J. Cogn. Neurosci.
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(Journal of Cognitive Neuroscience. 2006;18:2063-2076.)
© 2006 The MIT Press

Deficits in Movement Planning and Intrinsic Coordinate Control in Ideomotor Apraxia

Steven A. Jax1,2, Laurel J. Buxbaum1,3 and Adrienne D. Moll1

1 Moss Rehabilitation Research Institute, Philadelphia, 2 University of Pennsylvania Medical School, 3 Thomas Jefferson University, Philadelphia

Reprint requests should be sent to Laurel J. Buxbaum, Moss Rehabilitation Research Institute, Korman Building 213, 1200 W. Tabor Road, Philadelphia, PA 19141, or via e-mail: lbuxbaum{at}einstein.edu.

Two central issues in the field of motor control are the coordinate frame in which movements are controlled and the distinction between movement planning and online correction. In this study we used these issues to frame several hypotheses about the deficits underlying ideomotor apraxia (IMA). In particular, we examined whether ideomotor apraxics exhibited (1) deficits in movement control in intrinsic (body relative) coordinates with better control in extrinsic (workspace relative) coordinates, (2) deficits in movement planning that are compensated for by an overreliance on online correction, or (3) both deficits. Patients with IMA and two comparison groups performed movement tasks that relied preferentially on either intrinsic or extrinsic coordinate control when online correction was either possible or impossible. Participants performed posture imitation and grasp imitation movements to body- and object-relative end positions in the presence or absence of visual feedback. Consistent with the intrinsic coordinate control hypothesis, patients with IMA showed a significantly greater disparity than the other two groups between movements made to body-relative and object-relative targets as well as between imitation of meaningless postures and grasping. Consistent with the correction overreliance hypothesis, the IMA group was more disrupted than the other groups by the removal of vision. Thus, IMA patients exhibit behavioral patterns consistent with both deficient intrinsic coordinate control and overreliance upon visual feedback. Finally, lesion analysis suggests that damage to the left inferior parietal lobe (Brodmann's areas 39 and 40) may play a key role in both behavioral deficits.







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