Management of alcohol-induced peripheral neuropathy : Nursing made Incredibly Easy

Dr. Moawad regularly writes and edits health and career content for medical books and publications. Especially if you have been drinking heavily for many years, coping with alcohol use disorder is not easy. But with the proper resources to help you, you are better set up for success with sobriety. Nerve damage typically affects the axons, which are the projections that send electrical signals from one nerve to another, as well as the myelin, which is the fatty coating that protects the nerves. Heidi Moawad is a neurologist and expert in the field of brain health and neurological disorders. She has over a decade of direct patient care experience working as a registered nurse specializing in neurotrauma, stroke, and the emergency room.

Due to similar histologic and electrophysiological symptoms, it was believed that ALN may make up a subtype of beriberi [146]. Further research has confirmed the role of thiamine in the pathogenesis of ALN—the well-balanced diet and vitamin B1 supplementation significantly decreased the severity of ALN symptoms [147, 148]. However, the limitations of those studies include the lack of the possibility to measure the amount of vitamin B1 in the serum; further, patients who were involved in the study have received an unrefined form of the supplement. 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].

Progressed disease

The cause is a diverse multifactorial process caused from damage by free radicals, the release of inflammatory markers, and oxidative stress. Individuals with alcoholic neuropathy often make a partial or full recovery, depending on the extent and duration of their alcohol consumption. The best thing a person with alcoholic neuropathy can do is to stop or significantly reduce their alcohol intake.

Regarding the autonomic domain, our findings were just significant for piloerection. However, data from literature indicate additional autonomic alterations in long-term chronic users (Milovanovic et al., 2009). One of the tests was 24 h Holter monitoring, which evaluated short-term heart rate variability, showing a significant difference and an incidence of severe autonomic dysfunction in 56% of the patients (chronic alcohol users), (Milovanovic et al., 2009).

Conditions That May Mimic Alcoholic Neuropathy

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]. The demyelination is explained as the result of a slowing down (decceleration) of axoplasmic flow and a degradation of the quality of biological properties of axonal enzymes and proteins. This type of degeneration, so called ‘dying-back’, resembles Wallerian degeneration. Ethanol and its toxic degradation metabolites affect neuronal metabolism including the metabolic pathways of nucleus, lysosomes, peroxisomes, endoplasmatic reticulum and cytoplasm [21].

  • Alcoholic neuropathy is a severe condition that can lead to chronic pain, loss of some bodily functions, and permanent disability.
  • The authors hypothesized that vitamins B6 and B12 might have competed with the effects of vitamin B1 in the Milgamma-N group [97].
  • In studying the causes of polyneuropathy in alcoholics, most experts point to poor nutrition and the toxicity of long-term alcohol exposure.
  • A “very long investigation,” including a breath test, indicated she was significantly over the legal limit of 0.08.

Tricyclic antidepressants, including amitriptyline, desipramine, and nortriptyline, work similarly to the antiseizure medications. Duloxetine is a serotonin-norepinephrine reuptake inhibitor that may improve neuropathic pain. Desired outcomes of these medications include reduced pain and improved sleep.

Oxidative-nitrosative stress and alcoholic neuropathy

Recent studies show contradictory information about the role of malnutrition and micronutrients (thiamine) deficiency in the pathogenesis of ALN; however, it is assumed that these might induce the progression of ataxia or movement disorders [55, 57]. Nevertheless, heavy alcohol drinkers are usually significantly malnourished because of the improperly balanced diet and impaired absorption of the essential nutrients and elements [58, 59]. Benfotiamine (S-benzoylthiamine O-monophoshate) is a synthetic S-acyl derivative of thiamine (vitamin B1).