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D. Cao, A. J. Zele, J. Pokorny, S. M. Ksiazek, D. Lee, L. V. Messner, N. Chaudhary, J. W. Nicholas; Psychophysical Magnocellular and Parvocelluar Contrast Gain in Patients With Optic Neuritis. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1193. doi: https://doi.org/.
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To evaluate contrast threshold deficits in patients with optic neuritis under conditions designed to favor mediation by either the inferred Magnocellular (MC) or Parvocelluar (PC) pathway.
Luminance contrast discrimination was measured in 9 patients with unilateral or bilateral optic neuritis and 4 age-matched controls with normal vision, using steady- and pulsed-pedestal paradigms (Pokorny & Smith, JOSA A 14: 2477-2486, 1997) to bias performance toward the MC or PC pathway respectively. Additionally, L-M chromatic discrimination at equiluminance was evaluated using the steady-pedestal paradigm. The measured data were fitted by a physiologically plausible model that included parameters accounting for contrast gain and contrast sensitivity in the inferred MC or PC pathway. The fitted parameters from the affected eye were compared with those from the clinically non-affected eye in patients with unilateral optic neuritis, or with those from the controls.
For all affected eyes, the pulsed-pedestal data indicated a large decrease in PC contrast gain and contrast sensitivity. Interpretation of the steady-pedestal data was not clear-cut. There was a significant loss of sensitivity but it is uncertain whether detection under these conditions was mediated by the MC or PC pathway. We are certain that the loss of MC contrast gain was at least as great, or greater than the loss of PC contrast gain. In patients with unilateral optic neuritis, the contrast gain and contrast sensitivity in the affected eyes showed significant losses compared with the non-affected eyes. However, the non-affected eyes were not completely normal; they showed significantly lower contrast gain and sensitivity compared with the controls.
Optic neuritis produced large contrast gain and sensitivity losses for both inferred PC and MC mediated thresholds, suggesting that the disease in the optic nerve limits the information transfer from retina to cortex.
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