Appropriate and effective treatment for migraine first assumes an accurate diagnosis. In general, the treatment of migraine may be divided into two general pharmacologic approaches: treatment of the acute attack (abortive, symptomatic) or preventative (prophylactic ) therapy aimed at preventing the recurrence of headache. Patients often may need both treatments if their headaches are frequent and severe. As pointed out by Silberstein and Lipton {9}symptomatic treatment is appropriate for most acute attacks and should be used a maximum of two to three days per week. If attacks occur more frequently, treatment strategy should emphasize decreasing attack frequency with prophylactic medications. A full discussion of migraine therapy is reviewed by Baumel.{207}

Medications used in acute headache treatment include analgesics, antimedicanzietyalytics, nonsteroidal anti-inflammatory drugs (NSAIDs), ergots, steroids, major tranquillizers, narcotics, and more recently the selective 5HT1 (serotonin) agonists. The primary serotonin agonist is sumatriptan originally introduced in the United States in subcutaneous form but recently available in oral dosage. {208-211} Preventive therapy include a broad range of medications most notably calcium channel blockers, beta blockers, antidepressants, serotonin antagonists, and anticonvulsants.  A new agent, Lisinopril, an antihypertensive agent, is effective in migraine prophylaxis according to a report in the British Medical Journal in January 2001.

Headaches similar to migraine can be triggered by serotonergic drugs such as reserpine and m-chloralphenalpiprazine (serotonergic agonist).{27,28} Two agents effective in the acute treatment of migraine, are sumatriptan,{212-214} a serotonin analogue, and dihydroergotamine (DHE), {215,216} an ergot derivative. These agents block the development of neurogenically induced inflammation in rat dura mater. This in turn blocks the release of neuropeptides including substance P and calcitonin gene-related peptide, preventing neurogenic inflammation.{9 } The NSAIDs may also block neurogenic inflammation; the mechanism of this action, however, is less certain.