Early changes in optic disc compliance and surface position in experimental glaucoma
Early changes in optic disc compliance and surface position in experimental glaucoma
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DOI：
10.1016/s0161-6420(95)30791-9
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发表时间：
1995-12-01
期刊：
影响因子：
13.7
通讯作者：
Varma, R
中科院分区：
文献类型：
--
作者：
Burgoyne, CF;Quigley, HA;Varma, R
检测慢性实验性青光眼发病后猴视盘顺应性和基线位置（顺应性测试基线时间点的位置）的变化。方法：对13只猴子的26只眼进行66次顺应性测试。纵向研究。在七只正常猴子中，在一只眼睛（研究眼）中进行了三次依从性测试，在对侧眼睛中进行了一次。在其中五只猴子的研究眼中，诱发慢性实验性青光眼，并在以下部分或全部青光眼后测试间隔进行依从性测试：眼压（IOP）升高后1至2周、3至4周、5至8周、9至12周、13至18周和18周以上。在其余两只猴子的研究眼中，视神经被横断，并在横断后第 5、9 和 13 周测试依从性。进行方差分析（ANOVA）以检测每个测试间隔青光眼眼睛的顺应性的增加（过度顺应性）或减少（刚性）。进行第二次方差分析以检测每个椎间盘基线位置的慢性后变形的发生。横断面研究。在另外六只患有实验性青光眼的猴子中，以纵向研究中使用的青光眼后测试间隔之一对青光眼研究眼进行依从性测试。对侧正常眼进行一次顺应性测试。然后将这些数据以适当的青光眼前期和青光眼后期测试间隔添加到来自五只纵向研究的猴子的数据中。进行第三次方差分析，以将扩大的青光眼组在每个干预后测试间隔的依从性与 13 只正常对侧眼睛的依从性进行比较。结果：依从性。在纵向（Pr > F = 0.0005）和横向（Pr > F = 0.0001）研究的青光眼眼中，视盘顺应性在青光眼发病后 1 至 2 周内显着增加，然后在统计上恢复到与正常水平无法区分的水平。在横断眼中，横断后 5 周和 9 周时，与正常眼或青光眼眼中的视盘相比，视盘的顺应性显着降低（更坚硬）（Pr > F < 0.05）。基线视盘位置。在青光眼发病后 1 至 2 周内测试的三只眼睛中的一只和在青光眼发作后 3 至 4 周测试的四只眼睛中的三只中检测到椎间盘的慢性后变形（Pr > F < 0.05）。在任何横断后测试间隔，在任何横断眼的视盘中均未检测到慢性后部变形。结论：在猴眼实验性青光眼发病后 2 至 4 周内，通过数字化图像分析检测到视盘顺应性和表面位置的变化。这些发现不太可能仅归因于轴突损失，因为它们并未发生在视神经横断眼中（构成眼压保持正常的轴突损失模型）。结果表明，与眼内压相关的视神经乳头承重结缔组织损伤可能发生在实验性青光眼病程的早期。
To detect changes in the compliance and baseline position (position at the baseline time point of a compliance test) of the monkey optic disc after the onset of chronic experimental glaucoma.Methods: Sixty-six compliance tests were performed on 26 eyes of 13 monkeys. Longitudinal Study. In seven normal monkeys, compliance tests were performed three times in one eye (study eye) and once in the contralateral eye. In the study eye of five of these monkeys, chronic experimental glaucoma was then induced and compliance tests were performed at some or all of the following postglaucoma testing intervals: 1 to 2 weeks, 3 to 4 weeks, 5 to 8 weeks, 9 to 12 weeks, 13 to 18 weeks, and more than 18 weeks after the onset of elevated intraocular pressure (IOP). in the study eye of the remaining two monkeys, the optic nerve was transected, and compliance was tested at 5, 9, and 13 weeks after transection. An analysis of variance (ANOVA) was performed to detect an increase (hypercompliance) or decrease (rigidity) in the compliance of the glaucomatous eyes at each testing interval. A second ANOVA was performed to detect the onset of chronic posterior deformation of the baseline position of each disc. Cross-Sectional Study. In six additional monkeys with pre-existing experimental glaucoma, the glaucomatous study eye was compliance tested at one of the postglaucoma testing intervals used in the longitudinal study. The contralateral normal eye was compliance tested once. These data were then added to the data from the five longitudinally studied monkeys at the appropriate preglaucoma and postglaucoma testing intervals. A third ANOVA was done to compare the compliance of the expanded group of glaucomatous eyes at each postintervention testing interval with the compliance of the 13 normal contralateral eyes.Results: Compliance. In the longitudinally (Pr > F = 0.0005) and cross-sectionally (Pr > F = 0.0001) studied glaucomatous eyes, optic disc compliance increased significantly by 1 to 2 weeks and then returned to a level statistically indistinguishable from normal within 13 to 18 weeks after the onset of glaucoma. in the transection eyes, the optic discs were significantly less compliant (more rigid) at 5 and 9 weeks after transection compared with the discs in either the normal or the glaucomatous eyes (Pr > F < 0.05). Baseline Optic Disc Position. Chronic posterior deformation of the disc was detected in one of three eyes tested 1 to 2 weeks and three of four eyes tested 3 to 4 weeks after the onset of glaucoma (Pr > F < 0.05). Chronic posterior deformation was not detected in the discs of either of the transection eyes at any of the post-transection testing intervals.Conclusion: Changes in optic disc compliance and surface position were detected by digitized image analysis within 2 to 4 weeks of the onset of experimental glaucoma in the monkey eye. These findings are unlikely to be due to axon loss alone, because they did not occur in optic nerve transection eyes (which constitute a model of axon loss in which intraocular pressures remain normal). The results suggest that IOP-related damage to the load-bearing connective tissues of the optic nerve head may occur early in the course of experimental glaucoma.