Migraine results from dysfunction of the brain stem pathways that normally modulate sensory input. Abnormal metabolism of serotonin, a neurotransmitter found in brain cells, plays a major role. The headache is preceded by a rise in plasma serotonin, which dilates the cerebral vessels, but migraines are more than just vascular headaches. The exact mechanism of pain in migraine is not completely understood but is thought to be related to the cranial blood vessels, the innervation of the vessels, and the reflex connections in the brain stem.

Migraines can be triggered by menstrual cycles, bright lights, stress, depression, sleep deprivation, fatigue, overuse of certain medications, and certain foods containing tyramine, monosodium glutamate, nitrites, or milk products. Foods in these categories include aged cheese and many processed foods. Use of oral contraceptives may be associated with increased frequency and severity of attacks in some women.

Migraine with aura can be divided into four phases: prodrome, aura, headache, and recovery. Prodrome phase occurs hours to days before a migraine. Patient experiences irritability, depression, feeling cold, anorexia, diarrhea or constipation. Aura usually lasts less than hour. This period is characterized by focal neurologic symptoms. Visual disturbances are common. Other symptoms may include numbness and tingling of lips, face, or hands; mild confusion; slight weakness of an extremity; drowsiness; and dizziness. Headache occurs after the aura. Vasodilation and decrease in serotonin level causes headache. Headache is severe and incapacitating. Its duration varies from 4 to 72 hours. Then the pain gradually subsides.

Emotional or physical stress may cause contraction of the muscles in the neck and scalp, resulting in tension headache. The pathophysiology of cluster headache is not fully understood. One theory is that it is due to dilation of orbital and nearby extracranial arteries. Cranial arteries is thought to represent an immune vasculitis in which immune complexes are deposited within the walls of affected blood vessels, producing vascular injury and inflammation.

Therapy for migraine headache is divided into abortive and preventive approaches. The abortive approach, best employed in patients who suffer less frequent attacks, is aimed at relieving or limiting a headache at the onset or while it is in progress. The preventive approach is used in patients who experience more frequent attacks at regular or predictable intervals and may have medical conditions that preclude the use of abortive therapies.

The triptans, serotonin receptor agonists, are the most specific antimigraine agents available. These agents cause vasoconstriction, reduce inflammation, and may reduce pain transmission. The five triptans in routine clinical use include sumatriptan(Imitrex), naratriptan(Amerge), rizatriptan(Maxalt), zolmitriptan(Zomig), and almotriptan.

Ergotamine preparations may be effective in aborting the headache if taken early in the migraine process. They are low cost. Ergotamine tartrate acts on smooth muscle, causing prolonged contriction of the cranial blood vessels. Each patient's dosage is based on the individual needs. Side effects include aching muscles, paresthesias, nausea, and vomiting. Cafergot, combination of ergotamine and caffeine, can arrest or reduce the severity of the headache if taken at the first sign of an attack.

Perhaps the most widely used triptan is sumatriptan succinate(Imitrex); it is available in oral, intranasal, and subcutaneous preparations and is effective for the treatment of acute migraine and cluster headaches in adults. Subcutaneous form usually relieves symptoms within an hour and is available in an auto-injector for immediate patient use, although it is expensive in this form. Sumatriptan has been found to be effecting in relieving moderate to severe migraines in a large number of adult patients.

The medical management of an acute attack of cluster headache may include 100% oxygen by facemask for 15 minutes, ergotamine tartrate, sumatriptan, steroids, or a percutaneous sphenopalatine ganglion blockade.

The medical management for cranial arteritis consists of early administration of a corticosteroids to prevent the possibility of loss of vision due to vascular occlusion or rupture of the involved artery.