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Year : 2014  |  Volume : 4  |  Issue : 1  |  Page : 45-48

Topiramate-induced bilateral secondary angle closure and myopia shift☆

Department of Ophthalmology, Taipei City Hospital, Taipei, Taiwan

Date of Web Publication4-Mar-2014

Correspondence Address:
Shiow-Wen Liou
Department of Ophthalmology, Taipei City Hospital, RenAi Branch, Number 10, Section 4, Renai Road, Daan District, Taipei City 10629
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Source of Support: None, Conflict of Interest: None

DOI: 10.1016/j.tjo.2012.12.005

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A 41-year-old female with a history of migraine had no previous ocular problems except myopia with spherical refraction of −2.25 D OD and −1.75 D OS. She experienced sudden onset of bilateral blurred vision, ocular fullness sensation, and headache after undergoing topiramate therapy for 7 days (50 mg/ day). Her visual acuities with the presenting glasses were 20/200 OD and 20/50 OS. Intraocular pressures (IOPs) were 44 mmHg OD and 49 mmHg OS, respectively. Autorefraction measurement showed spherical refraction of −5.25 D OD and −4.75 D OS. Best-corrected visual acuities were 20/20 for both oculus dexter (OD) and oculus sinister (OS). Slit-lamp examination revealed bilateral conjunctival chemosis, very shallow anterior chambers, forward displacement of lens–iris diaphragm, round and sluggishly reacting pupils, and closed angles on gonioscopy. A B-scan ultrasound displayed choroidal thickening in both eyes. An ultrasound biomicroscopy demonstrated bilateral 360° ciliochoroidal effusions with forward rotation of ciliary body but no pupillary block. Impression of topiramate-induced bilateral angleclosure glaucoma and acute myopic shift was recorded. She was advised to discontinue topiramate immediately and was administered antiglaucoma medication and mydriatics. Two days later, IOP returned to normal limits and myopic shift resolved after 1 week. Her visual acuity with previous glasses improved to 20/20 OU. In addition, choroidal effusions also subsided gradually. The presented case highlights the possible side effects of topiramate, offers management and suggestion for such a condition, and brings awareness to sulfa drug complications.

Keywords: migraine, myopic shift, secondary angle closure, topiramate

How to cite this article:
Lin CC, Tseng PC, Chen CC, Woung LC, Liou SW. Topiramate-induced bilateral secondary angle closure and myopia shift☆. Taiwan J Ophthalmol 2014;4:45-8

How to cite this URL:
Lin CC, Tseng PC, Chen CC, Woung LC, Liou SW. Topiramate-induced bilateral secondary angle closure and myopia shift☆. Taiwan J Ophthalmol [serial online] 2014 [cited 2022 Jan 26];4:45-8. Available from: https://www.e-tjo.org/text.asp?2014/4/1/45/203925

  1. Introduction Top

Topiramate, a sulfamate-substituted monosaccharide, is generally prescribed as an antiepileptic and antidepressant medication. Several mechanisms elicit its antiseizure effect. For example, the drug serves as a state-dependent blocker of sodium channels, enhances γ-aminobutyric acid (GABA)-mediated chloride fluxes across the postsynaptic membrane, provides positive modulation of GABA-A receptors, and produces a mild effect by inhibiting the activity of carbonic anhydrase. Treatment with topiramate is found to be useful in migraine, bipolar disorder, weight loss, and neuropathic pain.[1] However, in July 2001, Banta et al. first reported a case of secondary angle-closure glaucoma associated with topiramate use. Thereafter, several cases of ocular adverse reaction related to topiramate administration have been published.[2] During the past 10 years, there were 39 case reports throughout the world. Although few cases were published in Chinese population, few such case reports were proposed in Taiwan population as well. Therefore, we herein present a case to highlight the possible side effects of topiramate, offer management and suggestion for such condition, and bring awareness to sulfa drug complications.

