Motion perception is abnormal in primary open-angle glaucoma and ocular hypertension
Several lines of evidence suggest that the large optic nerve fibers, which form the magnocellular retinocortical pathway, are preferentially susceptible to early glaucomatous damage. It is evident from studies of the functional architecture of the visual system that the magnocellular pathway underli...
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Published in | Investigative ophthalmology & visual science Vol. 31; no. 4; pp. 722 - 729 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Rockville, MD
ARVO
01.04.1990
Association for Research in Vision and Ophtalmology |
Subjects | |
Online Access | Get full text |
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Summary: | Several lines of evidence suggest that the large optic nerve fibers, which form the magnocellular retinocortical pathway, are preferentially susceptible to early glaucomatous damage. It is evident from studies of the functional architecture of the visual system that the magnocellular pathway underlies the global perception of motion. Therefore, we have developed a psychophysical technique for assessing motion detection thresholds in patients with ocular hypertension (OHT) and primary open-angle glaucoma (POAG). For this purpose we employed a dynamic random dot display that contained varying degrees of a coherent motion signal embedded within a background of random motion noise. We used this technique to measure motion thresholds in POAG patients (n = 37), OHT patients (n = 14), and age-matched controls (n = 39). Motion thresholds were elevated by 70% for the POAG group and 44% for the OHT group relative to controls. In the same patients, no significant deficit in form discrimination was found as measured by Pelli-Robson charts. Our results demonstrate that significant motion perception deficits are evident in POAG and OHT. These findings support the suggestion that significant and selective damage to the magnocellular pathway occurs in OHT and POAG and indicate that motion threshold testing may reveal preclinical optic nerve disease in early POAG. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0146-0404 1552-5783 |