Migraine headache is a highly prevalent and disabling neurological primary headache disorder. It is characterized by disabling, throbbing, episodic, unilateral headaches associated with neurologic features such as photophobia, phonophobia, or autonomic symptoms like nausea and vomiting lasting 4 to 72 hours at a time. Patients will often avoid bright lights or loud noises. About 30% of migraine patients experience auras which are unilateral focal neurological disturbances prior the headache onset, often manifested as visual, sensory, or motor symptoms. Pathophysiology of migraine headache is still unclear and is being studied; however, calcitonin gene-related peptide (CGRP) is believed to play a major and important role, and therefore has become a primary therapeutic target. This was supported by the finding of CGRP release during acute migraine attacks and then subsequent normalization of CGRP levels after efficacious sumatriptan treatment. These findings have been a focal point in recent pharmacological developments in managing migraine headaches.

Think of seizure mimics before you diagnose epileptic seizures. Some mimics such as syncope, transient ischemic attacks (TIA), and migraines may be associated with EEG abnormalities. Seizure mimics may be neurological, systemic, or psychological. Always confirm if the event in question is consistent with the patient’s typical event as the patient may have more than one type of event. Though uncommon, both epileptic and nonepileptic events may coexist; hence it is important to characterize each of the patient’s event types on video EEG.