TY - JOUR
T1 - Motor Adaptation Deficits in Ideomotor Apraxia
AU - Mutha, Pratik K.
AU - Stapp, Lee H.
AU - Sainburg, Robert L.
AU - Haaland, Kathleen Y.
N1 - Funding Information:
This work was funded by the Biomedical Laboratory Research and Development Service (101BX007080) and the Rehabilitation Research and Development Service (B4125R) grants from the VA Office of Research and Development to Kathleen Y. Haaland, and the National Institutes of Health (R01HD39311 and R01HD059783) grants to Robert L. Sainburg. This work was also supported by the Ramanujan Fellowship, and grants from the Health Sciences Committee and the Cognitive Science Research Initiative of the Department of Science and Technology (Government of India) to Pratik K. Mutha. We thank Jenna Keller, Sierra Widmer, Melissa Daniels, and Jennifer Hogan for assistance with data collection, Drs. Brad Cushnyr and Gammaliel Lorenzo for neuroradiological consultation, Drs. John Adair and Sally Harris, and HealthSouth Rehabilitation Hospital and Lovelace Medical Center for patient referral. The authors report no conflict of interest.
Publisher Copyright:
© Copyright The International Neuropsychological Society 2017.
PY - 2017/2/1
Y1 - 2017/2/1
N2 - 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.
AB - 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.
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U2 - 10.1017/S135561771600120X
DO - 10.1017/S135561771600120X
M3 - Article
C2 - 28205499
AN - SCOPUS:85013157566
SN - 1355-6177
VL - 23
SP - 139
EP - 149
JO - Journal of the International Neuropsychological Society
JF - Journal of the International Neuropsychological Society
IS - 2
ER -