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Papers of the Week


Papers: 2 Nov 2019 - 8 Nov 2019


Human Studies

PAIN TYPE:
Migraine/Headache


2020 Mar


Pain


161


3

Offset analgesia: somatotopic endogenous pain modulation in migraine.

Authors

Szikszay TM, Adamczyk WM, Carvalho GF, May A, Luedtke K
Pain. 2020 Mar; 161(3):557-564.
PMID: 31693545.

Abstract

The complex mechanisms underlying migraine are not entirely understood. It has been suggested that descending endogenous pain modulation is an important contributing factor, although research is controversial. A frequently used method to quantify the inhibitory pain modulation system is offset analgesia (OA), defined as a disproportionally large decrease in pain perception in response to a small decrease of painful stimulation. The aim of this study is to evaluate the OA response in patients with migraine and healthy controls, measured at the forehead (trigeminal, V1) and forearm (extra-trigeminal). Patients with episodic migraine during the headache free interval (n=26) and age and sex matched headache-free controls (n=26) were included in this cross-sectional study. All participants underwent an individualized OA paradigm consisting of three-stimulus offset trials and three constant temperature trials examined at both, a trigeminal and an extra-trigeminal test site. Items from the quantitative sensory testing protocol were additionally included. In contrast to the extra-trigeminal area, a reduced offset analgesia response was shown in the trigeminal area in patients with migraine compared to healthy controls (p<0.01, MD: 13.7, 95%CI: 3.8; 23.6). Statistically significant differences between the trigeminal area and the extra-trigeminal area were neither observed in healthy controls nor in patients with migraine (p>0.05). Mechanical detection, mechanical pain threshold, warm detection and heat pain threshold showed no significant differences between groups or test sites (p>0.05). In summary, patients with episodic migraine in the headache free interval exhibited somatotopically specific differences in endogenous pain modulation.