Central effects of acetylsalicylic acid on trigeminal-nociceptive stimuli

The Journal of Headache and Pain

Research Article

Arne May¹  Inga L Kröger¹ 

[1] Department of Systems Neuroscience, University Medical Center Hamburg- Eppendorf, Martinistr. 52, D-20246, Hamburg, Germany;

关键词: Aspirin;    ASA;    Trigeminal-nociception;    fMRI;    Pain;    Pharmacological modulation;    Cingulate cortex;   

DOI  :  10.1186/1129-2377-15-59

 received in 2014-07-16, accepted in 2014-08-19,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundAcetylsalicylic acid is one of the most used analgesics to treat an acute migraine attack. Next to the inhibitory effects on peripheral prostaglandin synthesis, central mechanisms of action have also been discussed.MethodsUsing a standardized model for trigeminal-nociceptive stimulation during fMRI scanning, we investigated the effect of acetylsalicylic acid on acute pain compared to saline in 22 healthy volunteers in a double-blind within-subject design. Painful stimulation was applied using gaseous ammonia and presented in a pseudo-randomized order with several control stimuli. All participants were instructed to rate the intensity and unpleasantness of every stimulus on a VAS scale. Based on previous results, we hypothesized to find an effect of ASA on central pain processing structures like the ACC, SI and SII as well as the trigeminal nuclei and the hypothalamus.ResultsEven though we did not find any differences in pain ratings between saline and ASA, we observed decreased BOLD signal changes in response to trigemino-nociceptive stimulation in the ACC and SII after administration of ASA compared to saline. This finding is in line with earlier imaging results investigating the effect of ASA on acute pain. Contrary to earlier findings from animal studies, we could not find an effect of ASA on the trigeminal nuclei in the brainstem or within the hypothalamic area.ConclusionTaken together our study replicates earlier findings of an attenuating effect of ASA on pain processing structures, which adds further evidence to a possibly central mechanism of action of ASA.

【 授权许可】

CC BY   
© Kröger and May; licensee Springer. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.