MAR 17, 2014
This article reviews the evidence surrounding the theory that myopic deformation of the eye and metabolic alterations of the nerve tissue of patients with diabetes may modify glaucomatous optic neuropathy (GON).
The authors explain that blockage of axonal transport of neurotrophic factors is the event crucial to understanding the factors that affect GON. The primary, but not sole, blockage site is at the lamina cribrosa.
Other than this primary site of damage at the lamina cribrosa, other factors may explain atypical nerve fiber layer defects and the vulnerability of the nerve fibers in eyes with high myopia and glaucoma: a second point of blockage at the edge of the posterior scleral foramen; ectatic strain on the nerve fiber layer; ectasia and distortion of the lamina cribrosa; association of a hypoplastic optic disc; thin and weak collagen fibers; peripapillary chorioretinal atrophy; and myopic neuropathy.
Among diabetic patients, diabetic neuropathy in the retinal nerve fiber layer is present initially and increased resistance to aqueous outflow leads to ocular hypertension. Superimposition of GON on diabetic neuropathy and ocular hypertension in patients with diabetes may enhance their susceptibility to nerve damage.
One meta-analysis suggested a positive association between diabetes mellitus and glaucoma whereas other reports suggested that leakage of vascular endothelial growth factor and enhanced stiffness of the lamina cribrosa as a result of diabetic glycation may protect neurons from apoptosis.
However, modification of GON as a result of diabetes remains controversial. The authors also note that if myopia is associated with glaucoma, a warning to the myopic population may be important for public health considerations.