Correspondence 7. Wong AM, Heon E. Helicoid peripapillary chorioretinal degeneration in abetalipoproteinemia. Arch Ophthalmol. 1998;116:250-1. 8. Runge P, Muller DPR, McAllister J, Calver D, Lloyd JK, Taylor D. Oral vitamin E supplements can prevent the retinopathy of abetalipoproteinemia. Br J Ophthalmol. 1986;70:166-73. 9. Gouras P, Carr RE, Gunkel RD. Retinitis pigmentosa in abetalipoproteinemia: effects of vitamin A. Invest Ophthalmol. 1971;10: 784-93.

Topiramate-induced myopic shift with associated retinal striae Drug-induced acute myopia, bilateral nonpupillary block angle closure, and retinal folds have been associated with sulfonamide-containing medications including topiramate and acetazolamide, among others.1,2 Although the mechanism remains elusive, anterior ultrasound biomicroscopy (UBM) has demonstrated ciliochoroidal effusion, anterior rotation of the ciliary body, and anterior displacement of the lens.3 There have been multiple reports of this syndrome after initiation of topiramate.1–9 Fraunfelder et al.6 demonstrated this finding of acute angle closure associated with topiramate to be bilateral in 83 patients and unilateral in 3 patients. In addition, the myopic shift is variable with a range of –2.00 to –8.75 D, likely correlating to the displacement of anterior lenticular migration.6 Macular striae in association with myopic shift and angle narrowing has been demonstrated as well.3–5,7–9 Initial reports demonstrated the reversibility of striae after cessation of the topiramate. In addition, of the cases described, all affected individuals were in the first 3 decades of life. In this article, we report a case of a 7-year-old boy

10. Li CM, Presley JB, Zhang X, et al. Retina expresses microsomal triglyceride transfer protein: implications for age-related maculopathy. J Lipid Res. 2005;46:628-40. Can J Ophthalmol 2015;50:e43–e46 0008-4182/15/$-see front matter & 2015 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2014.12.016

who presented with decreased vision and inner retinal macular striae, which we characterize with spectral-domain optical coherence tomography (SD-OCT). The subtle inner retinal findings seen on SD-OCT provide insights into possible mechanisms for retinal striae formation. A 7-year-old boy with history of migraines presented to the eye clinic after endorsing 2 days of sudden-onset blurry vision. Recent medical history was notable for initiation of topiramate 25 mg daily 7 days before presentation. On examination, uncorrected visual acuity (VA) was 20/50 OD and 20/60 OS with 20/20 best corrected VA after refraction to –1.00 D sphere and –1.25 D sphere in the right and left eye, respectively. Examination 4 months prior at the same clinic demonstrated 20/20 vision with plano refraction in both eyes. On presentation, his intraocular pressure was 17 mm Hg OU. Anterior segment examination was notable for uniform shallowing of the anterior chamber without pupillary block. Funduscopic examination demonstrated symmetric retinal striae limited to the posterior poles (Fig. 1A, 1B). SDOCT of the macula demonstrated attached hyaloid and fine corrugation of the internal limiting membrane (ILM) without disruption of the inner retina or choroid (Fig. 2A, 2B).

Fig. 1 — Colour fundus photo of the right (A) and left (B) eye depicting macular striae.

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Fig. 2 — Spectral-domain optical coherence tomography of the right (A) and left (B) eye demonstrating corrugations of the inner limiting membrane corresponding to the retinal striae.

Given the triad of acute myopia, bilateral shallowing of the anterior chamber, and macular striae consistent with topiramate toxicity, the medication was stopped. Two days

after cessation, the patient reported improved clarity of his vision. On repeat examination 1 month after cessation, his uncorrected VA was 20/20 OU. Examination was notable CAN J OPHTHALMOL — VOL. 50, NO. 3, JUNE 2015

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Fig. 3 — Colour fundus photo of the right (A) and left (B) eye depicting resolution of macular striae 1 month after cessation of topiramate.

for relative deepening of the anterior chamber and resolution of the macular folds (Fig. 3A, 3B). Correspondingly, SD-OCT demonstrated resolution of the inner retinal corrugations (Fig. 4A, 4B). The finding of retinal striae in conjunction with topiramate use has been previously reported.3–5,7–9 Of these cases, only Gualtieri and Janula7 and Natesh et al.3 presented OCT findings at the time of presentation and after cessation of topiramate. Gualtieri and Janula,7 using time-domain OCT, identified full-thickness retinal and choroidal folds in a 22year-old female.7 The authors attributed this finding to a posterior choroidal effusion, which induced the folds. Natesh et al.,3 using SD-OCT, demonstrated only ILM folds that resolved after cessation of topiramate. Similarly, the attribution of folds was to a posterior choroidal effusion. However, the mechanism by which a choroidal effusion would result in exclusively inner retinal folds without affecting the choroid or outer retina remains elusive.

