” The authors propose that this central neuronal hyperexcitability involves overactivity of the excitatory amino acids, glutamate, and possibly asparate. Stimuli that activate the migraine attack evoke neuronal depolarization, slow deplorization shifts, and spreading suppression of spontaneous neuronal activity possible by glutamate and K+dependent mechanisms. A low brain Mg2+ and consequent reduced gating of glutamatergic receptors may provide the link between the physiologic threshold for a migraine attack and the mechanisms of the attack itself by promoting glutamate hyperactivity, neuronal hyperexcitability, and susceptibility to glutamate-dependant spreading depression.” The Concept of Migraine as a State of Central Neuronal Hyperexcitability https://www.neurologic.theclinics.com/article/S0733-8619(18)30319-0/abstract [...]