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Show Joumal of Clinical Neuro-opllthalmology 6(2): 69-71, 1986. Migrainous Central Retinal Artery Occlusion Barrett Katz, M.D. 19 1986 Raven Press, New York A 29-year-old man experienced a migrainous central retinal artery occlusion coincident with the initiation of propranoiol therapy. The pharmacological effects of beta-blockade are discussed, and the use of betablockade in the acute management of anterior visual pathway migraine is examined. Key Words: Migraine-Central retinal artery occlusion -Retinal stroke- Beta-blockade-Inderal From the Departments of Ophthalmology and Neurosciences, University of California at San Diego. Address correspondence and reprint requests to Barrell Katz, M.D., Departments of Ophthalmology and Neurosciences, University of California, San Diego, UCSD Eye Center, M-018, La Jolla, CA 92093, U.S.A. 69 That the transient manifestations of migraine can become permanent has been documented since the time of Charcot (1). When migraine affects the anterior visual pathways and permanent sequelae result, retinal or optic nerve stroke can ensue (2). This report describes a migrainous central retinal artery occlusion in a patient treated with propranolol. CASE REPORT A laborer first experienced hemicranial and retro-orbital headaches in his twenties. They were heralded by bilateral central scotomas and fortification specter. They occurred on a monthly basis and were unchanged over a decade. At age 28, the patient noted transient loss of vision in the right eye associated with his migraines. This monocular visual loss lasted minutes, was described as "a central blurriness," and resolved without sequelae. The characteristics of the headache phase were not altered. At age 29, he experienced his typical hemicranial headache associated with prolonged monocular visual loss, and sought medical attention. When examined 3 h into his ictus, he reported a return of useful vision in the right eye. He was normotensive, with normal general and neurological examination save for his visual system. Acuity was described as "a blurry 20/200 0.0., 20/20 0.5." Pupils were described as normal, as were both posterior poles. The patient was diagnosed as "complicated migraine" and begun on propranolol, 20 mg b.i.d. Over the ensuing 12 h, acuity of his right eye returned to near normal. The following day, while awake, he suffered a catastrophic loss of vision. This was acute, unfolded over minutes, and was not accompanied by visual hallucination or headache. He had taken a total of three doses of propranolol. Upon re-evaluation, blood pressure was found to be normal, without orthostatic change. 70 B, KATZ Visual acuity was hand motion 0.0., 20/20 0.5. His neurological examination was unchanged. He was referred to a neurologist who, 5 days later, noted a macular "cherry red" spot and sent him for consultation, When seen 7 days after the event, his visual acuity was counting fingers 0.0.,20/20 0.5. Color vision was intact in the left eye only. A relative afferent pupillary defect was present on the right. Ocular motility was normal. The right optic nerve head was pale and full, with marked attenuation of the retinal arteriolar tree. There was retinal edema most severe within the vascular arcade, greater inferiorly than superiorly, and a prominent "cherry red" spot (Fig. 1). The peripheral retina appeared normal. The left fundus was normal and the left optic nerve head small, with crowding of the nerve fiber layer. Visual-field testing on tangent screen revealed only an inferior island remaining in the right eye, with normal field of the left eye. Medical evaluation yielded normal hemogram, serology, and lipid profiles without evidence of coagulopathy or collagen vascular disease. Cerebrospinal fluid was normal, as was a 2-D echocardiogram and intravenous digital cerebrovascular angiogram. Over the ensuing weeks, his retinal edema subsided but left him with vision of counting fingers O. D. DISCUSSION Our patient suffered a migrainous central retinal FIG. 1. Fundus photograph of right posterior pole ilI~ strates macular edema with cherry-red spot, pale diSC edema, and attenuation of the peripapillary retinal vasculature. , ,-'II' '\I,·lIrtJ-0l'l1Ilrolll/ol. Vol, 6, No, 2. 