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H. E. Killer, M. Harlev, U. Ziegler, P. Groscurth, N. R. Miller, P. Meyer, S. Dotan, G. Jaggi; Optic Nerve Compartment Syndrome. An Experimental Animal Model. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5666.
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© ARVO (1962-2015); The Authors (2016-present)
To report the results of experimental optic nerve compartmentation in sheep. This study was performed according to the ARVO guidelines for animal research and was approved by the local ethical committee
4 female Dorper sheep were selected. Age was between 1-1.5 years, weight between 30-35 kg. Orbitomy was performed under general anesthesia. The optic nerve on one side was gently ligated with a silicone sling near the optic canal and left in place in order to impair cerebrospinal fluid circulation. The optic nerves were removed after three weeks and were worked up for histology.
Light microscopy, transmission EM and scanning EM Light demonstrates loss of axons in the periphery of the nerve at the site of the ligature. Behind the globe, remote from the ligature, the axons loss is more pronounced, reaching in to the center of the cross section. Transmission electron microscopy shows destruction of myelin and axons while most of the cellular components of the optic nerve appear intact.
Light microscopy, transmission EM and scanning EM demonstrate axon loss after experimental compartmenation of the optic nerve. The cross section most involved is located distal to the ligation behind the globe. This pattern of axon loss is unlikely to be caused by local trauma via the ligature. We suggest that statis of CSF with accumulation of biologically active substances, such as L-PGDS my harm the the unmyelinated axons and mitochondria in the bulbar region behind the globe, causing anteriograde axon degeneration. Further studies including CSF analysis are necessary to elucidate the pathophysiology of the axon loss pattern.
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