Unilateral ocular malingering – a new test for the assessment of visual acuity

Abstract

ened. After the initial presentation, he discontinued 0.02% cyanocobalamin; the IOPs were between 16 and 20 mmHg OU, and no visual field progression occurred OU. Ten months after the initial presentation, corneal whitening OU developed. At the scheduled 11-month follow-up visit, the BCVAs were 1.0 OU; the IOPs were 20 mmHg OD and 18 mmHg OS. Slit-lamp examination (Fig. 1C, D) and anterior-segment optical coherence tomography (Fig. 1E,F) showed marked corneal opacities and invasion of vascular tissues from the corneal limbus to the temporal cornea at the level of the deep corneal stroma OU. The conjunctival injection remained OU. No ischaemic changes (angular rubeosis, peripheral anterior synechia) (Fig. 1G,H) or retinal haemorrhage were observed. Infectious keratitis, for example herpesviruses (herpes simplex viruses and varicella zoster virus), syphilis and tuberculosis, was ruled out, respectively, by polymerase chain reaction examination of tear samples, Treponema pallidum hemagglutination assay and tuberculosis antigen-specific interferon-gamma release assay. Interstitial keratitis with deep corneal vascularization possibly associated with topical medications was diagnosed (Maruyama et al. 2017). Brimonidine tartrate (BT) was discontinued, and 0.1% betamethasone (Sanbethasone, Santen Pharmaceutical Co. Ltd.) started three times daily; latanoprost and 1% dorzolamide hydrochloride/ 0.5% timolol maleate were continued. Three months after BT discontinuation, the vascularization regressed OU; betamethasone was discontinued, and oral acetazolamide (500 mg/day) was prescribed for 3 weeks for IOP elevations OU probably due to steroid use. At the final visit 7 months after BT discontinuation, the corneal vascularization regressed markedly and the corneal opacity decreased OU, while the extent of the corneal opacity was unchanged OU likely because of lipid deposition (Fig. 1I, J). The BCVAs were 1.0 OD and 1.2 OS, and the IOP was 16 mmHg OU with latanoprost and 1% dorzolamide hydrochloride/0.5% timolol maleate fixed combination. Maruyama et al. (2017) reported two cases of a severe corneal disorder that developed after BT use. Patient 1 used 0.005% latanoprost/0.5% timolol maleate fixed combination (Xalcom, Pfizer Japan, Tokyo, Japan) OU and BT OS, and corneal opacity developed nasally OS. Patient 2 developed an inferior corneal opacity OD and inferotemporal corneal opacity OS after using 0.005% latanoprost and the 1% dorzolamide hydrochloride/0.5% timolol maleate fixed combination and BT OU. The current case had deep corneal neovascularization, corneal infiltration and limbal corneal opacity after long-term use of the multiple antiglaucoma medications including BT. Collectively to the previous two cases, we speculate that long-term use of BT, its solvent or interaction between BT and other antiglaucoma medications associated with the corneal disorder in our case. All three cases with corneal disorders had follicular conjunctivitis, a wellknown side-effect of BT, that responded to steroid therapy and suggested a possible allergic reaction as the possible culprit after BT use. However, the exact mechanism(s) remains unknown. Since BT discontinuation is likely to be the most effective therapy, clinicians need to be aware of this disorder, which rarely develops with long-term BT use.