|Year : 2017 | Volume
| Issue : 5 | Page : 482-484
Topiramate-induced angle closure glaucoma in a case of chronic migraine
VA Arun, YS Sirohi, Yatharth Dixit
Department of Internal Medicine, Armed Forces Medical College, Pune, Maharashtra, India
|Date of Submission||28-Nov-2016|
|Date of Acceptance||13-Jan-2017|
|Date of Web Publication||14-Nov-2017|
V A Arun
Department of Internal Medicine, Armed Forces Medical College, Pune - 411 040, Maharashtra
Source of Support: None, Conflict of Interest: None
Topiramate is an oral sulfamate medication used primarily for epilepsy and migraine. The tolerability profile with its lack of significant metabolic side effects makes it a favorable drug for patients with comorbid lifestyle illnesses. Topiramate-induced angle closure is an idiosyncratic reaction and can occur in otherwise normal eyes with normal anterior chamber angles. Ocular examination before starting topiramate cannot identify eyes at risk. Prompt cessation of therapy alone can result in rapid resolution of most of these adverse effects, whereas failure to recognize can lead to permanent visual problems. The internists should be aware of the documented side effects of topiramate, particularly when presented with simultaneous bilateral acute angle-closure glaucoma. Neurologists initiating therapy with topiramate should also educate the patients of its potential side effects and importance of reporting back immediately in case of any visual disturbance. Prompt cessation of topiramate is the mainstay of treatment. Supportive treatment in the form of oral and topical antiglaucoma drugs to reduce the intraocular pressure (IOP), topical steroids to bring down the inflammation, and topical cycloplegics to retract the ciliary processes thus bringing down the IOP has been recommended, but a few would warrant laser iridotomy or surgical iridectomy. We report a case of topiramate-induced angle closure glaucoma in a young female being managed as a case of chronic migraine, highlighting the importance of increasing the awareness of this rare, idiosyncratic adverse effect of topiramate and the need for timely intervention to avoid irreversible visual loss.
Keywords: Topiramate, acute angle-closure glaucoma, gonioscopy
|How to cite this article:|
Arun V A, Sirohi Y S, Dixit Y. Topiramate-induced angle closure glaucoma in a case of chronic migraine. Med J DY Patil Univ 2017;10:482-4
| Introduction|| |
Topiramate, a sulfamate-substituted monosaccharide, is primarily used in the treatment of epilepsy; however, it has also demonstrated efficacy in the treatment of migraine, depression, bipolar disorders, neuropathic pain, posttraumatic stress disorder, postherpetic neuralgia, idiopathic intracranial hypertension, and as an “off-label application,” it has been used for weight loss, adjunctive therapy for alcoholism, and nicotine cessation. The tolerability profile with its lack of significant metabolic side effects makes it a favorable drug for patients with comorbid illnesses.
Launched into the market in 1996, 5 years later, Banta et al. reported the first case of acute angle-closure glaucoma (AACG) associated with the use of topiramate. On September 2001, Ortho-McNeil Pharmaceuticals, the protagonists, inserted a black box warning indicating that 23 cases of AACG had been reported to their safety division, and physicians should be aware of this adverse ocular drug reaction. The incidence of permanent vision loss in topiramate-associated bilateral AACG has been reported to be 8.1%. We report a case of topiramate-induced angle closure glaucoma (ACG) in a young female being managed as a case of chronic migraine, highlighting the importance of increasing the awareness of this rare, idiosyncratic adverse effect of topiramate and the need for timely intervention to avoid irreversible visual loss.
| Case Report|| |
A 25-year-old female, with a past medical history of migraine headaches, presented to the emergency department with a 1-day history of bilateral retro-orbital headache and sudden-onset progressive diminution of vision. She denied any history of fever, trauma, or focal neurological deficits. Further questioning revealed that the patient had been started on topiramate, 25 mg, 1 week before presentation for migraine headaches and had been instructed to double the dose 3 days before the onset of symptoms.
