Macular outer plexiform layer and outer nuclear layer thickness on spectral domain optical coherence tomography in central serous chorioretinopathy — a case of two patients

Increased thickness of the outer plexiform layer (OPL) of the fovea in central serous chorioretinopathy (CSC) has been previously reported. However, to our knowledge only one paper has given a concrete value of the thickness of the outer plexiform layer (OPL) of the macula in a patient with unilateral CSC. Here we report the outer plexiform and outer nuclear layer (ONL) thickness as measured with spectral domain optical coherence tomography (SD-OCT) in a patient with acute central serous chorioretinopathy in the left eye, and in a second patient with recurrent central serous chorioretinopathy in both eyes. Both patients received oral eplerenone treatment

Risk Factors and Symptoms of Meibomian Gland Loss in a Healthy Population

Purpose. The aim of this study was to investigate the relationships between MGL and ocular symptoms, several systemic conditions, and key markers of ocular surface health. Methods. We included into the study 91 healthy volunteers between the ages of 20 and 77 years. We analyzed meibomian gland morphology, function, and lid margin alterations. We correlated our findings with self-reported ocular symptoms, systemic medical history, lifestyle factors, and tear film abnormalities. Results. We observed that a high ocular surface disease index, a history of either chalazion or hordeolum, experience of puffy eyelids upon waking, and foreign body sensation all appeared to be predictors of an abnormal meiboscore after adjusting for age and sex (p=0.0007; p=0.001; p=0.02; p=0.001, resp.). Multivariate logistic regression model including age and sex showed that there were three independent predictors of abnormal meiboscore: older age (OR = 1.03, 95% CI = 1.01–1.04 per year, p=0.006), postmenopausal hormone therapy (OR = 4.98, 95% CI = 1.52–16.30, p=0.007), and the use of antiallergy drugs (OR = 5.85, 95% CI = 2.18–15.72, p=0.0004). Conclusion. Our findings extend current knowledge on the pathophysiology of MGL

Association between Asymptomatic Unilateral Internal Carotid Artery Stenosis and Electrophysiological Function of the Retina and Optic Nerve

Purpose. This study was designed to assess retinal and optic nerve bioelectrical function in patients with unilateral asymptomatic but hemodynamically significant internal carotid artery stenosis (ICAS). Methods. Forty-two subjects with a diagnosis of unilateral ICAS and 34 controls were analyzed. Full-field electroretinogram (ERG), pattern electroretinogram (PERG), and pattern visual-evoked potentials, as well as optical coherence tomography and ophthalmological examination, were performed. Data analysis included eyes ipsilateral to ICAS (EIS) and eyes contralateral to ICAS (ECS). Results. Intraocular pressure was significantly decreased in EIS and ECS compared to that in the controls. In the macula, both the cube average thickness and cube volume values were significantly reduced both in EIS and ECS compared to those in the controls. Similarly, PERG P50 and N95 wave amplitudes were significantly smaller in EIS and ECS compared to those in the controls. The ERG rod b-wave and rod-cone a-wave amplitudes were decreased, and implicit times were significantly prolonged, whereas the OP wave index was reduced in EIS compared to that in the controls. No differences in IOP, OCT, or ERG and PERG parameters were identified between EIS and ECS. Conclusions. Our study demonstrated that retinal bioelectrical function is negatively affected by ICAS despite the absence of objective clinical signs and symptoms of ocular ischemia

Ocular Manifestations of Systemic Diseases

LBL

Sodium Iodate Selectively Injuries the Posterior Pole of the Retina in a Dose-Dependent Manner: Morphological and Electrophysiological Study

Sequential morphological and functional features of retinal damage in mice exposed to different doses (40 vs. 20 mg/kg) of sodium iodate (NaIO3) were analyzed. Retinal morphology, apoptosis (TUNEL assay), and function (electroretinography; ERG) were examined at several time points after NaIO3 administration. The higher dose of NaIO3 caused progressive degeneration of the whole retinal area and total suppression of scotopic and photopic ERG. In contrast, the lower dose induced much less severe degeneration in peripheral part of retina along with a moderate decline of b- and a-wave amplitudes in ERG, corroborating the presence of regions within retina that retain their function. The peak of photoreceptor apoptosis was found on the 3rd day, but the lower dose induced more intense reaction within the central retina than in its peripheral region. In conclusion, these results indicate that peripheral area of the retina reveals better resistance to NaIO3 injury than its central part

