Alcohol Withdrawal-Induced Hyperalgesia in Young Adult Binge Drinkers

Abstract

Neuropathy is one of the many health consequences of long-term excessive alcohol consumption. To date, no effective treatment is available for alcoholic neuropathy and its pathogenesis remains unknown. Animal studies have proposed potential mechanisms underlying the association between alcohol abuse and pain conditions. Specifically, preclinical studies have demonstrated that exposure to a few cycles of alcohol withdrawal sensitizes pain pathways and that the two major stress hormones (i.e., epinephrine and cortisol) mediate the induction and maintenance of alcohol withdrawal-induced hyperalgesia. The current study was designed to determine the generality of this phenomenon and mechanisms of alcohol withdrawal-induced hyperalgesia in humans. Because alcohol withdrawal-induced hyperalgesia occurs after only four cycles of an ethanol binge diet in rats, the first objective of the current study was to determine whether alcohol withdrawal-induced hyperalgesia would occur in young adult binge drinkers with a relatively short history of drinking. The second objective was to determine whether stress hormones would be associated with this hyperalgesia. The third goal was to examine the role of negative affect in alcohol withdrawal-induced hyperalgesia because it is a common withdrawal symptom and is linked to enhanced physiological stress responses and pain sensitivity in humans. The last goal was to examine whether alcohol withdrawal and pain would enhance alcohol craving, and therefore, have the ability to motivate continued drinking. To achieve these objectives, two experiments were conducted. Experiment 1 was a cross-sectional design examining the effect of naturally occurring drinking episodes. Experiment 2 was a within-subject design with laboratory alcohol administration. Thecurrent study translated two of the animal findings to humans. First, binge drinkers showed hypersensitivity to muscle pressure pain and alcohol withdrawal further enhanced this hyperalgesia. Second, binge drinkers showed elevated basal levels of epinephrine, but withdrawal did not further increase epinephrine. All the other results were negative. In sum, the current results indicate that alcohol withdrawal-induced hyperalgesia occurs in young adult binge drinkers with a relatively short history of binge drinking and even before the development of alcoholic neuropathy. The study also suggests epinephrine may play a role in alcohol withdrawal-induced hyperalgesia.