Literature DB >> 19109546

Association between gait asymmetry and brain lesion location in stroke patients.

Lisa D Alexander1, Sandra E Black, Kara K Patterson, Fuqiang Gao, Cynthia J Danells, William E McIlroy.   

Abstract

BACKGROUND AND
PURPOSE: Associations between the site of brain injury and poststroke gait impairment are poorly understood. Temporal gait asymmetry after stroke is a salient index of gait dysfunction that has important functional consequences. The current study investigated whether subtraction lesion analysis could distinguish brain regions associated with persisting temporal gait asymmetry in chronic stroke patients.
METHODS: Analysis was conducted on 37 chronic ambulatory stroke patients (17 symmetrical gait, 20 asymmetrical gait). Spatiotemporal gait parameters were recorded using an instrumented walking surface. Lesions were traced from 3D T1-MRI, and region of interest images were generated. The lesion overlay of patients with symmetrical gait was subtracted from patients with asymmetrical gait to highlight voxels more frequently lesioned in asymmetrical patients and relatively spared in symmetrical patients.
RESULTS: Demographic data were comparable between the 2 groups. Asymmetrical patients exhibited significantly higher National Institute of Health Stroke Scale neglect scores and more severe motor impairment. Gait asymmetry was significantly correlated to Chedoke-McMaster Stroke Scale leg (r=-0.767, P<0.001) and foot (r=-0.759, P<0.001) scores, whereas gait speed correlated less strongly. After subtraction analysis, injury to the posterolateral putamen was evident 60% to 80% more frequently in the asymmetrical group compared to the symmetrical group.
CONCLUSIONS: In this sample of ambulatory chronic stroke patients, damage to the posterolateral putamen was associated with temporal gait asymmetry. Further advances in our understanding of the neural correlates of gait asymmetry may provide prognostic markers for future persistent gait dysfunction and lead to early targeted rehabilitation when key regions are damaged.

Entities:  

Mesh:

Year:  2008        PMID: 19109546     DOI: 10.1161/STROKEAHA.108.527374

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  35 in total

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