The proceedings of a symposium on “The scientific basis of migraine management” held Feb 1999 at Lake Louise, Alberta, Canada, are reported from the University of Calgary and other centers. [1]

Pathophysiology. Local vasodilatation of intracranial extracerebral blood vessels, and consequent stimulation of surrounding trigeminal sensory nervous pain pathways, causes release of vasoactive neuropeptides that sensitize neurons in the brain stem trigeminal nuclei and increase the pain response. The clinical effectiveness of 5-HT serotonergic agonists (triptan anti-migraine agents) is related to vasoconstriction, and inhibition of nociceptive transmission in peripheral nerve terminals in the meninges and in central terminals in brain stem sensory nuclei. [2]

Biology of Serotonin Receptors. Serotonin receptors are highly heterogeneous (5-HT, 1-7), and specific subtypes are associated with the pathogenesis or treatment of migraine headache. Availability of subtype selective 5-HT receptor agonists allow further proof of the neural/vascular hypothesis for migraine. [3]

Genetic basis of migraine. Migraine etiology is multifactorial and genetically complex, with aggregation in families due to environmental and genetic tendencies. Familial hemiplegic migraine (FHM) is autosomal dominant, with 50% of families linked to chromosome 19pl3 and mutations in a calcium channel alpha 1A subunit. FHM represents a CNS channelopathy. Migraine with or without aura may also be linked to chromosome 19p, or to Xq28 locus. [4]

Migraine prophylactic drug therapy. The scientific evidence based on randomized double-blind, placebo controlled trials, rates migraine prophylactics in the following order of efficacy: metoprolol has an average score of 4.3 (maximum 5); divalproex 3.8; amitriptyline 2.3; atenolol 2.3; flunarazine 2.2; and propranolol 1.4. The placebo response varies from a 32% reduction in migraine frequency to a 7% increase in frequency in various trials. Migraine prophylaxis is largely disappointing, a minority having significant benefits that make the risk of adverse effects worthwhile. Other newer antimigraine agents include the antiepileptics, gabapentin and topiramate, and riboflavin. A combination of an antidepressant and a B-blocker may act synergistically, but monotherapy is often preferred. [1]

COMMENT. This journal supplement provides an excellent review of the scientific advances in migraine mechanism and management. One paper also emphasizes the role of psychological treatments, especially relaxation training and biofeedback, in refractory migraine. The following report might also indicate the influence of psychological factors on the frequency of migraine attacks.

Pulsing electromagnetic fields (PEMF) in treatment. This novel therapy was studied by double-blind, placebo-controlled trial in 42 adults at the Orthopedic Surgery Service, Madigan Army Medical Center, Tacoma, WA [5]. Exposure of the inner thighs to PEMFs for at least 3 weeks was considered an effective, short-term prophylactic treatment for migraine, but not in patients with tension headaches.

Increased incidence of migraine headache in female subjects of all ages is reported from the Mayo Clinic, following a study in Olmsted County, Rochester, MN, comparing the 1979-1981 period and 1989-1990. The peak incidence at age 20-29 years increased from 634 new cases per 100,000 person-years to 986 in a decade. [6]

Increased brain serotonin synthesis in migraine was demonstrated using PET in 11 women patients in comparison to 8 healthy controls. The results are consistent with reports of systemic alteration of serotonin metabolism in patients with migraine without aura. [7]