Abstract
Walking dysfunction occurs at a very high prevalence in stroke survivors. Human walking is a phenomenon often taken for granted, but it is mediated by complicated neural control mechanisms. The automatic process includes the brainstem descending pathways (RST and VST) and the intraspinal locomotor network. It is known that leg muscles are organized into modules to serve subtasks for body support, posture and locomotion. Major kinematic mechanisms are recognized to minimize the center of gravity (COG) displacement. Stroke leads to damage to motor cortices and their descending corticospinal tracts and subsequent muscle weakness. On the other hand, brainstem descending pathways and the intraspinal motor network are disinhibited and become hyperexcitable. Recent advances suggest that they mediate post-stroke spasticity and diffuse spastic synergistic activation. As a result of such changes, existing modules are simplified and merged, thus leading to poor body support and walking performance. The wide range and hierarchy of post-stroke hemiplegic gait impairments is a reflection of mechanical consequences of muscle weakness, spasticity, abnormal synergistic activation and their interactions. Given the role of brainstem descending pathways in body support and locomotion and post-stroke spasticity, a new perspective of understanding post-stroke hemiplegic gait is proposed. Its clinical implications for management of hemiplegic gait are discussed. Two cases are presented as clinical application examples.
Highlights
Stroke is a leading cause of serious long-term disability (Benjamin et al, 2017)
Gait abnormality is characterized by a pronounced clinical presentation of gait asymmetry, as compared to healthy people (Olney and Richards, 1996; Richards and Olney, 1996)
Falls usually occur during walking in community-dwelling stroke survivors (Hyndman et al, 2002)
Summary
Stroke is a leading cause of serious long-term disability (Benjamin et al, 2017). Walking dysfunction occurs in more than 80% of stroke survivors (Duncan et al, 2005). Stroke survivors with fewer modules on the paretic limb walk more slowly and demonstrate more gait asymmetry (Routson et al, 2014).This modification of modular organization likely reflects the central nervous system’s response to muscle weakness and lack of voluntary muscle control on the affected side to improve body support and locomotion.
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