Migraine is a common, chronic, intermittently disabling neurovascular disorder. Migraine peaks between 15 and 24 years of age with the greatest prevalence between 35 and 45 years. The International Headache Society has classified migraine with six subtypes.
The presence of aura differentiates the first two sub-types of migraine. Migraine with aura is further sub-typed by familial or sporadic hemiplegic migraine. Hemiplegic migraine presents with motor weakness.
Migraine that attacks with monocular visual disturbances is subtyped as retinal migraine. Migraine sub-types are also classified according to associated complications: chronic migraine and status migrainosus, which is a debilitating migraine lasting more than 72 hours. Other complications include migraine-triggered seizures or a migrainous infarction, which requires neuroimaging to verify the presence of an ischemic brain lesion.
Patients often experience migraine without aura, typical aura with migraine headache, and typical aura without headache. Migraine risks increase when a patient presents with the following: asymmetry of pain; throbbing pain; pain that is moderate to severe in intensity; pain accompanied by nausea and sensitivity to light, sound, and often smell; the presence of typical migraine aura symptoms; and a family history of migraine.
A three-question screen can help with the diagnosis of migraine. The screen asks if the patient felt nauseated or sick to his or her stomach in the last 3 months. It asks if light has bothered him or her more when not experiencing headaches. Finally, it asks if headaches limited the patient’s ability to work, study, or complete daily tasks for at least 1 day.
The pathophysiology of migraine is due in part to the sensory input from the trigeminal nerve and the ninth and tenth cranial nerves, humoral factors (eg, blood glucose, ingested food, gonadotrophic hormones), environmental factors (sleep, stress, smells, light, and changes in barometric pressure), and other factors.
Auras are caused by a localized decrease of blood flow immediately followed by an increase of blood flow. This wave depolarization affects the parieto-occipital cortex. This complex neurological symptom typically presents just before a migraine attack.