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Show /lHl,,,,,1 of C/illie,,1 NCllw-0l'htllfllmolosy ('I(.! I: 72--7.1, J98b. Editorial Comments Migraine Migraine headache and equivalents are rubrics for symptom complexes which probably express themselves through two final common pathways (1). The first is seen in classic migraine and is associated with spreading oligemia (2-6), paralleling the spreading depression of Leao (7); the second underlies common migraine and is unassociated with oligemia. How the classic vasoactive theory of Wolff (8) and its physiologic relationship to the locus ceruleus (9) fits in, if at all, is not abundantly clear from the literature. Proof that multiple mechanisms exist that can trigger final common pathways is found in the literature where autonomic, immunologic, hematologic, and humoral mechanisms have been implicated as causative factors of migraine (10-12), and a large variety of drug classes have been shown to be effective in the acute and prophylactic treatment of various subpopulations of "migraine": nonsteroidal antiinflammatory agents-aspirin and indomethacin; alpha-adrenergic agents-isoproterenol; betablockers- propranolol and timolol; tricyclic antidepressants- amitriptyline; slow channel calcium blockers-nifedipine; antiserotonins- methysergide; parasympathomimetics-ergotamines (13); as well as acupuncture and biofeedback. In this issue of the Journal (page 69), Barrett Katz reports a patient with well-documented classic and ophthalmic migraine who developed an ophthalmic artery (?) occlusion following the institution of therapy with nonspecific betablocker propranolol. The patient had taken just three doses of propranolol of 20 mg each. Two previous reports in the literature cite similar catastrophic events in the setting of complicated migraine. Prendes (14) reported a patient with a history of transient left upper extremity weakness and subsequent left monocular blindness who developed right-sided weakness and dysphasia while on propranolol, aspirin, and dipyramidole. During the initial sequence of therapy propranolol was discontinued and when reinstituted was associated with a clinical worsening of his motor strength and dysphasia. Subsequently, Gilbert 72 © 1986 Raven Press, New York (15) reported a patient who was experiencing a crescendo in the number and severity of her classic migraine attacks. The patient was found to be mildly hypertensive, and therapy was instituted with propranolol, 20 mg t.Ld. Two weeks later, while taking a shower, she developed dysarthria, left hemiplegia, left sensory defect, and a dense left homonymous hemianopia. The question facing the informed clinician is whether the development of the permanent neurologic sequelae in these patients was related to the use of propranolol or was a chance occurrence unrelated to the use of the beta-blocking agent. It is clear from a careful review of the literature (16,17) that pharmacologically propranolol, in the appropriate clinical milieu, can aggravate adrenergically induced vasospasm by blocking the vasodilatory action of beta2-agonists and, to compound this effect, by directly decreasing cerebral blood flow cardiogenically or by inducing orthostatic hypotension (18,19). With rare exception (20), the available studies on the use of beta-blockers in migraine fail to differentiate between classic and common migraine in their results sections, and the only reasonable conclusion that can be drawn is that these drugs can decrease the frequency and occurrence of common migraine (21-26). Thus, it would seem prudent to recommend that in cases in which oligemia can be invoked as underlying part of the migraine complex, i.e., classic migraine, ophthalmic migraine, hemiplegic migraine, vertebrobasilar migraine, and complicated migraine, beta-blocking agents only be used with extreme caution. [Propranolol is approved only for use in the prophylaxis of common migraine (27).] R. M. Burde, M.D. Departments of Ophthalmology and Neurology and Neurological Surgery Washington University School of Medicine St. Louis, Missouri REFERENCES 1. Hachinski v: Common and classic migraine. One or two entities? Arch. Neural. 1985;42:277. EDITORIAL COMMENT: MIGRAINE 73 2. Olesen J, Helt-Hansen P, Henrikst'n L, Lars,'n B. Till' common migraine .lttack may not l,.. initiat"d by l'l'rl'l'r.ll ischaemia. 1."11"1'1 1981;2:438-40. 3. 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Saper J.R.: Migraine. 1. Classification and pathogenesis. lAMA 1978;239:2380-3. 11. Blau, J.N.: Migraine pathogenesis. The neural hypothesis reexamined. f. N,'lIrol Nellr"slIrg Psycilial 1984;47:437-42. 12. Linet MS, Stewart WF. Migraine headache. Epidemiologic perspectives. ["idemi,,1 R,'l' 1984;6:107-39. 13. Appenzeller 0, Feldman RG, Friedman AP. Migraine, headache, and related conditions-Panel 7. Arch NellTl,1 1979;36:784-805. 14. Prendes JJ. Considerations on the use of propranolol in complicated migraine. H"lIdache 1980;20:93-5. 15. Gilbert GJ. An occurrence of complicated migraine during propranolol therapy. llcadache 1982;22:81-3. 16. Frishman WHo Beta,adrenoceptor antagonists: new drugs and new indications. N EIISI I Med 1981;305:500-6. 17. Kup"rsmith MJ, Hass WK, Chase NE. Isoprotereno] treatmt'nt of visual symptoms in migraine. Slroke 1979;10:299305. Ill. M"yt'r JS, Okamoto S, Sari A, Koto A, Itoh Y, Ericsson AD. Effects of bl'la-adrenergic blockage with propranolol on the (l'rebral blood flow, autoregulation and CO2 responsiveness. Stroke 1974;5:167-9. 19. Weber RB, Reinmuth OM. The treatment of migraine with propranolol. Nellro/":<:'1f 1':172;22:366-8. 20. B~rgesen SE, Nidsen JL. Mf)lIer CE. Prophylactic treatment of migraine with propranolol. A clinical trial. Acta Nellrol Scalld 1974;50:651-6. 21. Lance JW. Headache. AIIII Nellrol 1981;10:1-10. 22. Raskin NH, Schwartz RK. Interval therapy of migraine. Long-term results. Headache 1980;20:336-40. 23. Rosen J. A.: Observations on the efficacy of propranolol for the prophylaxis of migraine. Anll. Nellrol. 1983;13:92-3. 24. Diamond S, Kudrow L, Stevens J, Shapiro DB. Long-term study of propranolol in the treatment of migraine. Headache 1982;22:268-71. 25. Helt-Hansen P, Standnes B, Kangasneimi P, Hakkarainen H, Olesen J. Timolol and propranolol for common migraine prophylaXis. Acta Nel/rol Scalld 1984;69(suppl 981:264-5. 26. Stellar S, Ahrens SP, Meibohm AR, Reines SA. Migraine prevention with timolol. A double-blind crossover study. lAMA 1984;252:2576-80. 27. Pilysiciall's desk re{awee, 39th ed. Oradell, NJ: ER Barnhart and Medical Economics Co., Inc., 1985:648. I (lin Neuro-ophl/laimol, Vol. 6, No 2. 1986 |