Transient and persistent neurological manifestations of migraine.

THE CLINICAL SYNDROME of migraine is estimated to affect 23 to 29% of women and 15 to 20% of men.' This very common condition is characterized by recurrent attacks of headache associated with photophobia, anorexia, nausea, vomiting, and other autonomic disturbances and frequently by striking focal neurological manifestations. The episodes are distinctly varied in frequency, severity, and duration and separated by symptom-free intervals. A family history of vascular headaches is obtained in about 75% of cases. While agreed upon diagnostic criteria are lacking, migraine is subdivided as follows: common type if there are no associated neurological signs or symptoms; classic migraine if characteristic visual or other sensory or motor disturbances precede or accompany the headache; cluster headaches; lower half (facial) headaches; and hemiplegic and ophthalmoplegic migraine in which the neurological deficits outlast the headache phase. Decreased and increased cerebral and extracerebral blood flow, increased platelet aggregation, and increased platelet release of serotonin have been demonstrated in migraine. Current theories of pathogenesis have recently been reviewed and include primary cerebrocortical depression, primary vascular hypenreactivity, altered neural control of cerebral blood flow, and disordered central monoamine transmission affecting autonomic function or pain perception. The several varieties of migraine may represent more than one closely related entity. This report will focus on the transient and persistent neurological manifestations of migraine.