Main aspects of etiopathogenesis, diagnosis and treatment of subhyaloid hemorrhages

Purpose. To present modern literature data on the main aspects of etiopathogenesis, diagnosis and treatment of subhyaloid hemorrhages. Material and methods. To perform the review, the search for literature sources on PubMed abstract databases was analyzed by the keywords «subhyaloid hemorrhages», «posterior hyaloidotomy» according to Russian publications on the topic of the article for the period up to 2020 inclusive. Results. Subhyaloid hemorrhage is a suspension of blood in a space bounded by a mesh membrane and a detached posterior hyaloid membrane. The most common cause of subhyaloid hemorrhages are retinal vascular diseases: diabetic retinopathy of the retina (30%), Valsalva hemorrhagic retinopathy (30%), central retinal vein thrombosis (20%). Subhyaloid hemorrhages are less common in hematological diseases, eye injury, rupture of the macroaneurysm, Terson syndrome. It has been established that the main complications due to untimely or inadequate treatment of subhyaloid hemorrhages are the formation of a premacular fibrous membrane, vitreoretinal fusion, traction retinal detachment, hemophthalmos, fibrosis and retinal atrophy, which require the right tactics in treatment. Conclusion. Thus, due to the prolonged presence of blood and fibrin in the premacular subhyaloidal space, there is a danger of mechanical and toxic effects on the retinal neuroepithelium of the macular region, which can lead to an irreversible decrease in visual functions. Key words: subhyaloid hemorrhages, Nd:YAG laser, posterior hyaloidotomy

Pattern Dystrophies

Pattern dystrophies have been known since 1950 which have autosomal dominant inheritance pattern. Pattern dystrophies have been classified based on the pattern of the pigment distribution. Despite significant retinal changes, good visual acuity is often maintained. However, complications such as choroidal neovascular membrane and retinal atrophy may develop in older patients and can significantly decrease visual acuity. There is no specific treatment, but when complications arise, treatment should be done by reason.

Association of retinal atrophy with cortical lesions and leptomeningeal enhancement in multiple sclerosis on 7T MRI

Background: Retinal atrophy in multiple sclerosis (MS) as measured by optical coherence tomography (OCT) correlates with demyelinating lesions and brain atrophy, but its relationship with cortical lesions (CLs) and meningeal inflammation is not well known. Objectives: To evaluate the relationship of retinal layer atrophy with leptomeningeal enhancement (LME) and CLs in MS as visualized on 7 Tesla (7T) magnetic resonance imaging (MRI). Methods: Forty participants with MS underwent 7T MRI of the brain and OCT. Partial correlation and mixed-effects regression evaluated relationships between MRI and OCT findings. Results: All participants had CLs and 32 (80%) participants had LME on post-contrast MRI. Ganglion cell/inner plexiform layer (GCIPL) thickness correlated with total CL volume ( r =−0.45, p < 0.01). Participants with LME at baseline had thinner macular retinal nerve fiber layer (mRNFL; p = 0.01) and GCIPL ( p < 0.01). Atrophy in various retinal layers was faster in those with certain patterns of LME. For example, mRNFL declined –1.113 (–1.974, –0.252) μm/year faster in those with spread/fill-pattern LME foci at baseline compared with those without ( p = 0.01). Conclusion: This study associates MRI findings of LME and cortical pathology with thinning of retinal layers as measured by OCT, suggesting a common link between meningeal inflammation, CLs, and retinal atrophy in MS.

Age-dependent favorable visual recovery despite significant retinal atrophy in pediatric MOGAD: how much retina do you really need to see well?

Background To investigate age-related severity, patterns of retinal structural damage, and functional visual recovery in pediatric and adult cohorts of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) optic neuritis (ON). Methods All MOGAD patients from the 5 participating centers were included. Patients with initial manifestation <18 years were included in the pediatric (MOGADped) cohort and patients with ≥18 years in the adult (MOGADadult) cohort. For patients with MOGAD ON, examinations at least ≥6 months after ON onset were included in the analyses. Using spectral domain optical coherence tomography (SD-OCT), we acquired peripapillary retinal nerve fiber layer thickness (pRNFL) and volumes of combined ganglion cell and inner plexiform layer (GCIPL). High- and 2.5% low-contrast visual acuity (HCVA, LCVA) and visual-evoked potentials (VEP) were obtained. Results Twenty MOGADped (10.3±3.7 years, 30 MOGAD ON eyes) and 39 MOGADadult (34.9±11.6 years, 42 MOGAD ON eyes) patients were included. The average number of ON episodes per ON eye was similar in both groups (1.8±1.3 and 2.0±1.7). In both pediatric and adult MOGAD, ON led to pronounced neuroaxonal retinal atrophy (pRNFL: 63.1±18.7 and 64.3±22.9 μm; GCIPL: 0.42±0.09 and 0.44±0.13 mm3, respectively) and moderate delay of the VEP latencies (117.9±10.7 and 118.0±14.5 ms). In contrast, visual acuity was substantially better in children (HCVA: 51.4±9.3 vs. 35.0±20.6 raw letters, p=0.001; LCVA: 22.8±14.6 vs. 13.5±16.4, p=0.028). Complete visual recovery (HCVA-logMAR 0.0) occurred in 73.3% of MOGADped and 31% MOGADadults ON eyes, while 3.3% and 31% demonstrated moderate to severe (logMAR > 0.5) visual impairment. Independent of retinal atrophy, age at ON onset significantly correlated with visual outcome. Conclusion Pediatric MOGAD ON showed better visual recovery than adult MOGAD ON despite profound and almost identical neuroaxonal retinal atrophy. Age-related cortical neuroplasticity may account for the substantial discrepancy between structural changes and functional outcomes.

Gene Panel Screening Across Canine Eye Disorders Highlights Genetic Heterogeneity and the Need for Molecular Discoveries

Blinding inherited eye diseases affect millions of people worldwide. Despite a large number of gene discoveries, many patients lack the molecular description of their condition. The domestic dog has become a widely used model to study inherited eye disease genetics and therapeutics during the past 15 years, and nearly 50 genes have been implicated across breeds. Despite a continuous discovery of new causative variants across canine eye disease groups, the genetic cause in most cases is expected to remain unknown. We tested this hypothesis by screening 49 known variants in 194 dogs from 71 breeds affected with progressive retinal atrophy (PRA), glaucoma, or lens luxation and validated the results in additional 1180 dogs. We found that eleven variants in ten genes explained 28% of the studied cases. We also observed new PRA-affected breeds for the RPGRIP1 c.340_341insA29GGAAGCAACAGGATG variant, and clinical support for the pathogenicity of the PDE6A c.1940delA and ADAMTS10 c.2231G>A variants for PRA and glaucoma in two new breeds, respectively. Our findings indicate extensive genetic heterogeneity and the lack of molecular descriptions in more than two-thirds of the LL, glaucoma, and PRA cases by the current gene tests. There is an urgent need for discoveries that would be critical not only for veterinary molecular diagnostics and breeding programs but also for establishing models to characterize pathophysiology and new therapeutic options for the corresponding human eye disorders.