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].
Progressive & Permanent Side Effects
It has been demonstrated that incubation of neural cells with advanced glycation end products of acetaldehyde (AA-AGE) induced dose-dependent degradation of neuronal cells while the addition of AA-AGE antibodies reduced neurotoxicity [51, 90]. Other findings showed that decreased activity of aldehyde dehydrogenase leads to peripheral neuropathy [76, 91]. 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. In general, the nerves in lower limbs were more affected than the upper limbs [3, 37–39].
History and Physical
The subgroup without thiamine deficiency, considered to be a pure form of alcoholic neuropathy, uniformly showed slowly progressive, sensory dominant symptoms. Superficial sensation, especially nociception, was predominantly impaired and painful symptoms were the primary complaint in most patients in this group. In contrast, the neuropathic symptoms of nonalcoholic thiamine deficiency neuropathy, considered to be identical to beriberi neuropathy [26], were variable, but typically were motor dominant and acutely progressive, affecting both superficial and deep sensation. The histologic features of sural nerve biopsy specimens demonstrated small fibre predominant axonal loss as characteristic of the pure form of alcoholic neuropathy.
Other areas of the body
Females, generally tend to drink less alcohol, are better abstainers, and present the smaller probability of the development of alcohol-related diseases [127, 128]. However, compared to males, the symptoms of excessive alcohol consumption manifest earlier in females [129, 130]. Alcohol-related liver cirrhosis may occur even a few years earlier in females compared to males [131]. The prevalence of alcoholic cardiomyopathy appears to be similar among males and females; however, males present a higher disease burden [132, 133].
Alcohol-related peripheral neuropathy: a systematic review and meta-analysis
The evidence of positive dynamics at peripheral and segmental nerve system level was supported by neurophysiological data. Benfotiamine was found to be beneficial in patients with alcoholic polyneuropathy [98]. Alcoholic neuropathy is a debilitating condition resulting from prolonged excessive alcohol consumption, leading to nerve damage throughout the body. This condition manifests when ethanol alcohol neuropathy stages in alcohol and its metabolites, like acetaldehyde, harm nerve tissues, disrupting their normal functions. Over time, chronic alcoholism can deplete the body of essential nutrients, particularly B vitamins like thiamine, which are crucial for nerve health. This deficiency, combined with the toxic effects of alcohol on nerve cells, precipitates the development of neuropathic symptoms.
Study characteristics
Neuropathy has multifactorial causes, ranging from nutritional deficiencies to the toxic effects that alcohol has on neurons. Because of the many effects that alcohol has on the organism, it is important that patients with alcoholic neuropathy be managed by a team of inter-professionals in the health industry. However, there is poor compliance on the part of https://ecosoberhouse.com/article/alcohol-and-dopamine-how-does-it-affect-your-brain/ patients, resulting in the progression of the condition and ultimately, poor quality of life. While one may find relief from conventional treatment, the addictive nature or side effects of some medications makes it undesirable to use it for the long term. These treatments, in some cases, only suppress the symptoms but do not treat the underlying pathology.
- This could lead to disability, chronic pain, and damage to your arms and legs.
- The Peripheral Neuropathy Research Registry (PNRR) is a unique and invaluable resource to researchers and patients alike.
- Peripheral neuropathy can have many causes unrelated to alcohol consumption, and it was previously thought that when it was found in alcoholics it was merely the result of poor nutrition in alcoholics as well as alcohol’s direct impact on nutrients.
- Axons are the groups of nerve fibers that carry impulses between the brain and the nervous system.
- Nerves that are part of the autonomic nervous system help to regulate heart rate, body temperature, respiration, and blood pressure.
- Subperineurial oedema is more prominent in thiamine deficient neuropathy, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier is more frequent in alcoholic neuropathy [3].
- This dual strategy is essential to manage the condition effectively and improve our quality of life.
- Symptoms of AAN are due to impairments in both sympathetic and parasympathetic autonomic fibers of the cardiovascular, digestive, and urogenital systems.
- 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).