Beruflich Dokumente
Kultur Dokumente
JapaneseJournalofOphthalmology
January 2014, Volume 58, Issue 1, pp 16-25
First online: 15 August 2013
Abstract
Myopic deformation of the eye and metabolic alterations of the nerve tissue of patients with diabetes may modify
glaucomatous optic neuropathy (GON). Blockage of axonal transport of neurotrophic factors (NTFs) is the event crucial to
understanding the factors that affect GON. The primary, but not sole, blockage site is at the lamina cribrosa (LC). Other
than this primary site of damage at the LC, 7 other factors may explain atypical nerve fiber layer (NFL) 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 NFL; ectasia and distortion of the LC; 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 NFL 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. Results of a meta-analysis study suggested a positive association between
diabetes mellitus and glaucoma whereas other reports suggested that leakage of vascular endothelial growth factor, a
survival mechanism of ischemic neural tissue, and enhanced stiffness of the LC as a result of diabetic glycation may protect
neurons from apoptosis. Thus, modification of GON as a result of diabetes remains controversial.
Keywords
Myopia Diabetes mellitus Diabetic neuropathy Glaucoma Optic disc
Part of this review article was presented as the Suda Memorial Lecture at the Japanese Glaucoma Society Meeting in
Kanazawa on September 30, 2012.
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Glaucoma
Optic disc
Industry Sectors
Biotechnology
Pharma
Authors
EtsuoChihara (1)
Author Affiliations
1. Sensho-Kai Eye Institute, Minamiyama 50-1, Iseda, Uji, Kyoto, 611-0043, Japan