  2. Case report Top

A 41-year-old healthy female presented to our hospital with sudden onset of bilateral ocular pain, ocular fullness sensation, blurred vision, and headache. On initial examination, her visual acuity with presenting glasses was 20/200 in the right eye and 20/ 50 in the left eye. Intraocular pressures (IOPs) as measured using an air puff tonometer were 44 mmHg OD and 49 mmHg OS. Central corneal thickness of both eyes was 540 μm (oculus dexter or OD) and 530 mm (oculus sinister or OS). Autorefraction measurement showed spherical refraction of −5.25 D OD and −4.75 D OS with acute myopic shift of 3.00 D in both eyes. The best-corrected visual acuity (BCVA) was 20/20 for both eyes. A slit-lamp examination revealed bilateral conjunctival chemosis and injection. Shallow anterior chambers measured using a Zeiss IOLMaster were 2.20 mm OU (average anterior chamber depth of adults: 3.15 mm) with iridocorneal touch for 360° and forward displacement of lens–iris diaphragm. Round and sluggishly reacting pupils without dilatation was also observed [Figure 1]A and [Figure 1]B. Axial length was 23.80 mm (OD) and 23.78 mm (OS). Average corneal curvature measured 44.23/44.82 D (OD) and 43.60/44.94 D (OS). Cystic corneal edema, peripheral anterior synechiae, or cellular inflammation in the anterior chambers was not detected. Gonioscopy showed closed angles in both eyes [Figure 1]C. A fundus photograph revealed normal retina and cup-disk ratio of 0.4 in both eyes.

Her medical history showed no previous ocular problems except myopia with spherical refraction of −2.25 D OD and −1.75 D OS. Shallow anterior chamber depth was noted due to forward displacement of lens–iris diaphragm during the slit-lamp examination. She had a past history of migraine under medication control. One week before her presenting symptoms, she was administered 50-mg topiramate daily for her migraine headache. She claimed no trauma history recently. There was no family history of glaucoma and her visual field was within normal limit. A Bscan ultrasound (SONOMED, B-5500) was performed, which revealed annular peripheral choroidal effusions in both eyes [Figure 2]A, while the lens thickness of both eyes was about 4.0 mm. At the same time, no characteristic T sign was demonstrated, and posterior scleritis (PS) is unlikely. Ultrasound biomicroscopy (UBM) (SONOMED, VuMAX) was arranged, which showed closed iridocorneal angles, bilateral 360° ciliochoroidal effusions, swelling and forward rotation of ciliary body; however, no pupillary block was seen [Figure 2]B.
Figure 1: At presentation, slit-lamp photograph revealed (A) shallow anterior chamber and forward displacement of the lenseiris diaphragm, (B) severe conjunctival chemosis, and marked shallow anterior chamber depth (2.20 mm) in both eyes, and (C) bilateral closed angles on gonioscopy. OD = oculus dexter; OS = oculus sinister.

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Figure 2: (A) On examination, B-scan ultrasound showed peripheral choroidal thickening and effusion (black arrows) in both eyes. (B) Ultrasound biomicroscopy (UBM) demonstrated ciliochoroidal effusions (white arrows) and forward rotation of edematous ciliary body (asterisks) in both eyes. (C and D) Three weeks later after discontinuation of topiramate, Bscan and UBM showed resolved choroidal effusions and edema of ciliary body in both eyes.

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She was advised to discontinue topiramate immediately and was prescribed antiglaucoma medication including intravenous infusion of mannitol, topical antiglaucoma eye drops, and mydriatics with 1% tropicamide b.i.d. (twice a day). Initial antiglaucoma eye drops were 0.5% timolol b.i.d. and 1% brinzolamide t.i.d. (thrice a day). The following day, much severe conjunctival chemosis andshallow anterior chamber persisted with 1OP mildly decreased to 25 and 30 mmHg, respectively. We stopped the brinzolamide usage due to suspicion of idiosyncratic reaction.

