Most of the histopathological and psychophysical studies in glaucoma reveal a preferential damage to the magnocellular (M) pathway although a few of them support a damage to the parvocellular (P) pathway as well. In glaucoma, the visual fields are usually evaluated by conventional perimetry. However, it has been demonstrated that 20-40% of ganglion cells are lost before field defects are detected using conventional perimetry. Therefore, new psychophysical tests have recently been designed in order to specifically isolate and evaluate the visual mechanisms that are impaired at the early stages of glaucoma. In this context, several authors have addressed the issue of motion perception under the hypothesis of a predominant damage of the M pathway in glaucoma, and that motion perception is mediated mainly by M pathway. The results of these studies depict a large variation in the percentage of patients showing anomalous motion perception. Overall, motion thresholds are elevated in both glaucoma and ocular hypertensive patients as compared to control subjects, irrespective of the stimulus size and eccentricity. The test which discriminates best between patients and normal subjects is motion perimetry. The visual field defects in glaucoma patients identified by conventional perimetry and motion perimetry are similar, but the sizes of the defects are usually larger with motion perimetry. However, motion tests in central vision have no correlation with visual field defect on conventional perimetry. In glaucoma, loss of performance on motion perception tests does not necessarily support the existence of a specific deficit in the M pathway, because some behavioral studies suggest that the P pathway can also mediate motion perception. It is also difficult to conclude that motion perception is specifically affected in glaucoma because most of these studies do not yield a comparison with other visual functions. Despite these difficulties, localized motion perception tests at eccentricities of more than 15 degrees can be considered as a promising diagnostic tool.
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http://dx.doi.org/10.1016/s0039-6257(02)00401-0 | DOI Listing |
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Johns Hopkins University, Department of Biomedical Engineering, 720 Rutland Avenue, Baltimore 21205, USA. Electronic address:
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