Family physicians frequently treat patients with migraine headaches successfully; however, some patients fail to respond and require emergency intervention. Kelly reviewed the physiology and emergency management of common migraine, or migraine without aura. This entity is described as an “idiopathic, recurring headache disorder manifesting in attacks lasting four to 72 hours. Typical characteristics are unilateral location; pulsating quality; moderate or severe intensity; aggravation by routine physical activity; and association with nausea, photophobia and phonophobia.” The less common migraine with aura is a similar recurring headache disorder preceded by attacks of neurologic symptoms localized to the cerebral cortex or the brain stem and lasting less than 60 minutes. Uncommon variants include ophthalmoplegic and abdominal migraines.

Knowledge about the pathophysiology of migraines continues to evolve. The headache pain seems to result from the activation of the trigeminovascular system with chemical triggers originating in the brain, blood vessel walls and the blood. The trigeminovascular axon stimulation causes pain and the release of vasoactive neuropeptides that act on mast cells, endothelial cells and platelets, increasing extracellular levels of arachidonate metabolites, amines, peptides and ions. These mediators and the related tissue injury prolong pain and hyperalgesia. Serotonin and magnesium also appear to have a role in migraine development.

Severe migraine that has been unresponsive to oral medications requires further treatment. Compilation of treatment efficacy is difficult because of absence of evidence or small studies. Phenothiazines are antipsychotic drugs acting as powerful antagonists of the neurotransmitter dopamine in the basal ganglia and limbic system. They also have anticholinergic and antiemetic properties and seem to change pain perception through neuroleptic action. Intravenous chlorpromazine (12.5 mg repeated at 20-minute intervals to a total dose of 37.5 mg) has good efficacy in aborting migraine headaches. Intravenous fluids may be given to avoid orthostatic hypotension.

Small studies of prochlorperazine have shown that 10 mg given intravenously provides good pain relief. Ergot alkaloids strongly bind to serotonin receptors inhibiting the trigeminal nerve–mediated neurogenic inflammation. Dihydroergotamine mesylate (DHE) can resolve migraine but has frequent gastrointestinal side effects. Comparisons with triptans are inadequate to define efficacy. Haloperidol, a dopamine antagonist, has antiserotonin effects, and patients treated with 5 mg intravenously after a bolus of 500 to 1,000 mL of intravenous fluid can achieve relief of migraine pain within one hour.

Ketorolac, a nonsteroidal anti-inflammatory agent that inhibits prostaglandin synthesis, platelet aggregation and serotonin release from platelets with a dose of 60 mg given intramuscularly has effectiveness similar to that of meperidine in headache relief. Meperidine is a synthetic narcotic analgesic that can be effective at a dose of 75 mg intravenously or intramuscularly but often does not provide lasting analgesia, and its use may lead to dependence. The triptans are specific and selective serotonin agonists that block serotonin receptors and the resultant neurogenic inflammation. Headache relief rates are good, but recurrence of headache within 24 hours is frequent. Magnesium sulfate infusion is most helpful in patients with migraine who have low ionized magnesium concentrations.

In conclusion, the author finds that the usefulness of haloperidol and magnesium sulfate requires more study. Ketorolac, metoclopramide and meperidine are useful, but there are better choices. Data on DHE are unclear, but this agent appears to be less useful than chlorpromazine and sumatriptan in treating acute migraine pain. The most effective medications at this time appear to be prochlorperazine, chlorpromazine and sumatriptan, each having a pain-relief efficacy in acute migraine of greater than 70 percent.