| OCR Text |
Show !ollnllli of CIi"ica! NCllrtl-0l'hOItlI1llo!O:{I/ b(3): uu-uu, !98b. Monocular Diplopia of Retinal Origin Frederick E. Lepore, M.D., and David L. Varian, M.D. IYH6 Raven Press, New York A 68-~'ear-nld man ~'"\periL'ncL'd mnl1\lCular diplopia rL'lated tn a subretinal chnwidal nL'ovascular mL'mbrane. His SYmptl1m rL'snlyed with lasL'r photncn,lgulatinn of the chowidal membranL'. Retinal disease is an uncnmmon cause nf this uncnmmnn symptnm. Key Words: Mononuclear diplopia - Subretinal choroidal neovascular membrane. From the Departments of Neurology and Ophthalmology, University of Medicine and Dentistry of Nl'w Jersey-Robert Wood Johnson Medical School. Academic Health Sciencl' Center, New Brunswick, New Jersey. Address correspondence and reprint reljuests to Dr. F. E. Lepore, Department of Neurology and Ophthalmology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School. Academic Health Science Cl'nter, CN 19, New Brunswick, NJ 08903, U.S.A. /81 Although monocular diplopia may occur with acquired lesions of the occipital lobe or central visual pathways (1), other causes of this unusual symptom are optical aberrations within the refracting media of the eye (2) or anomalous retinal correspondence, a rare sensory adaptation that may follow strabismus surgery (3). Retinal disease, which most typically causes metamorphopsia, blurred vision, and a positive scotoma can uncommonly cause monocular diplopia (4). We report a patient with the onset of monocular diplopia due to retinal disease and resolution following treatment with laser photocoagulation. CASE REPORT A 68-year-old college professor with a 20-year history of systolic hypertension noted blurred vision in his left eye in May 1985. Several weeks later he complained of (a) straight lines slanting to the right in the field just superonasal to fixation of the left eye, (b) objects appearing smaller when viewed with his left eye, and (c) double vision persisting despite closure of the right eye. While driving along a highway cloverleaf he would see a "false curb" displaced into the roadway or a pair of red automobile tail-lights would be accompanied by a pair of illusory greenish-white tail-lights below and to the right. No perseveration of images or polyopia was reported. The patient denied any prior ocular trauma or strabismus. Examination revealed visual acuity of 20115- 1 of the right eye and 20/50+ 1 of the left eye. Goldmann perimetry of the right eye was normal and showed a superotemporal constriction of the I2E isopter with involvement of fixation of the left eye. Superonasal metamorphopsia of the left eye was present on Amsler grid testing. The patient could identify 12 of 13 Ishihara color plates with the right eye and none with the left. Ocular ductions were full with a slight concomitant exophoria. The pupils measured 3 mm with a left trace afferent 182 I. L. LU'()I\f AND DAVID L. YARIAN dekct. Nu abnorm'llities uf till' anteriur segment Wt're seen on slit lamp l'xamin,ltiun. Indirect ophth,1lnll1scopy ITvl',lil'd peri PIll' r,lI rl'tinuschisis llf bllth eyes ,lIld a nl'UrPSl'nsury rl'tin,ll ddachnll'nt extt:nding frPm the tl'mpu;<ll m<lrgin uf the Idt disc tu involve the fuvea with deposition of deep rl'tin,lll'xudatt' just n,lsal tll the fovea. A thin I,lyer of subrl'tin,ll llL'morrhage was present at the sL;~1t'rior and inkrior bordns of the rdinal dl'tachment (Fig. 1). The remainder of the neurologic examination showed a slight reflex preponderance and mildly decreased pin perception on the right side. Fluorescein angiography demonstrated a peripapillary subretinal choroidal neovascular membrane extending from the left disc to within 400 f.Lm of the nasal margin of the foveal avascular zone (Fig. 2). Nonspecific retinal pigment epithelial window defects were found in the right eye. Seven weeks after the onset of symptoms the patient underwent krypton laser treatment of his subretinal choroidal neovascular membrane. The following day he noted complete resolution of his monocular diplopia, diminished micropsia and metamorphopsia, and a persistent superotemporal scotoma of the left eye. Five weeks after laser therapy, visual acuity of the left eye had improved to 20/40- 1 Fluorescein angiographv showed effective obliteration of the subretinal choroidal neovascular membrane. Three and one-half months later visual acuity of the left eye was 20/20- 2, and the patient remained free of diplopia although micropsia and photopsias "like silverfish" in the paracentral scotoma of the left eye persisted. FIG. 1. Retinal detachment of the left eye extending from temporal disc margin to fovea. Deep perimacular exudates and subretinal hemorrhage at the