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Show j. Clin. Neuro-ophthalmol. 3: 157-162, 1983. Transient Retinal Striae BAIRD S. GRIMSON, M.D. KENNETH B. SIMONS, M.D. MEIMEI CHANG, M.D. Abstract Transient retinal folding was observed in a 28-yearold woman presenting with bilateral uveal inflammation. These retinal striae resolved within 5 weeks as the anterior uveal inflammation responded to topical cycloplegic and corticosteroid therapy. Ultrasonographic findings demonstrated choroidal thickening as a contributing factor in the production of these temporary retinal folds. We present this unusual case since transient retinal folding has been rarely documented, and as far as we are aware, has not been previously investigated by ultrasonography. Introduction Retinal folds (striae) are usually permanent and are most often seen with contracting epiretinal membranes, surrounding chorioretinal scars or areas of subretinal neovascularization, associated with retinal detachments, during or following intraocular surgery. Transient retinal folds have been rarely documented, and their etiology remains enigmatic. We report transient retinal striae occurring in a 28-year-old woman experiencing bilateral uveal inflammation. We present serial ultrasonographic findings indicating choroidal thickening as a prominent underlying factor in the production of this temporary retinal folding. Case Report A 28-year-old black woman experienced sudden irritation of both eyes. Her present and past medical history revealed no significant illness, and she denied taking any recent medications. Her visual acuity was 20/40 right eye and 20/30 left eye; the ocular motility was full bilaterally, and no proptosis, periorbital lid edema, or orbital mass lesions were detected. External examination revealed mild conjunctival hyperemia in both eyes but the cornea, anterior chamber, and lens were unremarkable on slit lamp biomicroscopy. No cell or flare reac- From the Department of Ophthalmology. University of North Carolina. Chapel Hill. North Carolina. September 1983 tion was visualized within the anterior chamber. Direct and indirect ophthalmoscopy with scleral depression revealed pathology confined to the posterior poles, appearing as a peculiar configuration of striae in both posterior poles radiating centrifugally from the disc and macula (Figs. 1 and 2). These folds appeared confined to the retina. No retinal edema, retinitis, or retinal vasculitis was observed. Biomicroscopy of the vitreous was normal, revealing no cells, vitreous debris, posterior vitreous detachment, or abnormal vitreoretinal traction. She was given Albacon-A for symptomatic relief of a "viral" conjunctivitis and returned 3 days later complaining of photophobia bilaterally. Applanation intraocular pressures were 18 mm Hg right eye and 20 mm Hg left eye. A moderate nongranulomatous anterior chamber flare and cell reaction was then visualized, but otherwise the ocular examination remained unchanged. She was started on atropine 1%, 1 drop both eyes twice daily, and prednisolone acetate 1%, 1 drop both eyes four times a day, for management of her bilateral anterior uveitis. Fluorescein angiograms (Figs. 3a and 3b ) failed to reveal the alternating bands of hypofluorescence and hyperfluorescence characteristically seen in folds involving the choroid and retinal pigment epithelium, supporting the clinical impression that the configuration of these folds were confined to the retina. Late staining of both optic discs was observed during fluorescein angiography, but no other breakdown in the blood-retinal or pigment epithelial-retinal barriers was noted. Ocular sonography (Ocuscan 400, 10 mg hz Bscan probe; 8 mg hz A-scan probe) documented an irregular, flattened, vitreoretinal interphase (Bscan) with spike heights (A-scan) of medium low reflectivity, occurring between the highly reflective retinal and scleral acoustical spikes (Fig. 4). A wider sector B-scan (Ultrascan 11) readily detected a corresponding crescent of relative echolucency between the retina and sclera in both posterior poles. Orbital A- and B-scan ultrasonography revealed no evidence of a posterior scleritis or retrobulbar orbital edema which would have demonstrated flattening of the curvature or increased thickness of the posterior sclera, fluid in subtenon's space, enlargement of the extraocular muscles or optic nerve sheaths, and mottling or prolongation of the 157 Transient Retinal Striae Figure 1. A 60° angle photograph of the posterior pole of the right eye showing retinal striae radiating centrifugally from the optic disc and macula. The prominent light reflex inferiorly arises from the abnormally flattened and elevated retina. Figure 2. Magnified view of the retinal folding, left eye. Journal of Clinical NeuTo-ophthalmology Crimson, Simons, Chang Figures 3a and 3b. Fluorescein angiograms of the (a) right and (b) left eve show no eVIdence of alternating hypofluorescent and hyperfluorescent bands. indicating the folds Me confined to the retina and do not involve the retina pigment epithelium or choroid. September 1983 159 Transient Retinal Striae Figure 4. B-scan ultrasound (top, left): The Irregular, flattened vitreoretinal acoustical interphase disappears following resolution of the retinal folds (bottom, left). A-scan echography (top, right) Initial Iv revealed separation of the highly reflective retinal (arrow) and scleral acoustical spike height~ by low reflective spikes