The diagnosis of alcoholic neuropathy involves a combination of medical history, physical examination, and possibly blood tests or nerve tests such as electromyography (EMG) and nerve conduction studies (NCV). In this study, we observed that Wistar rats that consumed alcoholic solution (20%; v/v) for eight weeks showed initial signs of demyelinating lesions in the peripheral nervous system. Furthermore, based on the mean severity score (MSS) of FOB, dysfunctions in the AL group in neurological, autonomic, and behavioral domains over untreated animals were also shown.
Neurological Conditions Affect 1 in 3 Globally – Healthline
Neurological Conditions Affect 1 in 3 Globally.
Posted: Thu, 21 Mar 2024 07:00:00 GMT [source]
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. This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency. Treatment may involve nutritional supplementation, pain management, and abstaining from alcohol.
Coping With Alcoholic Neuropathy
Later, the results have been supported by Victor and Adams (1961)—among 12 patients with ALN, neuropathic symptoms were alleviated just after thiamine supplementation, even though the alcohol consumption was previously completely reduced [149]. Koike et al. (2003) compared clinical and histological differences between ALN with and without thiamine deficiency [65]. Also, the results of the group of 32 patients with non-alcoholic thiamine deficiency neuropathy were considered. Thiamine deficiency resulted in the progression of sensory dysfunctions; further, histological examination of the sural nerves revealed the loss of small nerve fibers and segmental demyelination. Patients with non-alcoholic thiamine deficiency neuropathy showed more abrupt onset of symptoms, mainly in a form of motor dysfunctions; biopsy showed damage to greater fibers with subperineurial edema. ALN with thiamine deficiency was manifested as a variable mixture of these symptoms.
Once alcohol use has been addressed, your doctor can focus on the neuropathy itself. Nerve damage can also make it difficult for you to carry out the functions of daily life. The most important thing you can do to treat alcohol neuropathy this condition is to stop drinking. Others may be able to stop drinking with outpatient therapy or social support. It is important to share any history of alcohol use with your doctor to get an accurate diagnosis.
Alcohol-related peripheral neuropathy: a systematic review and meta-analysis
This can be achieved by complete alcohol abstinence and a balanced diet primarily supplemented by B6, B12, and E vitamins, as well as folate, thiamine, and niacin. Benzodiazepines are commonly used to reduce the symptoms of alcohol withdrawal syndrome; acamprosate and naltrexone are effective to treat alcohol dependence; however, the latter usually induces withdrawal symptoms [175]. Further, serotonin-norepinephrine reuptake inhibitors are prescribed to treat alcohol-induced neuropathic pain via exerting antinociceptive properties by increasing serotonergic and noradrenergic neurotransmissions [71]. In an animal model, Kaur et al. (2017) showed that curcumin and sildenafil administrated alone or in combination represent a therapeutic advantage in alcohol-induced neuropathic pain [176]. Chronic alcohol consumption leads to malnutrition with dysfunctions in protein and lipid metabolism which affect the metabolic pathways and progression of ALN symptoms within the central and peripheral nervous systems [89].