Seeing Beyond Retinopathy in Diabetes: Electrophysiological and Psychophysical Abnormalities and Alterations in Vision

Ewing, Fiona M.E; Deary, Ian J.; Strachan, Mark W. J.; Frier, Brian M.

doi:10.1210/edrv.19.4.0340

Cited by 84 publications

(57 citation statements)

References 88 publications

(148 reference statements)

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“…Interestingly, in our study we found that only contrast sensitivities at high spatial frequencies were positively correlated with macular GCC and peripapillary RNFL thickness. These correlations are expected because previous studies indicated that the selective losses at high spatial frequencies may be due to the dysfunction in the parvocellular pathway [35,37], and approximately 80% of ganglion cells are parvocellular cells [40].…”

Section: Discussionmentioning

confidence: 68%

“…We hypothesize that the slight macular GCC loss in NDR patients may be insufficient to detect significant BCVA changes. Previous contrast sensitivity tests revealed abnormal functions before visual acuity tests, and correlated positively with the presence and the degree of diabetic retinopathy [35]. Several contrast sensitivity studies in diabetic patients showed a general decrease of sensitivity across low, medium, and high spatial frequencies, suggesting that both the parvocellular and magnocellular systems involved in contrast processing were affected by the disease [12,3537].…”

Section: Discussionmentioning

confidence: 98%

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Association between retinal neuronal degeneration and visual function impairment in type 2 diabetic patients without diabetic retinopathy

Zhu

et al. 2015

Sci. China Life Sci.

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The changes in retinal thickness and visual function in type 2 diabetic patients without clinical evidence of diabetic retinopathy were evaluated. A total of 141 diabetic subjects without retinopathy and 158 healthy subjects were enrolled in this study. Superior macular ganglion cell complex thicknesses were significantly decreased in diabetic cases, and no significant peripapillary retinal nerve fiber layer thickness changes were observed. The contrast sensitivities at all space frequencies were significantly different between diabetic patients and controls. The mean P50 amplitude from pattern electroretinogram results was reduced significantly in the diabetic group. In the diabetic group, average superior ganglion cell complex thicknesses positively correlated with both contrast sensitivities at high spatial frequencies and P50 amplitudes. The results indicated that ganglion cell complex thickness and visual function changes could be observed in diabetic subjects before the onset of any significant diabetic retinopathy. Macular ganglion cell complex reduction occurred much earlier than peripapillary retinal nerve fiber layer thinning in diabetic patients without retinopathy. diabetes mellitus, diabetic retinopathy, retinal nerve fiber layer, retinal ganglion cell, contrast sensitivity, electroretinogram Citation:Zhu TP, Ma J, Li YH, Zhang Z. Association between retinal neuronal degeneration and visual function impairment in type 2 diabetic patients without diabetic retinopathy. Sci China Life Sci, 2015, 58: 550 -555,

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Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 98%

Association between retinal neuronal degeneration and visual function impairment in type 2 diabetic patients without diabetic retinopathy

Zhu

et al. 2015

Sci. China Life Sci.

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“…Neuroretinal damage produces functional abnormalities such as colour vision defects, reduced contrast sensitivity and abnormalities in dark adaptation. These alterations can occur before microvascular lesions are detectable in ophthalmological examinations, but they tend to be predictive of PDR, which ultimately leads to degenerative changes and significant visual impairment [24][25][26]. The design of our study does not allow us to say whether the lower IRBP content in diabetic retinas is a cause or a consequence of retinal neurodegeneration.…”

Section: Discussionmentioning

confidence: 93%

Interphotoreceptor retinoid-binding protein (IRBP) is downregulated at early stages of diabetic retinopathy

et al. 2009

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Aims/hypothesis Interphotoreceptor retinoid-binding protein (IRBP) plays a major role in the visual cycle and is essential to the maintenance of photoreceptors. The aim of this study was to determine whether a decrease in IRBP production exists in the early stages of diabetic retinopathy. Methods Vitreous samples from diabetic patients with proliferative and non-proliferative diabetic retinopathy (PDR, NPDR), and from non-diabetic patients with macular hole (control group) were selected for IRBP quantitative assessment by proteomic analysis (fluorescence-based difference gel electrophoresis) and western blot. Human post mortem eyes (n=16) from diabetic donors without clinically detectable retinopathy and from non-diabetic donors (n=16) were used to determine IRBP (also known as RBP3) mRNA levels (RT-PCR) and protein content (western blot and confocal microscopy). Retinal neurodegeneration was assessed by measuring glial fibrillar acidic protein (GFAP) and the apoptotic rate. Y79 human retinoblastoma cells were used to test the effects of glucose, TNF-α and IL-1β on IRBP expression and IRBP levels. Results Intravitreous IRBP concentration was significantly lower in PDR

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“…Indeed, growing evidence indicates that a significant neuroglial dysfunction also occurs during diabetic retinopathy in unison with blood flow abnormalities, and before the appearance of microvascular lesions (reviewed by Antonetti et al 5 ). In diabetic patients and short-term animal models of diabetes reversible alterations are evident in the electroretinogram (such as loss of oscillatory potentials 6 ) together with defects in colour perception 7 and impaired contrast sensitivity. 8 These well-characterized electrophysiological deficits may represent a progressive 'neuropathic' aetiology to diabetic retinopathy.…”

Section: Introductionmentioning

confidence: 99%

Microvascular lesions of diabetic retinopathy: clues towards understanding pathogenesis?

Curtis

Gardiner

Stitt

2009

Eye

311

231

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Retinopathy is a major complication of diabetes mellitus and this condition remains a leading cause of blindness in the working population of developed countries. As diabetic retinopathy progresses a range of neuroglial and microvascular abnormalities develop although it remains unclear how these pathologies relate to each other and their net contribution to retinal damage. From a haemodynamic perspective, evidence suggests that there is an early reduction in retinal perfusion before the onset of diabetic retinopathy followed by a gradual increase in blood flow as the complication progresses. The functional reduction in retinal blood flow observed during early diabetic retinopathy may be additive or synergistic to proinflammatory changes, leucostasis and vasoocclusion and thus be intimately linked to the progressive ischaemic hypoxia and increased blood flow associated with later stages of the disease. In the current review a unifying framework is presented that explains how arteriolar dysfunction and haemodynamic changes may contribute to late stage microvascular pathology and vision loss in human diabetic retinopathy.

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Seeing Beyond Retinopathy in Diabetes: Electrophysiological and Psychophysical Abnormalities and Alterations in Vision

Cited by 84 publications

References 88 publications

Association between retinal neuronal degeneration and visual function impairment in type 2 diabetic patients without diabetic retinopathy

Association between retinal neuronal degeneration and visual function impairment in type 2 diabetic patients without diabetic retinopathy

Interphotoreceptor retinoid-binding protein (IRBP) is downregulated at early stages of diabetic retinopathy

Microvascular lesions of diabetic retinopathy: clues towards understanding pathogenesis?

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