Abstract
Abstract: :
Purpose: To describe a novel idiopathic, bilateral optic nerve (ON) atrophy in rhesus monkeys that may confound interpretation of primate models. Methods: Six monkeys, among a "normal" population, were evaluated with in vivo structural imaging, ON stereophotos and confocal scanning laser tomography. Functional examination was performed with photopic full–field ERG, pattern ERGs (PERG) and multifocal ERGs (mfERG). After euthanasia, semi–thin ON sections were stained with Toluidine blue and phenylenediamine and were examined. Pooled normal ONs served as controls. Results: Fundus photographs revealed extensive temporal ON pallor. The temporal nerve fiber layer was markedly thin and often absent between the vascular arcades. Functional examination was consistent with retinal ganglion cell (RGC) disease. ERG parameters, including a–wave, b–wave, photopic negative response, and oscillatory potential amplitudes were relatively unaffected. The results are consistent with isolated RGC loss from central retina, with relative preservation of cone photoreceptor and bipolar cell function. PERG changes were also consistent with RGC disease, with larger reduction of the N95 amplitude and N95:P50 slope parameters, relative to P50 amplitude. Central retinal mfERG responses showed selective loss of high–frequency components, a marker of RGC dysfunction and additional evidence of normal cone photoreceptor and bipolar cell function. Histologically, the density of RGC axons in the temporal ON was dramatically decreased and in regions axons were unidentifiable. In regions of axonal degeneration, axonal bundles shrank significantly and many were filled with glial cells. Astrocytes with enlarged processes and cell bodies were seen at the edges of damaged regions. Conclusions: Recognition of this idiopathic temporal ON atrophy is crucial and mandates screening before employing primates in ophthalmic research. The structural and functional evaluation showed predominantly temporal inner retina and ON damage. Results are all consistent with pathological findings in human optic atrophy, such as toxic/nutritional, Leber’s hereditary, and dominant optic atrophy.
Keywords: optic disc • ganglion cells • electrophysiology: clinical