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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.

Purpose: The aim of this experimental study was to investigate the pathogenesis of Terson syndrome (TS), which currently is controversial. Methods: The central retinal artery (in 39 orbits), posterior ciliary arteries (in 8 orbits), and central retinal vein (CRV in 21 orbits) were occluded in rhesus monkeys by exposing them to lateral orbitotomy. Fundus examination and fluorescein fundus angiography were performed before and immediately after cutting the vessels and serially thereafter during the follow-up period. The rationale of the experimental study design is discussed. Results: In eyes with central retinal artery occlusion, retinal hemorrhages were seen soon after the procedure in 7 eyes, and on follow-up in a total of 15 eyes. In posterior ciliary artery occlusion, retinal hemorrhages were seen soon after the procedure in one eye, and on follow-up in a total of three eyes. In eyes with CRV, all eyes had extensive scattered retinal hemorrhages. Conclusion: The findings of this experimental study, and my basic, experimental, and comprehensive clinical studies on CRVO, suggest the following concept of the pathogenesis of TS: Compression of the CRV plays a crucial role in the development of TS. The CRV is compressed, as it lies in the subarachnoid space of the optic nerve sheath, by raised cerebrospinal fluid pressure and/or accumulated blood. This results in retinal venous stasis and raised venous pressure in the retinal veins, leading to venous engorgement, rupture of the retinal capillaries and retinal hemorrhages. The clinical importance of compression of the CRV and not occlusion of CRV in TS is that optic nerve sheath decompression by opening it and releasing the blood and raised cerebrospinal fluid (CSF) pressure, would result in immediate decompressing of the CRV in the subarachnoid space and restoration of normal circulation and prevent visual loss.

Ischemic optic neuropathies (IONs) consist primarily of two types: anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). AION comprises arteritic AION (A-AION: due to giant cell arteritis) and non-arteritic AION (NA-AION: due to other causes). PION consists of arteritic PION (A-PION: due to giant cell arteritis), non-arteritic PION (NA-PION: due to other causes), and surgical PION (a complication of several systemic surgical procedures). These five types of ION are distinct clinical entities etiologically, pathogenetically, clinically and from the management point of view. In the management of AION, the first crucial step with patients aged 50 and over is to identify immediately whether it is arteritic or not because A-AION is an ophthalmic emergency and requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. Patients with NA-AION, when treated with systemic corticosteroid therapy within first 2 weeks of onset, had significantly better visual outcome than untreated ones. Systemic risk factors, particularly nocturnal arterial hypotension, play major roles in the development of NA-AION; management of them is essential in its prevention and management. NA-PION patients, when treated with high-dose systemic steroid therapy during the very early stages of the disease, showed significant improvement in visual acuity and visual fields, compared to untreated eyes. A-PION, like A-AION, requires urgent treatment with high-dose steroid therapy to prevent any further visual loss in one or both eyes. There is no satisfactory treatment for surgical PION, except to take prophylactic measures to prevent its development.

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.

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

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.