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Bilateral Retinal Infarction Br J Ophthalmol: First Published As 10.1136/Bjo.76.3.189 on 1 March 1992

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Bilateral Retinal Infarction Br J Ophthalmol: First Published As 10.1136/Bjo.76.3.189 on 1 March 1992 BritishJournal ofOphthalmology, 1992,76, 189-190 189 Complicated migraine resulting in blindness due to bilateral retinal infarction Br J Ophthalmol: first published as 10.1136/bjo.76.3.189 on 1 March 1992. Downloaded from Andrew M Glenn, Pamela J Shaw, John W Howe, David Bates Abstract macula (Fig 1). On this occasion she was treated Retinal migraine is not uncommon, but perma- with the calcium channel blocker nimodipine nent sequelae in the anterior visual pathway are and intravenous methyl prednisolone 1 g daily rare. We describe the case ofa young woman in for three days. No visual recovery occurred. whom blindness developed over a six-year The patient had not been taking an oral period due to recurrent episodes of migraine- contraceptive agent and had never been pre- related occlusions of a branch retinal artery. scribed ergot derivatives. Her father, brother, and niece also suffer from migraine. Migraine occurs in 10-25% of the population' and is more common in women than in men. EXAMINATION 'Complicated migraine' occurs in 1% ofcases and A general medical examination revealed no sig- is defined as an episode of classical migraine nificant abnormalities. In particular she was which results in a persisting neurological deficit.2 normotensive, the heart was clinically normal, Persisting visual morbidity in migraineurs is and there were no carotid or orbital bruits. Slit- usually caused by posterior cerebral hemisphere lamp examination revealed normal anterior seg- ischaemia.3 Permanent anterior visual pathway ments, and the intraocular pressures were 14 mm damage related to migraine has been reported Hg in both eyes. After the most recent BRAO her rarely. Several types of migraine-related retinal visual acuity was counting fingers in the right eye vascular lesions have been described, including and hand movements in the left. There was loss branch retinal artery occlusion (BRAO),"8 cen- of the central and superotemporal visual field of tral retinal artery occlusion,47 "'ciliary artery the right eye and loss of all but the superotem- occlusion,'2 anterior ischaemic optic neuropa- poral quadrant of the left. Funduscopy showed thy,'"" and central retinal vein thrombosis.'2 16 an acute occlusion ofthe inferotemporal arteriole Other retinal abnormalities described as on the right and optic atrophy plus attenuation of migraine related include; optic nerve haemor- the superior and inferior temporal arterioles on rhage,'7 disc oedema and retinal haemorrhage,'8 the left. A fluorescein angiogram, performed on inner retinal layer damage,'9 optic atrophy,4 and the right eye two days after the inferior temporal neuroretinitis.' BRAO (Fig 2) showed occlusion of the infero- http://bjo.bmj.com/ We report a case of a young woman who had temporal arteriole and evidence of the previous recurrent attacks of migraine-related BRAO superior macular branch arteriolar occlusion. affecting both eyes and resulting in legal blind- ness INVESTIGATIONS The following investigations gave normal or Case report negative results: full blood count, erythrocyte on September 27, 2021 by guest. Protected copyright. A 20-year-old housewife began experiencing sedimentation rate, routine biochemical screen- classical migraine at the age of 14 years. She was initially treated with propranolol as a prophylac- tic agent. At the age of 15 in association with a typical migraine attack she developed profound and persisting loss of vision in the left eye. The visual actuity of the affected eye was reduced to Royal Victoria Infirmary, Newcastle upon Tyne, perception of light, and only the superotemporal and University of quadrant ofvision remained intact. Funduscopy Newcastle upon Tyne revealed an acute occlusion of the superotem- Department of Ophthalmology poral, superonasal, and inferotemporal arteries. A M Glenn The left sided visual loss persisted despite treat- J W Howe ment with acetazolamide, amyl nitrate, and CO2 Department of rebreathing. Neurology Eight months later, following an increase in P J Shaw the frequency of her migraine, she developed an D Bates occlusion of a macular branch of the right Correspondence to: Mr Andrew M Glenn, FRCS, superotemporal arteriole which resulted in a Department of permanent scotoma and a reduction of visual Ophthalmology, Pavilion Two, Royal Victoria acuity on the right to 6/9. Infirmary, Queen Victoria At the age of 20, again following an increase in Road, Newcastle upon Tyne the of her she Figure I Photograph ofthe rightfundus showing occlusion NEI 4LP. frequency migraine, suddenly ofthe inferior temporal arteriole and atrophy ofthe superior Accepted for publication developed further loss of vision in the right eye temporal disc corresponding to the previous macular branch 30 May 1991 due to an inferotemporal BRAO affecting the occlusion. 