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“COMPLICATED MIGRAINE” ITS ASSOCIATION WITH INCREASED PLATELET AGGREGABILITY AND ABNORMAL PLASMA COAGULATION FACTORS

Z. Kalendovsky, J. Austin
Published 1975 · Medicine

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The reasons for the prolonged and selective focal cerebral ischemia in complicated migraine remain to be clarified. The results of this study of coagulation mechanisms suggest that small thromboemboli may further compromise the cerebral perfusion in migraine. Platelet aggregability to ADP, epinephrine and serotonin was studied in seven patients with complicated migraine 2 weeks to 1 year after an episode of focal cerebral dysfunction. In addition, twelve patients who had uncomplicated migraine were also studied in between headaches. The patients with complicated migraine also had, during the acute stage of their focal cerebral ischemic episode, a detailed analysis of plasma factors that promote and inhibit coagulation. Each of the clotting abnormalities tended to correlate with the neurological outcome of the ischemic episode: 1. Patients with the most hyperaggregable platelets, but normal plasma coagulation factors had many transient episodes dating from childhood and early adolescence, compatible with fragile, white platelet thrombi. 2. Patients with dual coagulation abnormalities presented with a completed stroke as one of their first episodes of focal cerebral dysfunction, and they did so significantly later in life, after they had had many uncomplicated migraine attacks. Their platelets were no more hyperaggregable than those of many patients with uncomplicated migraine. It is therefore postulated that the decisive new element was the plasma hypercoaguability. Most of these patients had taken estrogens for many months, but not necessarily immediately before their stroke. Their family history was strongly positive for conditions predisposing to early disease of the vessel wall. Such conditions were absent in relatives of the patients with complicated migraine who had normal plasma coagulation factors. The high incidence of platelet hyperaggregability in these series of patients with complicated and uncomplicated migraine is discussed. The direct and indirect effects of estrogens on coagulation mechanisms are noted. In these patients, complicated migraine appears to be an association of the genetic disorder migraine together with platelet, plasma, or vessel wall abnormalities which may accentuate the ischemic process. REFERENCES 1. Brendshaw, P., and Parsons, M.: Hemiplegic migraine, a clinical study, Quart. J. Med., 34:65, 1965. 2. Whitty, C. W. M.: Familial hemiplegic migraine, J. Neurol. Neurosurg. Psychiat., 16:172, 1953. 3. Bickerstaff, E. R.: Basilar artery migraine, Lancet, 1:15, 1961. 4. Rosenbaum, H. E.: Familial hemiplegic migraine, Neurol., 10:164, 1960. 5. Simard, D., and Paulson, O. B.: Cerebral vasomotor paralysis during migraine attack, Arch. Neurol., 29:207, 1973. 6. O'Brien, M. D.: Cerebral blood changes in migraine, Headache, 10:139, 1971. 7. 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ACKNOWLEDGEMENT The following tests were performed in the Coagulation Laboratory of the Department of Medicine through the kindness of Kurt von Kaulla, M.D.: thrombin generation, antithrombin III activity, euglobulin lysis time, spontaneous platelet aggregation in platelet-rich plasma, thromboelastograms. Zdenka Kalendovsky, M.D., is the recipient of a Neurology Traineeship as part of Veterans Administration Training Program TR-176. The screen filtration pressure apparatus was purchased with a grant from the Japan Arteriosclerosis Research Foundation. Reprint requests to: Zdenka Kalendovsky, M.D. Department of Neurology University of Colorado Medical Center 4200 East 9th Avenue Denver, Colorado 80220
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