Effect of Visual Search Training on Saccades in Age-related Macular Degeneration Subjects.

OBJECTIVE: To compare the impact of unilateral versus bilateral Age-related Macular Degeneration (AMD) on saccadic movements, and to show the effect of visual search training on these eye movement performances in AMD subjects. We hypothesized that unilateral and bilateral AMD subjects had abnormal saccadic performances, and that visual search training could improve their performances. METHODS: Three groups participated in visual search training: 13 elderly unilateral AMD subjects (mean age: 74.6 ± 1.6 years), 15 elderly bilateral AMD subjects (mean age: 74.2 ± 1.2 years), and 15 healthy age-matched control subjects (mean age: 70.9 ± 1.3 years). Horizontal saccadic performances were recorded before and after visual search training (Metrisquare®) with the Mobile Eye Tracker (Mobile EBT®). We analyzed the saccadic movement performances: latency, mean velocity and gain. We measured the training performances for each exercise: the time, the number of omissions and the number of errors. We analyzed the performances with Kruskal-Wallis and posthoc tests. RESULTS: The latency of saccades in AMD subjects is significantly longer compared to healthy elderly for 15° (p<0.03), 10° (p<0.003) and 5° (p<10-3). Unilateral and bilateral AMD subjects normalized their latency of saccades after training for small saccades (respectively p=0.30 and p=0.23 for 10°, and p=0.09 and p=0.52 for 5°). In elderly, performances depend on the saccade's amplitude. CONCLUSION: AMD subjects' saccadic movements are disrupted: the execution needs more time but is efficient. The visual search training improved the saccadic performances in AMD subjects. Further studies will aim to improve knowledge on such issues and to explore the benefit of training over time in unilateral AMD subjects.

Mineralocorticoid receptor antagonism in the treatment of chronic central serous chorioretinopathy: a pilot study.

PURPOSE: Based on experimental data showing that central serous chorioretinopathy could result from overactivation of mineralocorticoid receptor pathway in choroid vessels, the authors studied eplerenone, a mineralocorticoid receptor antagonist, as a potential treatment for chronic central serous chorioretinopathy. METHODS: This nonrandomized pilot study included 13 patients with central serous chorioretinopathy of at least 4-month duration, treated with 25 mg/day of oral eplerenone for a week followed by 50 mg/day for 1 or 3 months. The primary outcome measure was the changes in central macular thickness recorded by optical coherence tomography, and the secondary outcomes included changes in foveal subretinal fluid (SRF) measured by OCT, in best-corrected visual acuity (BCVA) and the percentage of eyes achieving complete resolution of subretinal fluid during the treatment period. RESULTS: Central macular thickness decreased significantly from 352 ± 139 µm at baseline to 246 ± 113 µm and 189 ± 99 µm at 1 and 3 months under eplerenone treatment (P < 0.05 and P < 0.01, respectively). At 3 months, the subretinal fluid significantly decreased compared with baseline subretinal fluid (P < 0.01) and best-corrected visual acuity significantly improved compared with baseline best-corrected visual acuity (P < 0.001). CONCLUSION: Eplerenone treatment was associated with a significant reduction in central macular thickness, subretinal fluid level, and an improvement in visual acuity. Randomized controlled trials are needed to confirm these encouraging results.

Mineralocorticoid receptor is involved in rat and human ocular chorioretinopathy.

Central serous chorioretinopathy (CSCR) is a vision-threatening eye disease with no validated treatment and unknown pathogeny. In CSCR, dilation and leakage of choroid vessels underneath the retina cause subretinal fluid accumulation and retinal detachment. Because glucocorticoids induce and aggravate CSCR and are known to bind to the mineralocorticoid receptor (MR), CSCR may be related to inappropriate MR activation. Our aim was to assess the effect of MR activation on rat choroidal vasculature and translate the results to CSCR patients. Intravitreous injection of the glucocorticoid corticosterone in rat eyes induced choroidal enlargement. Aldosterone, a specific MR activator, elicited the same effect, producing choroid vessel dilation -and leakage. We identified an underlying mechanism of this effect: aldosterone upregulated the endothelial vasodilatory K channel KCa2.3. Its blockade prevented aldosterone-induced thickening. To translate these findings, we treated 2 patients with chronic nonresolved CSCR with oral eplerenone, a specific MR antagonist, for 5 weeks, and observed impressive and rapid resolution of retinal detachment and choroidal vasodilation as well as improved visual acuity. The benefit was maintained 5 months after eplerenone withdrawal. Our results identify MR signaling as a pathway controlling choroidal vascular bed relaxation and provide a pathogenic link with human CSCR, which suggests that blockade of MR could be used therapeutically to reverse choroid vasculopathy.

A case of acute retinal pigment epithelitis: spectral domain optical coherence tomography time course and physiopathologic hypothesis.

PURPOSE: To report the time course of retinal morphologic changes in a patient with acute retinal pigment epithelitis (ARPE) using spectral domain optical coherence tomography (SD-OCT). METHODS: A 30-year old man was referred for blurred vision of his right eye after five days that appeared suddenly 15 days after recovery from a flu-like syndrome. SD-OCT was performed immediately, followed by fluorescein and infracyanine angiography at eight days and then at three weeks. RESULTS: At presentation, a bubble of sub-macular deposit was observed on the right macula with central golden micronodules in a honeycomb pattern. SD-OCT showed an "anterior dislocation" of all the retinal layers up to the inner/outer segment (IS/OS) line and irregular deposits at the OS level together with thickening of the retinal pigment epithelial (RPE) layer. As visual acuity increased, eight days later, the OCT showed reduction of the sub-retinal deposits and an abnormal hyperflectivity of the sub-retinal and RPE layers was observed. The patient showed a positive serology for picornavirus. DISCUSSION: The acute SD-OCT sections of this patient with ARPE were compared with histological sections of a 35 day old Royal College of Surgeons rat. Similar findings could be observed, with preservation of the IS/OS line and accumulation of debris at the OS level, suggesting that ARPE symptoms could result from a transient phagocytic dysfunction of the RPE at the fovea, inducing reversible accumulation of undigested OS. Picornaviruses comprising enterovirus and coxsachievirus described as being associated with acute chorioretinitis. In this case, it was responsible for ARPE. CONCLUSION: We hypothesize that ARPE syndrome results from a transient dysfunction of RPE, which can occur as a post viral reaction.

Full-thickness macular hole in a patient with diabetic cystoid macular oedema treated by intravitreal triamcinolone injections.

PURPOSE: Full-thickness macular hole associated with diabetic macular oedema is a rare feature and its pathogenesis remains incompletely elucidated. We report the occurrence of a full-thickness macular hole, documented with optical coherence tomography (OCT), in a patient with diabetic cystoid macular oedema treated by intravitreal triamcinolone injections. CASE REPORT: A 48-year-old woman with refractory diabetic cystoid macular oedema underwent successive intravitreal triamcinolone injections, which were followed by a progressive thinning of the neurosensory retina at the fovea, and then by a full-thickness macular hole, associated with a perifoveal posterior hyaloid detachment, visible on OCT. During pars plana vitrectomy, a thin epiretinal macular membrane was diagnosed and removed. DISCUSSION: Pathogenesis of the present full-thickness macular hole associated with diabetic macular oedema is different from that of idiopathic macular holes because anteroposterior vitreous tractions were not involved in its formation. Recurrent intravitreal triamcinolone injections may have had an indirect role in the development of the macular hole, by favouring the rupture of distended Muller cells and intraretinal pseudocysts.