EN
Migraine is an episodic neurovascular disorder typically characterized by attacks of unilateral throbbing headache, autonomic dysfunctions and focal neurological symptoms. The initiation of migraine attacks is still enigmatic. While an essential role for the intracranial afferent innervation is widely accepted, the importance of cortical spreading depression inducing neurovascular inflammatory responses is disputed. Recent animal experiments indicate that a cascade of nociceptive events including the generation of gaseous mediators like nitric oxide species, which activate transient receptor potential channels and increase the release of calcitonin gene-related peptide, is involved in the trigeminal processing of nociceptive information possibly leading to migraine pain. A periodic weakening of endogenous inhibitory control systems may enable the dysregulation of central pain processing and constitutes a challenge for future routes of migraine therapy.