Essock E A, Fechtner R D, Zimmerman T J, Krebs W K, Nussdorf J D
Department of Psychology, University of Louisville, KY 40292, USA.
J Glaucoma. 1996 Dec;5(6):395-405.
This study investigated whether certain binocular mechanisms are disrupted in early glaucoma.
Glaucoma patients, suspects, and normals were tested on a battery of psychophysical tests consisting of flicker sensitivity (5 and 34 Hz), temporal cut-off frequency (CFF), contrast sensitivity (Pelli-Robson chart), and stereoacuity. Monocular channels were evaluated with tests of monocular flicker performance and spatial contrast sensitivity. Binocular summation on spatial and temporal tests was used to reflect integrity of binocular neural interactions. Stereoacuity was taken as a measure of performance of disparity processing mechanisms.
The groups differed in terms of binocular flicker sensitivity at both temporal rates, binocular and monocular peak contrast sensitivity, and stereoacuity. Binocular summation of both spatial and temporal sensitivity was normal. The glaucoma suspect group was distinguishable from the age-matched normal group on binocular contrast sensitivity and stereoacuity.
The binocular mechanisms that mediate stereoacuity appear to be heavily disrupted, whereas the binocular mechanisms that mediate central neural interaction of monocular inputs are normal. Although monocular spatiotemporal abilities are disrupted, the binocular processes combine the monocular input normally. In addition, our results suggest a benefit of binocular testing for routine assessment of glaucoma patients. The profound disruption of stereoacuity appears to result from disorder in the spatial sampling array at the ganglion-cell level similar to the disorder reported in the normal periphery and the central retina of strabismic amblyopes. These and previous findings were reviewed to evaluate the supposition of preferential M-pathway disruption in early glaucoma. Such a model can not be reconciled with the present findings. We conclude that measurements of temporal modulation sensitivity fit well with such a model, but that the current evidence of spatiotemporal contrast sensitivity disruption is less supportive of such a model.
本研究调查了早期青光眼患者某些双眼机制是否受到破坏。
对青光眼患者、疑似青光眼患者和正常人进行了一系列心理物理学测试，包括闪烁敏感度（5和34赫兹）、时间截止频率（CFF）、对比敏感度（佩利-罗布森视力表）和立体视锐度。通过单眼闪烁性能测试和空间对比敏感度测试评估单眼通道。在空间和时间测试中使用双眼总和来反映双眼神经相互作用的完整性。立体视锐度被用作视差处理机制性能的指标。
在两个时间频率下的双眼闪烁敏感度、双眼和单眼峰值对比敏感度以及立体视锐度方面，各组存在差异。空间和时间敏感度的双眼总和均正常。青光眼疑似组在双眼对比敏感度和立体视锐度方面与年龄匹配的正常组有区别。
介导立体视锐度的双眼机制似乎严重受损，而介导单眼输入的中枢神经相互作用的双眼机制正常。尽管单眼时空能力受损，但双眼过程能正常整合单眼输入。此外，我们的结果表明双眼测试对青光眼患者的常规评估有益。立体视锐度的严重破坏似乎是由于神经节细胞水平的空间采样阵列紊乱所致，类似于斜视性弱视患者正常周边和中央视网膜中报道的紊乱情况。回顾了这些及先前的研究结果，以评估早期青光眼患者优先M通路受损的假设。这样的模型与目前的研究结果不一致。我们得出结论，时间调制敏感度的测量结果与这样的模型相符，但目前关于时空对比敏感度受损的证据不太支持这样的模型。