On examination, she was oriented, afebrile, and hemodynamically stable. Her neck was supple and there were no focal deficits. Bilateral lid edema, conjunctival chemosis, and shallow anterior chamber were seen. The cornea was clear and pupil was mid-dilated, bilaterally sluggishly reacting to light. The best-corrected visual acuity (BCVA) was 1/60 in the right eye and 2/60 in the left eye. The intraocular pressures (IOPs) by applanation tonometry were 56 mmHg and 38 mmHg in the right and left eyes, respectively. Gonioscopy with and without compression revealed appositional angles. Funduscopy revealed normal optic discs. The patient was diagnosed with ACG, secondary to topiramate idiosyncrasy. After discontinuation of topiramate, the patient was treated with topical timolol maleate, cyclopentolate, and oral acetazolamide 500 mg. After 1 h, the topical treatment was repeated with the same combination, and no change in IOP was noted. Intravenous 20% mannitol, 100 g in 500 ml, was administered, and 3 h later, IOP was 46 mmHg in the right eye and 32 mmHg in the left eye. A second dose of mannitol was given and the previously outlined regimen was continued. By the next morning, the patient's pain score was 4/10 in the right eye and 2/10 in the left eye. The BCVA was 6/60 in both eyes. At that visit, the IOP values were 38 mmHg in the right eye and 37 mmHg in the left eye. Anterior segment examination showed persistent bilateral shallowing of the anterior chamber with microcystic epithelial edema and bullae bilaterally with Descemet's folds in the right eye only. The patient was followed up daily with gradual reduction of IOPs. On day 3 of admission, her IOP had normalized; 9 mmHg in the right eye and 8 mmHg in the left eye. The BCVA was 6/9 in both eyes, and gonioscopy showed open angles bilaterally. The anterior chamber depth improved, and cornea was clear. She was discharged on day 5, follow-up 2 weeks later revealed normal anterior segment, and dilated fundus examination showed that the cup-to-disk ratio was 0.2 with intact rim and a full visual field in both eyes.
| Discussion|| |
We report on a case of bilateral topiramate-induced ACG. Fraunfelder et al. reviewed 115 reports of topiramate-induced ACG and found that 85% of cases occurred within the first 2 weeks of treatment (range: 1–49 days). This is consistent with the presentation in this patient, who had been on treatment for 10 days and experienced the onset of symptoms within 3 days of doubling her dose. Previous reports have not identified a minimal dose of topiramate associated with ACG consistent with idiosyncratic nature of the reaction. Nonetheless, the study by Fraunfelder et al. showed that almost 50% of cases occur with doses of 50 mg or less.
The principal step in appropriate management is making a correct diagnosis. We believe that a prompt diagnosis and treatment at the time of the patient's presentation to the emergency department might have allowed faster resolution of the episode of angle closure in our case. The ocular adverse reaction consists of peripheral ciliochoroidal effusion with ciliary body edema and anterior rotation of the ciliary body. There is an anterior shifting of the lens iris diaphragm shallowing the anterior chamber in the periphery, causing the ACG without pupillary block. The exact mechanism of the ciliochoroidal effusion is unknown.,
The anterior displacement of the iris lens diaphragm causes a myopic shift in the patient's refraction and, as illustrated by the temporal course in this patient, the myopic shift may take several weeks to resolve, despite normalization of IOP. This might be a useful observation to discuss with the patient during the recovery phase.
The treatment of topiramate-induced ACG is tailored to the severity of IOP elevation.,, The first step is immediate discontinuation of topiramate. This step combined with topical hypotensive medications and cycloplegics is most often sufficient to reduce the IOP. In a large retrospective case series, the typical course of IOP normalization was reported to be within hours to days after cessation of topiramate and initiating of conventional IOP-reducing therapy. In contrast, our case necessitated further treatment with mannitol to correct the marked elevation of IOP that appeared to be refractory to conventional therapy over many hours. Rhee et al. suggested that, in cases that do not respond to conventional therapy, systemic corticosteroids and hyperosmolar agents should be used to speed the recovery and to avoid the need for surgical intervention. Laser peripheral iridotomy used in some cases reported in literature has not been uniformly effective in relieving the secondary angle closure and should be reserved for cases where the above treatment fails. Iridotomy may not be advisable as acute glaucoma is caused by uveal effusion without pupillary block; when performed, it can aggravate glaucoma by pushing forward iris and lens. We used mannitol in our patient, and recovery followed after administration of two doses of the same in addition to the ongoing use of topical medications and acetazolamide.
| Conclusion|| |
Topiramate-induced angle closure is an idiosyncratic reaction and can occur in otherwise normal eyes with normal anterior chamber angles. Ocular examination before starting topiramate cannot identify eyes at risk. The internists should be aware of the documented side effects of topiramate, particularly when presented with simultaneous bilateral AACG. Neurologists initiating therapy with topiramate should also educate the patients of its potential side effects and the importance of reporting back immediately in case of any visual disturbance. Prompt cessation of therapy alone can result in the rapid resolution of most of these adverse effects, whereas failure to recognize can lead to permanent visual problems.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
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.
Fraunfelder FW, Fraunfelder FT, Keates EU. Topiramate-associated acute, bilateral, secondary angle-closure glaucoma. Ophthalmology 2004;111:109-11.
Lee GC, Tam CP, Danesh-Meyer HV, Myers JS, Katz LJ. Bilateral angle closure glaucoma induced by sulphonamide-derived medications. Clin Exp Ophthalmol 2007;35:55-8.
Rhee DJ, Ramos-Esteban JC, Nipper KS. Rapid resolution of topiramate-induced angle-closure glaucoma with methylprednisolone and mannitol. Am J Ophthalmol 2006;141:1133-4.