Lesion Localization of Poststroke Lateropulsion
BACKGROUND AND PURPOSE—Hemispheric stroke studies associating lateropulsion (pusher syndrome) with the location of brain lesions have had mixed results from small, unmatched samples. This study was designed to determine whether lateropulsion localizes to specific brain regions across patients with s...
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Published in: | Stroke (1970) Vol. 50; no. 5; pp. 1067 - 1073 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
American Heart Association, Inc
01-05-2019
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Subjects: | |
Online Access: | Get full text |
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Summary: | BACKGROUND AND PURPOSE—Hemispheric stroke studies associating lateropulsion (pusher syndrome) with the location of brain lesions have had mixed results from small, unmatched samples. This study was designed to determine whether lateropulsion localizes to specific brain regions across patients with stroke using a case-control design.
METHODS—Fifty patients with lateropulsion after stroke were matched with 50 stroke patients without lateropulsion using age, time since onset of stroke, admission motor Functional Independence Measure score, lesion side, and gender. The primary analysis included multivariate lesion symptom mapping using sparse canonical correlations to identify regions most associated with lateropulsion as assessed with the Burke Lateropulsion Scale. Secondary analyses included evaluating paired comparisons for lesion volume, degree of motor impairment, motor and cognitive Functional Independence Measure scores.
RESULTS—The lesion symptom mapping analysis of all lesions mapped onto a common hemisphere produced an overall significant model (P<5×10) with a regional peak at the inferior parietal lobe at the junction of the post-central gyrus (Brodmann Area 2) and Brodmann Area 40 as the lesion location most associated with lateropulsion. Lesion volume was larger for patients with lateropulsion. Despite adequate matching, motor performance and total Functional Independence Measure scores differed at a group level between patients with and without lateropulsion.
CONCLUSIONS—This analysis implicated lesion involvement of the inferior parietal lobe as a key neuroanatomical determinant of developing lateropulsion. A better understanding of the anatomic underpinnings of lateropulsion may improve rehabilitation efforts, including the potential for informing noninvasive neuromodulation approaches. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0039-2499 1524-4628 |
DOI: | 10.1161/STROKEAHA.118.023445 |