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Diabetic maculopathy is characterized by the accumulation of extracellular fluid in Henle's layer and the inner nuclear layer of the retina. The localization of the edema is likely to be due, in part, to the relative barrier properties of the inner and outer plexiform layers. The origin of the extracellular fluid is from the intravascular compartment. Although changes to retinal blood flow may partly explain the extravasation of fluid, the most important mechanism is breakdown of the blood retinal barriers. Both the inner blood retinal barrier formed by the retinal capillary endothelial cell tight junctions and the outer barrier formed by the retinal pigment epithelial cell tight junctions can be affected. The mechanism of breakdown of the blood retinal barriers is likely to be changes to the tight junction proteins including occludin and ZO-1. The biochemical messenger inducing these changes may be vascular endothelial growth factor. The origin of this or other cofactors may be the retinal glial cells. The underlying biochemical stimulus to the production of vascular endothelial growth factor is chronic hyperglycaemia, but it is uncertain by what pathway this is effected.

In humans, the inner and outer plexiform layers are sites of high resistance to the diffusion of large molecules, resulting in an REL of 76.5 kDa. There was only moderate interspecies variation in the REL of the animals studied, suggesting that they provide adequate models for the study of human transretinal macromolecular diffusion.

Although childhood-onset LHON carries a relatively better visual prognosis, approximately 1 in 5 patients will remain within the visual acuity criteria for legal blindness in the UK. The clinical presentation can be insidious and LHON should be considered in the differential diagnosis when faced with a child with unexplained subnormal vision and optic disc pallor.