Influence on intraocular pressure of anti-inflammatory treatments after selective laser trabeculoplasty.

INTRODUCTION: Selective laser trabeculoplasty (SLT) is an effective and safe procedure to lower intraocular pressure (IOP) in the management of open-angle glaucoma. The post-laser inflammatory reaction could be positively implicated in SLT efficacy and the relevance of postoperative use of topical anti-inflammatory remains controversial. The goal of this study is to determine the effect of various anti-inflammatory treatments on intraocular pressure and on side effects following SLT. MATERIAL AND METHODS: A prospective, randomized, double-blind study with a control group was conducted. Ninety-six eyes of 67 patients with primary open-angle glaucoma who underwent SLT were enrolled in this study between March 2009 and March 2012. Eyes recruited in the study were randomized to receive either prednisolone acetate 1%, diclofenac 0.1% or a placebo. The 3 treatments were administered 4 times a day for 5 days following SLT. The intraocular pressures were measured at regular intervals during the 6-months follow-up period. Side effects were also evaluated with a questionnaire as well as with the ocular exam. RESULTS: The analysis of the relative IOP decrease over the 6-months period revealed a significant difference between the time points of follow-up (P<0.0001), but no group effect (P=0.2980). No significant difference regarding anterior chamber inflammation and discomfort was observed between the 3 groups. CONCLUSION: There was no difference in intraocular pressure reduction, intraocular inflammation or ocular discomfort post-SLT when comparing the 3 treatment modalities.

A common gene for juvenile and adult-onset primary open-angle glaucomas confined on chromosome 1q.

Primary open-angle glaucoma (POAG), which causes progressive loss of the visual fields, was subdivided into two groups according to age at onset: (1) chronic open-angle glaucoma (COAG) diagnosed after age 40 years and (2) juvenile open-angle glaucoma (JOAG) diagnosed between 3 years of age and early adulthood. A JOAG gene (GLC1A) was recently mapped to chromosome 1q. We studied 142 members of a huge multigenerational French Canadian family affected with autosomal dominant POAG. Either JOAG or COAG was diagnosed in 40 patients. Six subjects were also diagnosed with ocular hypertension (OHT), which may lead to POAG. To localize a common disease gene that might be responsible for both glaucoma subsets, we performed linkage analysis considering JOAG and COAG under the same phenotypic category. JOAG/COAG was tightly linked to seven microsatellite markers on chromosome 1q23-q25; a maximum lod score of 6.62 was obtained with AF-M278ye5. To refine the disease locus, we exploited a recombination mapping strategy based on a unique founder effect. The same characteristic haplotype, composed of 14 markers spanning 12 cM between loci D1S196 and D1S212, was recognized in all persons affected by JOAG, COAG, or OHT, but it did not occur in unaffected spouses and in normal family members > 35 years of age, except for three obligatory carriers. Key recombination events confined the disease region within a 9-cM interval between loci D1S445 and D1S416/D1S480. These observations demonstrate that the GLC1A gene is responsible for both adult-onset and juvenile glaucomas and suggest that the JOAG and COAG categories within this family may be part of a clinical continuum artificially divided at age 40 years.

Early foveal involvement and generalized depression of the visual field in glaucoma.

We selected for study 35 patients with glaucomatous visual field loss or cupping that was asymmetric between the two eyes, concentrating on cases in which the glaucomatous damage was mild. We found that 15 patients had a reduced foveal sensitivity usually associated with either a scotoma impinging on fixation or a depression in the central field. In addition, 19 of the 35 patients had a subtle reduction in visual acuity. Thus, the fovea is often mildly affected early in glaucoma, even though the point of fixation is typically among the last regions of visual field to have a severe loss of visual sensation. We also observed that there is often a diffuse visual field loss early in glaucoma, represented as a generalized depression, and this may occur before there are discrete nerve fiber-bundle defects (paracentral scotomas and the like).

Dethecting glaucomatous damage with the Friedmann analyzer compared with te Goldmann perimeter and evaluation of stereoscopic photographs of the optic disk.

We used a Friedmann visual field analyzer with a 98-hole plate to test 32 normal control eyes and to establish highly specific criteria for abnormality. When these criteria were later applied to the testing of 50 additional normal control eyes, there were no false-positive abnormalities. With these criteria, the Friedmann visual field analyzer proved to be at least as sensitive as careful manual perimetry with the Goldmann perimeter in detecting early glaucomatous visual field defects. In addition to having high sensitivity and specificity, the Friedmann visual field analyzer with the 98-hole plate is rapid and requires very little training to operate. By way of comparison, examination of stereoscopic photographs of the optic disk was also sensitive in detecting or suggesting glaucomatous damage with visual field loss, but some of the normal control optic nerves were also considered suspect. Ignoring the suspect disks in order to reduce false-positive results improved specificity but simultaneously reduced sensitivity for detecting definite visual field loss. The combination of optic disk evaluation and visual field testing (with wither the Goldmann or the Friedman instrument) better detected early cases than did either test alone, because each method picked up some early cases missed by the other.