Multifocal Electroretinogram and Short-Wavelength Automated PerimetryMeasures in Diabetic Eyes With Little or No Retinopathy

Han, Ying

doi:10.1001/archopht.122.12.1809

Cited by 97 publications

(75 citation statements)

References 24 publications

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“…86 The blue-yellow functional loss in early ARM might also reflect ischaemic conditions at postreceptoral levels. 69 A selective early loss of S-cone postreceptoral pathways has been shown in other ischaemic diseases such as, for example, in diabetes with 69,87 or without retinopathy. 87,88 Additional evidence of primary postreceptoral involvement might be reflected by impaired high contrast-, low contrast-, low luminance (SKILL) visual acuity and contrast sensitivity as demonstrated in other studies in early ARM.…”

Section: Eyementioning

confidence: 98%

“…69 A selective early loss of S-cone postreceptoral pathways has been shown in other ischaemic diseases such as, for example, in diabetes with 69,87 or without retinopathy. 87,88 Additional evidence of primary postreceptoral involvement might be reflected by impaired high contrast-, low contrast-, low luminance (SKILL) visual acuity and contrast sensitivity as demonstrated in other studies in early ARM. 21,89 Although these are mainly L-and M-photoreceptor properties, a loss of these functions is thought to relate to decreased efficiency in lateral inhibitory mechanisms that are mediated by horizontal and amacrine cells at the postreceptoral level (Figure 1d and e).…”

Section: Eyementioning

confidence: 98%

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Functional loss in early age-related maculopathy: the ischaemia postreceptoral hypothesis

Feigl

Brown

Lovie‐Kitchin

et al. 2006

Eye

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We review proposed models and psychophysical and electrophysiological tests performed in many studies for early agerelated maculopathy (ARM). We suggest that ischaemia is the trigger for impaired retinal pigment epithelium function causing imbalance of secretion of vascular growth factors, reduced disc degradation capability and reduced metabolic activity and possible inflammatory response. This results in increased deposition of cell debris, such as drusen and thickens Bruch's membrane causing even more ischaemia of the overlying neurosensory retina. The photoreceptors are more resistant to ischaemia given their proximity to the choroid. Furthermore, being 'upstream' from the inner retinal layers, they act as an oxygen sink depriving retinal layers further from the choroid. Postreceptoral cell layers and especially parts of the inner nuclear layer that are located in the watershed zone between two sources of blood supply are preferentially vulnerable to ischaemia. Based on psychophysical and electrophysiological findings we propose that most of the function impairment in early ARM starts postreceptorally.

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Section: Eyementioning

confidence: 98%

Section: Eyementioning

confidence: 98%

Functional loss in early age-related maculopathy: the ischaemia postreceptoral hypothesis

Feigl

Brown

Lovie‐Kitchin

et al. 2006

Eye

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“…Clinical studies have demonstrated altered electroretinograms and impairment of color vision, and contrast sensitivity even before the clinical diagnosis of diabetic retinopathy (Ghirlanda et al, 1997;Han et al, 2004). Recent studies using visual field testing have shown field defects in patients with little of no vascular signs of retinopathy.…”

Section: Clinical Features Of Diabetic Retinopathymentioning

confidence: 99%

Vascular endothelial growth factor in eye disease

Penn

Madan

Caldwell

et al. 2008

Progress in Retinal and Eye Research

636

527

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Collectively, angiogenic ocular conditions represent the leading cause of irreversible vision loss in developed countries. In the U.S., for example, retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration are the principal causes of blindness in the infant, working age and elderly populations, respectively. Evidence suggests that vascular endothelial growth factor (VEGF), a 40 kDa dimeric glycoprotein, promotes angiogenesis in each of these conditions, making it a highly significant therapeutic target. However, VEGF is pleiotropic, affecting a broad spectrum of endothelial, neuronal and glial behaviors, and confounding the validity of anti-VEGF strategies, particularly under chronic disease conditions. In fact, among other functions VEGF can influence cell proliferation, cell migration, proteolysis, cell survival and vessel permeability in a wide variety of biological contexts. This article will describe the roles played by VEGF in the pathogenesis of retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. The potential disadvantages of inhibiting VEGF will be discussed, as will the rationales for targeting other VEGF-related modulators of angiogenesis.

