Regarding the biological mechanisms, in the present work, we focused on the role of hyperactivation of GABAergic neurons in CSD propagation, which could result from hemiplegic migraine mutations of the SCN1A gene, causing gain of function of NaV1.1 voltage-gated sodium channels leading to hyperexcitability of GABAergic neurons [11, 13, 25, 26]. The gene discussed is SCN1A; the disease is familial or sporadic hemiplegic migraine.