What is the pathogenesis of pediatric migraine headache?

Updated: Jan 02, 2019
  • Author: J Ivan Lopez, MD, FAAN, FAHS; Chief Editor: George I Jallo, MD  more...
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Answer

Although much remains to be discovered, the pain in migraine attacks is multifactorial. One mechanism suggests activation of the trigeminovascular system. Synaptic boutons of the perivascular branches of the trigeminal nerve at the level of meningeal and basal cerebral vessels release the following proinflammatory mediators when the nerve is stimulated:

  • Substance P

  • Calcitonin gene-related peptide (CGRP)

  • Vasoactive intestinal peptide (VIP)

The initial triggers are still poorly understood. The mediators create neurogenic inflammation, including local rupture of the blood-brain barrier, and trigger vasodilatation, further stimulating the trigeminal nerve terminals. (See the image below.)

Trigeminovascular system. The trigeminal nerve fib Trigeminovascular system. The trigeminal nerve fibers around basal cerebral and meningeal vessels are triggered (various stimuli are possible), and a vicious cycle starts in which the nerve terminals release calcitonin gene-related peptide (CGRP), substance P, vasoinhibitory peptide (VIP), and other mediators of local neurogenic inflammation and vasodilatation. The latter further stimulates the nerve endings. On the other end of the nerve, painful messages are transmitted toward central centers, including thalamus and cortex, and the sensation of pain arises. Modern drugs, such as the triptans, act at 3 levels, via 5-HT 1 B and D receptors; they vasoconstrict the vessels, reduce the release of the above-mentioned mediators, and decrease the central transmission of pain impulses.

On the other end, pain afferent messages are transmitted centrally. Whether this system is abnormal in migraineurs versus healthy people, and whether it is genetically determined, is not known. Evidence exists of cortical hyperexcitability in migraineurs, which may be linked to a defect in the central catecholaminergic systems. Low magnesium levels also may play a role.

White-matter T2 MRI hyperintensities are observed in higher frequency in migraineurs with aura, especially in the posterior circulation territories. The pathophysiologic implication of this remains unclear.

Chronic transformation of migraine is believed to be due to spatial and temporal, central and peripheral sensitization, which correlates clinically with cutaneous allodynia.


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