Jonas J B, Hayreh S S
Department of Ophthalmology and Eye Hospital, Friedrich-Alexander-University Erlangen-Nürnberg in Erlangen, Germany.
Am J Ophthalmol. 1999 May;127(5):523-30. doi: 10.1016/s0002-9394(99)00030-6.
To evaluate longitudinally the optic disk morphology of nonglaucomatous optic nerve damage secondary to retinal nerve fiber damage, using experimental central retinal artery occlusion in rhesus monkey eyes as a model.
This prospective study included 24 eyes of 16 monkeys. In eight eyes of eight animals, central retinal artery occlusion was produced by clamping the central retinal artery in the retrobulbar space. Occlusion was verified by fluorescein fundus angiography. The same eyes at baseline as well as the eight contralateral healthy eyes and eight monkey eyes with experimental high-pressure glaucoma served as control groups. Serially taken optic disk photographs were morphometrically evaluated.
The area and shape of the neuroretinal rim and alpha zone and beta zone of parapapillary chorioretinal atrophy of eyes after central retinal artery occlusion did not vary significantly (P > .30) from the same eyes before central retinal artery occlusion nor from the normal contralateral eyes. In the glaucomatous eyes, the neuroretinal rim was significantly (P < .001) smaller and parapapillary atrophy significantly (P = .01) larger than in the eyes after central retinal artery occlusion.
Experimental central retinal artery occlusion, in contrast to glaucoma, does not markedly change the size and shape of parapapillary atrophy and neuroretinal rim; this confirms previous clinical studies. Thus, assessment of parapapillary atrophy and neuroretinal rim may be helpful to differentiate between glaucomatous optic neuropathy and nonglaucomatous optic neuropathy secondary to retinal nerve fiber damage. Parapapillary atrophy is independent of decreased retinal blood perfusion and development of nonglaucomatous optic nerve atrophy following experimental central retinal artery occlusion.
以恒河猴眼实验性视网膜中央动脉阻塞为模型,纵向评估视网膜神经纤维损伤继发的非青光眼性视神经损伤的视盘形态。
这项前瞻性研究纳入了16只猴子的24只眼。在8只动物的8只眼中,通过在球后间隙夹闭视网膜中央动脉造成视网膜中央动脉阻塞。通过荧光素眼底血管造影术验证阻塞情况。将基线时的同一只眼以及8只对侧健康眼和8只实验性高压青光眼猴眼作为对照组。对连续拍摄的视盘照片进行形态测量评估。
视网膜中央动脉阻塞后,患眼的神经视网膜边缘、视乳头旁脉络膜视网膜萎缩的α区和β区的面积和形状,与视网膜中央动脉阻塞前的同一只眼以及对侧正常眼相比,差异均无统计学意义(P>.30)。在青光眼眼中,神经视网膜边缘明显小于视网膜中央动脉阻塞后的眼睛(P<.001),视乳头旁萎缩明显大于视网膜中央动脉阻塞后的眼睛(P=.01)。
与青光眼不同,实验性视网膜中央动脉阻塞不会显著改变视乳头旁萎缩和神经视网膜边缘的大小和形状;这证实了先前的临床研究。因此,对视乳头旁萎缩和神经视网膜边缘的评估可能有助于区分青光眼性视神经病变和视网膜神经纤维损伤继发的非青光眼性视神经病变。视乳头旁萎缩与实验性视网膜中央动脉阻塞后视网膜血流灌注减少及非青光眼性视神经萎缩的发生无关。