[Pathophysiology of migraine and clinical implications].
Migraine pathophysiology is determined by genetic and environmental factors. Based on altered cerebral habituation and low serotonin levels, certain triggers can elicit a migraine attack. Following initial unspecific prodromi, an aura follows in many patients which most often consists of visual symptoms. Cortical spreading depression is the electrophysiological correlate of the aura and can activate the trigemino-vascular system. This is one potential mechanism initiating the pain process. The characteristic unilateral pulsating headache is caused by a neurogenic inflammation in the meninges. Neck pain as reported by some patients is a migraine-specific feature, the anatomical basis being the trigemino-cervical complex. Functional changes in the pain processing system maintain the headache. Among these are sensitization of trigeminal nucleus caudalis neurons and an altered antinociception descending from the periaquaductal grey. Triptans have a peripheral and central mode of action, but they are no longer effective once central sensitization has occurred.
Schürks
M
M
Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 900 Commonwealth Avenue East, 3rd fl, Boston, MA 02215-1204, USA. mschuerks@rics.bwh.harvard.edu
Diener
H-C
HC
D000700:Analgesics / Q000009:adverse effects / Q000627:therapeutic use; D001921:Brain / Q000503:physiopathology; D013181:Cortical Spreading Depression / Q000187:drug effects / Q000502:physiology; D052246:Cyclooxygenase 2 Inhibitors / Q000009:adverse effects / Q000627:therapeutic use; D004087:Dihydroergotamine / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D008578:Meninges / Q000098:blood supply; D008881:Migraine Disorders / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D020325:Migraine with Aura / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D009434:Neural Pathways / Q000187:drug effects / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology; D012307:Risk Factors; D012701:Serotonin / Q000378:metabolism; D017366:Serotonin Receptor Agonists / Q000009:adverse effects / Q000627:therapeutic use; D013126:Spinal Nerve Roots / Q000187:drug effects / Q000503:physiopathology; D014276:Trigeminal Nerve / Q000187:drug effects / Q000503:physiopathology; D014363:Tryptamines / Q000009:adverse effects / Q000627:therapeutic use; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
D000700:Analgesics; D052246:Cyclooxygenase 2 Inhibitors; D017366:Serotonin Receptor Agonists; D014363:Tryptamines; D012701:Serotonin; D004087:Dihydroergotamine