ABSTRACT
The pathophysiology of migraine is complex. Even less is known about the genesis of tension-type headache. The migraine aura is probably due to cortical spreading depression (CSD). CSD is a spreading decrease in electrical activity that moves across the cerebral cortex at 2 to 3 mm/min. It is characterized by shifts in cortical steady state potential, transient increases in potassium, nitric oxide, and glutamate, and transient increases in CBF, followed by sustained decreases. Functional MRI studies of patients with migraine show that a period of hyperemia precedes the oligemia present during the migraine aura and the headache itself can begin before hyperemia, while blood flow in the cerebral cortex is still reduced. Headache probably results from activation of meningeal and blood vessel nociceptors combined with a change in central pain modulation. Headache and its associated neurovascular changes are subserved by the trigeminal system. Stimulation results in the release of substance P and calcitonin gene related peptide (CGRP) from sensory C-fiber terminals and neurogenic inflammation (4). Neurogenic inflammation sensitizes nerve fibers (peripheral sensitization), which now respond to previously innocuous stimuli, such as blood vessel pulsations, causing, in part, the pain of migraine. Central sensitization of trigeminal nucleus caudalis neurons can also occur. Central sensitization may play a key role in maintaining the headache. The migraine aura can trigger headache: CSD activates trigeminovascular afferents. This replaces the older theories of migraine pathophysiology of aura caused by vasoconstriction and headache caused by vasodilation.
