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Arseny Sokolov, Michael Erb, Wolfgang Grodd, Marcos Tatagiba, Richard Frackowiak, Marina Pavlova; Recovery of biological motion processing and network plasticity after cerebellar lesion. Journal of Vision 2013;13(9):762. doi: https://doi.org/10.1167/13.9.762.
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Visual body motion perception is essential for social competence and everyday life activities. The left lateral cerebellum is involved in visual biological motion processing and interacts with the right superior temporal sulcus, STS (Sokolov et al. Neuroimage 2012), a key structure within the action observation network. Lesions to the left lateral cerebellum may cause deficits in body motion perception (Sokolov et al. Cereb Cortex 2010). Yet alterations in sensitivity to body motion and the underlying neural network after cerebellar tumor removal remain unknown. Psychophysical assessment of visual sensitivity to point-light biological motion was conducted before, and 8 and 24 months after neurosurgery in a patient SL with left cerebellar dysplastic gangliocytoma (WHO grade I), and in six healthy controls. Functional magnetic resonance imaging (fMRI) was used to assess postoperative activity and connectivity during visual body motion processing. Preoperative visual sensitivity to biological motion in patient SL was significantly lower than in healthy matched controls. Sensitivity substantially improved at 8 months and approached the level of controls at 24 months after neurosurgery. As compared to healthy controls, fMRI reveals activation of left cerebellar lobules III and IX to biological motion, implying a midline shift of cerebellar activation. Psychophysiological interaction (PPI) analysis shows that, as in normalcy, the left cerebellum interacts with a region in the right STS, which is located more anteriorly than in healthy participants. The psychophysical findings indicate a remarkable potential for recovery of biological motion perception after removal of a left cerebellar tumor. Brain imaging data reveal topographical cerebro-cerebellar network reorganization as underlying compensatory mechanism, and suggest that cerebellar lesions may induce plasticity in the cerebral cortex.
Meeting abstract presented at VSS 2013
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