Retinal Ganglion Cell Complex Changes Using Spectral Domain Optical Coherence Tomography in Diabetic Patients Without Retinopathy

Neuroretinal damage in diabetes produces functional abnormalities such as the loss of chromatic discrimination,contrast sensitivity and dark adaptation. These alterations can be detected by means of electrophysiological studies in diabetic patients with diabetes duration of less than two years, i.e. before microvascular lesions can be detected in ophthalmologic examination. Neurodegeneration seems to be a generalized process that occurs throughout the macula and is not confined to local abnormalities, in the cases with visible signs of retinopathy.

The debate is still open as to whether diabetic retinal neuropathy is the effect of vascular diabetic retinopathy or is primarily caused by direct neurologic damage from chronic hyperglycemia. The hypothesis that diabetes causes retinal neuro-pathy independent of retinopathy is intriguing and potentially links retinal neuropathy to other diabetic neuropathies.

Neuroretinal degeneration initiates and/or activates several metabolic and signalling pathways which participates in the microangiopathic process as well as in the disruption of the blood-retinal barrier which is a crucial element in the pathogenesis of diabetic retinopathy.

Retinal ganglion cells are the earliest cells affected and have the highest rate of apoptosis. However, an elevated rate of apoptosis has been also observed in the outer nuclear layer (photoreceptors) and in the retinal pigment epithelium (RPE). The use of spectral domain OCT (SD-OCT) makes it possible to measure the thickness of individual layers at higher resolution and indicates that the thinning of the inner retina in the macula is primarily due to loss of ganglion cells.