Document Type
Article
Publication Date
12-31-2010
Abstract
Background
The mechanism of veisalgia cephalgia or hangover headache is unknown. Despite a lack of mechanistic studies, there are a number of theories positing congeners, dehydration, or the ethanol metabolite acetaldehyde as causes of hangover headache.
Methods
We used a chronic headache model to examine how pure ethanol produces increased sensitivity for nociceptive behaviors in normally hydrated rats.
Results
Ethanol initially decreased sensitivity to mechanical stimuli on the face (analgesia), followed 4 to 6 hours later by inflammatory pain. Inhibiting alcohol dehydrogenase extended the analgesia whereas inhibiting aldehyde dehydrogenase decreased analgesia. Neither treatment had nociceptive effects. Direct administration of acetate increased nociceptive behaviors suggesting that acetate, not acetaldehyde, accumulation results in hangover-like hypersensitivity in our model. Since adenosine accumulation is a result of acetate formation, we administered an adenosine antagonist that blocked hypersensitivity.
Discussion
Our study shows that acetate contributes to hangover headache. These findings provide insight into the mechanism of hangover headache and the mechanism of headache induction.
Recommended Citation
Maxwell, Christina R.; Spangenberg, Rebecca Jay; Hoek, Jan B.; Silberstein, Stephen D.; and Oshinsky, Michael L., "Acetate Causes Alcohol Hangover Headache in Rats" (2010). Department of Neurology Faculty Papers. Paper 35.
https://jdc.jefferson.edu/neurologyfp/35
Comments
This article has been peer reviewed. It was published in PLoS ONE. Volume 5, Issue 12, December 2010, e15963. The published version is available at doi:10.1371/journal.pone.0015963. Copyright © 2010 Maxwell et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.