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Pathogenesis of migraine

K M Welch1

  • 1Department of Neurology, Henry Ford Hospital and Health Sciences Center, Detroit, Michigan 48202, USA.

Seminars in Neurology
|January 1, 1997
PubMed
Summary

Migraine mechanisms are reviewed, exploring aura via ischemia and spreading depression, and headache via trigeminovascular and brainstem pathways. Neuronal hyperexcitability may trigger attacks, potentially linked to mitochondrial issues or magnesium deficiency.

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Magnetoencephalographic fields from patients with spontaneous and induced migraine aura.

Annals of neurology·2001

Area of Science:

  • Neurology
  • Neuroscience
  • Pathophysiology

Background:

  • Migraine is a complex neurological disorder with poorly understood underlying mechanisms.
  • Current hypotheses involve various central and peripheral pathways contributing to migraine attacks.

Purpose of the Study:

  • To review and synthesize prevailing hypotheses regarding the mechanisms of migraine aura and headache.
  • To discuss potential factors contributing to brain hyperexcitability between migraine attacks.

Main Methods:

  • Literature review of current scientific hypotheses and models of migraine.
  • Analysis of proposed mechanisms for migraine aura (e.g., transient cerebral ischemia, spreading depression).
  • Examination of proposed mechanisms for migraine headache (e.g., trigeminovascular, brainstem pathways).

Main Results:

  • Aura mechanisms are hypothesized to involve transient cerebral ischemia and spreading depression.
  • Headache mechanisms are linked to trigeminovascular activation and brainstem involvement.
  • Neuronal hyperexcitability between attacks may be influenced by mitochondrial dysfunction, magnesium deficiency, or calcium channel abnormalities.

Conclusions:

  • The precise generation centers for migraine attacks (cortical vs. brainstem) require further investigation.
  • Understanding these mechanisms is crucial for developing targeted migraine therapies.

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