Abstract
The activity of neurons in the spinal trigeminal nucleus (STN) is thought to reflect the activity of central trigeminal nociceptive pathways that underlie facial pain and headache in man. About 40% of human trigeminal neurons contain the neuropeptide calcitonin gene-related peptide (CGRP), which is released from these primary afferents upon activation. The CGRP levels in the jugular venous blood are elevated during migraine attacks and cluster headache, and the time course of CGRP plasma levels parallels headache intensity. The functional relevance of mechanisms downstream of CGRP has been demonstrated by headache generation following CGRP infusion and the successful treatment of spontaneous migraine by a CGRP receptor antagonist. The functional relevance of CGRP in the pathophysiology of headache is further supported by animal experiments in which a CGRP receptor antagonist reduced nociceptive signaling in the STN.
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