Alcoholic neuropathy is one of the most common adverse effects of chronic alcohol consumption. There is damage to the nerves due to the direct toxic effect of alcohol and the malnutrition induced by it. Patients present with pain, ataxia, and paresthesias in the lower extremities. 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.
Acetaldehyde
The authors concluded that malnutrition, including low blood concentrations of B vitamins, is not a prerequisite for the development of alcoholic neuropathy, and ethanol per se plays a role in the pathogenesis of alcoholic neuropathy. Coasting is a major feature of alcoholic neuropathy, largely due to chronic alcohol abuse. Even though much research was done in this area, still we do not have a full understanding of the mechanism of alcoholic neuropathy.
Role of caspases in alcoholic neuropathy
Patients were admitted and treated with a diet containing thiamine, nicotinic acid, pantothenic acid, pyridoxine, folic acid, and vitamin B12. This study found that the response to treatment depended upon the severity of neuropathy and whether there was severe cirrhosis. No patients with grade III (severe sensory impairment, absent reflexes, foot drop, muscle wasting) neuropathy showed clinical improvement over the 4-week period, but 4/8 did show an improvement over 3–6 months.
Treatment for alcoholic neuropathy
- Early diagnosis and treatment can help increase your chances of fully recovering.
- The only way to prevent alcoholic neuropathy is not to drink excessive amounts of alcohol.
- 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 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.
Thirteen studies provided data from the biopsy of the sural nerve or the skin in patients with alcohol-related peripheral neuropathy. Alcohol-related peripheral neuropathy appears to be characterised by severe loss of myelinated fibres; and although profound small fibre loss can also be present, this appears to occur more variably [3, 51, 53, 59, 85]. 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]. Peripheral neuropathy refers to damage or disease of the nerves that carry messages to and from the brain or spinal column and the rest of the body. More recent research, however, suggests that alcohol can directly damage nerves.
How is alcohol-related neurologic disease treated?
The medical community has recognized that addiction is a disease and some people are predisposed to it. As a result, it is usually necessary to get medical help to manage alcohol use disorder. In general, it takes years for alcoholic neuropathy to develop, alcohol neuropathy stages so a long-standing history of heavy alcohol use is typical. Some people experience a faster onset and progression of alcoholic neuropathy than others. It’s not completely clear why some people are more prone to this complication than others.
Effects due to nutritional deficiency
The majority of patients were middle-class, working men, and continuous drinkers were more affected than episodic drinkers. Women are more likely to develop alcohol polyneuropathy and suffer from a more rapid onset and greater severity. Biomarkers of alcohol abuse include carbohydrate-deficient transferrin (CDT) and phosphatidylethanol (PEth). 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. Alcoholic neuropathy, also called alcohol-induced peripheral neuropathy, is nerve damage in the body caused by the toxic effects of alcohol.
It has been recognized that spinal cord glial cells, astrocytes and microglia are activated by neuropathic pain or peripheral inflammation [42]. It is important to stop drinking if you suffer from alcoholic polyneuropathy in order to stop the disease from getting worse and to correct the nutritional imbalance that is damaging the nerves and interfering with the nervous system. A medical detox program followed by a comprehensive alcohol rehab program can manage alcoholism and help a person to get sober and stay that way. Many alcohol rehab programs help to manage co-occurring disorders, such as alcoholic polyneuropathy.
Alcohol can have significant negative effects on the central nervoussystem (CNS). Drinking alcohol can also have negative effects on the peripheral nervous system (PNS). The primary risk factor for alcoholic neuropathy is chronic consumption of large amounts of alcohol. The damage from alcohol neuropathy can affect the nerves that control movement, senses, and organ function. This can result in a variety of symptoms that affect different areas of the body. This article provides an overview of alcoholic neuropathy, including symptoms, causes, and diagnosis.
- Miyoshi et al. found that 5 weeks after ethanol treatment, the mechanical nociceptive threshold was significantly decreased and is further reduced up to 10 weeks [80].
- Vitamin E is used to refer to a group of fat-soluble compounds that include both tocopherols and tocotrienols.
- In 47 of these patients sural nerve biopsy was performed, with discrimination in terms of their thiamine status [3].
- Alcohol abuse causes a wide range of disorders that affect the nervous system.
- Alcoholic neuropathy is a condition in which the nerves become damaged as a result of years of heavy alcohol consumption.
- When significantly limiting or stopping alcohol consumption, receiving ongoing support is essential.