APPLICATION OF PSYCHOPHYSICAL MODELS TO VISUAL DISORDERS

描述（由申请人提供）：本研究的长期目标 是将视觉障碍患者的功能缺陷与 潜在的细胞病理生理学这项拟议中的研究使用心理物理学方法， 制定新的评估昏迷进展方法的措施 视力丧失，以及一个定量模型， 神经节细胞损伤具体目标是： (1)开发新的刺激，旨在提高对渐进性 神经节细胞损伤神经节细胞嵌合体对 常规的周边刺激表明青光眼进展的测试 可以改善，如果刺激使用的皮层机制， 大量视网膜神经节的介导检测联合收割机响应 细胞这一目标将通过使用动态噪声掩模来开发这样的刺激， 具有大空间总和区域的隔离机制。 (2)通过测量这些新刺激的临床潜力， 昏迷性缺陷的重测变异性和空间总和。与 常规视野检查，刺激大小增加会降低重测 变异性，但也降低了对昏迷性损伤的敏感性。这一目标 将评估在具体目标1中开发的新刺激， 假设最小化重测变异性，同时保持对 昏迷性缺陷。将收集重测和空间汇总数据 为了找到最佳的条件，使用这些 刺激以检测视力丧失的进展。 (3)为了模拟对这些新刺激的敏感性， 正常和青光眼眼的神经节细胞反应。定量模型 已经开发了神经节细胞损失对常规的 视野检查，这表明需要考虑皮质的影响， 神经节细胞反应的总和。该模型将扩展到适用于 具体目标1和2中开发的新刺激。这个模型将有助于 从神经节细胞的角度解释具体目标1和2的结果 损害，并将指导新的周边方法的发展。 这些目标将为开发新形式的视野检查奠定基础， 这将提供更强大的评估进展的方法， 评价治疗效果。

DESCRIPTION (provided by applicant): The long-term objective of this research is to relate functional deficits in patients with visual disorders to underlying cellular pathophysiology. The proposed research uses psychophysical measures to develop new methods for evaluation of progression of glaucomatous visual loss, and a quantitative model to relate glaucomatous visual defects to ganglion cell damage. The specific aims are: (1) To develop new stimuli designed to improve sensitivity to progressive ganglion cell damage. Modeling of responses of ganglion cell mosaics to conventional perimetric stimuli indicate that tests for progression of glaucoma could be improved if stimuli were used for which the cortical mechanisms mediating detection combine responses of large numbers of retinal ganglion cells. This aim will develop such stimuli by using dynamic noise masks to isolate mechanisms with large spatial summation areas. (2) To evaluate the clinical potential of these new stimuli by measuring test-retest variability and spatial summation in glaucomatous defects. With conventional perimetry, increase in stimulus size decreases test-retest variability, but also decreases sensitivity to glaucomatous damage. This aim will evaluate the new stimuli developed in specific aim 1, which are hypothesized to minimize test-retest variability while retaining sensitivity to glaucomatous defects. Test-retest and spatial summation data will be gathered in glaucomatous defects in order to find optimal conditions for using these stimuli to detect progression of visual loss. (3) To model sensitivity to these new stimuli in terms of cortical summation of ganglion cell responses in normal and glaucomatous eyes. A quantitative model has been developed of the effects of ganglion cell loss on conventional perimetry, which has demonstrated the need to consider effects of cortical summation of ganglion cell responses. The model will be extended to apply to the new stimuli developed in specific aims 1 and 2. This modeling will help interpret the results of specific aims 1 and 2 in terms of ganglion cell damage, and will guide the development of new perimetric methods. These aims will lay the foundation for development of new forms of perimetry, which will provide more powerful methods of assessing progression and evaluating effects of treatment.