ABSTRACT
This chapter presents a short introduction to the clinical picture of migraine, the hypothesis on migraine pathology, and proposed signaling pathways involved as well as the possible role of phosphodiesterases (PDE) in migraine, focusing on the role of cyclic guanosine monophosphate and PDE5. The basis for migraine pathogenesis has for some time been a matter of some controversy where divergent standpoints were taken as to whether migraine was vascular or neurogenic in origin. The key neuropeptide involved in migraine pathophysiology is calcitonin gene-related peptide, which is present in both the human and the animal brains, as well as in the perivascular sensory nerves and trigeminal ganglion. Selective inhibitors of PDEs appear to provide specific tools to pinpoint the role of cyclic nucleotides in the pathophysiology of migraine. PDE5 inhibitors induce headache in patients suffering from migraine without aura; this mirrors a usual migraine attack including accompanying symptoms similar to what is seen with nitric oxide donors.