Stem cell treatment of degenerative eye disease

Stem cell therapies are being explored extensively as treatments for degenerative eye disease, either for replacing lost neurons, restoring neural circuits or, based on more recent evidence, as paracrine-mediated therapies in which stem cell-derived trophic factors protect compromised endogenous retinal neurons from death and induce the growth of new connections. Retinal progenitor phenotypes induced from embryonic stem cells/induced pluripotent stem cells (ESCs/iPSCs) and endogenous retinal stem cells may replace lost photoreceptors and retinal pigment epithelial (RPE) cells and restore vision in the diseased eye, whereas treatment of injured retinal ganglion cells (RGCs) has so far been reliant on mesenchymal stem cells (MSC). Here, we review the properties of non-retinal-derived adult stem cells, in particular neural stem cells (NSCs), MSC derived from bone marrow (BMSC), adipose tissues (ADSC) and dental pulp (DPSC), together with ESC/iPSC and discuss and compare their potential advantages as therapies designed to provide trophic support, repair and replacement of retinal neurons, RPE and glia in degenerative retinal diseases. We conclude that ESCs/iPSCs have the potential to replace lost retinal cells, whereas MSC may be a useful source of paracrine factors that protect RGC and stimulate regeneration of their axons in the optic nerve in degenerate eye disease. NSC may have potential as both a source of replacement cells and also as mediators of paracrine treatment

Bloodstream-To-Eye Infections Are Facilitated by Outer Blood-Retinal Barrier Dysfunction

This work was funded by National Institutes of Health (NIH; http://www.nih.gov) Grants R01EY024140 and R21EY022466 (to M.C.C.) and R01EY019494 (to M.H.E.). Our research is also funded in part by NIH Core Grant P30EY021725 (to Robert E. Anderson, OUHSC) and an unrestricted grant from Research to Prevent Blindness Inc. (http://www.rpbusa.org) to the Dean A. McGee Eye Institute. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.We thank Bolanle Adebayo (Cameron University, Lawton OK), Craig Land (Oklahoma State University, Stillwater OK), Nathan Jia (Oklahoma Christian University, Edmond OK), Kobbe Wiafe (Oklahoma School of Science and Mathematics, Oklahoma City OK), and Amanda Roehrkasse and Madhu Parkunan (OUHSC) for intellectual discussions and technical assistance. The authors also acknowledge thank Nanette Wheatley, Dr. Feng Li, and Mark Dittmar (OUHSC Live Animal Imaging Core, P30EY021725) for their invaluable technical assistance.This work was presented in part at the 2014 Association for Research in Vision and Ophthalmology Annual Conference in Orlando FL.The blood-retinal barrier (BRB) functions to maintain the immune privilege of the eye, which is necessary for normal vision. The outer BRB is formed by tightly-associated retinal pigment epithelial (RPE) cells which limit transport within the retinal environment, maintaining retinal function and viability. Retinal microvascular complications and RPE dysfunction resulting from diabetes and diabetic retinopathy cause permeability changes in the BRB that compromise barrier function. Diabetes is the major predisposing condition underlying endogenous bacterial endophthalmitis (EBE), a blinding intraocular infection resulting from bacterial invasion of the eye from the bloodstream. However, significant numbers of EBE cases occur in non-diabetics. In this work, we hypothesized that dysfunction of the outer BRB may be associated with EBE development. To disrupt the RPE component of the outer BRB in vivo, sodium iodate (NaIO3) was administered to C57BL/6J mice. NaIO3-treated and untreated mice were intravenously injected with 108 colony forming units (cfu) of Staphylococcus aureus or Klebsiella pneumoniae. At 4 and 6 days postinfection, EBE was observed in NaIO3-treated mice after infection with K. pneumoniae and S. aureus, although the incidence was higher following S. aureus infection. Invasion of the eye was observed in control mice following S. aureus infection, but not in control mice following K. pneumoniae infection. Immunohistochemistry and FITC-dextran conjugate transmigration assays of human RPE barriers after infection with an exoprotein-deficient agr/sar mutant of S. aureus suggested that S. aureus exoproteins may be required for the loss of the tight junction protein, ZO-1, and for permeability of this in vitro barrier. Our results support the clinical findings that for both pathogens, complications which result in BRB permeability increase the likelihood of bacterial transmigration from the bloodstream into the eye. For S. aureus, however, BRB permeability is not required for the development of EBE, but toxin production may facilitate EBE pathogenesis.Yeshttp://www.plosone.org/static/editorial#pee