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Kenneth R. Alexander, Claire S. Barnes, Gerald A. Fishman, Joel Pokorny, Vivianne C. Smith; Contrast-Processing Deficits in Melanoma-Associated Retinopathy. Invest. Ophthalmol. Vis. Sci. 2004;45(1):305-310. doi: https://doi.org/10.1167/iovs.03-0840.
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purpose. To evaluate the hypothesis that patients with melanoma-associated retinopathy (MAR) have a selective functional loss within the magnocellular (MC) pathway of the cone system, with sparing of parvocellular (PC) pathway function.
methods. Two patients with MAR, ages 57 and 61 years, with normal Snellen visual acuity, participated in the study. Contrast sensitivity was measured at spatial frequencies ranging from 0.25 to 8 cycles per degree (cpd), using two paradigms (steady pedestal and pulsed pedestal) designed to assess the functional integrity of the MC and PC pathways, respectively. Results in patients with MAR were compared with those in 10 visually normal observers, aged 23 to 57 years.
results. Both patients with MAR showed a loss of contrast sensitivity compared to normal observers, but the pattern of loss differed for the two testing paradigms. For the steady-pedestal paradigm (presumed MC-pathway mediation), the patients’ sensitivity loss was greatest at the lowest spatial frequency (0.25 cpd) and the sensitivity loss decreased systematically with increasing spatial frequency. For the pulsed-pedestal paradigm (presumed PC-pathway mediation), the sensitivity loss was greatest at an intermediate spatial frequency of 1 cpd. For both paradigms, the patients’ sensitivities were within the normal range at the highest spatial frequency (8 cpd), consistent with their normal visual acuity.
conclusions. The contrast sensitivity deficits of patients with MAR under photopic conditions are not specific to the MC pathway, as proposed previously, but instead are related to the spatial frequency of the test target. The overall pattern of contrast sensitivity loss shown by the patients with MAR is consistent with the dysfunction at the level of the retinal bipolar cells that is presumed to underlie the MAR syndrome.
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