Electroretinogram Alterations in Diabetes?

Abstract

Diabetes mellitus is a heterogeneous metabolic disorder characterized by hyperglycemia resulting from defective insulin secretion (type 1), resistance to insulin action (type 2), or both. It is often associated with complications, such as cardiovascular disease, kidney failure, retinopathy, as well as peripheral and autonomic neuropathies. Retinopathy is the most common microvascular complication of diabetes, and it remains a major cause of visual impairment worldwide. Vascular lesions in the early stages of diabetic retinopathy are characterized by the presence of capillary microaneurysms, pericyte deficient capillaries, and obliterated and degenerated capillaries. Proliferative diabetic retinopathy is the more advanced form of the disease, when circulation problems cause the retina to become oxygen deprived. As a result, new fragile blood vessels can begin to grow in the retina and into the vitreous. Therefore, diabetic retinopathy has long been recognized as a vascular disease. However, it is becoming increasingly clear that neuronal cells of the retina are also affected by diabetes. Electroretinogram (ERG) is the neurophysiological test used in order to measure electric changes that happen in the retina after a light stimulus. Changes in the ERG may be due to an impairment of any of the retinal cell types: photoreceptors (a-wave ERG), and amacrine, bipolar, and, mainly, Muller cells (b-wave ERG). Moreover, oscillatory potentials are likely to be due to inner retinal neurotransmission. Though it may seem that diverse studies have presented contradictory results, it is important to point that most of the studies in diabetic experimental animals point to a very early alteration in the b-wave amplitude and reductions in oscillatory potentials. The nervous potential originated in the retina after a light stimulus is transmitted to the visual cortex via the optic nerve. Retinal ganglion cells (RGCs), which form this optic nerve, are the best studied of the retinal neurons with respect to the effect of diabetes. The aim of this work is to summarize recent clinical and laboratory findings about several experimental therapies that have been used to minimize neural changes in retina of different animal models of diabetes.