Two days later, 1OP returned to normal limits with resolution of the conjunctival chemosis. On Day 7, her myopic shift has resolved, and her visual acuity with previous glasses improved to 20/20 OU. Results of B-scan and UBM revealed mild residual choroidal effusions in both eyes that subsided 3 weeks later (Figure 2C and D). However, relative shallow anterior chamber depth was noted at her 3-month follow-up (2.68 mm OD and 2.62 mm OS). At this point, the BCVA readings were 20/20 OU, with 1OP and anterior chamber depth remaining stable. Topical aqueous suppressants were discontinued.

  3. Discussion Top

Bilateral simultaneous secondary acute angle-closure glaucoma is rare, and has been reported relating to drugs, general anesthesia, snake bite, microspherophakia, and Vogt–Koyanagi–Harada syndrome.[3] Among these, sulfonamide drug and its derivatives have been documented to cause transient myopia, ciliary body edema, choroidal effusions, and anterior rotation of the lens–iris diaphragm inducing secondary angle closure.[4]

In this case, bilateral acute myopic shift of 3.0 D was noted besides secondary angle closure. The differential diagnoses were primary angle-closure glaucoma (PACG), acute attack of chronic angle-closure glaucoma, PS, and drug-induced secondary angleclosure glaucoma. Given her younger age and myopic refractive status, plus no family history, PACG could be excluded. Besides, rarely are bilateral case and myopic progression reported in primary angle closure. A few factors, such as no history of glaucoma, no peripheral anterior synechiae, no progressive cupping of the optic nerve head, and no characteristic glaucomatous loss of visual field, excluded the possibility of acute attack of chronic angleclosure glaucoma. PS could give rise to angle-closure glaucoma without pupillary block due to choroidal effusions. PS is painful and may be associated with choroidal folds and serous elevation of the retina. 1n addition, bilateral PS can occur, but is rare. B-scan ultrasonography is quite characteristic, due to the presence of the T sign that occurs from collection of fluid in the sub-Tenon’s space. Therefore, PS needs to be considered. Topiramate-induced bilateral acute angle-closure glaucoma and myopic shift had been reported in several literatures. There were ocular findings of high myopia, shallow anterior chambers with anterior iris and lens displacement, microcystic edema, elevated IOP, closed anterior chamber angles, and ciliochoroidal effusions/detachment.[4]

Topiramate, a sulfa derivative, would cause potentially serious ocular side effects including blurred vision, acute 1OP elevation, acute myopia, diplopia, nystagmus, and shallow anterior chamber with angle closure.[5] 1n placebo-controlled trials, myopia was seen in 1% of children and abnormal vision in 13% of adults. Overall ocular adverse effects >1% was noted from the literature review.[6] These patients were predominantly female (89%) with a mean age of 34 years. Most cases have been reported to occur within the first 2 weeks (3–21 days) of starting topiramate administration, or within hours of doubling the doses.[7] Few cases were presented as unilateral episodes.[8] Symptoms were bilateral blurred vision, eye pain, sudden loss of vision with myopic shift, pressure sensation, headache, nausea, and vomiting. Ocular findings are high myopia, shallow anterior chambers with anterior iris and lens displacement, microcystic edema, elevated IOP, a closed anterior chamber angle, and a ciliochoroidal effusions/detachment.[4],[5],[6]

Nevertheless, the eye structures are not the risk factors to induce the malignant glaucoma after having topiramate. The underlying mechanism of topiramate-induced acute 1OP elevation is not clear yet. 1t may be an idiosyncratic reaction and can occur in otherwise normal eyes with normal anterior chamber angles, resulting in ciliochoroidal effusions with ciliary body swelling and induce forward rotation of the iris–lens diaphragm, causing myopia and angle-closure glaucoma.[4],[5] The management of topiramaterelated acute angle-closure glaucoma requires immediate cessation of topiramate, and institution of medical therapy including oral and topical aqueous suppressants. Use of pilocarpine can lead to further narrowing of the angles and worsening of signs and symptoms. Traditional treatment for angle-closure glaucoma such as laser iridotomy or surgical peripheral iridectomy may not be of value as precipitating mechanism is not a pupillary block. Topical cycloplegic agents can be given as they lower 1OP by relaxing the ciliary muscle and deepening anterior chamber.[4],[5],[6],[7],[8]

