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.