Abstract

Diabetic vasculopathy is still, despite all efforts to treat its late complications, the leading cause of blindness among the working-age adults in the Western world, and in the developing countries, a similar situation is created due to the catching up in welfare and in its wake an identical unhealthy diabetes-promoting lifestyle (1). The definition of diabetic retinopathy is based on observation of vascular changes. The first recognizable vascular abnormalities are microaneurysms and small hemorrhages, followed by more severe signs of vascular leakage, such as hard exudates and larger hemorrhages; vascular dropout, such as cotton wool spots; more widespread hemorrhages; and neovascularizations. The severity of the vascular changes has been graded to guide ophthalmologists in monitoring patients and treating patients in a timely fashion to prevent loss of vision (2). It has been long known that the neuroretina is affected at an early stage by diabetes-induced metabolic changes. This diabetic neuroretinal degeneration has been demonstrated in histological studies and through the measurement of functional loss with a number of functional tests (3), such as contrast vision, color vision, visual field, and dark adaptation. An important test demonstrating neuroretinal degeneration is the multifocal electroretinogram (mfERG) (4,5). Recently, with spectral domain optical coherence tomography, structural changes could be shown with decreased thickness of the ganglion cell layer and retinal nerve fiber layer (6). Signs of neuroretinal degeneration, measured with all these methods, were present in eyes even before any visible vascular pathology could be detected. This highlights the interesting concept of neuroretinal degeneration playing a role in the development of diabetic retinal vasculopathy (7–9). If neuroretinal degeneration does play a role in the subsequent development of diabetic vasculopathy, one would expect neuroretinal degeneration to precede vasculopathy. …

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