In our case, we administered intravenous mannitol, topical aqueous suppressants, and mydriatics for treatment, in addition to topiramate cessation. Oral acetazolamide, a sulfa-derivative medication, was avoided as treatment for the elevated IOP, because it has been reported to cause secondary angle-closure glaucoma.[9] Topical antiglaucoma eye drops were given with 0.5% timolol and 1% brinzolamide. However, on the next day, conjunctival chemosis worsened, with only mild improvement in IOP. Brinzolamide administration was suspected due to its sulfonamide-derived property, and possible idiosyncratic reactions, although no previous case reports were presented. As such, it was stopped. Two days later, her 1OP returned to normal ranges with resolution of the conjunctival chemosis. 1n our opinion, any systemic or topical sulfa-derivative drugs should be avoided when clinical suspicion of topiramate-associated acute angle-closure glaucoma is encountered.[9],[10]

Topiramate/sulfa-derivative medication can induce ocular adverse effects of bilateral acute myopia and angle-closure glaucoma secondary to choroidal effusions.[4],[5],[6],[7],[8] Ophthalmologist should be aware of this potential complication. The quick identification of sulfaderivative medication and subsequent discontinuation can expedite resolution of the angle closure. 1f the causative medication is not recognized, persistent high 1OP may result in permanent visual loss. Neurologist and psychiatrist prescribing topiramate for their patients should be alert to such side effects, and be advised immediate referral to ophthalmology service under clinical suspicion.

Conflicts of interest: The authors have no conflicts of interest relevant to this article.

  References Top

Medeiros FA, Zhang XY, Bernd AS, Weinreb RN. Angle-closure glaucoma associated with ciliary body detachment in patients using topiramate. Arch Ophthalmol. 2003;121:282–285.  Back to cited text no. 1
Banta JT, Hoffman K, Budenz DL, Ceballos E, Greenfield DS. Presumed topiramate-induced bilateral acute angle-closure glaucoma. Am J Ophthalmol. 2001;132:112–114.  Back to cited text no. 2
Senthil S, Garudadri C, Rao HB, Maheshwari R. Bilateral simultaneous acute angle closure caused by sulphonamide derivatives: a case series. Indian J Ophthalmol. 2010;58:248–252.  Back to cited text no. 3
Desai CM, Ramchandani SJ, Bhopale SG, Ramchandani SS. Acute myopia and angle closure caused by topiramate, a drug used for prophylaxis of migraine. Indian J Ophthalmol. 2006;54:195–197.  Back to cited text no. 4
Lee GC, Tam CP, Danesh-Meyer HV, Myers JS, Katz LJ. Bilateral angle closure glaucoma induced by sulphonamide-derived medications. Clin Experiment Ophthalmol. 2007;35:55–58.  Back to cited text no. 5
Cereza G, Pedrós C, Garcia N, Laporte JR. Topiramate in non-approved indications and acute myopia or angle closure glaucoma. Br J Clin Pharmacol. 2005;60: 578–579.  Back to cited text no. 6
Thambi L, Kapcala LP, Chambers W, et al. Topiramate-associated secondary angle-closure glaucoma: a case series. Arch Ophthalmol. 2002;120:1108.  Back to cited text no. 7
Fraunfelder FW, Fraunfelder FT, Keates EU. Topiramate-associated acute, bilateral, secondary angle-closure glaucoma. Ophthalmology. 2004; 111: 109–111.  Back to cited text no. 8
Narayanaswamy AK, Antrolikar M, Vijaya L. Acetazolamide-induced glaucoma. Asian J Ophthalmol. 2007;9:213–215.  Back to cited text no. 9
Blain P, Paques M, Massin P, Erginay A, Santiago P, Gaudric A. Acute transient myopia induced by indapamide. Am J Ophthalmol. 2000;129:538–540.  Back to cited text no. 10


  [Figure 1], [Figure 2]


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1. Introduction
2. Case report
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