Abstract
BackgroundMigraine and trigemino-autonomic cephalalgia attacks are associated with an increase of α-calcitonin-gene related peptide levels in the ipsilateral jugular vein. It is however unknown whether trigeminal pain stimulation in healthy subjects without headache disorders also induces increase of calcitonin-gene related peptide levels.FindingsWe measured α-calcitonin-gene related peptide levels in eight healthy subjects after subcutaneous injection of capsaicin in the forehead and in the mandibular region and after injection of sodium chloride in the forehead. We observed a significant increase of α-calcitonin-gene related peptide level only after injection of capsaicin in the forehead (i.e. first trigeminal branch). We also observed trigemino-autonomic activation (lacrimation, rhinorrhea etc.) only after injection of capsaicin in the forehead.ConclusionIncrease of α-calcitonin-gene related peptide levels do not only occur in primary headache attacks but also after experimental trigeminal pain of the first branch. This finding suggests that α-calcitonin-gene related peptide elevation is, at least an additional, unspecific effect of first trigeminal branch stimulation following pain activation and not a specific mechanism of idiopathic headache disorders.
Highlights
Calcitonin-gene related peptide (CGRP) is regarded today as the most important and central molecule/neuropeptide in migraine pathophysiology
After injection of capsaicin in the forehead, the a-CGRP level in the ipsilateral jugular vein increased from 28 þ/- 5 to 40 þ/- 7 pmol/l (p1⁄40.043), whereas no significant increase was observed in the contralateral jugular vein and in the cubital vein
Our main finding is a significant a-CGRP release into the blood of the ipsilateral external jugular vein when evoking severe trigeminal pain in the first trigeminal branch but not in the third trigeminal branch. This finding is supported by a placebo control and suggests that the a-CGRP release in headache disorders is mainly due to first branch trigeminal pain activation and not a specific mechanism of only idiopathic headache disorders
Summary
Calcitonin-gene related peptide (CGRP) is regarded today as the most important and central molecule/neuropeptide in migraine pathophysiology This is based, initially, on clinical studies on elevated a-CGRP levels in trigeminal pain disorders such as trigeminal neuralgia, migraine, cluster headache, and paroxysmal hemicrania. Migraine and trigemino-autonomic cephalalgia attacks are associated with an increase of a-calcitoningene related peptide levels in the ipsilateral jugular vein It is unknown whether trigeminal pain stimulation in healthy subjects without headache disorders induces increase of calcitonin-gene related peptide levels. Conclusion: Increase of a-calcitonin-gene related peptide levels do occur in primary headache attacks and after experimental trigeminal pain of the first branch This finding suggests that a-calcitonin-gene related peptide elevation is, at least an additional, unspecific effect of first trigeminal branch stimulation following pain activation and not a specific mechanism of idiopathic headache disorders
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