Areas Of Retinal Atrophy Research Articles

CHARACTERIZING THE NATURAL HISTORY OF FOVEAL-SPARING ATROPHIC LATE-ONSET RETINAL DEGENERATION.

To identify quantifiable markers of disease progression in patients with foveal-sparing atrophic late-onset retinal degeneration using fundus autofluorescence and spectral-domain optical coherence tomography imaging. Natural history study evaluating patients within a 3-year interval. Disease progression was assessed based on the area of retinal atrophy, macular topographic distribution of lesions, retinal and choroidal thickness and volume, and choroidal vascularity index. Twenty-four eyes (12 individuals) were included for fundus autofluorescence, and 31 eyes (16 individuals) for spectral-domain optical coherence tomography studies. Measurements were symmetrical between eyes of the same patient. The area of atrophy significantly enlarged (P = 0.002), with a growth rate of 2.67 mm2/year (SD: 2.13; square rooted: 0.57 mm/year, SD = 0.34). Baseline area of atrophy and progression both correlated with age. Most atrophic lesions were found in the temporal macula and progressed nasally at follow-up. Central choroidal and retinal thicknesses and volume in late-onset retinal degeneration cases were significantly reduced compared with controls, but only central retinal thickness decreased significantly at follow-up. This study identifies the area of atrophy and central retinal thickness, but not chorioretinal volume or choroidal thickness, as markers of short-term progression in late-onset retinal degeneration. These findings may be useful for disease monitoring and late-onset retinal degeneration interventional studies.

Retinal tubulations in geographic atrophy associated with age‐related macular degeneration

AbstractPurpose To describe the presence of retinal tubulations at the boundaries and within areas of retinal atrophy in patients with geographic atrophy (GA) associated with age‐related macular degeneration (AMD) by spectral‐domain optical coherence tomography (SD‐OCT).Methods 82 consecutive patients, 50 years or older with GA associated with AMD were examined between January 2012 and July 2012. Patients were evaluated by SD‐OCT and fundus autofluorescence (FAF). Patients with single or multiple and well‐defined areas of atrophy in whom retinal layers could be visualized were included. FAF was performed at the same time that OCT (Spectralis, Heidelberg Eng). Three acquisition protocols were performed: high‐resolution horizontal B‐scan for foveal study and two macular cubes to evaluate the whole macular surface (19 horizontal and 19 vertical B‐scans centred on the fovea). Main Outcomes Measures: Presence of spherules/tubulations within the atrophic area in patients with GA associated with AMD.Results 50/82 patients with GA presented with single or multiple areas of atrophy with identifiable retinal layers. Clearly visible and slightly hyper/hyporeflective round, rosette‐like, spherule‐shaped structures were localized in the outer nuclear layer (ONL). These structures occasionally contacted the external limiting membrane. They were adjacent to the margin between preserved retina and atrophic area and within the atrophic area. In these cases, uniformly hypereflective, hyporeflective and isoreflective spherules surrounded by hyperreflective halo that might correspond with retinal tubulation were present in the same eye.Conclusion Retinal tubulations can be observed in the ONL in patients with GA associated with AMD.

Spectral domain optical coherence tomography and in vivo confocal microscopy imaging of a case of Bietti's crystalline dystrophy

BackgroundThe aim was to describe the morphology and localisation of crystals in a case of Bietti's crystalline corneo‐retinal dystrophy (BCD) by means of spectral domain optical coherence tomography (SD‐OCT) and in vivo confocal microscopy (IVCM).MethodsClinical examination, SD‐OCT and IVCM evaluation of a 35‐year‐old woman with BCD.ResultsOptical coherence tomography examination of the macular region revealed multiple crystals in the retinal pigment epithelium (RPE)‐choriocapillaris, some crystals within the full thickness of the neurosensory retina and less numerous crystals in the choroid. Crystals were present peripherally in areas of retinal atrophy, predominantly in the choroid and to a lesser extent in the RPE‐choriocapillaris and the neuroepithelium. In vivo confocal microscopy showed multiple crystals of varying morphology in the peripheral and paralimbal cornea, mainly located in the anterior stroma over 360°.ConclusionsSD‐OCT provided greater precision in the localisation of crystals, found mainly in the choroid and RPE‐choriocapillaris rather than the neuroepithelium. In vivo confocal microscopy revealed a higher number of crystals compared to those visible using conventional slitlamp biomicroscopy and showed a different crystal morphology.

Recent advances in the treatment of age-related macular degeneration

Loss of central vision with age-related macular degeneration (ARMD) is a devastating reality for 8% of adults aged over 65 years in the UK,1 but new therapies with the potential to halt and improve visual loss have emerged. As a result, the NHS faces some difficult choices in terms of provision of and access to treatments. ARMD is thought to be a group of genetically- and environmentally-determined retinal degenerative diseases: in ARMD there is an age-related dysfunction of the retinal pigment epithelial cells, which are essential for photoreceptor metabolism and removal of waste products. Dysfunctional cells accumulate undigested waste, which is clinically evident as focal yellow subretinal clumps, termed drusen. Drusen are the herald of ARMD, and large or numerous drusen are poor prognostic factors for future visual loss.2 The disruption of photoreceptor metabolism eventually causes areas of retinal atrophy: the macula, the ‘high definition’ central point of the retina with the highest density of photoreceptors, is consequently more susceptible to this progressive dysfunction. In the majority of patients, ARMD occurs as atrophic or ‘dry’ macular degeneration. This is a relatively slow process, and at the present time there is no effective treatment. In the remaining patients with ‘wet’ or neovascular disease there is aberrant growth of choroidal blood vessels beneath the dysfunctional retina: haemorrhage and oedema from these neovascular membranes causes sudden central visual loss. Retinal angiography is needed to identify and classify the membranes as ‘classic’ well-defined lesions or amorphous ‘occult’ membranes, as the classification has an impact on the treatments available. A current estimate of the incidence of wet ARMD in the UK is around 21 000 new cases each year.3 Patients with ARMD who need referral to ophthalmic services present …

Retinopathy in diabetic hypertensive monkeys: a pathologic study.

No satisfactory primate model of diabetic retinopathy has been produced. The clinical picture of microangiopathic retinopathy in diabetic hypertensive monkeys has been previously reported. The present study describes the pathologic findings of these animals. Eleven eyes of six monkeys (five rhesus, one cynomolgus) were studied. Diabetes mellitus was either spontaneous or induced by streptozocin; mild arterial hypertension was either spontaneous or induced by fludrocortisone acetate. In two monkeys, the horseradish peroxidase tracer technique was employed. Trypsin flat preparations of the nasal retinal vasculature were prepared. The material was studied by light and electron microscopy. We divided the development of the microangiopathic retinopathy into three stages. In the early stage, background retinopathy was characterized by microvascular abnormalities and capillary dropout. Massive vascular leakage, intraretinal exudates and hemorrhage, cystoid degeneration, and cotton-wool spots were features of an exudative retinopathy in the second stage. In the final stage, chronic ischemic retinopathy was characterized by vascular occlusions and areas of retinal atrophy. Microangiopathic retinopathy in diabetic monkeys with mild hypertension presented many features of human diabetic and hypertensive retinopathy, except vitreous neovascularization.