Similarly, a recent large cohort study of diabetic patients without DR demonstrated an association between functional deficits on frequency doubling technology (FDT) perimetry or mesopic microperimetry and retinal ganglion cell count, as inferred from GCL thickness on OCT. A correlation between GCL thinning and visual field deficits on Rarebit perimetry was demonstrated in type 1 DM patients with no DR. In addition to inner retinal thinning, functional deficits in contrast sensitivity, perimetry testing, multifocal electroretinogram (mfERG), and dark adaptation have also been described in diabetic patients without DR or with very early DR. Decreased peripapillary RNFL thickness has been described in diabetic patients with or without DR, with RNFL thickness inversely associated with glycated hemoglobin (HbA1c), duration of diabetes, and severity of DR. These structural changes are not limited to the macula. To date, many studies have now used OCT to demonstrate thinning of the inner retina including the retinal nerve fiber layer (RNFL), ganglion cell layer (GCL), and more variably the inner plexiform layer (IPL) in patients with type 1 or type 2 DM without DR. While the diagnostic criteria for DR were developed at a time when clinical exam, color fundus photographs, and fluorescein angiography were the mainstays of retinal evaluation, the introduction of optical coherence tomography (OCT) imaging to noninvasively and rapidly visualize the layers of the macula in cross-section has revealed alterations in retinal structure prior to the onset of DR. This review will discuss the evidence for early diabetic retinal neurodegeneration from patients as well as experimental models, suggest potential molecular mechanisms and relevant cell types involved, and highlight the implications for the diagnosis and treatment of diabetic retinal disease.Įvidence for Retinal Neurodegeneration in Pre-clinical DR Understanding the onset, pathogenesis, and progression of these “preclinical” manifestations of DR may uncover novel strategies for earlier detection and treatment. However, during the past several years, an increasing body of evidence suggests that retinal neurodegeneration represents an additional component of diabetic retinal disease that may precede the retinal vascular abnormalities. A recent study using the American Academy of Ophthalmology’s Intelligent Research in Sight (IRIS) registry demonstrated that in eyes with good initial vision, severity of DR at first diagnosis was a risk factor for the development of blindness, reflecting the persistent clinical utility of this classification scheme. DR stage guides treatment recommendations and monitoring intervals due to increasing risk of severe vision loss as the disease progresses. These findings range from the microaneurysms, cotton-wool spots, intraretinal hemorrhages, venous beading, and intraretinal microvascular abnormalities that define the spectrum of nonproliferative DR to the extensive ischemia, neovascularization, and subsequent potential vitreous hemorrhage and tractional retinal detachments that define more advanced proliferative DR. DR has long been considered a disease of the retinal microvasculature and indeed is still diagnosed and staged by microvascular manifestations evident on clinical examination. Diabetes mellitus (DM) remains a growing epidemic worldwide with significant morbidity and mortality, and diabetic retinopathy (DR) represents the leading cause of blindness in the working-age population.
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