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The pathogeneses, clinical features, and management of central retinal artery occlusion (CRAO) are discussed. CRAO consists of the following four distinct clinical entities: non-arteritic CRAO (NA-CRAO), transient NA-CRAO, NA-CRAO with cilioretinal artery sparing, and arteritic CRAO. Clinical characteristics, visual outcome, and management very much depend upon the type of CRAO. Contrary to the prevalent belief, spontaneous improvement in both visual acuity and visual fields does occur, mainly during the first 7 days. The incidence of spontaneous visual acuity improvement during the first 7 days differs significantly (P < 0.001) among the four types of CRAO; among them, in eyes with initial visual acuity of counting finger or worse, visual acuity improved, remained stable, or deteriorated in NA-CRAO in 22%, 66%, and 12%, respectively; in NA-CRAO with cilioretinal artery sparing in 67%, 33%, and none, respectively; and in transient NA-CRAO in 82%, 18%, and none, respectively. Arteritic CRAO shows no change. Recent studies have shown that administration of local intra-arterial thrombolytic agent not only has no beneficial effect but also can be harmful. Investigations to find the cause and to prevent or reduce the risk of any further visual problems are discussed. Prevalent multiple misconceptions on CRAO are discussed.

Giant cell arteritis (GCA) is the most important medical emergency in ophthalmology, because its most dreaded complication is visual loss, which is preventable if these patients are diagnosed early and treated immediately and aggressively. This is a brief review of GCA, its ophthalmic manifestations, and how to diagnose and manage them.

ObjectiveThere has long been a great interest in neuroprotection therapy for ischaemic stroke and various types of optic neuropathies. In view of that, I reviewed the literature on the role of neuroprotection for non-arteritic anterior ischaemic optic neuropathy (NA-AION).MethodsThe review is based on a PubMed search of literature about the use of neuroprotectors in stroke and optic neuropathies and about current clinical trials of RPh201 and QPI-1007 in NA-AION.ResultsSeveral neuroprotection agents for ischaemic stroke and various types of optic neuropathies have been evaluated extensively in experimental studies in animals and benefits claimed. However, translation of therapeutic strategies for neuroprotection from experimental research to humans has invariably been fraught with failure. Two currently ongoing studies dealing with neuroprotection by RPh201 and QPI-1007 in NA-AION may have limitations in their rationale and study designs.ConclusionsUnfortunately, in spite of all the experimental and clinical research on neuroprotection agents in NA-AION so far, we have no scientifically proven evidence of neuroprotection agents showing any benefit in the human clinical studies so far.

We investigated the clinical characteristics, time to resolution and the factors that influence it, and evolutionary pattern of optic disc edema (ODE) in non-arteritic anterior ischemic optic neuropathy (NA-AION). Our study was conducted in 591 consecutive patients (749 eyes) with NA-AION who fulfilled our inclusion criteria. On their first visit to our clinic, all patients had a detailed ophthalmic and medical history, a comprehensive ophthalmic evaluation, and stereoscopic color fundus photography and fluorescein fundus angiography. On each follow-up visit, the same ophthalmic evaluation was performed, except for fluorescein fundus angiography. The effect of steroid therapy on ODE was evaluated in a \"patient choice study\" in 723 eyes, i.e., patients who voluntarily opted to have (343 eyes) or not have (380 eyes) this therapy. To identify the factors that influence time to ODE resolution, parametric regression models for interval-censored data were fitted by maximum likelihood estimation using an SAS procedure. Our results indicate that the overall median time (25-75th percentile) to spontaneous resolution of ODE from the onset of visual loss was 7.9 (5.8-11.4) weeks. The ODE resolution time was longer in diabetics than in non-diabetics (p = 0.003) in the single factor model. Multi-factor analysis showed that worse initial visual field defects (p < 0.0001) and worse visual acuity (p = 0.04) were associated with a faster resolution of ODE. Those treated with steroid therapy within 2 weeks after onset of NA-AION had significantly (p = 0.0006) faster ODE resolution than untreated cases. Severity of initial visual loss and systemic diseases were identical in steroid treated and untreated patients. A characteristic evolutionary pattern of ODE in NA-AION was observed. In conclusion, our study showed that in NA-AION the time course for resolution of ODE is shorter with greater severity of initial visual field and visual acuity loss, which may relate to the number of axons permanently damaged during the acute stage. Steroid therapy was associated with shorter time to resolution of ODE. Resolution of ODE goes through a characteristic evolutionary process.

