The elusive nature of migraine attacks makes them difficult to study under controlled conditions. However, the human migraine models offer a way around this, were you can successfully induce attacks in a research environment and examine whatever aspect of migraine pathophysiology, you are interested in. Furthermore, the very nature of the models allows for studies within patients as they traverse from a pain-free interictal state into attacks, making them their own controls in these state-of-the-art experiments.

Numerous pharmacological substances have been used in migraine provocation and they generally elicit their effects through modulation of nucleotides in two cellular pathways; either cyclic adenosine monophosphate or cyclic guanosine monophosphate. Calcitonin gene-related peptide (CGRP) activates the cyclic adenosine monophosphate pathway and triggers migraine attacks in two thirds of migraine patients while sildenafil promotes the cyclic guanosine monophosphate pathway and triggers attacks in 83% of patients. Both substances are vasoactive, but while CGRP triggers attacks with concomitant cranial vasodilation, sildenafil has showed no cranial vasoreactivity alongside attacks.

The role of the vasculature in migraine has been heavily studied and it is still unknown whether the vessels play a role in attack genesis, pain origination or modulation or something else entirely. Despite speculations of trigeminal.... 

Supervisor: Professor Messoud Ashina.

Supervisor: Professor Henrik Bo Wiberg Larsson.

Supervisor: Dr. Faisal Mohammad Amin.