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M. Castelo-Branco, M. Mendes, F. Silva, G. Januário, J. Massano, C. Januário, A. Freire; Hierarchical and Parallel Visual Processing in Parkinson Disease: Magnocellular Impairment and Motion Integration Deficits Are Independent. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5848.
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© ARVO (1962-2015); The Authors (2016-present)
Motion processing involves multiple hierarchical steps, from the magnocellular pathway, sensitive to high temporal frequency modulations, to subsequent motion integration within magno recipient regions in the visual cortical dorsal stream. We have asked the question whether motion integration deficits in Parkinson Disease (PD) can be explained by visual deficits in earlier processing nodes. An alternative hypothesis is that convergence of magno inputs may be sufficient to compensate for peripheral loss of these inputs.
Deficits in the afferent magnocellular pathway, measured with a contrast sensitivity task that uses a sinusoidal grating stimulus at high temporal (25 Hz) and low spatial frequencies (0.25 cycles per degree) were compared with speed discrimination of local dots moving in random directions, speed and direction discrimination of moving surfaces, direction discrimination and motion integration as measured by 2D coherence thresholds.
We have found that low-level magnocellular impairment in PD does not explain deficits in subsequent steps in motion processing. In fact, high-level performance was abnormal only for tasks requiring perception of coherently moving tasks, with partial compensation being observed for other tasks requiring processing of motion attributes.
We conclude that dorsal stream deficits in PD have a high-level visual cortical basis are not explained by low level magnocellular damage. These findings further challenge visual magnocellular theories in dyslexia that postulate that magnocellular dysfunction is causally related to motion integration deficits.
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