Investigative ophthalmology & visual science · 2004
Psychophysical measurement of neural adaptation abnormalities in magnocellular and parvocellular pathways in glaucoma.
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McKendrick Allison M, Badcock David R, Morgan William H
Аннотация
PURPOSE: It is well established that contrast sensitivity is reduced in glaucoma. This study explored whether such contrast processing abnormalities consist of an absolute threshold level difference or a problem with contrast gain control.
METHODS: Seventeen patients with primary open-angle glaucoma and 17 approximately age-matched control subjects participated. Subjects were tested foveally and midperipherally (12.5 degrees ). Subjects with glaucoma were tested in a peripheral region of relatively normal visual field (neighboring locations required to be within the normal 95% confidence limit on the total deviation plot of their most recent SITA/full threshold Humphrey Field Analyzer assessment; Carl Zeiss Meditec, Dublin, CA). Control subjects were tested in matching locations. Contrast discrimination was assessed using the steady-pedestal (magnocellular [M] pathway) and pulsed-pedestal (parvocellular [P] pathway) stimuli of Pokorny and Smith for seven pedestal luminances between 15 and 75 cd/m(2), presented on a background of 30 cd/m(2).
RESULTS: Glaucoma group thresholds were significantly elevated compared with control subjects foveally and peripherally on both the pulsed-pedestal (P) and steady-pedestal (M) tasks (P < 0.01). Effect size statistics revealed slightly greater deficits on the P pathway task and greater deficits for pedestals that were decrements, rather than increments, from the surround luminance. Foveal deficits were of a magnitude to be explained by a reduction in contrast sensitivity; however, the peripheral deficits were greater than predicted by this factor alone.
CONCLUSIONS: Foveal and midperipheral dysfunction of both M and P pathways was identified in people with glaucoma, in areas of relatively normal visual field performance. These findings are supportive of nonselective neural adaptation abnormalities in early glaucoma.
METHODS: Seventeen patients with primary open-angle glaucoma and 17 approximately age-matched control subjects participated. Subjects were tested foveally and midperipherally (12.5 degrees ). Subjects with glaucoma were tested in a peripheral region of relatively normal visual field (neighboring locations required to be within the normal 95% confidence limit on the total deviation plot of their most recent SITA/full threshold Humphrey Field Analyzer assessment; Carl Zeiss Meditec, Dublin, CA). Control subjects were tested in matching locations. Contrast discrimination was assessed using the steady-pedestal (magnocellular [M] pathway) and pulsed-pedestal (parvocellular [P] pathway) stimuli of Pokorny and Smith for seven pedestal luminances between 15 and 75 cd/m(2), presented on a background of 30 cd/m(2).
RESULTS: Glaucoma group thresholds were significantly elevated compared with control subjects foveally and peripherally on both the pulsed-pedestal (P) and steady-pedestal (M) tasks (P < 0.01). Effect size statistics revealed slightly greater deficits on the P pathway task and greater deficits for pedestals that were decrements, rather than increments, from the surround luminance. Foveal deficits were of a magnitude to be explained by a reduction in contrast sensitivity; however, the peripheral deficits were greater than predicted by this factor alone.
CONCLUSIONS: Foveal and midperipheral dysfunction of both M and P pathways was identified in people with glaucoma, in areas of relatively normal visual field performance. These findings are supportive of nonselective neural adaptation abnormalities in early glaucoma.