Castelo-Branco Miguel, Mendes Mafalda, Silva Fatima, Massano João, Januário Gustavo, Januário Cristina, Freire António
Visual Neuroscience Laboratory, IBILI, Faculty of Medicine, 3000-458 Coimbra, Portugal.
Neuropsychologia. 2009 Jan;47(2):314-20. doi: 10.1016/j.neuropsychologia.2008.09.003. Epub 2008 Sep 7.
Motion processing involves multiple hierarchical steps, from the magnocellular pathway, sensitive to high temporal frequency modulations, to subsequent motion integration within the visual cortical dorsal stream. We have tested whether motion integration deficits in mild Parkinson disease (PD) can be explained by visual deficits in earlier processing nodes. Contrast sensitivity deficits in the magnocellular pathway, were compared with speed discrimination of local dots moving in random directions, speed and direction discrimination of moving surfaces and motion integration as measured by 2D coherence thresholds (n=27). We have found that low-level magnocellular impairment in PD does not explain deficits in subsequent steps in motion processing. High-level performance was abnormal in particular for tasks requiring perception of coherently moving surfaces. Motion coherence deficits were predictive of visuomotor impairment, corroborating a previous magnetic stimulation study in normal subjects. We conclude that dorsal stream deficits in PD have a high-level visual cortical basis independent of low-level magnocellular damage.
运动处理涉及多个层次步骤，从对高时间频率调制敏感的大细胞通路，到视觉皮层背侧流内随后的运动整合。我们测试了轻度帕金森病（PD）中的运动整合缺陷是否可以由早期处理节点中的视觉缺陷来解释。将大细胞通路中的对比敏感度缺陷与随机方向移动的局部点的速度辨别、移动表面的速度和方向辨别以及通过二维相干阈值测量的运动整合进行了比较（n = 27）。我们发现，PD中的低水平大细胞损伤并不能解释运动处理后续步骤中的缺陷。特别是对于需要感知连贯移动表面的任务，高水平表现异常。运动连贯性缺陷可预测视觉运动障碍，这证实了先前对正常受试者的磁刺激研究。我们得出结论，PD中的背侧流缺陷具有独立于低水平大细胞损伤的高级视觉皮层基础。
