Praxic functions are frequently altered following brain lesion, giving rise to apraxia, a complex pattern of impairments that is difficult to assess or interpret. In this chapter, we review the current taxonomies of apraxia and related cognitive and neuropsychological models. We also address the questions of the neuroanatomical correlates of apraxia, the relation between apraxia and aphasia and the analysis of apraxic errors. We provide a possible explanation for the difficulties encountered in investigating apraxia and also several approaches to overcome them, such as systematic investigation and modeling studies. Finally, we argue for a multidisciplinary approach. For example, apraxia should be studied in consideration with and could contribute to other fields such as normal motor control, neuroimaging and neurophysiology.

The processing of biological motion is a critical, everyday task performed with remarkable efficiency by human sensory systems. Interest in this ability has focused to a large extent on biological motion processing in the visual modality (see, for example, Cutting, J. E., Moore, C., & Morrison, R. (1988). Masking the motions of human gait. Perception and Psychophysics, 44(4),[339][340][341][342][343][344][345][346][347]. In naturalistic settings, however, it is often the case that biological motion is defined by input to more than one sensory modality. For this reason, here in a series of experiments we investigate behavioural correlates of multisensory, in particular audiovisual, integration in the processing of biological motion cues. More specifically, using a new psychophysical paradigm we investigate the effect of suprathreshold auditory motion on perceptions of visually defined biological motion. Unlike data from previous studies investigating audiovisual integration in linear motion processing [Meyer, G. Research, 19,[185][186][187][188][189][190][191][192][193][194], we report the existence of direction-selective effects: relative to control (stationary) auditory conditions, auditory motion in the same direction as the visually defined biological motion target increased its detectability, whereas auditory motion in the opposite direction had the inverse effect. Our data suggest these effects do not arise through general shifts in visuo-spatial attention, but instead are a consequence of motion-sensitive, direction-tuned integration mechanisms that are, if not unique to biological visual motion, at least not common to all types of visual motion. Based on these data and evidence from neurophysiological and neuroimaging studies we discuss the neural mechanisms likely to underlie this effect.

Human motion studies have focused primarily on modeling straight point-to-point reaching movements. However, many goal-directed reaching movements, such as movements directed towards oneself, are not straight but rather follow highly curved trajectories. These movements are particularly interesting to study since they are essential in our everyday life, appear early in development and are routinely used to assess movement deficits following brain lesions. We argue that curved and straight-line reaching movements are generated by a unique neural controller and that the observed curvature of the movement is the result of an active control strategy that follows the geometry of one's body, for instance to avoid trajectories that would hit the body or yield postures close to the joint limits. We present a mathematical model that accounts for such an active control strategy and show that the model reproduces with high accuracy the kinematic features of human data during unconstrained reaching movements directed toward the head. The model consists of a nonlinear dynamical system with a single stable attractor at the target. Embodiment-related task constraints are expressed as a force field that acts on the dynamical system. Finally, we discuss the biological plausibility and neural correlates of the model's parameters and suggest that embodiment should be considered as a main cause for movement trajectory curvature.

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Abstract. This paper investigates the neural mechanisms of visuo-motor imitation in humans through convergent evidence from neuroscience. In particular, we consider a deficit in imitation following callosal brain lesion, based on the rational that looking at how imitation is impaired can unveil its underlying neural principles. We ground the functional architecture and information flow of our model in brain imaging studies and use findings from monkey brain neurophysiological studies to drive the choice of implementation of our processing modules. Our neural model of visuo-motor imitation is based on self-organizing maps with associated activities. Patterns of impairment of the model, realized by adding uncertainty in the transfer of information between the networks, account for the scores found in a clinical examination of imitation [1]. The model also allows several interesting predictions.