Abstract
Migraine is increasingly recognized as a disorder of altered neuronal excitability, in part based on genetically mediated and environmentally modified aberrations of ionic exchange across the brain neuronal membrane. To this end, migraine pharmacotherapy aids in restoring the abnormally low threshold for neuronal excitation. Indeed, modulation of neuronal excitability is a common property of several established migraine preventive drugs such as propranolol, valproate, amitriptyline, and topiramate. Future migraine preventive pharmacologic therapies likely will aim at restoring the neuronal threshold for excitation by targeting such processes as cortical spreading depression and intracellular calcium influx. Also, strategies aimed at enhancing descending antinociceptive inhibition will yield effective antimigraine drugs.
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