Migraine pathogenesis: the neural hypothesis reexamined.
The hypothesis that migraine is a primary neurological disturbance with secondary vascular manifestations is tested by analysing the five phases of migraine attacks and the eight groups of recognised precipitating factors. Accessory evidence from cerebral blood flow and EEG recordings taken during attacks is also considered. The evidence supports the concept that the sensory cortex and hypothalamus could be initiating sites for migraine attacks, and indicates that a neurological mechanism, suggested by Liveing and Gowers 100 years ago, remains viable and needs to be considered in future research.
D000818:Animals; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D013181:Cortical Spreading Depression; D004569:Electroencephalography; D004777:Environment; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006257:Head; D006801:Humans; D006815:Hunger; D006967:Hypersensitivity / Q000150:complications; D008598:Menstruation; D008881:Migraine Disorders / Q000209:etiology / Q000503:physiopathology*; D009333:Neck; D009424:Nervous System Physiological Phenomena; D010146:Pain / Q000150:complications; D005082:Physical Exertion; D011817:Rabbits; D012890:Sleep / Q000502:physiology; D012892:Sleep Deprivation; D013312:Stress, Physiological / Q000150:complications
D012739:Gonadal Steroid Hormones