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Background: Calcitonin gene-related peptide (CGRP) plays a major role in the pathogenesis of migraine and other primary headaches. Spinal trigeminal neurons integrate nociceptive afferent input from trigeminal tissues including intracranial afferents, and their activity is thought to reflect facial pain and headache in man. CGRP receptor inhibitors and anti-CGRP antibodies have been demonstrated to be therapeutically effective in migraine.

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The mechanisms underlying conditioned pain modulation (CPM) are multifaceted. We searched for a link between individual differences in prefrontal cortex activity during multi-trial heterotopic noxious cold conditioning and modulation of the cerebral response to phasic heat pain. In 24 healthy female subjects, we conditioned laser heat stimuli to the left hand by applying alternatively ice-cold or lukewarm compresses to the right foot.

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In eight patients with chronic paroxysmal hemicrania (CPH), forehead sweating was measured after various provocation tests-body heating, exercise, and subcutaneous pilocarpine administration (0.1 mg/kg body weight). Evaporation was measured bilaterally on the forehead with an Evaporimeter (in g/m2/h).

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The responses of supraorbital (SA), superficial temporal (TA), and digital (F) arterial beds and heart rate were studied in 5 normal subjects and 10 migraineurs when hand temperature was increased by volition and/or by heat. In normal subjects, volitional digital arterial dilation coincided with vasoconstriction in SA and TA. In migraineurs, the response varied.

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