Migraine and epilepsy share many characteristics with the broader group of episodic disorders that include the various forms of the congenital long QT syndrome (disorders of cardiac muscle) and different myotonias and periodic paralyses (disorders of skeletal muscle).17Although they affect diverse organ systems and have different outward manifestations, such episodic disorders have a number of common features. They often occur in otherwise healthy individuals and the attacks may be precipitated by factors such as stress, fatigue, or diet. Episodic disorders often have a genetic component and are first experienced in infancy, childhood, or adolescence. As the genetic bases of the syndromes have been identified, it has become clear that many episodic disorders are caused by defects in membrane ion channels or, more broadly, ion (or neurotransmitter) transport molecules. Disorders associated with defects in ion channels have become known as channelopathies. Since ion channels are the principal mediators of cellular excitability properties, it can be presumed that the underlying pathophysiologic basis of diverse channelopathies is altered cellular excitability. For some episodic disorders—for example, some genetic epilepsies, long QT syndromes, and periodic paralyses—it has been possible to define the specific nature of the change in cellular excitability that results from the mutations that cause the disorders. Often this is a gain-of-function increase in excitability, but in some instances there may be a reduction in excitability in a specific cell population (for example, in inhibitory interneurons) that leads to a net increase in circuit excitability (as in severe myoclonic epilepsy in infancy18). Additional evidence for a common pathophysiologic basis among the episodic disorders is that they may occur together. In particular, there is strong evidence of comorbidity between migraine and epilepsy.19Moreover, in at least 1 episodic disorder, childhood epilepsy with occipital paroxysms, the attacks have features of both migraine and epilepsy. In this syndrome, partial seizures begin with a visual migrainelike aura and in some cases are followed by postictal migrainelike headache. The comorbidity does not necessarily imply that epilepsy and migraine share a common genetic basis in all instances.20Rather, in cases in which there are environmental contributions to the pathogenesis (for example, in a head injury, which is a risk factor for both epilepsy and migraine), it is possible that the state of brain hyperexcitability causes some individuals to manifest both epileptic seizures and migraine attacks. It is also the case that migraine attacks may, albeit rarely, trigger epileptic seizures (preictal headache), and seizures often initiate headache (postictal headache), which patients may recognize as similar to their migraines.