Alcohol-induced polyneuropathy is typically characterized by diffuse neuropathy with an absent Achilles tendon reflex1. Initially, disturbances of sensation occur with or without neuropathic pain. In the later course, distal-predominant pareses and autonomic dysfunction may develop. Nerve conduction studies demonstrate an axonal sensorimotor neuropathy2. Alcohol-associated polyneuropathy has a prevalence of 22 – 66 % among individuals with chronic alcohol use disorder3. The most important risk factors for the development of alcohol-induced polyneuropathy are the duration of alcohol abuse and lifetime alcohol consumption.
Pathophysiology of alcohol-induced polyneuropathy
The pathophysiology of alcohol-associated polyneuropathy consists of malnutrition, for example with regard to the B vitamins, and direct toxic effects of alcohol and its metabolites, such as acetaldehyde. Oxidative stress also plays a role. Liver values and the concentration of “Carbohydrate deficient transferrin” (CDT) are generally elevated. In addition, laboratory testing usually reveals macrocytosis4.
Treatment of alcohol-induced polyneuropathy
Treatment includes alcohol abstinence and dietary modification to correct the malnutrition. With sustained abstinence, the neuropathy may resolve over a period of months to years5.
References
Greenberg MS, Abel N, Agazzi S. Handbook of Neurosurgery. Georg Thieme Verlag; 2020. doi:10.1055/b-006-161147 ↩ ↩
Sommer C, Geber C, Young P, Forst R, Birklein F, Schoser B: Polyneuropathies—etiology, diagnosis, and treatment options. Dtsch Arztebl Int 2018; 115: 83–90. DOI: 10.3238/arztebl.2018.0083 ↩ ↩ ↩ ↩ ↩ ↩ ↩ ↩