What is the trigemino-vascular theory of migraine etiology?

Updated: Aug 15, 2019
  • Author: William C Robertson, Jr, MD; Chief Editor: Amy Kao, MD  more...
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At present, the most widely accepted model of migraine is the trigemino-vascular theory. This theory proposes that migraine results from depolarization of cortical neurons followed by a reduction in posterior cerebral blood flow.

According to the trigemino-vascular theory, migraineurs have a hyperexcitable cerebral cortex. Genetic factors cause disturbances in neuronal ion channels, which allow a variety of external and/or internal factors to trigger episodes of regional neuronal excitation followed by cortical depression.

The initial phase is a wave of spreading cortical depression, which is associated with suppression of spontaneous electroencephalographic (EEG) activity and regional oligemia. The cortical depression begins in the occipital region, moves anteriorly during the course of an attack, and is thought to be responsible for the patient's aura, focal neurologic symptoms, or both.

This wave of cortical depression is preceded by brief ionic changes in neurons and glia causing prolonged depolarization and depression of EEG activity. These ionic changes move across the cortical gyri at 2-3mm/min, resulting in decreased neuronal activity.

The cortical depression stops at the central sulcus and then spreads ventrally to the meningeal trigeminal fibers, causing headache. Brain ion homeostasis falters, allowing an efflux of excitatory amino acids from nerve cells and enhanced energy metabolism. Activation of N -methyl-D-aspartate receptors may be involved. Decreased blood flow to the occipital cortex follows in response to the decreased neuronal activity.

A reactive hyperemic phase follows. This increased blood flow does not precisely follow the timing of the head pain.

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