Spreading depression: from serendipity to targeted therapy in migraine prophylaxis

被引:58
作者
Ayata, C. [1 ,2 ,3 ]
机构
[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol,Stroke & Neurovasc Regulat Lab, Boston, MA USA
[2] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Stroke Serv, Boston, MA USA
[3] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neurosci Intens Care Unit,Dept Neurol, Boston, MA USA
关键词
Spreading depression; migraine; prophylaxis; experimental models; drug screening; FAMILIAL HEMIPLEGIC MIGRAINE; CEREBRAL-BLOOD-FLOW; EXCITATORY SYNAPTIC-TRANSMISSION; GLUTAMATE-RECEPTOR BLOCKADE; C-FOS EXPRESSION; NMDA-RECEPTOR; CA2+ CHANNEL; DOUBLE-BLIND; CALCIUM-CHANNELS; NITROUS-OXIDE;
D O I
10.1111/j.1468-2982.2009.01982.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Despite the relatively well-characterized headache mechanisms in migraine, upstream events triggering individual attacks are poorly understood. This lack of mechanistic insight has hampered a rational approach to prophylactic drug discovery. Unlike targeted abortive and analgesic interventions, mainstream migraine prophylaxis has been largely based on serendipitous observations (e.g. propranolol) and presumed class effects (e.g. anticonvulsants). Recent studies suggest that spreading depression is the final common pathophysiological target for several established or investigational migraine prophylactic drugs. Building on these observations, spreading depression can now be explored for its predictive utility as a preclinical drug screening paradigm in migraine prophylaxis.
引用
收藏
页码:1095 / 1114
页数:20
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