190 Glenn, Shaw, Howe, Bates occlusion in migraine is incompletely under- stood. The most widely accepted theory is that there is an episodic reduction in retinal blood Br J Ophthalmol: first published as 10.1136/bjo.76.3.189 on 1 March 1992. Downloaded from flow, due to vasospasm and/or vessel wall oedema.24 This may be associated with a throm- botic predilection because of abnormalities of platelets, plasma, and/or blood vessels.25 In our case after episodes of BRAO vasodila- tors, calcium channel blockers, intravenous steroids, and measures to reduce intraocular pressure were ineffective in ameliorating the visual loss. Furthermore antimigraine pro- phylaxis with 13 blockers and serotonin antago- Figure 2 Fluorescein nists did not prevent further attacks. The angiogram ofthe right eye showing occlusions of the usefulness of antiplatelet agents, particularly for inferotemporal and superior prevention of migraine related infarcts, requires macular branch arterioles. evaluation. There is recent animal experimental evidence that glutamate antagonists given after ing tests, VDLR/TPHA, autoantibodies includ- cerebrovascular occlusion may reduce the area of ing anticardiolipin antibodies and DNA binding, cerebrovascular damage.26 Such agents may be of fasting blood lactate and pyruvate and lactate/ value in limiting the area of infarcts following pyruvate ratio, serum angiotensin converting retinal vascular occlusions. enzyme, full clotting studies including pro- thrombin time, activated partial thrombo- 1 Waters WE, O'Conner PS. Prevalence of migraine. J Neurol plastin time, platelet function studies, protein NeurosurgPsychiatry 1975; 38: 613-6. 2 Pearce JMS, Foster JB. An investigation of complicated C, protein S, levels of factors V and VIII and migraine. ] Neurol Sci 1965; 15: 333-40. lupus anticoagulant, fasting cholesterol, and tri- 3 Broderick JP, Swanson JW. Migraine-related strokes. Clinical profiles and prognosis in 20 patients. Arch Neurol 1987; 44: glycerides. A chest radiograph and electrocardio- 868-71. graph were normal, and M-mode and two 4 Galezowski X. Ophthalmic megrim. Lancet 1882; i: 176-7. 5 Brown GC, Magargal LE, Shield JA, Goldberg RE, Walsh dimensional echocardiography gave normal find- PN. Retinal artery obstruction in children and young adults. ings, with no evidence of a cardiac embolic Ophthalmology 1981; 88: 18-25. 6 Gronvall H. On changes in the fundus oculi and persisting source. A cranial CT scan was normal and the injuries to the eye in migraine. Acta Ophthalmol (Kbh) 1983; cerebrospinal fluid showed normal levels of pro- 16: 602-11. 7 Graveson GS. Retinal artery occlusion in migraine. BM7 tein, IgG, glucose, and cells. A Colour Flow 1949; ii: 838-40. Duplex Scan (an ultrasound and doppler haemo- 8 Pearce J The ophthalmological complications of migraine. J NeurolSci 1968; 6: 73-81. dynamic study) revealed normal flow and mor- 9 Walsh FB. Clinical neuro-ophthalmology. Baltimore: Williams phology in 'the carotid arteries. and Wilkins, 1947. 10 Krapin D. Occlusion of the central retinal artery in migraine. N Med EnglJ3 1964; 270: 359-60. http://bjo.bmj.com/ 11 Katz B Migrainous central retinal artery occlusion. J Clin Neuro Ophthalmol 1986; 6: 69-70. Discussion 12 Coppeto JR, Lessel S, Sciarra R, Bear L. Vascular retinopathy In the elderly BRAO is usually due to emboli in migraine. Neurology 1986; 36: 267-70. 13 Katz B. Bilateral sequential migrainous ischemic optic neuro- from atheroma at the carotid bifurcation.202' In pathy. Am]rOphthalmol 1985; 99: 489. younger patients systemic disorders associated 14 Weinstein JM, Feman SS. Ischemic optic neuropathy in migraine. Arch Ophthalmol 1982; 100: 1097-100. with retinal vasculitis, such as sarcoidosis and 15 Katz B. Migrainous ischemic optic neuropathy. Neurology collagen vascular disease, may lead to BRAO.22 1985; 35: 112-14. 16 Friedman MW. Occlusion of the central retinal vein in on September 27, 2021 by guest. Protected copyright. In a series of27 cases ofretinal artery occlusion migraine. Arch Ophthalmol 1951; 45: 678-82. occurring under the age of 30 years risk factors 17 Gaynes PM, Towle PA. Haemorrhage in hyaline bodies (drusen) of the optic disc during an attack of migraine. Am] were identified in the majority and included Ophthalmol 1967; 63: 1693-6. coagulation or platelet disorders, heart disease, 18 Victor DI, Welch RB. Bilateral retinal hemorrhages and disk edema in migraine. Am]tOphthalmol 1977; 84: 555-8. or the use of oral contraceptive agents.5 Migraine 19 Dubois LG, Sadun AA, Lawton TB. Inner retinal layer loss in was the sole risk factor for retinal stroke in only complicated migraine. Case report. Arch Ophthalmol 1988; 106: 1035-7. two (7%). Gass et a123 recently reported on a 20 Kollarits CR, Lubow M, Hissang SL. Retinal strokes. I. series of nine patients (age range 24-69 years) Incidence of carotid atheroma. JAMA 1972; 222: 1273-5. 21 Heges TR, Giliberti 01, Magargal LE. Intravenous digital with idiopathic recurrent BRAO. The fundal subtraction angiography and its role in ocular vascular appearances were suggestive offocal arteritis and disease. Arch Ophthalmol 1985; 103: 666-9. 22 Haskjold E, Froland S, Egge K. Ocular polyarteritis nodosa: arteriolitis. Most of these patients retained good report of a case. Acta Ophthalmol (Kbh) 1987; 65: 749. central vision, and none developed evidence of 23 Gass JDM, Tiedeman J, Thomas MA.
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