Sign up for free and stay up to date on research advancements, health tips, current health topics, and expertise on managing health. Lauren Smith has worked as a journalist and copywriter for the last decade, covering a range of topics including health, energy, and technology in the US and UK. Some tests can be performed by a doctor to rule out other causes of neurologic symptoms. But according to the Centers for Disease Control and Prevention (CDC), drinking less or not at all may help you avoid neurological harm.
- The reason for better results in the benfotiamine alone group than in the Milgamma-N group, despite the fact that the benfotiamine dosage was equivalent, is not completely understood.
- 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].
- Ethanol and its toxic degradation metabolites affect neuronal metabolism including the metabolic pathways of nucleus, lysosomes, peroxisomes, endoplasmatic reticulum and cytoplasm [21].
- There are no medications that can help improve loss of sensation, strengthen muscle weakness, or assist with the coordination and balance problems caused by alcoholic neuropathy.
Medical Professionals
Electromyography and nerve conduction tests are performed in order to reveal signs of ALN. Sensory functions and reflexes can be tested during a neurological examination. Once you stop alcohol intake, a doctor can address your specific symptoms. Doctors tailor specific treatments and alcohol abstinence programs to the individual. The alcohol will continue to circulate in the bloodstream and eventually affect other organs.
History and Physical
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]. Recently findings from our laboratory also suggest the benefecial effects of both α-tocopherol and tocotrienol, isoforms of vitamin E, in the prevention of hyperalgesia and allodynia in rats administered ethanol for 10 weeks [55]. We found more potent effects with tocotrienol as compared with α-tocopherol [55].
Prevalence of alcoholic neuropathy
To determine the functions of the sympathetic division of the autonomic nervous system (ANS), sympathetic skin response (SSR) is used; the abnormal results of this test suggest subclinical transmission impairments [162]. Navarro et al. (1993) showed that nearly half of the alcohol-dependent patients without AAN symptoms and any aberrations in electrophysiologic studies presented abnormal alcohol neuropathy stages SSR results [163]. In a similar study, SSR was used to assess the number of reactive sweat glands (SGN), which turned out to be decreased in alcohol-dependent patients [164]. 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.
- Thus, deficiency of these vitamins was felt to be unlikely in Danish beer drinkers at that time and, indeed, measured vitamin concentrations were mostly normal.
- Several treatment options and interventions can help a person recover from alcohol dependence.
- 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.
- Not only mGluRs but ionotropic glutamate (NMDA) receptors are also involved in alcoholic-induced neuropathic pain.
- It was shown that patients with liver cirrhosis (regardless of its etiology) present dysfunctions in ANS, primarily within the vagus nerve [170].
Further, alcohol impairs vitamin B1 absorption and its storage in the liver [151,152,153]. ALN is characterized by spontaneous burning pain, hyperalgesia, and allodynia. Besides, the key mechanism of chronic pain includes the long-term potentiation of glutamatergic transmission. The percentage of alcohol-dependent patients affected by ALN is estimated to be 66% [50, 51]. 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]. An essential risk factor regarding the etiology of ALN is the amount of alcohol consumed throughout the years since alcohol displays direct toxicity on nerve fibers [55].
Malnutrition and Micronutrients Deficiency
Nerves that are part of the autonomic nervous system help to regulate heart rate, body temperature, respiration, and blood pressure. Polyneuropathy involves damage to more than one nerve at the same time, usually multiple nerves throughout the peripheral nervous system and all over the body. Thiamine serves as an important coenzyme in carbohydrate metabolism and neuron development. The lack of thiamine in the nervous system affects the cellular structure and can cause cell membrane damage and irregular ectopic cells. Other vitamin deficiencies seen with alcohol abuse include but are not limited to, B vitamins, folic acid, and vitamin E. Poor absorption and low intake of these vitamins have clinical features of dermatitis, neuropathy, and anorexia.
- 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.
- Dr. Moawad regularly writes and edits health and career content for medical books and publications.
- Painful sensations with or without burning quality represent the initial and major symptom of alcoholic neuropathy [2, 4].
- 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.
- The primary axonal damage and secondary demyelination of motor and sensory fibres (especially small diameter fibres) are considered to constitute the morphologic basis of alcoholic damage to nerve tissue at present [20].