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“…In fact, loss of oscillatory potentials on electroretinograms predicts the onset of proliferative retinopathy better than vascular lesions seen on fundus photographs or capillary nonperfusion visualized by fluorescein angiograms (40). Electroretinograms and psychophysical tests are primarily used in research settings, but recent reports using clinically available visual field test modifications (short-wave automated perimetry and frequency doubling perimetry) reveal field defects in patients with little or no vascular retinopathy (41,42), and visual fields predict the severity of retinopathy better than visual acuity (43). Together, these findings strongly suggest that functional tests are more sensitive indicators of retinal integrity than fundus photographs or optical coherence tomography and may serve as useful end points for clinical trials, but they must be validated first.…”

Section: Diabetic Retinopathy: Beyond Glucose-induced Microvascular Dmentioning

confidence: 99%

Diabetic Retinopathy

et al. 2006

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Diabetic retinopathy remains a frightening prospect to patients and frustrates physicians. Destruction of damaged retina by photocoagulation remains the primary treatment nearly 50 years after its introduction. The diabetes pandemic requires new approaches to understand the pathophysiology and improve the detection, prevention, and treatment of retinopathy. This perspective considers how the unique anatomy and physiology of the retina may predispose it to the metabolic stresses of diabetes. The roles of neural retinal alterations and impaired retinal insulin action in the pathogenesis of early retinopathy and the mechanisms of vision loss are emphasized. Potential means to overcome limitations of current animal models and diagnostic testing are also presented with the goal of accelerating therapies to manage retinopathy in the face of ongoing diabetes. Diabetes 55:2401-2411, 2006 D espite years of clinical and laboratory investigation, diabetic retinopathy remains the leading cause of vision impairment and blindness among working-age adults, yet the fundamental cause(s) remains uncertain. Retinal photocoagulation to reduce neovascularization and macular edema was developed in the 1950s and is still the standard of care (1). The number of people worldwide at risk of developing vision loss from diabetes is predicted to double over the next 30 years (2), so it is imperative to develop better means to identify, prevent, and treat retinopathy in its earliest stages rather than wait for the onset of vision-threatening lesions. Progress in these areas requires a new perspective on the problem that includes the roles of the neural retina, impaired insulin action, and inflammation. In this way, established neurobiological principles can inform us how diabetes impairs vision, and knowledge of metabolism, inflammation, and regenerative medicine may lead to new treatments.This perspective will discuss how the unique anatomy and physiology of the retina may render it vulnerable to the metabolic derangements of diabetes and lead to impaired vision. The intent of this unconventional approach is to encourage consideration of new opportunities for investigations that will advance the field. NORMAL RETINAL STRUCTURE AND PHYSIOLOGY Topographic and cellular organization of the retina.It is instructive to consider the functional organization of the retina (literally a network) to better understand the impact of diabetes (http://webvision.med.utah.edu). The retina is a transparent layer of neural tissue between the retinal pigmented epithelium and the vitreous body. Normal vision depends on intact cell-cell communication among the neuronal, glial, microglial, vascular, and pigmented epithelial cells of the retina. The fundamental functions of the retina are to capture photons, convert the photochemical energy into electrical energy, integrate the resulting action potentials, and transmit them to the occipital lobe of the brain, where they are deciphered and interpreted into recognizable images. The retina is partitioned from the syst...

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Multifocal Electroretinogram and Short-Wavelength Automated PerimetryMeasures in Diabetic Eyes With Little or No Retinopathy

Cited by 97 publications

References 24 publications

Functional loss in early age-related maculopathy: the ischaemia postreceptoral hypothesis

Functional loss in early age-related maculopathy: the ischaemia postreceptoral hypothesis

Vascular endothelial growth factor in eye disease

Diabetic Retinopathy

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