Table 1 summarizes the characteristics of patients in the literature and the present case who presented with retinal folds. A similarity in presentation is the young age (range 7– 26 years) and attached posterior hyaloid. All cases described a myopic shift secondary to presumed anterior displacement of the crystalline lens. This would, in turn, shift the anterior hyaloid forward, and in the setting of a taught posterior hyaloid, effectively increase the anterior-posterior diameter of the vitreous cortex. This shift may potentially cause traction on the inner retina inducing folds at the level of the ILM (where the posterior hyaloid interdigitates) and manifest superficial striae on clinical examination. The findings by Natesh et al.3 and the present case are similar with subtle ILM folds responsible for the retinal striae on examination. These findings are juxtaposed to Gualtieri and Janula’s7 case in which full-thickness retinal and choroidal folds are present, suggesting varied mechanisms responsible for the heterogeneous presentations. It is

Table 1—Review of cases with topiramate-associated macular striae Age (y), Sex

Days of Topiramate Use

Myopic Shift

OCT Findings

UBM Findings

Sen, 20019 Lin,10 2007 Natesh et al.,3 2010 Dorronzoro et al.,5 2011 Kumar et al.,8 2012 Kumar et al.,8 2012

15, M 26, F 23, M 23, F 25, F 20, F

7 — 5 1 14 —

4D — 6D 3.25 D 5D 4.5 D

— Inner retinal striae* ILM folds — — —

Gualtieri and Janula,7 2013 Present case

22, F 7, M

— 7

— 1.00–1.25 D

Chorioretinal folds ILM folds

— — Anteverted ciliary processes with ciliochoroidal effusion — Anteverted ciliary processes with ciliochoroidal effusion Anteverted ciliary processes with 360-degree ciliochoroidal effusion (extending posteriorly) — —

Author, Year

OCT, optical coherence tomography; UBM, ultrasound biomicroscopy; M, male; F, female; D, diopter; ILM, internal limiting membrane. *The inner retinal striae were demonstrated shortly after discontinuation. There is no initial OCT in this report.

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Fig. 4 — Spectral-domain optical coherence tomography of the right (A) and left (B) eye demonstrating resolution of the internal limiting membrane corrugations 1 month after cessation of topiramate.

plausible that the subtle cases of ILM folds may be due to vitreoretinal traction and the more advanced cases secondary to a combination of vitreoretinal traction inducing inner

retinal change, as well as a posterior choroidal effusion inducing choroidal and outer retinal changes. Despite the varied presentations and purported mechanisms, discontinuation of CAN J OPHTHALMOL — VOL. 50, NO. 3, JUNE 2015

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Disclosures: The authors have made the following disclosures: R.S. received a grant from Regeneron and consulting fees from Alcon, Regeneron, and Genentech.

Nathaniel Sears, Yasha S. Modi, Robert Engel, Rishi P. Singh Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio Correspondence to: Rishi P. Singh, MD: [email protected] REFERENCES 1. Banta JT, Hoffman K, Budenz DL, Ceballos E, Greenfield DS. Presumed topiramate-induced bilateral acute angle-closure glaucoma. Am J Ophthalmol. 2001;132:112-4. 2. Garland MA, Sholk A, Guenter KE. Acetazolamide-induced myopia. Am J Obstet Gynecol. 1962;84:69-71.

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3. Natesh S, Rajashekhara SK, Rao AS, Shetty B. Topiramate-induced angle closure with acute myopia, macular striae. Oman J Ophthalmol. 2010;3:26-8. 4. Beyenburg S, Weyland C, Reuber M. Presumed topiramate-induced maculopathy. Epilepsy Behav. 2009;14:556-9. 5. Dorronzoro E, Santos-Bueso E, Vico-Ruiz E, Sáenz-Frances F, Argaya J, Gegúndez-Fernández JA. Myopia and retinal striae induced by topiramate [in Spanish]. Arch Soc Esp Oftalmol. 2011;86:24-6. 6. Fraunfelder FW, Fraunfelder FT, Keates EU. Topiramate-associated acute, bilateral, secondary angle-closure glaucoma. Ophthalmology. 2004;111:109-11. 7. Gualtieri W, Janula J. Topiramate maculopathy. Int Ophthalmol. 2013;33:103-6. 8. Kumar M, Kesarwani S, Rao A, Garnaik A. Macular folds: an unusual association in topiramate toxicity. Clin Exp Optom. 2012;95:449-52. 9. Sen HA, O'Halloran HS, Lee WB. Case reports and small case series: topiramate-induced acute myopia and retinal striae. Arch Ophthalmol. 2001;119:775-7. 10. Lin C-C, et al. Topiramate induced bilateral secondary angle closure and myopia shift. Taiwan. Ophthalmology. 2014;4:45-8. Can J Ophthalmol 2015;50:e46–e50 0008-4182/15/$-see front matter & 2015 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2015.02.008

Topiramate-induced myopic shift with associated retinal striae.

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