Migraine's Premonitory Phase: What Can We Learn From It?
In this review, we have discussed the prevalence of premonitory symptoms and postulated their potential mechanisms. Although these symptoms seem to be common, we need prospective studies in unselected patient populations to ascertain their true frequency. The nature of these symptoms and their potential mechanisms suggests the earliest changes in migraine, before headache comes on, are likely to be in the brain. The imaging findings in the premonitory phase are in keeping with such a central origin. Various brain areas including subcortical areas like the hypothalamus, dorsal raphe nuclei, PAG and locus coeruleus, and cortical areas like the frontal, occipital, and limbic cortex are involved. Hypothalamic involvement can explain many of the premonitory symptoms. Involvement of the brainstem structures mentioned here along with the hypothalamus may lead to facilitation of trigeminocervical complex activity and in turn the perception of pain. Symptoms of increased sensitivity to external stimuli are likely to result from direct involvement of brain structures, at least in part, independent of pain.
We now need well-designed, controlled, double-blinded trials to investigate if treatment during the premonitory phase can reliably prevent headache in selected patients who can predict a migraine headache. Researching this earliest clinical phase of migraine is likely to yield rich dividends for our understanding of the disorder and for the benefit of our patients.
Conclusion
In this review, we have discussed the prevalence of premonitory symptoms and postulated their potential mechanisms. Although these symptoms seem to be common, we need prospective studies in unselected patient populations to ascertain their true frequency. The nature of these symptoms and their potential mechanisms suggests the earliest changes in migraine, before headache comes on, are likely to be in the brain. The imaging findings in the premonitory phase are in keeping with such a central origin. Various brain areas including subcortical areas like the hypothalamus, dorsal raphe nuclei, PAG and locus coeruleus, and cortical areas like the frontal, occipital, and limbic cortex are involved. Hypothalamic involvement can explain many of the premonitory symptoms. Involvement of the brainstem structures mentioned here along with the hypothalamus may lead to facilitation of trigeminocervical complex activity and in turn the perception of pain. Symptoms of increased sensitivity to external stimuli are likely to result from direct involvement of brain structures, at least in part, independent of pain.
We now need well-designed, controlled, double-blinded trials to investigate if treatment during the premonitory phase can reliably prevent headache in selected patients who can predict a migraine headache. Researching this earliest clinical phase of migraine is likely to yield rich dividends for our understanding of the disorder and for the benefit of our patients.
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