• Tibor M Szikszay, Waclaw M Adamczyk, Gabriela F Carvalho, Arne May, and Kerstin Luedtke.
• Medical Section, Department of Orthopaedic and Trauma Surgery, Academic Physiotherapy, Pain and Exercise Research Luebeck (P.E.R.L), University of Luebeck, Luebeck, Germany.
• Pain. 2020 Mar 1; 161 (3): 557-564.

AbstractThe 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 (extratrigeminal). 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 3 stimulus offset trials and 3 constant temperature trials examined at both, a trigeminal and an extratrigeminal test site. Items from the quantitative sensory testing protocol were additionally included. In contrast to the extratrigeminal area, a reduced OA response was shown in the trigeminal area in patients with migraine compared with healthy controls (P < 0.01, mean difference: 13.7, 95% confidence interval: 3.8-23.6). Statistically significant differences between the trigeminal area and the extratrigeminal 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.

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