Purpose. To evaluate the changes in thickness of individual inner and outer macular and peripapillary retinal layers in diabetes. Methods. 124 subjects (124 eyes) were enrolled: 74 diabetics and 50 controls. Macular edema, proliferative diabetic retinopathy (DR), any intraocular treatment and refractive error diopters were the main exclusion criteria. Full ophthalmic examination, stereoscopic fundus photography, and spectral domain-OCT were performed. After automatic retinal segmentation (layering) in 5 layers, the thickness of each layer was calculated, and values compared among groups. Results. Thirty patients had no DR, 44 patients had non proliferative DR. A significant increase of inner plexiform and nuclear layers was found in DR eyes versus controls ( ). A significant decrease ( ) of retinal nerve fiber layer (RNFL) and at specific sites of retinal ganglion cell layer ( ) was documented in the macula. In the peripapillary area there were no differences between diabetics and controls. Conclusions. Decreased RNFL thickness and increased INL/OPL thickness in diabetics without DR or with initial DR suggest early alterations in the inner retina. On the contrary, the outer retina seems not to be affected at early stages of DM. Automatic intraretinal layering by SD-OCT may be a useful tool to diagnose and monitor early intraretinal changes in DR. 1. Introduction Diabetic retinopathy (DR) is the first cause of visual impairment and blindness in the adult working-age population [1]. For a long period of time, DR has been considered primarily a retinal microvascular disorder caused by the direct effects of hyperglycemia and by the metabolic pathways it activates [2]. Nevertheless, some recent studies have demonstrated that retinal neurodegeneration (the result of a negative balance between neurotoxic and neuroprotective factors) is present even before the development of clinically detectable microvascular damage. Retinal neurodegeneration may therefore represent an early event in the pathophysiology of DR and may anticipate the onset of microvascular changes [2–4]. The term neurodegeneration used in this paper encompasses pathologic phenomena affecting both the pure neuronal component and the glial one. The hypothesis according to which neurodegeneration precedes the vascular one is confirmed by some electrophysiological and psychophysical studies, which show that the alterations are present even before the microvascular damage becomes ophthalmoscopically or angiographically visible. Such retinal function alterations mainly consist in contrast sensitivity
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