Motor Adaptation Deficits in Ideomotor Apraxia

Pratik K. Mutha, Lee H. Stapp, Robert L. Sainburg, Kathleen Y. Haaland

Research output: Contribution to journalArticle

5 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)139-149
Number of pages11
JournalJournal of the International Neuropsychological Society
Volume23
Issue number2
DOIs
StatePublished - Feb 1 2017

Fingerprint

Ideomotor Apraxia
Learning
Apraxias
Parietal Lobe
Healthy Volunteers
Extremities
Stroke

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Clinical Psychology
  • Clinical Neurology
  • Psychiatry and Mental health

Cite this

Mutha, Pratik K. ; Stapp, Lee H. ; Sainburg, Robert L. ; Haaland, Kathleen Y. / Motor Adaptation Deficits in Ideomotor Apraxia. In: Journal of the International Neuropsychological Society. 2017 ; Vol. 23, No. 2. pp. 139-149.
@article{fe8b3e52bf74416286cfeb76117e2fe7,
title = "Motor Adaptation Deficits in Ideomotor Apraxia",
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.",
author = "Mutha, {Pratik K.} and Stapp, {Lee H.} and Sainburg, {Robert L.} and Haaland, {Kathleen Y.}",
year = "2017",
month = "2",
day = "1",
doi = "10.1017/S135561771600120X",
language = "English (US)",
volume = "23",
pages = "139--149",
journal = "Journal of the International Neuropsychological Society",
issn = "1355-6177",
publisher = "Cambridge University Press",
number = "2",

}

Motor Adaptation Deficits in Ideomotor Apraxia. / Mutha, Pratik K.; Stapp, Lee H.; Sainburg, Robert L.; Haaland, Kathleen Y.

In: Journal of the International Neuropsychological Society, Vol. 23, No. 2, 01.02.2017, p. 139-149.

Research output: Contribution to journalArticle

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.

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.

UR - http://www.scopus.com/inward/record.url?scp=85013157566&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85013157566&partnerID=8YFLogxK

U2 - 10.1017/S135561771600120X

DO - 10.1017/S135561771600120X

M3 - Article

C2 - 28205499

AN - SCOPUS:85013157566

VL - 23

SP - 139

EP - 149

JO - Journal of the International Neuropsychological Society

JF - Journal of the International Neuropsychological Society

SN - 1355-6177

IS - 2

ER -