APPLICATION OF PSYCHOPHYSICAL MODELS TO VISUAL DISORDERS

描述(申请人提供)：本研究的长期目标 是将视力障碍患者的功能缺陷与 潜在的细胞病理生理学。这项拟议的研究使用了心理物理学。 开发评估青光眼进展的新方法的措施 视力损失，以及青光眼视觉缺陷与 神经节细胞受损。具体目标是： (1)开发新的刺激，旨在提高对进步的敏感度 神经节细胞受损。神经节细胞嵌合体的反应模型 传统的视野刺激表明青光眼进展的测试 如果使用皮质机制的刺激，可以改善 介导性检测结合大量视网膜神经节的反应 细胞。这个目标将通过使用动态噪声掩模来开发这样的刺激 隔离具有较大空间总和区域的机构。 (2)通过测量来评估这些新刺激的临床潜力 青光眼缺陷的测试-复测变异性和空间总和。使用 常规视野检查，增加刺激大小会减少重测 变异性，但也降低了对青光眼损害的敏感性。这一目标 将评估在特定目标1中开发的新刺激，这些刺激是 假设将重测变异性降至最低，同时保持对 青光眼的缺陷。将收集重测和空间总和数据 青光眼的缺陷，以便找到使用这些药物的最佳条件 刺激以检测视力丧失的进展。 (3)根据大脑皮质对这些新刺激的敏感度建模 正常眼和青光眼的神经节细胞反应。一种量化模型 已经研究了神经节细胞丢失对传统的 视野检查，这表明有必要考虑皮质的影响 神经节细胞反应总和。该模型将扩展到适用于 在特定目标1和2中发展的新刺激。这个模型将有助于 从神经节细胞的角度解释特定目标1和2的结果 损害，并将指导开发新的周长方法。 这些目标将为开发新形式的视野奠定基础， 它将提供更强大的方法来评估进展和 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.