Discussion

Topiramate-induced angle closure is usually bilateral and occurs in the absence of pupillary block. It is due to cilio-choroidal effusions causing anterior rotation of the ciliary body and anterior displacement of the lens–iris diaphragm, occluding the angle.6 It has been theorised that topiramate (or other sulpha medications) can disrupt the ocular blood brain barrier through an inflammatory mechanism, causing an increase in the protein content of the cerebrospinal fluid. When large amounts of protein leak into the ciliochoroidal extravascular space, the osmotic pressure difference allows for choroidal expansion. The enlargement of the choroid displaces the lens–iris diaphram forward.7 This anterior rotation of anatomic structures induces a myopic shift, causing bilateral blurring of vision. In addition, ciliary body swelling allows for relaxation of the zonules, causing thickening of the lens. This also contributes to the forward displacement of anterior segment structures.

UBM is a valuable tool in diagnosis of this condition as it is able to provide high-resolution (35 mHz) imaging of middle and anterior chamber anatomy and the angle. Gonioscopy can only be used to identify the closure of the angle and although B-scan can occasionally identify posterior segment or ciliary body structures creating forward pressure, the 10 mHz probe does not provide adequate visualisation of the anterior chamber. UBM is the optimal technology for visualising the anterior chamber structures and their relative anatomy and positioning. It is the only one of these three modalities that can confirm the presence of secondary angle closure and diagnose the aetiology as choroidal effusions.8 We therefore recommend that any suspected cases of topiramate or other sulpha medication-induced secondary angle closure be evaluated using UBM.

The ability to differentiate between varying aetiologies of angle closure glaucoma is crucial to initiating appropriate management; in this case, confirmation of diagnosis via UBM directed therapy. Treatment begins with the immediate discontinuation of the offending agent (topiramate or other sulpha medication) and the subsequent administration of ocular hypotensives and cycloplegic agents. Importantly, cycloplegics function to tighten the zonules and displace the lens–iris diaphragm posteriorly. Miotics such as pilocarpine, the gold standard for the treatment of primary angle closure glaucoma, are actually contraindicated in the case of choroidal effusions—contraction of the ciliary body can cause additional zonular relaxation and further forward displacement the lens–iris diaphragm.9 Oral steroids, mannitol, choroidal drainage and laser peripheral iridoplasty have also been described in the treatment of acute angle closure.1–10 However, in secondary angle closure due to choroidal effusions, miotics and laser iridectomy are not indicated, as pupillary block is not the underlying pathophysiology.10

Finally, sulpha-based medications other than topiramate have been known to cause similar phenomena and effected patients may experience cross-reactivity to these other medications.9 Therefore, the confirmation of topiramate-induced choroidal effusions should serve as a warning—even in those patients without appositional angle closure—to avoid both the offending agent and all sulpha-based medications in the future.