Biomedical subjects

Ronald S Harwerth

Publications and source records attributed to Ronald S Harwerth.

5 recordsLinked to original sources

PubMed2003

Stereopsis is perturbed by vergence error.

Fixation disparity or vergence noise produce instantaneous vergence errors. These errors are analogous to the imposition of a pedestal disparity, which is known to elevate stereothresholds. In this study, stereothresholds were measured as a function of induced vergence errors in subjects with normal binocular vision. Stereo half-images were viewed in the dark through a custom mirror haploscope. Vergence constant error and vergence variability were induced by introducing horizontal disconjugate position offsets in a pair of moveable mirrors within the haploscope, resulting in forced vergence demands of 6(Delta) base-in to 12(Delta) base-out. In addition, vergence variability was simulated by producing oscillatory disconjugate retinal image motion via motion of the moveable mirrors. The motion of the mirrors was either sinusoidal (frequency=2-6 Hz) or random, with peak-to-peak amplitudes of 0 degrees -0.5 degrees per eye. Stereopsis worsened systematically with induced or simulated VV that exceeded approximately 1.5' disparity. The results were similar regardless of whether the vergence error was induced by forced vergence or was simulated by periodic or random disconjugate retinal image motion. Stereothresholds were invariant with the frequency of disconjugate oscillation, within the range of frequencies and amplitudes tested. Hence, the simulated vergence velocity is not the essential factor that limits stereopsis within Panum's fusional area. The results indicate that the stereothreshold is elevated if the vergence error exceeds a critical value.

Adult↗

PubMed2003

Stereothresholds with simulated vergence variability and constant error.

Stereothresholds are elevated by vergence constant error (fixation disparity), vergence noise, or both. This study investigated the separate and combined effects of simulated vergence constant error and variability on stereothresholds in four normal observers. Targets were 30 arc min bright vertical lines presented separately to the two eyes for 150 ms in darkness. Vergence constant error, simulated as a pedestal disparity, was induced by altering the screen positions of the stereo half-images relative to a previously visible binocular fixation point. Vergence variability was simulated simultaneously by disconjugate motion (amplitude=0-0.5 deg per eye; frequency=2 or 4 Hz) of a pair of scanning mirrors in a Wheatstone stereoscope that was used to present the images to each eye. Various combinations of pedestal disparity and simulated vergence variability produce equivalent stereothresholds whenever the calculated mean deviation (sigma/instantaneous vergence errors//N) of the stimulus from the fixation plane is the same. In particular, stereothresholds are optimal for mean deviations up to approximately 1.4 arc min and then increase according to a power function with an exponent of 0.61. The results imply that vergence constant errors and vergence variability impair stereothresholds because of the resulting mean deviation from the horopter.

Adult↗

PubMed2003

Temporal integration for stereoscopic vision.

With normal binocular vision, maximal stereoacuity requires an extended viewing duration, but the relationship between the critical viewing duration for stereopsis and other variables affecting stereoacuity is unknown. The purposes of the study were to investigate the properties of normal temporal integration for stereoscopic vision with respect to the effects of contrast and spatial frequency of the stimuli and to determine whether the temporal summation of disparity is affected in deficient stereopsis caused by abnormal binocular vision during infancy. Psychophysical methods were used to measure stereothresholds in human and monkey subjects with either normal binocular vision or abnormal binocular vision. The results showed that the critical viewing duration for stereoscopic depth discrimination was independent of variations in basic stimulus parameters and/or the subject's stereoacuity. A critical duration of approximately 100 ms was found for both local (narrowband Gabor and broadband line targets) and global (dynamic random dots) stimuli. Although stereothresholds increased with decreasing stimulus contrast, the properties of temporal integration did not. Stereothresholds were substantially elevated for monkeys and humans with abnormal binocular vision, but the critical durations for these subjects were not significantly different from those of subjects with normal binocular vision. Overall, the results demonstrate that the general properties of temporal integration for stereopsis are similar to other detection and discrimination tasks that do not require binocular processing. In addition, increased integration time does not account for the elevated stereothresholds of subjects with abnormal binocular vision.

Animals↗

PubMed2002

Visual field defects and neural losses from experimental glaucoma.

Glaucoma is a relatively common disease in which the death of retinal ganglion cells causes a progressive loss of sight, often leading to blindness. Typically, the degree of a patient's visual dysfunction is assessed by clinical perimetry, involving subjective measurements of light-sense thresholds across the visual field, but the relationship between visual and neural losses is inexact. Therefore, to better understand of the effects of glaucoma on the visual system, a series of investigations involving psychophysics, electrophysiology, anatomy, and histochemistry were conducted on experimental glaucoma in monkeys. The principal results of the studies showed that, (1) the depth of visual defects with standard clinical perimetry are predicted by a loss of probability summation among retinal detection mechanisms, (2) glaucomatous optic atrophy causes a non-selective reduction of metabolism of neurons in the afferent visual pathway, and (3) objective electrophysiological methods can be as sensitive as standard clinical perimetry in assessing the neural losses from glaucoma. These experimental findings from glaucoma in monkeys provide fundamental data that should be applicable to improving methods for assessing glaucomatous optic neuropathy in patients.

Animals↗

PubMed2002

Vitreal glutamate concentration in monkeys with experimental glaucoma.

PURPOSE: To investigate the hypothesis that the pathophysiology for the death of retinal ganglion cells in glaucoma involves excitotoxic effects from elevated concentrations of vitreal glutamate. METHODS: Experimental glaucoma was induced in the right eyes of 18 rhesus monkeys by argon laser treatments to the trabecular meshwork. After significant visual field defects and/or typical clinical glaucomatous changes had developed (1.5-13 months), the eyes were removed, and a sample (0.1-0.2 mL) of posterior vitreous was collected. Similar vitreous samples also were collected from eight untreated monkeys. The vitreous samples were analyzed in a masked fashion by high-pressure liquid chromatography in two independent laboratories. Mean levels of vitreal glutamate were determined for the treated and control eyes and differences between groups of eyes were evaluated by Student's t-test. RESULTS: The mean level (+/- SD) of vitreal glutamate in the eight untreated monkeys was 5.0 +/- 2.0 microM. A similar level of 5.7 +/- 1.8 microM was measured in the untreated eyes of monkeys with experimental glaucoma. In the glaucomatous eyes, the mean concentration of vitreal glutamate was 5.7 +/- 2.6 microM, which was not significantly different from the concentrations in the control eyes. CONCLUSIONS: Vitreal glutamate concentrations were not elevated in eyes with anatomic and functional damage from experimental glaucoma. This finding is in contradiction to previous reports that vitreal glutamate increases to toxic levels and probably contributes to glaucomatous damage of retinal ganglion cells.

Amino Acids↗