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Neuronal plasticity and macular edema
Author(s) -
TICK S,
GIRMENS JF,
SAHEL JA,
PAQUES M
Publication year - 2008
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2008.6335.x-i1
Subject(s) - outer nuclear layer , retinal , retina , outer plexiform layer , ophthalmology , visual acuity , medicine , anatomy , pathology , biology , neuroscience
Purpose The aim of this study is to analyze the retinal structure of the macula of patients having recovered from ME due to perfused retinal vein occlusion(RVO) and compare it to histology of experimental RVO in rats. Methods In 26 patients with perfused RVO having recovered from ME, averaged high resolution OCT cross scans were acquired. The aspect of retinal layering was analyzed and compared to that of fellow eyes. In parallel, the retinal structure of rats subjected to transient RVO was analyzed by immunohistochemistry and electron microscopy. Results All eyes had a normal macular profile. In 7 out of 14 eyes with normal visual function, disorganization of the layers presumably corresponding to the outer plexiform layer(OPL) was detected associated with variable thinning of the outer and inner nuclear layer (ONL, INL). Loss of central vision occurred was present only when disruption of the OS reflectance was apparent. In rats, a similar profile of OPL dizorganisation and ONL and INL thinning was observed. Electron microscopy objectivated synaptic migration into the ONL. Conclusion Neuroglial plasticity is challenged during macular edema. Remodeling of retinal layers may be detected by OCT even when visual acuity is normal. Post‐RVO ME neuroglial remodeling initially affects the OPL. Loss of cone OS is a crucial milestone during the course of ME, being the first event leading to irreversible visual loss. The fact that OPL damage precede cone OS loss may suggest that deafferentation participates to cone OS loss.