BACKGROUND: Migraine is a common headache disorder that can vary menstrually in women and has been linked to an impairment of endogenous pain inhibitory systems. One of these endogenous pain inhibitory systems, namely conditioned pain modulation (CPM; formerly diffuse noxious inhibitory controls-like), has been shown to be affected by the menstrual cycle. The aim of this study was to examine CPM over the menstrual cycle in migraineurs and healthy controls. METHODS: Twenty healthy women and 32 female migraineurs were examined on days 1, 4, 14 and 22 of the menstrual cycle. Detection and pain thresholds for electrocutaneous stimuli were first assessed at baseline. Second, tonic heat stimuli were applied concurrently to the electrical stimuli, and the difference in electrical thresholds to baseline were analysed as indicating CPM inhibition. RESULTS: Migraineurs revealed higher detection thresholds than the control group but similar pain thresholds for the electrical current. Likewise, pain sensitivity for tonic heat stimulation also did not differ between groups. With regard to our main hypotheses, we found that CPM inhibition neither differed between migraineurs and healthy volunteers nor varied over the menstrual cycle. CONCLUSIONS: Our findings suggest that CPM inhibition is not altered in female migraineurs; thus, it is questionable whether CPM really plays a role in the development of migraine or whether migraine leads to a dysfunctional CPM inhibition.
BACKGROUND:Migraine is a common headache disorder that can vary menstrually in women and has been linked to an impairment of endogenous pain inhibitory systems. One of these endogenous pain inhibitory systems, namely conditioned pain modulation (CPM; formerly diffuse noxious inhibitory controls-like), has been shown to be affected by the menstrual cycle. The aim of this study was to examine CPM over the menstrual cycle in migraineurs and healthy controls. METHODS: Twenty healthy women and 32 female migraineurs were examined on days 1, 4, 14 and 22 of the menstrual cycle. Detection and pain thresholds for electrocutaneous stimuli were first assessed at baseline. Second, tonic heat stimuli were applied concurrently to the electrical stimuli, and the difference in electrical thresholds to baseline were analysed as indicating CPM inhibition. RESULTS:Migraineurs revealed higher detection thresholds than the control group but similar pain thresholds for the electrical current. Likewise, pain sensitivity for tonic heat stimulation also did not differ between groups. With regard to our main hypotheses, we found that CPM inhibition neither differed between migraineurs and healthy volunteers nor varied over the menstrual cycle. CONCLUSIONS: Our findings suggest that CPM inhibition is not altered in female migraineurs; thus, it is questionable whether CPM really plays a role in the development of migraine or whether migraine leads to a dysfunctional CPM inhibition.
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