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Show ]. Clin. Neuro-ophthalmol. 3: 75-76, 1983. The article in this issue entitled "Amaurosis Fugax for a Long Duration," by T. FUjino, S. Akiya, S. Takagi, and H. Shiga was published because it describes in detail the universally poorly recognized syndrome of ocular migraine. The syndrome of migraine has been recognized for over 2000 years. l Migraine is best described in terms of recurrent attacks of headache, commonly unilateral in onset, associated with anorexia, nausea, and vomiting. These attacks may be preceded by or associated with conspicuous neurologic and mood disturbances.2 There are many types of migraine, but the ophthalmologist generally relates the expected symptomatology to that of classic migraine which occurs in only about 10% of patients. There is an acute onset of a prodromal phase which lasts 10-30 minutes and is classically visual in nature. The hemianopic scintillating scotoma was best described by Sir William Gowers in 1895.:1 These scotomas usually begin just eccentric to fixation. They are sharply defined, white or multicolored, picket-like lines that may have a shimmering quality and, for the most part, are relatively localized. These scintillations then begin to slowly expand simultaneously moving peripherally. The center of the fortification specter is variously described as being blurred, grayed-out, or blank. As the scintillating scotoma begins to fade the patient notes the onset of the headache phase. A much less common and much less publicized variety of migraine is the 50-called "ocular migraine." Ocular migraine may be defined as a transient or permanent monocular visual disturbance occurring in an individual with a strong history of migraine episodes. 4 In this unique form of migraine, vasospasms of the retinal vessels have been postulated to be the cause of the unilateral visual loss experienced by the patientS As reviewed by Kline and Kelly," a variety of ocular manifestations have been reported including retinal and vitreous hemorrhages, ischemic optic neuropathy, branch and central retinal artery and vein occlusions, central serous retinopathy, and unexplained bouts of transient visual loss. These attacks of transient visual loss last for minutes to hours and are rarely accompanied by a headache phase. With repeat episodes the patients may develop permanent visual 1055. Kline and Kelly" had the opportunity to document the fundus findings in such a patient with fundus photographs and fluorescein angiography. They demonstrated narrowing of the retinal veins during the attack similar t<;> the findings reported by Wolter and Burchfield.' There was also delay March 1983 Editorial Comment in appearance of fluorescein dye in the branches of the central retinal artery, but no delay in choroidal filling. They postulated that the visual 1055 in their patient was due to reduced arteriolar flow into the retinal circulation, possibly due to arteriolar spasm between the branching of the ciliary vessels and the surface of the optic disc. A marked variation in the amplitude, but not in the latency, of the visual-evoked response in this patient was mentioned by Kline and Kelly" and subsequently discussed in detail by Kline and Glaser.8 The variation in amplitude paralleled the recovery of visual function. They suggest that the loss of the visual evoked response signal reflects the loss of inner retinal function, the inner retina being supplied by the central retinal artery. With the resumption of central retinal artery perfusion, there is a return of inner retinal activity and a gradual and progressive return of the visual evoked response signal. Since there was no permanent damage to the myelinated ganglion cells in this patient, there was no change in latency. The parallel between the patient reported in this issue by Fujino et al. and the one reported by Kline and Kelly" and Kline and Glaser8 is remarkable. As in the previous reports, the major change is in the caliber of the veins, not the artery (see Fig. 1, Fujino et aLl. There is a suggestion of a relative delay in the venous return during this attack as demonstrated by the differences in laminar flow between various vessels (see Fig. 2, Fujino et aLl, although this type of sequence is also occasionally noted in normal individuals. In the patient reported by Fujino et al. there was a general delay in the filling of the arteries and a more profound delay, at least during one episode, in the filling of the choroid (see Fig. 3, Fujino et aLl. These findings suggest the occurrence of a vasospastic phenomenon occurring proximal to the branching of the long posterior ciliary artery somewhere in the course of the ophthalmic artery. We concur, therefore, with the postulated site of occlusion as proposed by FUjino et aL We believe the mechanism of the "occlusion" is vasospasm secondary to a migraine diathesis. Since Kline and Kelll reported the prompt cessation of visual symptoms in their patient with the use of propranolol, we believe that such a trial is warranted in this patient. We do not believe that the congenital abnormality noted on angiography is of significance. FUjino et aL pose a last question with respect to how the retina survives ischemic attacks of such long duration. It is highly likely that the ischemia 75 Editorial Comment: Amaurosis Fugax is relative-severe but not total occlusion occurring with arteriolar vasospasm. The ischemia induces a physiologic block of retinal ganglion cell function producing a loss of vision reflected electrophysiologically by the loss of the visual-evoked response signal. If the spasm is severe enough or recurrent in the same distribution, permanent damage may be induced insidiously, as in the patient reported by Fujino et aI., or cataclysmically in those patients who develop true branch9 or central 10, 11 retinal artery occlusions or ischemic optic neuropathy.12 The points to remember are: 1) migraine can affect the anterior visual system, and 2) these attacks may last for minutes to hours in contrast to the fixed pattern of 15-40 minutes for the fortification specter of classic migraine. Ronald M. Burde, M.D. Washington University School of Medicine St. Louis, Missouri References 1. Aretaeus Capbodox: Heterocrania In Hude est Corpus Medicorum Graecorum, Vol. 3. Teubuer, Leipzig, 1923, p. 37. 76 2. Ad Hoc Committee on Classification of Headache: Classification of headache. Arch. Neural. 6: 123-176, 1962. 3. Gowers, W.R.: A Manual of Diseases of the Nervous System, Vol. 2. Blakiston & Son, Philadelphia, 1960, p. 838 4. Troost, B.T.: Migraine. In Clinical Ophthalmology, Vol. 2. T.B. Duane, Ed. Harper & Row, Hagerstown, 1976, Chap. 19, pp. 11, 12. 5. Walsh, F.B., and Hoyt, W.F.: Clinical Neura-Ophthalmology (3rd ed.) Williams & Wilkins, Baltimore, 1969, pp. 1671-1678; 1707; 1806. 6. Kline, L.B., and Kelly c.L.: Ocular migraine in a patient with cluster headaches. Headache 20: 253-257, 1980. 7. Wolter, J.R., and Burchfield, W.J.: Ocular migraine in a young man resulting in unilateral transient blindness and retinal edema. ]. Pediatr. Ophthalmol. 8: 173-176, 1971. 8. Kline, L.G., and Glaser, J.5.: Visual evoked response in transient monocular visual loss. Br.]. Ophthalmol. 66: 382-385, 1982. 9. Gronvall, H.: On changes in the fundus oculi and persisting injuries to the eye in migraine. Acta Ophthalmol. 16: 602-611, 1938. 10. Graveson, C.S.: Retinal arterial occlusion in migraine. Br. Med.]. 2: 838-840, 1949. 11. Krapin, D.: Occlusion of the central retinal artery in migraine. N. Engl. ]. Med. 270: 359-360, 1964. Journal of Clinical Neuro-ophthalmology |