This is a case report of 'familial giant cell arteritis' in three siblings from northwest India. This is the first case report of 'familial giant cell arteritis' in a non-Caucasian family.This is a case report of 'familial giant cell arteritis' in three siblings from northwest India. This is the first case report of 'familial giant cell arteritis' in a non-Caucasian family.

Objective To investigate systematically the role of systemic corticosteroid therapy in non-arteritic anterior ischemic optic neuropathy (NA-AION). Methods The study consists of a cohort of 613 consecutive patients (696 eyes), first seen in our clinic from 1973 to 2000. Of this cohort, 312 patients (364 eyes) voluntarily opted for systemic steroid therapy, and 301 (332 eyes) for no treatment. At first visit, all patients in both groups had a detailed ophthalmic and medical history, and comprehensive ophthalmic evaluation. Visual evaluation was done by recording Snellen visual acuity, and visual fields with a Goldmann perimeter. The same ophthalmic evaluation was performed at each follow-up visit. Patients in the steroid-treated group were initially given 80 mg Prednisone daily for 2 weeks, and then tapered down to 70 mg for 5 days, 60 mg for 5 days, and then cutting down by 5 mg every 5 days. Visual outcome in the two groups was compared Results Median follow-up was 3.8 years. At 6 months from onset of NA-AION, of the eyes with initial visual acuity 20/70 or worse and seen within 2 weeks of onset, there was visual acuity improvement in 69.8% (95% confidence interval (CI): 57.3%, 79.9%) in the treated group, compared to 40.5% (95% CI: 29.2%, 52.9%) in the untreated group (odds ratio of improvement: 3.39; 95% CI:1.62, 7.11; p  = 0.001). Comparison of visual field defect at 6 months from onset of NA-AION, among those seen within 2 weeks of NA-AION onset with moderate to severe initial visual field defect, there was improvement in 40.1% (95% CI: 33.1%, 47.5%) of the treated group, and 24.5% (95% CI: 17.7%, 32.9%) of the untreated group (odds ratio: 2.06, 95% CI: 1.24, 3.40; p  = 0.005). In both treated and untreated groups, the visual acuity and visual fields kept improving up to about 6 months from onset of NA-AION, and very little thereafter. Conclusion This study suggested that NA-AION eyes treated during the acute phase with systemic corticosteroids resulted in a significantly higher probability of improvement in visual acuity ( p  = 0.001) and visual field ( p  = 0.005) than in the untreated group. Both visual acuity and visual fields improved up to 6 months after onset of NA-AION.

Since 1985,[5] based on my FFA studies in NA-AION, I have published many articles showing the presence of distinct filling defects in the peripapillary choroid as well as in the choroidal watershed zones passing through the peripapillary choroid [Figure 1]. For evaluation of the peripapillary and the rest of the choroid, FFA provides superior information, because it covers a much bigger field than optical coherence tomography angiography. The misconception that an altitudinal visual field defect is characteristic in NA-AION has emerged from the use of automated static threshold perimetry rather than manual kinetic perimetry performed with a Goldmann perimeter.

[...]scientific research was never discussed or taught in medical colleges. [...]at age 37 with my Ph.D. from University of London, research credentials, and the prestigious Beit fellowship, I went back and started as a clinical trainee. Contrary to the popular belief, I found that the retina suffers no permanent damage with CRAO lasting for about 100 min; after that, the longer the occlusion, the more progressive the damage, so that CRAO lasting for 4 h results in permanent retinal damageMalignant arterial hypertension: Since Bright described it in 1836, there had been no comprehensive studies about its ophthalmic manifestations. [...]the conclusions are totally reliable, being based purely on what the observations reveal. Because of this policy, I feel, my studies have revealed a lot of new information, which has contradicted prevalent dogmas, conventional wisdom and misconceptions, and stood the test of timeContrary to popular belief and my own before I started research, serious scientific research is rarely glamorous, except for an occasional glimpse.

The author relates an unlikely journey from his rural village in India, through medical school, a prestigious fellowship with Sir Stewart Duke-Elder, and a colorful career in the United Kingdom and the USA, as a clinician and researcher, particularly in the area of vascular disease of the eye and optic nerve