title: Ventral aspect of the visual form pathway is not critical for the perception of biological motion.
abstract: Identifying the movements of those around us is fundamental for many daily activities, such as recognizing actions, detecting predators, and interacting with others socially. A key question concerns the neurobiological substrates underlying biological motion perception. Although the ventral "form" visual cortex is standardly activated by biologically moving stimuli, whether these activations are functionally critical for biological motion perception or are epiphenomenal remains unknown. To address this question, we examined whether focal damage to regions of the ventral visual cortex, resulting in significant deficits in form perception, adversely affects biological motion perception. Six patients with damage to the ventral cortex were tested with sensitive point-light display paradigms. All patients were able to recognize unmasked point-light displays and their perceptual thresholds were not significantly different from those of three different control groups, one of which comprised brain-damaged patients with spared ventral cortex (n > 50). Importantly, these six patients performed significantly better than patients with damage to regions critical for biological motion perception. To assess the necessary contribution of different regions in the ventral pathway to biological motion perception, we complement the behavioral findings with a fine-grained comparison between the lesion location and extent, and the cortical regions standardly implicated in biological motion processing. This analysis revealed that the ventral aspects of the form pathway (e.g., fusiform regions, ventral extrastriate body area) are not critical for biological motion perception. We hypothesize that the role of these ventral regions is to provide enhanced multiview/posture representations of the moving person rather than to represent biological motion perception per se.
authors.affiliation: Institute of Cognitive Neuroscience and Wellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, London, WC1N 3AR, United Kingdom; shagido@gmail.com.
authors.forename: Sharon
authors.initials: S
authors.lastname: Gilaie-Dotan
authors.affiliation: Department of Cognitive Science and Neurosciences Program, University of California, San Diego, CA 92093-0515; and.
authors.forename: Ayse Pinar
authors.initials: AP
authors.lastname: Saygin
authors.affiliation: Department of Psychology and.
authors.forename: Lauren J
authors.initials: LJ
authors.lastname: Lorenzi
authors.affiliation: Institute of Cognitive Neuroscience and Wellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, London, WC1N 3AR, United Kingdom;
authors.forename: Geraint
authors.initials: G
authors.lastname: Rees
authors.affiliation: Department of Psychology and Center for the Neural Basis of Cognition, Carnegie Mellon University, Pittsburgh, PA 15213.
authors.forename: Marlene
authors.initials: M
authors.lastname: Behrmann
mesh_terms: D000328:Adult; D000368:Aged; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009039:Motion Perception; D014793:Visual Cortex / Q000473:pathology / Q000503:physiopathology*; D014795:Visual Pathways / Q000473:pathology / Q000503:physiopathology*; D014796:Visual Perception
keywords: EBA; action perception; point-light displays; ventral stream; visual form agnosia