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Impaired pain
inhibitory responses (including conditioned pain modulation) may be associated
with development of migraine.
An impaired conditioned pain modulation (CPM) inhibition of the nociceptive blink reflex (nBR) leads to a deficiency in trigeminal nociception inhibition, and this deficiency shows a close association with migraine development, evident from a cross-sectional assessment of experimental pain.
A total of
thirty-two without and twenty-three adults with a history of migraine headaches
were selected for the analysis. The supraorbital branch of the left trigeminal
nerve was given four elcetrocutaneous stimulations at 150% of an individually
determined pain threshold. Further, the noxious counter stimulus was applied to
assess the CPM, and four more electrocutaneous stimulations were delivered.
Evaluation of nociceptive blink reflex and pain was done after each
stimulation. Pain catastrophizing and depression were assessed for their
influence on pain modulation.
Similar baseline
pain responsivity without meaningful differences in nociceptive blink reflexes
or pain report was noticed within patients with or without migraine headaches.
Control and migraine, both groups showed inhibition of pain report. Although
inhibition of nociceptive blink reflexes during the ischemia task was exclusive
to nonmigraine controls. Even after controlling pain catastrophizing and
depression, this pattern remained to persist. All these findings indicate that
impaired conditioned pain modulation of the nociceptive blink reflex may
contribute to developing migraine headaches.
Pain Medicine
Impairment of Inhibition of Trigeminal Nociception via Conditioned PainModulation in Persons with Migraine Headaches.
Amy E. Williams et al.
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