Migraine and Epilepsy—Shared Mechanisms within the Family of Episodic Disorders

摘要: Migraine and epilepsy are episodic disorders that share many clinical features underlying pathophysiological mechanisms. Cortical spreading depression (CSD), a wave of profound cellular depolarization, is believed to underlie migraine aura be trigger for the headache pain in migraine. However, initial event preceding CSD hyperexcitability associated with localized epileptiform discharges. Glutamate critical mediator both focal seizures In epilepsy, seizure generation spread mediated by synaptically released glutamate acting on AMPA receptors, whereas triggering depends NMDA receptors does not require synaptic transmission. Some antiepileptic drugs prevent occurrence attacks, supporting view neuronal an initiating event. Epidemiological studies demonstrate comorbid conditions. This likely due shared genetic or environmental factors (such as head injury) lead brain hyperexcitability. Strong support basis comes from familial hemiplegic (FHM), autosomal dominant syndrome characterized severe migraine, arises result mutations genes membrane ion transport proteins CACNA1A (P/Q-type voltage-gated calcium channel), ATP1A2 (Na+-K+ ATPase), SCN1A (voltage-gated sodium channel). Allelic all three also cause generalized some cases epilepsy. Certain each co-occurrence FHM same family members; cases, occur during attacks (“migralepsy”). While hypersynchronous discharges present key unanswered question why activity propagates transitions Insights into commonalities pathophysiology may suggest new treatment approaches