Visual detection of body motion is of immense importance for daily-life activities and social nonverbal interaction. Although neurobiological mechanisms underlying visual processing of human locomotion are being explored extensively by brain imaging, the role of structural brain connectivity is not well understood. Here we investigate cortical evoked neuromagnetic response to point-light body motion in healthy adolescents and in patients with early periventricular lesions, periventricular leukomalacia (PVL), that disrupt brain connectivity. In a simultaneous masking paradigm, participants detected the presence of a point-light walker embedded in a few sets of spatially scrambled dots on the joints of a walker. The visual sensitivity to camouflaged human locomotion was lower in PVL patients. In accord with behavioral data, root-mean-square (RMS) amplitude of neuromagnetic trace in response to human locomotion was lower in PVL patients at latencies of 180–244 msec over the right temporal cortex. In this time window, the visual sensitivity to body motion in controls, but not in PVL patients, was inversely linked to the right temporal activation. At later latencies of 276–340 msec, we found reduction in RMS amplitude in PVL patients for body motion stimuli over the right frontal cortex. The findings indicate that disturbances in brain connectivity with the right temporal cortex, a key node of the social brain, and with the right frontal cortex lead to disintegration of the neural network engaged in visual processing of body motion. We suspect that reduced cortical response to body motion over the right temporal and frontal cortices might underlie deficits in visual social cognition.

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