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Show ]. Clin. Neuro-ophthalmol. 3: 9-12, 1983. Amaurosis Fugax for a Long Duration* TADASHI FUJINO, M.D. SHINOBU AKIYA, M.D. SHUICHIRO TAKAGI, M.D. HAYAO SHIGA, M.D. Abstract A 31-year-old Japanese male with unilateral bouts of transient visual loss lasting for variable periods of time has been observed. In spite of the prolonged duration of some of these attacks (the longest attack lasted 7Y2 hours), the patient sustained a relatively small amount of functional damage to the retina. Although the exact mechanism underlying these bouts of transient visual loss remains unknown, a discussion of the possible causes of such episodes, as well as the reasons for the relative preservation of vision in spite of the length of these attacks, is included. Permanent retinal damage occurs within a relatively short period of time following a total ischemic event. We recently saw a patient with attacks of unilateral transient visual loss of variable duration. The peculiarity of the attacks was such that his visual function was not impaired severely, in spite of lasting a long period of time. Case Report A 31-year-old Japanese male engineer had his first attack of transient unilateral visual loss on October 30, 1977, after three glasses of beer. He noted that during the attack his right eye was blind for 50 minutes, after which time his vision slowly improved but never returned to the level preceding the attack. Since that time he has had similar attacks once or twice per week (Table 1). The patient has been known to suffer from right hemicrania since the age of 6 years, but has otherwise been healthy. The patient was seen in the Department of Ophthalmology at Keio University on January 11, 1978. His best corrected visual acuity was 20/40 in the From the Departments of Ophthalmology (TF, SA). Psychiatry (ST), and Radiology (HS), Keio University School of Medicine, Shinanomachi, Tokyo, Japan. • This paper was presented at the 17th Annual Residents' Days, Bascom Palmer Eye Institute, on June 20, 1981. March 1983 right eye and 20/15 in the left eye. With the exception of a small central depression in the right visual field, the remainder of the ophthalmologic examination, including ophthalmodynamometry, was normal. The fundus and fluorescein angiograms were normal. No carotid bruits were noted. The neurological examination was normal. Laboratory tests, including a complete blood count, serology, and glucose tolerance test, were normal. Skull and chest x-rays, CT-scan, and EKG were unremarkable. Subsequent to his visit to our office the patient kept a log of his attacks (Table 1). On February 20, 1978, while in our office, the patient noted the onset of one of his attacks (Table 1). He was examined by one of us. Sludging was noted in one of the veins (Fig. 1, arrow). A fluorescein angiogram was performed, at which time the patient noted improvement in his vision. The angiogram was interpreted as normal (Fig. 2). The lack of venous collapse on the angiogram led us to question our original speculation of decreased flow. Subsequent examinations revealed a relative central scotoma and a decrease in the visual acuity of the right eye to 20/200. Because of the peculiarity of the patient's complaints and the patient's personality, psychiatric TABLE 1. Record of Attack Reported by Patient ViSUdl Loss [)ur.ltlOn Jan. 11,1978 5:00 to 6:00 P.M. 1 hour Jan. 13, 1978 5:00 to 6:00 P.M. 1 hour Jan. 21, 1978 2:00 to 3:00 P.M. 1 hour Jan. 27, 1978 2:00 to 6:00 P.M. 4 hours Feb. 6, 1978 10:20 A.M. to 12:35 r.M. 2 hours 15 min.1I Feb. 11, 1978 3:20 to 5:30 P.M. 2 hours ID min. Feb. 15, 1978 8:00 to 9:30 P.M. 1 hour 30 min. Feb. 20, 1978 2:40 to 2:50 r.M. ID min." 6:30 to 9:00 P.M. 2 hours 30 min. Feb. 25, 1978 11:30 A.M. to 2:00 P.M. 30 min. Mar. I, 1978 8:30 to 9:15 P.M. 45 min. .. Completely blind for the first 30 minutes Vision gradually returned over the next I hour 45 minutes. h See in text. 9 Amaurosis Fugax 10 Figure 1. Right fundus, normal appearance, on May 14, 1978. (Same findings on January 11, 1978 and February 20,1978.) Journal of Clinical Neuro-ophthalmology Fujll1o, Aklyd, T,lkagi, 5higd Figure 3. Fluorescein angiogram on February 18, 1980. At 46 seconds, the medial half of the choroid is dark and slow retinal arterial flow is just begInnIng, consultation was obtained. Tranquilizers were prescribed which seemed to reduce the frequency of the attacks. His subsequent visits to our office were sporadic. On September 29, 1978, he experienced his longest attack