The long-term objective of this research is to relate visual deficits in patients to the underlying cellular pathophysiology. The proposed research uses new psychophysical measures for monitoring cell dysfunction, and quantitative modeling to relate glaucomatous visual defects with ganglion cell damage.
These aims will lay the foundation for development of new forms of perimetry.
The Specific Aims are: 1) To develop a clinically useful version of a new method for evaluating ganglion cell dysfunction. Over the past decade a new functional technique has been developed in terms of saturation of ganglion cell spike generation, and has been applied to the study of foveal dysfunction. The proposed research will develop a version of this technique for evaluating dysfunction throughout the visual field. The clinical version will be used to follow patients in Specific Aim 2, and will be modeled in Specific Aim 4. 2) To follow patients being treated for glaucoma, using methods with sufficient precision to detect improvement in visual function. We have demonstrated that test-retest variability can be reduced by using stimuli for which cortical mechanisms summate responses of large numbers of ganglion cells. These stimuli, along with the method developed in Specific Aim 1, will be used to monitor visual function in glaucomatous defects. In this Aim we will use these methods to follow patients undergoing treatment for glaucoma, in order to evaluate the potential role of ganglion cell dysfunction in determining depth of defect. 3) To evaluate structural and functional data on glaucomatous defects using quantitative modeling of effects of ganglion cell death and dysfunction. Functional data for conventional perimetry and for our new tests will be compared with structural measures of ganglion cell loss, to more precisely define the potential roles of cell dysfunction and cell death in structure/function comparisons. 4) To extend our quantitative modeling by analyzing potential effects of neural noise in terms of population dynamics and spike train analysis. We will use both neurometric analysis of macaque ganglion cell spike trains and simulation of population dynamics to incorporate physiologically plausible sources of neural noise and distinguish between decreased sensitivity of ganglion cells vs. increased neural noise, and provide an improved understanding of the effects of different aspects of cellular pathophysiology.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
5R01EY007716-16
Application #
7049430
Study Section
Biology and Diseases of the Posterior Eye Study Section (BDPE)
Program Officer
Liberman, Ellen S
Project Start
1999-03-01
Project End
2006-05-31
Budget Start
2006-04-01
Budget End
2006-05-31
Support Year
16
Fiscal Year
2006
Total Cost
$25,147
Indirect Cost
Name
State College of Optometry
Department
Other Clinical Sciences
Type
Schools of Optometry/Ophthalmol
DUNS #
152652764
City
New York
State
NY
Country
United States
Zip Code
10036
Alluwimi, Muhammed S; Swanson, William H; King, Brett J (2018) Identifying Glaucomatous Damage to the Macula. Optom Vis Sci 95:96-105
Ramezani, Koosha; Marín-Franch, Iván; Hu, Rongrong et al. (2018) Prediction Accuracy of the Dynamic Structure-Function Model for Glaucoma Progression Using Contrast Sensitivity Perimetry and Confocal Scanning Laser Ophthalmoscopy. J Glaucoma 27:785-793
Swanson, William H; Dul, Mitchell W; Horner, Douglas G et al. (2017) Individual differences in the shape of the nasal visual field. Vision Res 141:23-29
Price, Derek A; Swanson, William H; Horner, Douglas G (2017) Using perimetric data to estimate ganglion cell loss for detecting progression of glaucoma: a comparison of models. Ophthalmic Physiol Opt 37:409-419
Gardiner, Stuart K; Swanson, William H; Demirel, Shaban (2016) The Effect of Limiting the Range of Perimetric Sensitivities on Pointwise Assessment of Visual Field Progression in Glaucoma. Invest Ophthalmol Vis Sci 57:288-94
Ashimatey, Bright S; Swanson, William H (2016) Between-Subject Variability in Healthy Eyes as a Primary Source of Structural-Functional Discordance in Patients With Glaucoma. Invest Ophthalmol Vis Sci 57:502-7
Swanson, William H; Dul, Mitchell W; Horner, Douglas G et al. (2016) Contrast sensitivity perimetry data from adults free of eye disease. Data Brief 8:654-8
Dul, Mitchell; Ennis, Robert; Radner, Shira et al. (2015) Retinal adaptation abnormalities in primary open-angle glaucoma. Invest Ophthalmol Vis Sci 56:1329-34
Swanson, William H; Horner, Douglas G (2015) Assessing assumptions of a combined structure-function index. Ophthalmic Physiol Opt 35:186-93
Huang, Gang; Luo, Ting; Gast, Thomas J et al. (2015) Imaging Glaucomatous Damage Across the Temporal Raphe. Invest Ophthalmol Vis Sci 56:3496-504

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