Abstract
Purpose :
Inner retinal blood vessels that are interposed between light entering the eye and the photoreceptors generate an entoptic effect called an angioscotoma. The prevailing view is that the shadows cast by these vessels generate imperceptible, discrete, areas of blindness. Although angioscotomas were described 195 years ago, observations of what else the vasculature does to the retinal layers is absent. In fact, the inner retinal vasculature, over time, also damages the inner and outer nuclear layers and the peripheral nerve fiber layer.
Methods :
Observations and measurements were made in paraffin sections of the retinas of 20 macaque monkeys ranging in age from fetal day 64 to adulthood. Sections were microscopically scanned looking for vessels that were associated with outward bowing (deformations) of the inner (INL) & outer (ONL) nuclear layers. Ten sections were used for this analysis. INL & ONL thicknesses were measured both at the deformation and at both sides of the deformation. Deformed vs. undeformed (normal) laminar thicknesses were compared using paired t-tests and power analysis.
Results :
Mean thickness of undeformed INL was 27.3 μm and that of the deformed INL was 16.8 μm. This 48% reduction in INL thickness caused by vessels was significant (P<1.3E-3; power=0.97). Mean ONL undeformed thickness was 35.3 μm and that for the deformed ONL was 29.8 μm. This 16% reduction in ONL thickness was also significant (P<1.3E-7; power=0.94). Laminar thickness reduction magnitude was always greater for the INL than for the ONL and was therefore directly related to proximity to the vessel. Mean vessel diameter was 47.3 μm for 9 arteries and 65.5 μm for 3 veins.
Conclusions :
The inner retina is bounded on one side by vitreous through which it is subjected to an IOP force of 10-15 mm Hg. Intraretinal arteries and veins also generate pressure waves that radiate through the retinal tissue with each pulse. By age 60, at a heart rate of 60 bpm, 1.9 billion pulses have been delivered to a human retina. The amplitudes of such local pulses have yet to measured. High blood pressure would also increase the pressure generated by vascular pulsation. The retinal nerve fiber layer adjacent to the vessels was hypodense for all but one artery. This suggests that vascular pulsations may also batter and damage retinal ganglion cell axons. Lastly, angioscotomas are contributed to by both light blockage and nerve fiber layer damage due to vascular pulsations.
This is a 2020 ARVO Annual Meeting abstract.