inferior and superior borders of the detachment are present. I Clill NCllyo-ophtlw/}}/ol, Vol. (', No . .1, 198t1 FIG. 2. Fluorescein angiogram of the left eye at 21 s reveals the hyperfluorescent peripapillary subretinal choroidal neovascular membrane extending to within 400 f.lm of the nasal margin of the avascular zone. Much of the hypofluorescence of the subretinal choroidal neovascular membrane is blocked by the overlying subretinal hemorrhage. COMMENT Although slight degrees of monocular diplopia can be physiologic (5), significant monocular diplopia can signal disease any\\'here from the precorneal tear film to the occipital lobes (Table 1). However, refractive disorders of the anterior segment and ocular media are the most frequent causes of monocular diplopia and can be confirmed when the "ghost" or secondary image is eliminated bv the use of a pinhole (2). With the exclusion of visual pathway pathology, monocular diplopia must be regarded as a symptom of psychiatric disease or malingering. The cardinal svmptoms of metamorphopsia, micropsia, scotoma, and decreased visual acuity unequivocallv denoted our patient's macular disease. His monocular double vision, which is seldom a svmptom of retinal disease, did conform to the typical pattern of monocular diplopia in which a faint and undistorted secondary image is displaced from a primary bright clear image (4). Our patient's subretinal choroidal neovascular membrane elicited monocular diplopia in a manner analogous to that reported with macular cysts or cystoid change (4). Choroidal neovascularization consists of a sheet of new capillaries extending from the choroid into the subretinal pigment epithelial or subretinal space via a break in Bruch's membrane or around its peripapillary termination. It occurs most commonly in association with macular drusen in agerelated macular degeneration. It can also OCcur in MONOCLlLA/~ DlflUl/'/1t or RET/NAL ORIGIN 183 TABLE 1. Organic causes of monocular diplopia Cornea Oil droplet in precorneal tear film Epithelial irregularity 2" eyelid disease or contact lens Corneal dystrophy Corneal astigmatism Keratoconus Iris Polycoria Iridodialysis Lens Subluxation Multirefractile cataract Aqueous humor'vitreous body Foreign body. e.g., air bubbles, glass, parasites Retina Giant retinal tear with folded over retina Macular cyst Subretinal choroidal neovascular membrane Neurologic Suprasellar tumor Occipital lobe lesions Dissociative lesions between frontal eye fields and occipital associative areas Tonic conjugate daze deviation Anomalous retinal correspondence Superior oblique myokymia? Palinopsia the presumed ocular histoplasmosis syndrome, with angioid streaks, optic nerve drusen, high myopia, healed choroiditis, choroidal tumors, or idiopathically. Visual loss is often precipitated by serous and hemorrhagic detachment of the macula (6). Resolution of our patient's diplopia and improvement of his micropsia and metamorphopsia stemmed from cessation of exudation and hemorrhage after the entire subretina I choroidal neo-vascular membrane was obliterated by laser photocoagulation. Whereas monocular diplopia caused by disturbances of the refracting media of the eye can be explained "as a simple consideration of light and optics," a purely retinal mechanism for the same symptom is more problematic. Possibly this mechanism is similar to cerebral diplopia for which it is hypothesized that the functional equivalent of a new macula is created by impaired fixation due to defective central vision (1,7), or the shift of image from normally to abnormally functioning macula with microsaccades may create a displaced and false image. Retinal disease in general and choroidal neovascularization in particular remain potentially treatable and infrequently considered causes of monocular diplopia. REFERENCES I. Bender MB. Polvopia and monocular diplopia 01 cerebral origin. Arcl1 N'·111'll119"5;5·t323-38. 2. Burde R, Savino PJ. Tmbe J. Clililcal dfCis/llllS ill Ilcllro-opl1tha//)/ olosy. 5t. Louis: C. V. Mosbv Co. 198-+:151-2. 3. Van Noorden GK. Bllriall-Vo" Noord",,', /JiIlO(III11r ,';S;tlIllllld o(lilar /)/otilill/ 2nd I'd. 51. Louis: C. V. Mosbv Co. 1980:26-+-6. . ... Records RE. Monocular diplopia. SlIn' Opl1tl1al1l1l1/ 1980;24:303-6. 5. Fincham EF. Monocular diplopia. Br I 0l'htha//)/(}/ 1963; ..7:705-12. 6. Gass JDM. Chllmidal necwascular membranes. In: Fraunielder FT, Roy FH, eds. Cllrrcllt o(lIlar theral'l/. Philadelphia: WB Saunders, 1980:33.. -6. 7. Sairan AB, Kline LB, Glaser JS, Daroii RB. Tele\'ision-induced iormed visual hallucinations and cerebral diplopia. Br I OphthallllOl 1981;65:707-11. I Gill NClIro-0l'ltllltlll//ol. Vol. 6. No.3. 1986 |
