Abstract：
OBJECTIVES:To review conjectured modes of action of migraine triggers and to present a new hypothesis about them. BACKGROUND:Migraine attacks are initiated in many migraineurs by a variety of "triggers," although in some patients no external trigger can be identified. Many triggers provoke attacks with such a short latency that only some kind of neural mechanism can explain the triggering. RESULTS:We present here a hypothesis that the pain of migraine has its ultimate origin in the cortex, but that the immediate generator is in the brainstem. Our hypothesis is that most migraines have triggers that produce excitation of cortical neurons and that this directly causes withdrawal of descending sensory inhibition originating in the brainstem. A wide range of evidence from the literature that cortical activation induced by a number of different mechanisms often produces headache is presented to support this notion. Several nuclei in the brainstem appear to participate in the selective control of trigeminovascular sensation through descending inhibitory mechanisms that arise in the cortex. In this review we focus on 2 of them, the periaqueductal gray matter and nucleus raphe magnus. Our own past results and those of others show that this inhibition is specific for craniovascular sensation and involves the neurotransmitter 5-hydroxytryptamine. Finally, we summarize our own recent experiments, which show that cortical activation by migraine triggers (including cortical spreading depression) inhibits neuronal discharge in the brainstem and facilitates trigeminovascular sensation. CONCLUSION:If the hypothesis can be proven and the neurotransmitters involved in the hypothetical trigger pathway can be identified, it may be possible to develop novel migraine preventative therapies.
journal_name
Headachejournal_title
Headacheauthors
Lambert GA,Zagami ASdoi
10.1111/j.1526-4610.2008.01230.xsubject
Has Abstractpub_date
2009-02-01 00:00:00pages
253-75issue
2eissn
0017-8748issn
1526-4610pii
HED1230journal_volume
49pub_type
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