1986 artery occlusion. This was coincident with the initiation of propranolol therapy and perhaps influenced by it. Cerebral infarction has been reported in migrainous patients taking propranolol (3,4). Central retinal artery occlusion has been documented in migraine (5). To our knowledge, retinal stroke coincident with propranolol therapy has not been reported. Propranolol has been used successfully in both acute and prophylactic treatment of migraine, suggesting that adrenergic mechanisms are involved in the migraine pathophysiology (6). Experimental evidence suggests that alpha-adrenergic receptors mediate vasoconstriction and betaadrenergic receptors mediate vasodilation. The obvious pharmacologic effect of beta-blockade in peripheral vascular beds is to allow alpha-adrenergic action to be unopposed and thereby cause vasoconstriction. Such beta-blockade potentiation of vasoconstriction has been demonstrated in the digital circulation of man (7). The primate central retinal artery in its intraorbital course has been shown to have a heavy mesh of adrenergic fibers superimposed on its muscular coats (8-10). Betablockade in our patient with anterior visual pathway migraine may have changed the autonomic tone of the microcirculation of the eye and contributed to the central retinal artery occlusion by exacerbating the vasoconstrictive phase of his migraine. Other mechanisms for the role of propranolol can be implicated. Though the existence of betaadrenergic central retinal artery receptors in humans is controversial, the cvclic AMP-induced relaxation of vascular smooth ~uscle appears established in animal models (11,12). That levels of cyclic AMP are beta-adrenergic agonist-dependent has been demonstrated (11,12), so beta-antagonism would be expected to decrease levels of cyclic AMP and thereby contribute to vasoconstriction. Propranolol also may prevent the uptake of serotonin by platelets and thereby increase the amount of extracellular serotonin, which then becomes available for vasotonic action on a peripheral vascular bed (13). The role of beta-adrenergic blockade in worseni~ g our patient's vasoconstriction remains speculative. Indeed, one might argue that propranolol would inhibit thromboxane synthesis and platelet ~ggregation, thus affording some protective effect 10 the setting of impending vascular thrombosis (14). Our patient received a modest dose of propranolol. As much as 50-70% of an oral dose is extracted and metabolized in the liver, so the bioavailability of single small doses has to be very low, most of the drug haVing been removed during the MIGRAINOUS RETINAL STROKE 71 first pass through the liver (15). Peak blood levels do not occur until hepatic binding is saturated; certainly our patient had not reached that point yet. Propranolol is and will appropriately remain a gold standard in the clinical management of migraine. Our patient's course does raise questions about the management of anterior visual pathway migraine. Perhaps such patients ought to be treated differently from those with predominantly posterior circulation symptomatology (2). Avoidance of beta-blockade may be a therapeutic concern. Indeed, active intervention with a beta-agonist, such as isoproterenol, may offer protection from the transient visual symptoms becoming permanent (16). Acknowledgment: The author thanks Dr. Jose Laguna for bringing this case to his attention. REFERENCES 1. Fere c.: Contribution Ii /'etude de la migraine ophthalmiqlle. Paris, 1881. 2. Katz B., Bamford c.: Migrainous ischemic optic neuropathy. Neurology 1985;35:112-4. 3. Prendes J. L.: Considerations on the use of propranolol in complicated migraine. Headache 1980;20:93-S. 4. Gilbert G. J.: An occurrence of complicated migraine during propranolol therapy. Headache 1982;21:81-3. 5. Galezowski X.: Ophthalmic megrim. Lancet 1882;1:176. 6. Tokola R., Hokkanen E.: Propranolol for acute migraine. Br Med 11978;2:1089. 7. Yasue H., Touyana M., Shimamoto M., Kato H., Tanaka 5., Akiyama F.: Role of autonomic nervous system in the pathogenesis of Prinzmetal's variant form of angina. Circula! iOll 1974;50:S34-9. 9. Ehinger B.: Adrenergic nerves to the eye and to related structures in man and in the cynomolgus monkey. Invest Ophthalmol Vis Sci 1966;5:42-52. 9. Laties A. M.: Central retinal artery innervation. Arch OphthalmoI1967; 77:40S-9. 10. Laties A. M., Jacobowitz D.: A comparative study of the autonomic innervation to the eye in monkey, cat, and rabbit. Anat Res 1966;156:383-96. 11. Flamm E. 5., Kim J., Lin J., Ransahoff J.: Phosphodiesterase inhibitors and cerebral vasospasm. Arch Neurol 1975;32:569-71. 12. Flamm E. 5., Viau A. T., Ransahoff J., Naftchi N. E.: Experimental alterations in cyclic AMP concentrations in the cat basilar artery. Neurology 1967;26:646-6. 13. Frishman W. H.: Beta-adrenoceptor antagonists: new drugs and indications. N Engll Med 1981;305(9):500-S. 14. Campbell W. B., Callahan K. 5., Johnson A. R., et al.: Antiplatelet activity of beta-adrenergic antagonist: inhibition of thromboxane synthesis and platelet aggregation in patients receiving long-term propranolol treatment. Lancet 1981;2:1382-4. IS. Evans G. H., Shand D. G.: Disposition of propranolol. V. Drug accumulation and steady state concentrations during chronic oral administration in man. Clin Pharmacol Ther 1973;14:487-93. 16. Kupersmith M. J., Hass W. K., Chase N. E.: Isoproterenol treatment of visual symptoms in migraine. Stroke 10(3):299-30S, 1979. 1CJiIl Neuro-ovhthalmol. Vol. 6. No.2. 19i1i1 |
