The proposed research will determine the extent to which diseased visual systems can be pushed selectively beyond the limits of their effective adaptation capabilities so that their sensitivities become categorically different from normal. The emphasis will be on glaucoma-related visual dysfunction that cannot be attributed directly to the loss of optic nerve cells. This dysfunction involves adaptation processes that actively maintain visual response. It occurs for people who have a slight degree of glaucomatous optic neuropathy combined with high blood pressure, and could be due to either condition. The research will help clarify the relation between high blood pressure and glaucoma-related visual dysfunction. It will focus on how to exceed the limits of the visual system's adaptation capabilities so that subtle physiologic compromise can be amplified into large sensitivity changes. A major emphasis will concern the visual system's ability to maintain a stable effective operating range for resolving temporally modulated stimuli, i.e. for detecting flicker. Psychophysical tests of visual function after adaptation-field onset will be compared with clinical assessments of early glaucomatous damage. The prevalence of visual adaptation abnormalities will be examined for four clinically-defined groups of middle-age subjects: 1) glaucoma subjects with positive medical histories of high blood pressure, 2) glaucoma subjects with negative medical histories of high blood pressure, 3) non-glaucoma subjects with positive medical histories of high blood pressure and negative clinical histories of ocular hypertension, and 4) healthy normal subjects. Young healthy subjects will be tested also. The experiments will identify the types of processes that underlie flicker response abnormalities and will integrate a diverse set of existing results concerning suppression of flicker response under taxing adaptation conditions.
The specific aims are 1) to determine whether people with high blood pressure have a higher-than-normal prevalence of visual dysfunction, 2) to determine how often foveal visual adaptation is abnormal for people who have high blood pressure but do not have glaucoma, and vice versa, 3) to determine whether certain subtypes or stages of glaucoma are associated with certain types of foveal adaptation abnormalities, 4) to identify the mechanisms by which glaucoma and/or high-blood-pressure alter foveal flicker response, and 5) to determine if the limits of the visual system's flicker-response operating-range can be specified as precisely at bright ambient light levels as they have been at dim ambient light levels.
