ATP1A2 and familial hemiplegic migraine: Taken together, the three different forms of FHM indicate the existence of a main pathophysiological pathway that, starting from excessive neuronal release of glutamate (CACNA1A), impaired glutamate reuptake by glial cells (ATP1A2), or enhanced glutamatergic activity due to impaired GABAergic inhibition (SCN1A), ultimately leads to altered glutamatergic neurotransmission, with consequent neuronal hyperexcitability and increased susceptibility to CSD (Ferrari et al., 2015).