papilledema/hypoxia

Hypoxia-induced retinal edema primarily induced by vascular lesion is seen in various conditions such as diabetic retinopathy (DR) and retinal vein occlusion (RVO). The edematous changes in these conditions occur mainly in intermediate and deep layers of retina as a result of disruption of the inner

The aim of this study was to investigate the effects of Avastin on aquaporin4 (AQP4) expression in human retinal Müller cells in vitro under hypoxia, so as to explore the mechanism of Avastin treating retinal edema. The human Müller cells were cultured using the enzymatic digestion method. Müller

In miniature pigs, retinal veins were experimentally occluded using argon laser coagulation. Microvascular modifications leading to retinal hemorrhages and retinal edema were observed some hours after the occlusion. These lesions resolved progressively within 3 weeks after the occlusion, but in most

Müller cells are closely related to diabetic retinopathy (DR). Aquaporin-4 (AQP4) can effectively promote the diffusion of water across cellular membranes. However, the dynamic balance of water plays key role in many diseases, such as cerebral edema. Meanwhile, the unusual expression and

To demonstrate the utility of a novel in vivo molecular imaging probe, HYPOX-4, to detect and image retinal hypoxia in real time, in a mouse model of retinal vein occlusion (RVO). Retinal vein occlusion was achieved in adult mice by photodynamic retinal vein thrombosis (PRVT). One or two major

Müller cells support the integrity of the blood-retinal barrier, whereas their dysfunction under pathological conditions may contribute to retinal edema formation. The apelin peptide, as the endogenous ligand of G protein-coupled receptor APJ, participates in numbers of physiological and

Retinal hypoxia is the potentially blinding mechanism underlying a number of sight-threatening disorders including central retinal artery occlusion, ischemic central retinal vein thrombosis, complications of diabetic eye disease and some types of glaucoma. Hypoxia is implicated in loss of retinal

OBJECTIVE To characterize the pathogenesis and clinical features of optic disc edema associated with obstructive sleep apnea syndrome (SAS). METHODS A series of 4 patients with SAS and papilledema (PE) underwent complete neuro-ophthalmologic evaluation and lumbar puncture. In 1 patient, continuous

Retinal hemorrhages may occur at high altitudes. They occur more commonly in association with acute mountain sickness and particularly with high-altitude cerebral edema. We describe a 27-year-old man who experienced retinal hemorrhages as well as papilledema and coma at 5,330-m altitude and who died

BACKGROUND Visual disturbances after high altitude exposure were first reported in 1969. Later, the term "High Altitude Retinal Hemorrhage-HARH" has been used for the ensuing retinal hemorrhages and vascular engorgement. METHODS A 31-year-old Caucasian male presented to our outpatient department 1

The investigation was carried out in 168 cases thus selected as chronic anaemia to be the only affection. In 49 patients (20%) the following changes, single or associated, were found: retinal pallor in 15% of the cases, superficial retinal bleedings in 6%, deep bleedings in 3.5%, retinal exudates in

A 46-year-old extremely obese black woman presented with headaches, blurred vision, and visual obscurations. Her exam was notable for bilateral severe papilledema, retinal hemorrhages, and lethargy. Her CAT scan was normal, and a spinal tap revealed a very high opening pressure. Although this

Sleep-disordered breathing may make the eye vulnerable due to the direct effect of hypoxia or it can involve pathways that lead to impaired autoregulation of optic nerve perfusion. In this review, we discuss our present understanding of the interactions that occur between sleep-disordered breathing

Regulation of vascular permeability plays a major role in the pathophysiology of visually threatening conditions such as retinal vein occlusion and diabetic retinopathy. Principally, several factors such as vascular endothelial growth factor (VEGF), are up-regulated or induced in response to hypoxia