injected at the site of nociceptive testing.

Once a person has stopped drinking, they can receive continued care for their nerve damage in addition to treatment for alcohol addiction. Alcohol use leaves no one immune to nerve damage and other health-related issues. If you or someone you know struggles with alcohol use and addiction, the best way to prevent neuropathy is to seek professional treatment. Symptoms of alcohol-related nerve damage develop gradually over time, and can become worse without treatment. Until symptoms become serious, many people may ignore or neglect their neuropathy. Steven Collier RN is one of the co founders of the Hemet Valley Recovery Center and owner of Addiction Medicine Services Inc.

Treatment for Alcoholic Neuropathy

Without these transmissions, one can experience reduced sensation or a complete lack of sensation, among other symptoms. Myelin sheath is an insulating layer around the nerves that allows electrical alcoholic neuropathy recovery time impulses to transmit quickly and efficiently along the nerve cells. As Chief Financial and Legal Officer, Mrs. Clark is responsible for all financial planning, reporting and treasury functions.