The similarity between beriberi and alcoholic neuropathy had long been noted, but Shattuck in 1928 was the first to seriously discuss the relationship. He suggested that "polyneuritis of chronic alcoholism" was caused chiefly by failure to take or assimilate food containing a sufficient quantity of vitamin Bx and might properly be regarded as true beriberi. However, this theory may be only partly true.
Pathophysiology: The precise pathogenesis of alcohol neuropathy remains unclear. Separating ethanol use from nutritional and vitamin deficiencies, especially thiamine, has always been difficult and a source of long-standing debate. Nutritional deficiency (frequently associated with alcohol neuropathy) and/or the direct toxic effect of alcohol or both have been implicated and studied. In Wernicke-Korsakoff syndrome, a clear association between reduction of thiamine levels or thiamine-mediated enzyme activity (transketolase) has been established, though this has not been conclusively established in the case of peripheral neuropathy.
In their comparison of alcoholics and nonalcoholic control subjects, Behse and Buchthal concluded that nutritional deficiencies alone did not produce the neuropathy.
Monforte et al concluded that alcohol appears to be toxic to autonomic and peripheral nerves in a dose-dependent manner, on the basis of heart rate, blood pressure, and electrophysiologic examination.
In a study of macaque monkeys, Hallet et al failed to produce clinical and electrophysiologic signs of neuropathy in monkeys that were given a certain amount of alcohol for 3-5 years.
Studies in rats also failed to demonstrate a direct toxic effect of alcohol on the peripheral nerves.
Most studies of peripheral neuropathy in humans and animals implicate nutritional deficiency as an etiology as opposed to the direct toxic effect of alcohol.
Frequency:
- Internationally: Depending on criteria and patient selection, incidence of peripheral neuropathy ranging from 10-50% 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 (Monforte, 1995). When electrodiagnostic criteria are added, neuropathy detection increases to 25-90% (Vittadini, 2001).
Mortality/Morbidity: Johnson and Robinson studied the mortality rate of alcoholics with autonomic neuropathy.
- 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.
Sex:
- A high incidence of alcoholic polyneuropathy has been observed in women.
Medical Care: Treatment is directed toward stopping further damage to the peripheral nerves and returning to normal functioning. These can be achieved by alcohol abstinence, a nutritionally balanced diet supplemented by all B vitamins, and rehabilitation. However, in the setting of ongoing ethanol use, vitamin supplementation alone has not been convincingly shown to be sufficient for improvement in most patients.
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