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• W2024286290 abstract "Research has shown that some chronic pain conditions, including headache disorders, are associated with a dysfunction of pain inhibitory systems. To date, no known study has examined this issue using a physiological measure of trigeminal nociception in human participants. The current study assessed whether diffuse noxious inhibitory controls (DNIC), a form of endogenous inhibition, was disrupted in persons suffering from severe headaches. DNIC involves the application of a tonic, noxious, conditioning stimulus that inhibits phasic pain evoked from a distant body site. Animal research suggests this inhibition is mediated by a spino-bulbo-spinal circuit that inhibits nociceptive processing as well as pain perception. For the present study, tonic pain was induced by 2-min of forearm ischemia. Before, during, and after ischemia, suprathreshold electrocutaneous stimulations were delivered to the supraorbital branch of the trigeminal nerve. Pain and trigeminal nociception were assessed from these stimulations via pain ratings and the electrophysiologically-determined nociceptive blink reflex (nBR), respectively. We hypothesized that persons with severe headaches would exhibit a disruption of endogenous inhibition. The headache group was comprised of 11 individuals with migraine and/or tension-type headaches who were categorized as having moderate or severe disability according to the Migraine Disability Assessment Scale (MIDAS). Controls were 11 individuals with no headaches or infrequent tension-type headaches (all with minimal or mild disability according to MIDAS). All procedures were IRB approved. Results indicated DNIC-inhibition of pain ratings was similar in both groups. However, DNIC-inhibition of nBR was noted in the control group, but not the headache group. These findings suggest a dysfunction of endogenous inhibition of trigeminal nociception in persons suffering from severe headaches. Further research is needed to determine whether inhibitory dysfunction is a precursor or a consequence of disabling headaches. Research has shown that some chronic pain conditions, including headache disorders, are associated with a dysfunction of pain inhibitory systems. To date, no known study has examined this issue using a physiological measure of trigeminal nociception in human participants. The current study assessed whether diffuse noxious inhibitory controls (DNIC), a form of endogenous inhibition, was disrupted in persons suffering from severe headaches. DNIC involves the application of a tonic, noxious, conditioning stimulus that inhibits phasic pain evoked from a distant body site. Animal research suggests this inhibition is mediated by a spino-bulbo-spinal circuit that inhibits nociceptive processing as well as pain perception. For the present study, tonic pain was induced by 2-min of forearm ischemia. Before, during, and after ischemia, suprathreshold electrocutaneous stimulations were delivered to the supraorbital branch of the trigeminal nerve. Pain and trigeminal nociception were assessed from these stimulations via pain ratings and the electrophysiologically-determined nociceptive blink reflex (nBR), respectively. We hypothesized that persons with severe headaches would exhibit a disruption of endogenous inhibition. The headache group was comprised of 11 individuals with migraine and/or tension-type headaches who were categorized as having moderate or severe disability according to the Migraine Disability Assessment Scale (MIDAS). Controls were 11 individuals with no headaches or infrequent tension-type headaches (all with minimal or mild disability according to MIDAS). All procedures were IRB approved. Results indicated DNIC-inhibition of pain ratings was similar in both groups. However, DNIC-inhibition of nBR was noted in the control group, but not the headache group. These findings suggest a dysfunction of endogenous inhibition of trigeminal nociception in persons suffering from severe headaches. Further research is needed to determine whether inhibitory dysfunction is a precursor or a consequence of disabling headaches." @default.
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• W2024286290 date "2010-04-01" @default.
• W2024286290 modified "2023-09-23" @default.
• W2024286290 title "Endogenous inhibition of trigeminal nociception is impaired in persons with severe headaches" @default.
• W2024286290 doi "https://doi.org/10.1016/j.jpain.2010.01.144" @default.
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