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Motor Adaptation Deficits in Ideomotor Apraxia

Published online by Cambridge University Press:  16 February 2017

Pratik K. Mutha*
Affiliation:
Department of Biological Engineering and Center for Cognitive Science, Indian Institute of Technology Gandhinagar, Palaj, Gandhinagar, Gujarat, India
Lee H. Stapp
Affiliation:
New Mexico VA Healthcare System, Albuquerque, New Mexico
Robert L. Sainburg
Affiliation:
Department of Kinesiology, Pennsylvania State University, University Park, Pennsylvania Department of Neurology, Pennsylvania State University, Hershey, Pennsylvania
Kathleen Y. Haaland
Affiliation:
Departments of Psychiatry & Behavioral Sciences and Neurology, University of New Mexico, Albuquerque, New Mexico
*
Correspondence and reprint requests to: Pratik K. Mutha, Indian Institute of Technology Gandhinagar, Block 5, Room 316A, Palaj, Gandhinagar, Gujarat, India – 382355. E-mail: [email protected]

Abstract

Objectives: The cardinal motor deficits seen in ideomotor limb apraxia are thought to arise from damage to internal representations for actions developed through learning and experience. However, whether apraxic patients learn to develop new representations with training is not well understood. We studied the capacity of apraxic patients for motor adaptation, a process associated with the development of a new internal representation of the relationship between movements and their sensory effects. Methods: Thirteen healthy adults and 23 patients with left hemisphere stroke (12 apraxic, 11 nonapraxic) adapted to a 30-degree visuomotor rotation. Results: While healthy and nonapraxic participants successfully adapted, apraxics did not. Rather, they showed a rapid decrease in error early but no further improvement thereafter, suggesting a deficit in the slow, but not the fast component of a dual-process model of adaptation. The magnitude of this late learning deficit was predicted by the degree of apraxia, and was correlated with the volume of damage in parietal cortex. Apraxics also demonstrated an initial after-effect similar to the other groups likely reflecting the early learning, but this after-effect was not sustained and performance returned to baseline levels more rapidly, consistent with a disrupted slow learning process. Conclusions: These findings suggest that the early phase of learning may be intact in apraxia, but this leads to the development of a fragile representation that is rapidly forgotten. The association between this deficit and left parietal damage points to a key role for this region in learning to form stable internal representations. (JINS, 2017, 23, 139–149)

Type
Research Articles
Copyright
Copyright © The International Neuropsychological Society 2017 

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