TY - JOUR
T1 - Lesion location alters brain activation in chronically impaired stroke survivors
AU - Luft, Andreas R.
AU - Waller, Sandy
AU - Forrester, Larry
AU - Smith, Gerald V.
AU - Whitall, Jill
AU - Macko, Richard F.
AU - Schulz, Jörg B.
AU - Hanley, Daniel F.
N1 - Funding Information:
We thank Andrew Goldberg, Jim Boyd, Christina Stephenson and Jill England for their support. Thanks also to Dr. John Sorkin for his expert help with statistical analyses. We thank the F.M. Kirby Center for Functional Brain Imaging, Kennedy Krieger Institute (Baltimore, MD, USA), and its staff, especially Terry Brawner, Dr. James Pekar, and Dr. Peter van Zijl. Dr. Luft is supported by grants from Deutsche Forschungsgemeinschaft (Lu 748/2, 748/3). Funding for this study was obtained from the National Institutes of Health (P60AG 12583 NIA University of Maryland Claude D. Pepper Older Americans Independence Center H133G010111) the Baltimore Department of Veterans Affairs Geriatrics Research, Education and Clinical Center (GRECC), Dr. Hanley is supported by 1RO1 NS 24282-08 and the France-Merrick Foundation, the Johns Hopkins GCRC (grant NCRR #MO1-00052), the National Center for Research Resources, MO1 RR-00052, and the Eleanor Naylor Dana Charitable Trust.
PY - 2004/3
Y1 - 2004/3
N2 - Recovery of motor function after stroke is associated with reorganization in central motor networks. Functional imaging has demonstrated recovery-dependent alterations in brain activation patterns when compared to healthy controls. These alterations are variable across stroke subjects. Factors identified as contributing to this variability are the degree of functional impairment, the time interval since stroke, and rehabilitative therapies. Here, the hypothesis is tested that lesion location influences the activation patterns. Using functional magnetic resonance imaging, the objective was to characterize similarities or differences in movement-related activation patterns in patients chronically disabled by cortical plus subcortical or subcortical lesions only. Brain activation was mapped during paretic and non-paretic movement in 11 patients with subcortical stroke, in nine patients with stroke involving sensorimotor cortex, and in eight healthy volunteers. Patient groups had similar average motor deficit as measured by a battery of scores and strength measures. Substantial differences between patients groups were found in activation patterns associated with paretic limb movement: Whereas contralateral motor cortex, ipsilateral cerebellum (relative to moving limb), bilateral mesial (cingulate, SMA), and perisylvian regions were active in subcortical stroke, cortical patients recruited only ipsilateral postcentral mesial hemisphere regions, and areas at the rim of the stroke cavity. For both groups, activation in ipsilateral postcentral cortex correlated with motor function; in subcortical stroke, the same was found for mesial and perisylvian regions. Overall, brain activation in cortical stroke was less, while in subcortical patients, more than in healthy controls. For non-paretic movement, activation patterns were similar to control in cortical patients. In subcortical patients, however, activation patterns differed: the activation of non-paretic movement was similar to that of paretic movement (corrected for side). The data demonstrate more differences than similarities in the central control of paretic and non-paretic limb movement in patients chronically disabled by subcortical versus cortical stroke. Whereas standard motor circuitry is utilized in subcortical stroke, alternative networks are recruited after cortical stroke. This finding proposes lesion-specific mechanisms of reorganization. Optimal activation of these distinct networks may require different rehabilitative strategies.
AB - Recovery of motor function after stroke is associated with reorganization in central motor networks. Functional imaging has demonstrated recovery-dependent alterations in brain activation patterns when compared to healthy controls. These alterations are variable across stroke subjects. Factors identified as contributing to this variability are the degree of functional impairment, the time interval since stroke, and rehabilitative therapies. Here, the hypothesis is tested that lesion location influences the activation patterns. Using functional magnetic resonance imaging, the objective was to characterize similarities or differences in movement-related activation patterns in patients chronically disabled by cortical plus subcortical or subcortical lesions only. Brain activation was mapped during paretic and non-paretic movement in 11 patients with subcortical stroke, in nine patients with stroke involving sensorimotor cortex, and in eight healthy volunteers. Patient groups had similar average motor deficit as measured by a battery of scores and strength measures. Substantial differences between patients groups were found in activation patterns associated with paretic limb movement: Whereas contralateral motor cortex, ipsilateral cerebellum (relative to moving limb), bilateral mesial (cingulate, SMA), and perisylvian regions were active in subcortical stroke, cortical patients recruited only ipsilateral postcentral mesial hemisphere regions, and areas at the rim of the stroke cavity. For both groups, activation in ipsilateral postcentral cortex correlated with motor function; in subcortical stroke, the same was found for mesial and perisylvian regions. Overall, brain activation in cortical stroke was less, while in subcortical patients, more than in healthy controls. For non-paretic movement, activation patterns were similar to control in cortical patients. In subcortical patients, however, activation patterns differed: the activation of non-paretic movement was similar to that of paretic movement (corrected for side). The data demonstrate more differences than similarities in the central control of paretic and non-paretic limb movement in patients chronically disabled by subcortical versus cortical stroke. Whereas standard motor circuitry is utilized in subcortical stroke, alternative networks are recruited after cortical stroke. This finding proposes lesion-specific mechanisms of reorganization. Optimal activation of these distinct networks may require different rehabilitative strategies.
KW - Cerebellum
KW - Chronic
KW - Functional imaging
KW - Hemiparesis
KW - Sensorimotor cortex
KW - Stroke
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U2 - 10.1016/j.neuroimage.2003.10.026
DO - 10.1016/j.neuroimage.2003.10.026
M3 - Article
C2 - 15006659
AN - SCOPUS:1542346245
SN - 1053-8119
VL - 21
SP - 924
EP - 935
JO - NeuroImage
JF - NeuroImage
IS - 3
ER -