which lasted for 71;2 hours. On February 18, 1980, we were fortunate to be able to examine his fundus during an attack. At this time the retinal blood flow appeared completely arrested. However, fluorescein angiography revealed extremely slow filling of the vessels. A representative picture of the angiogram 46 seconds after injection demonstrated minimal filling of the arterial tree with choroidal circulation present only temporally (Fig. 3). At 86 seconds (Fig. 4), all of the retinal arteries were filled, but the veins were just beginning to show some laminar flow. The slowed retinal circulation suggested a possible circulatory abnormality, so a cardiovascular angiographic study was obtained. A congenital anomaly of the origin of the ophthalmic artery was found. In July 1982, the patient was still in the same condition, but his right visual acuity had reduced to 20/400. The cause of the attack, however, remained unknown. Comment Where is the site of occlusion? On the fluorescein angiogram both the central artery and the medial posterior ciliary arteries were occluded. March 1983 According to HayrehI the most common origin of these arteries is initially a single branch from the ophthalmic artery. The site of occlusion in this case is postulated to be at this point. What is the mechanism of the arterial occlusion? It is still undetermined. Attacks were never precipitated by pressure on the globe or carotid artery. The attack often was accompanied by headache, but t~e use of ~ntimi~ra~ne medi.cations inc~udin~ Mignstene@ (dlmetohazme mesllate), Kalhkren (kallidinogenase), and Nitrol@ (isosorbide dinitrate), did not abort the attacks. Three stellate ganglion blocks were also not effective in preventing the attacks. However, the inhalation of carbon dioxide did improve the vision slightly during an attack. Unfortunately, the vision decreased immediately when the patient was allowed to breathe room air. Is there any relationship between the attack and the congenital vascular anomaly? This type of anomaly of extradural origin of the ophthalmic artery is an extremely rare congenital anomaly and occurs at the 20-mm embryo stage. The anomaly was recently reported by Vignaud et al.2 and Dilenge and Ascherl/ but has not been noted to have ophthalmologic significance. In any case, the site of the postulated blockage of flow is distal to the site of origin, i.e., the origin of the central retinal artery and medial long posterior ciliary artery. 11 Amaurosis Fugax Figure 4. At 86 seconds, all the retinal arteries are filled and some laminar flow is beginning in the vein. Therefore, the relationship to the congenital vascular anomaly, if any, remains unknown. How does the retina survive ischemic attacks of such long duration (up to 7 1h hours)? Longfellow et al. 4 report a similar case in which an attack lasted 10 hours. It was believed that the tolerance of retinal nerve cells to ischemia was measured in terms of minutes, but it has been shown recently that retinal cells seem to be more tolerant than previously believed." Experimental evidence in primates supports this contention.6 There is also some supporting evidence in humans. 7 In the present case, it is most likely that the blood flow, although severely decreased, was sufficient for survival of the retina but not sufficient to maintain physiologic function. References 1. Hayreh, 5.5.: The ophthalmic artery. III. branches. Br. f. Ophthalmol. 46: 212-247, 1962. 12 2. Vignaud, J., Hasso, A.N., Lasjaunias, P., and Clay, c.: Ocular vascular anatomy and embryology. Radiology 111: 617-626, 1974. 3. Dilenge, D., and Ascher!, G.F., Jr.: Variations of the ophthalmic and middle meningeal arteries: Relation to the embryonic stapedid artery. Am. f. Neural Radiol. 1: 45-53, 1980. 4. Longfellow, D.W., Davis, F.5., and Walsh, F.B.: Unilateral intermittent blindness with dilatation of retinal veins. Arch. Ophthalmol. 67: 554-555, 1962. 5. Plum, F.: The clinical problem: How much anoxiaischemia damages the brain? Arch. Neural. 29: 359-360, 1973. 6. FUjino, T.: Vascular disorder in the visual pathway. Ophthalmology (Tokyo) 14: 234-240, 1972. 7. Hayreh, 5.5., Kolder, H.E., and Weingeist, T.A.: Central retinal artery occlusion and retinal tolerance time. Ophthalmology 87: 75-78, 1980. 8. Bock, J., Bornschein, H., and Hommer, K.: Die Wieder! ebungszeit der menschlichen Netzhaut. Albrecht Graefes Arch. Ophthalmol. 165: 437-451, 1963. Write for reprints to: Tadashi FUjino, M.D" 3-3-5-304 5himo-Ochiai, 5hinjuku, Tokyo 161, Japan. Journal of Clinical Neuro-ophthalmology |
