Alcohol (Ethanol) Related Neuropathy

Updated: Sep 07, 2021
  • Author: Danette C Taylor, DO, MS, FACN; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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Practice Essentials

Alcoholic neuropathy is common, impacting an average of 44% of chronic alcohol users. [1]

Although commonly seen together, alcoholic neuropathy is separate from other nutritional deficiencies. Treatment is symptomatic; at present, there is no way to completely reverse alcoholic neuropathy. [2, 3]

Identication of alcoholic neuropathy is based on history; there is no specific test that can specifically identify alcoholic neuropathy.



The clinical symptoms of alcoholic peripheral neuropathy (ALN) were first described more than 200 years ago. The descriptions by Lettsom (1787) [4] and Jackson (1822) [5]  led to the recognition and association of peripheral nerve disease with excessive ethanol use. 

Although patients with alcoholic neuropathy often have associated nutritional deficiencies, it has been identified that these deficiencies are not the cause of the neuropathy. While the exact etiology of the neuropathy hasn't yet been identified, many theories have been raised, ranging from a direct toxic effect of alcohol on peripheral nerves to spinal enzymes or impact of alcohol on the central opioid system. [2]




The precise pathogenesis of alcohol neuropathy remains unclear. Many theories have been raised as to the cause of alcohol-related peripheral neuropathy (ALN). While nutritional deficiencies can contribute to progression of ALN, these are not the primary cause leading to neuropathy.

It has been identified that alcohol use can lead to thiamine deficiency, However, animal studies have shown that when thiamine levels are normal, alcohol exposure can still induce neuropathy. [6]

Monforte et al. concluded that alcohol appears to be toxic to autonomic and peripheral nerves in a dose-dependent manner, based on heart rate, blood pressure, and electrophysiologic examination. [7]

Independent of thiamine deficiency, ethanol now appears to have a direct toxic effect on the peripheral nerves. Dina et al suggest that catecholamines in nociceptors are metabolized to neurotoxic products by monoamine oxidase-A (MAO-A). This can cause neuronal dysfunction, which leads to neuropathic pain. [8]

Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status is well known. The clinicopathologic features of painful symptoms and small axon loss are distinct from those of beriberi neuropathy. This supports the view of direct neurotoxic effect by alcohol or its metabolites. [9]

Axonal transport and cytoskeletal properties are impaired by ethanol exposure. Protein kinase A and protein kinase C may also play a role in the pathogenesis, especially in association with painful symptoms. [10]

In utero alcohol exposure predisposes to a major risk factor for lifelong aberrant neuroimmune function. Behavioral and physiological sequelae occur throughout life and include cognitive developmental disabilities as well as disease susceptibility related to aberrant immune and neuroimmune actions, in particular significant alterations in the neuroimmune axis occur. [11, 12]




Depending on criteria and patient selection, incidence of peripheral neuropathy ranging from 25% to 66% has been reported. These studies included alcoholics hospitalized for other reasons or for detoxification. Neuropathy is more prevalent in frequent, heavy, and continuous drinkers compared to more episodic drinkers. [7]


Johnson and Robinson studied the mortality rate of individuals with alcoholism who had autonomic neuropathy. [11]

Their findings suggested that evidence of vagal neuropathy in long-term alcoholics is associated with a significantly higher mortality rate than in the general population (a reported 88% survival rate at 7 years in alcoholics with autonomic neuropathy as compared to 94% in the general population).

Deaths due to cardiovascular disease are a major factor.

Many deaths were attributed to strokes, since heavy alcohol consumption is a significant risk factor for stroke.


A high incidence of alcoholic polyneuropathy has been observed in women and men. Women, when compared to men, are more predisposed to alcohol-induced damage, and the susceptibility extends to hepatic, cardiac, cerebral, and muscular changes. Also, there appears to be a greater sensitivity of females to the toxic effects of alcohol on peripheral nerve fibers unrelated to malnutrition. [3]



The prognosis of alcoholic neuropathy generally is good, as reported by Hillbom and Wennberg in their series of 10 patients. [13]

Provided that alcohol intake is discontinued and other causes of neuropathy (eg, malignancy, diabetes, nerve trauma) are excluded, clinical and electrophysiologic examinations may return to near normal; however, residual neuropathy may be seen even after years of abstinence. [3]

Prognosis is generally better in patients who are healthy and well nourished. Recovery is presumed to be due to regeneration and collateral sprouting of damaged axons.