Stroke-related differences in axial body segment coordination during preplanned and reactive changes in walking direction

• Published in: Experimental brain research Vol. 202; no. 3; pp. 591 - 604
• Main Authors: Hollands, Kristen L, van Vliet, Paulette, Zietz, Doerte, Wing, Alan, Wright, Christine, Hollands, Mark A
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Berlin/Heidelberg : Springer-Verlag 01.05.2010; Springer-Verlag; Springer; Springer Nature B.V
• Subjects: Aged; Aged, 80 and over; Biomechanics; Biomedical and Life Sciences; Biomedicine; Brain Infarction - pathology; Brain Infarction - physiopathology; Female; Gait; Gait - physiology; Gait Disorders, Neurologic - diagnosis; Gait Disorders, Neurologic - etiology; Gait Disorders, Neurologic - physiopathology; Humans; Male; Middle Aged; Neurology; Neurosciences; Orientation - physiology; Paresis - etiology; Paresis - physiopathology; Physiological aspects; Research Article; Stroke; Stroke (Disease); Stroke - complications; Walking; United Kingdom; United Kingdom > UK; Hemiparesis; Walking; Locomotion; Basal ganglia; Cerebrovascular; Steering
• ISSN: 0014-4819; 1432-1106
• DOI: 10.1007/s00221-010-2162-1

This study quantitatively describes differences between participants with hemiparetic stroke and age-matched healthy participants in axial body segment and gait kinematics during a direction change task. Participants were required to change walking direction by 45°, either to their left or right, at the midpoint of a 6-m path. Participants were visually cued either at the start of the walk (pre-planned) or one stride before they reached the turn point (reactive). The sequence and inter-segmental timing of axial orientation onset was preserved in participants with stroke. Analysis of a subgroup of stroke survivors indicated that participants with lesions affecting the basal ganglia (BG) took significantly longer time than control participants to initiate the reorientation synergy when making turns to their non-paretic side. We hypothesize that these differences are a product of asymmetrical activity of dopaminergic pathways in the brain resulting from compromised BG function.