Ganglion cell losses underlying visual field defects from experimental glaucoma.
Ganglion cell losses underlying visual field defects from experimental glaucoma.
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DOI：
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发表时间：
1999-09
影响因子：
4.4
通讯作者：
R. Harwerth;L. Carter-Dawson;F. Shen;Earl L. Smith;M. Crawford
中科院分区：
文献类型：
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作者：
R. Harwerth;L. Carter-Dawson;F. Shen;Earl L. Smith;M. Crawford
目的探讨青光眼所致视野损害与神经节细胞丢失的关系。方法收集10只恒河猴单侧实验性青光眼的行为学和组织学资料，用Ar激光照射小梁网。在出现明显的视野缺陷后，收集视网膜进行组织学分析。用光学显微镜对甲酚紫染色的视网膜切片中的神经节细胞进行计数，并将相应视网膜和视野测试位置的神经节细胞丢失百分比(经处理以控制眼数)与视野缺陷的深度(经处理以控制眼阈值)进行比较。分析了Goldmann III、White和Goldmann V以及短波和长波视野测试刺激下神经节细胞损失的敏感度损失。结果无论是白色刺激还是有色刺激，神经节细胞的比例损失与视觉敏感度之间均呈非线性关系。在白色刺激下，神经节细胞损失小于30%到50%时，视觉敏感度损失相对恒定(约6分贝)，然后随着细胞损失的增加，视觉缺陷与神经节细胞损失更系统地相关(约0.42分贝/百分比细胞损失)。当视觉阈值被归一化以补偿白色和有色视野检查刺激的预期正常阈值的差异时，用短波长或长波长视野检查刺激测量的视觉缺陷的神经敏感性关系的形式相似。结论：目前使用白色或单色刺激的视野检查方案在相当大比例的神经节细胞死亡之前不能提供对神经节细胞丢失的有用估计。神经节细胞丢失的差异很大，对于诊断早期青光眼的轻度缺陷和中心凹附近的视野位置，敏感度丧失发生在疾病过程的相对较晚的地方。对于白色和单色测试刺激，神经敏感性关系基本上是相同的，因此，似乎不太可能用单色刺激检测青光眼的较高敏感性是基于神经节细胞对青光眼损伤的大小依赖的敏感性。
PURPOSE To investigate the relationship between ganglion cell losses and visual field defects caused by glaucoma. METHODS Behavioral perimetry and histology data were obtained from 10 rhesus monkeys with unilateral experimental glaucoma that was induced by argon laser treatments to their trabecular meshwork. After significant visual field defects had developed, the retinas were collected for histologic analysis. The ganglion cells were counted by light microscopy in cresyl violet-stained retina sections, and the percentage of ganglion cell loss (treated to control eye counts) was compared with the depth of visual field defect (treated to control eye thresholds) at corresponding retinal and perimetry test locations. Sensitivity losses as a function of ganglion cell losses were analyzed for Goldmann III, white and Goldmann V, and short- and long-wavelength perimetry test stimuli. RESULTS The relationship between the proportional losses of ganglion cells and visual sensitivity, measured with either white or colored stimuli, was nonlinear. With white stimuli, the visual sensitivity losses were relatively constant (approximately 6 dB) for ganglion cell losses of less than 30% to 50%, and then with greater amounts of cell loss the visual defects were more systematically related to ganglion cell loss (approximately 0.42 dB/percent cell loss). The forms of the neural-sensitivity relationships for visual defects measured with short- or long-wavelength perimetry stimuli were similar when the visual thresholds were normalized to compensate for differences in expected normal thresholds for white and colored perimetry stimuli. CONCLUSIONS Current perimetry regimens with either white or monochromatic stimuli do not provide a useful estimate of ganglion cell loss until a substantial proportion have died. The variance in ganglion cell loss is large for mild defects that would be diagnostic of early glaucoma and for visual field locations near the fovea where sensitivity losses occur relatively late in the disease process. The neural-sensitivity relationships were essentially identical for both white and monochromatic test stimuli, and it therefore seems unlikely that the higher sensitivity for detecting glaucoma with monochromatic stimuli is based on the size-dependent susceptibility of ganglion cells to injury from glaucoma.