Migraine

• Published in: Handbook of experimental pharmacology no. 194; p. 75
• Main Authors: Benemei, Silvia, Nicoletti, Paola, Capone, Jay G, De Cesaris, Francesco, Geppetti, Pierangelo
• Format: Journal Article
• Language: English
• Published: Germany 2009
• Subjects: Afferent Pathways - metabolism; Afferent Pathways - physiopathology; Analgesics - therapeutic use; Animals; Calcitonin Gene-Related Peptide - metabolism; Cerebrovascular Circulation; Efferent Pathways - metabolism; Efferent Pathways - physiopathology; Humans; Migraine Disorders - complications; Migraine Disorders - drug therapy; Migraine Disorders - metabolism; Migraine Disorders - physiopathology; Neurogenic Inflammation - metabolism; Neurogenic Inflammation - physiopathology; Pain - drug therapy; Pain - etiology; Pain - metabolism; Pain - physiopathology; Receptors, Calcitonin Gene-Related Peptide - antagonists & inhibitors; Receptors, Calcitonin Gene-Related Peptide - metabolism; Sensory Receptor Cells - drug effects; Sensory Receptor Cells - metabolism; Trigeminal Nerve - drug effects; Trigeminal Nerve - metabolism; Trigeminal Nerve - physiopathology; Vasodilation
• ISSN: 0171-2004
• DOI: 10.1007/978-3-540-79090-7_3

Migraine is a neurovascular disorder which affects one fifth of the general population. Disability due to migraine is severe and involves patients from infancy through senescence and it is aggravated by the fact there is no complete cure. However, various drugs for the symptomatic or prophylactic treatment of the disease are available. Recently, better knowledge of the neurobiological and pharmacological aspects of a subset of trigeminal primary sensory neurons has provided key information for the development of effective molecules that specifically target the activation of the trigeminovascular system and may represent a significant advancement in the treatment of the disease. These novel antagonists block the receptor for the sensory neuropeptide calcitonin gene-related peptide (CGRP), which upon release from peripheral terminals of trigeminal perivascular neurons dilates cranial arterial vessels. Whether neurogenic vasodilatation is the major contributing factor to generate the pain and the associated symptoms of the migraine attack or whether other sites of action of CGRP receptor antagonists are responsible for the antimigraine effect of these compounds is the subject of current and intense research.