Structural and functional neuroimaging of the pathophysiology of apraxia

A better understanding of the neural bases of apraxia is an important prerequisite to develop new therapeutic strategies for the disabling apraxic deficits after left-hemisphere stroke, like disturbed imitation of gestures, deficient pantomime, and object use deficits. Recently, functional and structural imaging methods allowed deeper insights into the pathophysiology of apraxia: While apraxic object use deficits result from the dysfunction of an extended fronto-parietal network within the left hemisphere, pantomime deficits are caused by impaired functioning of the left inferior frontal cortex. Further apraxia-related, motor cognitive processes (i.e., gesture imitation, integration of temporal and spatial movement information, and intentional movement planning) depend on the integrity of the left parietal cortex. Newly developed functional and structural imaging methods, like dynamic causal modelling (DCM) and diffusion tensor imaging (DTI), promise to further elucidate the pathophysiology of apraxia at the network level