Evaluation of lower limb cross planar kinetic connectivity signatures post-stroke.

J Biomech

Northwestern University Interdepartmental Neuroscience, Northwestern University, Chicago, IL, USA; Department of Biomedical Engineering, Northwestern University, Chicago, IL, USA; Sensory Motor Performance Program, Rehabilitation Institute of Chicago, Chicago, IL, USA.

Published: March 2014

Following stroke, aberrant three dimensional multijoint gait impairments emerge that present in kinematic asymmetries such as circumduction. A precise pattern of cross-planar coordination may underlie abnormal hemiparetic gait as several studies have underscored distinctive neural couplings between medio-lateral control and sagittal plane progression during walking. Here we investigate potential neuromechanical constraints governing abnormal multijoint coordination post-stroke. 15 chronic monohemispheric stroke patients and 10 healthy subjects were recruited. Coupled torque production patterns were assessed using a volitional isometric torque generation task where subjects matched torque targets for a primary joint in 4 directions while receiving visual feedback of the magnitude and direction of the torque. Secondary torques at other lower limb joints were recorded without subject feedback. We find that common features of cross-planar connectivity in stroke subjects include statistically significant frontal to sagittal plane kinetic coupling that overlay a common sagittal plane coupling in healthy subjects. Such coupling is independent of proximal or distal joint control and limb biomechanics. Principal component analysis of the stroke aggregate kinetic signature reveals unique abnormal frontal plane coupling features that explain a larger percentage of the total torque coupling variance. This study supports the idea that coupled cross-planar kinetic outflow between the lower limb joints uniquely emerges during pathological control of frontal plane degrees of freedom resulting in a generalized extension of the limb. It remains to be seen if a pattern of lower limb motor outflow that is centrally mediated contributes to abnormal hemiparetic gait.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4073298PMC
http://dx.doi.org/10.1016/j.jbiomech.2014.01.025DOI Listing

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