originating with the region of the choroid. With resolution of the retinal striae (bottom, right ), the retinal spike height has returned to its normal anatomical position adjacent to the highly reflective spikes from the choroid and sclera. orbital fat pattern. Axial length measurements (Sonometric DBR-300) were 19.40 mm right eye and 18,78 mm left eye. Within 5 weeks of starting topical ocular therapy (atropine sulfate, prednisolone acetate), a mild iritis remained, but the retinal folding had resolved (Figs, Sa and 5b ). The best-corrected visual acuity had returned to 20/20 both eyes, and her refractive error was +0,50 +0,50 X 90° right eye and +0.75 + 0,50 X 90° left eye. The normally smooth concavity of the posterior vitreoretinal acoustical interphase on B-scan echography was now present and the retinal/choroidal/scleral spike heights (Ascan) were no longer separated abnormally (Fig. 4). Repeated biometric echography revealed an increase in the axial length of 1.85 mm right eye (from 19,40 mm to 21.25 mm) and 2.53 mm left eye (from 18,78 mm to 21,31 mm), This increase in the axial lengths was not associated with changes in the depth of the anterior chamber angle or lens thickness. Throughout the 5 weeks that retinal folding was observed, ocular hypotony was never documented by repeated applanation pressures. In the following 10 months since the resolution of her transient retinal striae, she continues to manifest a mild anterior uveal inflammation, but remains adequately controlled with topical atropine and corticosteroids. She has not developed meningeal or other neurological symptoms or signs, The uveitis evaluation included a normal PA and lateral chest x-ray, a normal complete blood count, an angiotensin converting enzyme of 18,40 (n 11-29), a nonreactive VORL, a negative serum FTA-ABS, and a normal serum electrophoresis. TB skin testing was negative and the mumps skin testing was positive. Complement levels reveal a Cl of 145 mg/dl (n 90-185 mg/dl) and a C of 23 mg/dl (n 10-40 mg/dl). Discussion Retinal striae are best separated from chorioretinal folding by their normal fluorescein angiogram pattern. l The characteristic, alternating hypofluorescent and hyperfluorescent bands seen in folding of the choroid and retinal pigment epithelium are absent when the folding is confined solely to the retina. The resolution of striae which are restricted to the retina has been rarely documented, Gass~ observed ephemeral retinal folding with normal fluorescein angiograms in a 22-year-old white woman taking chlorthalidone. Within 48 hours of Journal of Clinical Neuro-ophthalmology September 1983 (;rim~()n Simons, Chang Figures Sa and sb. Resolution of the retina folds in the (a) right and (b) left eye 5 weeks after initial presentation. 161 Transient Retinal Striae cessation of this drug therapy, the retinal folds had disappeared completely. The duration of transient retinal striae in our case was longer, the retinal folds resolving in 5 weeks as her uveitis responded to topical corticosteriods and atropine. Our serial ultrasonographic examinations uncovered choroidal thickening as a contributing factor in the development of temporary retinal striae. As far as we are aware, such echographic findings have not been reported in folds confined to the retina, although ultrasonographic evaluation of choroidal folding has been well-studied. B-scan ultrasonograms in patients with benign choroidal folds (idiopathic, posterior scleritis) have shown flattening and thickening of the retina, choroid, and sclera.:l - 5 Our patient, in whom transient folds were confined to the retina, demonstrated A- and B-scan echographic features of thickening of the posterior choroid, but no changes in the curvature of the sclera. The axial length measurements increased 1.85 mm in the right eye and 2.53 mm in the left eye following ultrasonographic resolution of the choroidal thickening with concomittant clinical disappearance of the retinal folding. We found these echographic findings striking, and recommend ocular ultrasonography in future patients developing folding of the retinal to see if choroidal thickening is a common finding in other cases of transient retinal striae. We suspect that the total surface area normally covered by the retina in our patient was reduced by significant thickening of the choroid, thus allowing the redundant retinal tissue to transiently fold onto itself. References 1. Norton, E.W.D.: A characteristic fluorescein angiographic pattern in choroidal folds. Proc. R. Soc. Med. 62: 119-128, 1969. 2. Gass, J,D.M.: Stereoscopic atlas of macular diseases: Diagnosis and treatment. In Textbook of Macular Disease (2nd ed.). C.V. Mosby Co., St. Louis, 1977, pp. 147-154. 3. Cappaert, W.E., Purnell, E. W., and Frank, K.E.: Use of B-sector scan ultrasound in the diagnosis of benign choroidal folds. Am. f. Ophthalmol. 84: 375379,1977. 4. Kalina, R.E., and Mills, R.P.: Acquired hyperopia with choroidal folds. Ophthalmology 87: 44-50, 1980. 5. Benson, W.E., Shields, J.A., Tasman, W., and Crandall, A.S.: Posterior scleritis. A cause of diagnostic confusion. Arch. Ophthalmol. 97: 1482-1486, 1979. Acknowledgment This work was supported in part by a grant from Research to Prevent Blindness, Inc., New York, New York. Write for reprints to: Baird S. Grimson, MD., Department of Ophthalmology, 617 Clinical Sciences Bldg. 29H, Chapel Hill, North Carolina 27514. Journal of Clinical Neuro-ophthalmology |
