Cluster headache is a primary headache disorder featuring attacks of unilateral pain so severe patients often describe it as excruciating. Attack pain is accompanied by notable ipsilateral cranial autonomic symptoms (CAS) and attacks often occur with circadian rhythmicity. The pathophysiology of cluster headache remains incompletely understood much like the mechanisms behind available attack abortive and preventive medications. Several sensory and parasympathetic signaling molecules such as calcitonin gene-related peptide (CGRP), pituitary adenylate cyclase-activating peptide-38 (PACAP38) and vasoactive intestinal peptide (VIP) have gained interest in cluster headache due to their potential involvement in attack initiation. This was indicated by findings of increased concentration of these signaling molecules during cluster headache attacks. Whether infusion of CGRP, PACAP38 and VIP triggers cluster-like attacks in cluster headache patients is unknown.

In study I we investigated the headache inducing abilities of CGRP in 32 cluster headache patients (9 episodic cluster headache in active phase, 9 episodic cluster headache remission phase and 14 chronic cluster headache) in the first placebo-controlled provocation study in cluster headache. We found that CGRP induced attacks in cluster headache patients in active disease phase (i.e. episodic cluster headache active phase (89%) and chronic cluster headache (50%)) but not in episodic cluster headache remission phase…..

Supervisor Professor Messoud Ashina, PhD, DMSc.

Supervisor Professor Rigmor Højland Jensen, DMSc.

Supervisor Song Guo, MD, PhD.