Open AccessTopographic Evolution of Anterior Cerebral Artery Infarction and Its Impact on Motor Impairment
Author(s) -
Tharani Thirugnanachandran,
Henry Ma,
Jason Vuong,
Melissa Mitchell,
Chloe Wong,
Shaloo Singhal,
LeeAnne Slater,
Richard Beare,
Velandai Srikanth,
Thanh G. Phan
Publication year - 2021
Publication title -
cerebrovascular diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.221
H-Index - 104
eISSN - 1421-9786
pISSN - 1015-9770
DOI - 10.1159/000519134
Subject(s) - medicine , supplementary motor area , sma* , interquartile range , magnetic resonance imaging , stroke (engine) , anterior cerebral artery , premotor cortex , lesion , middle cerebral artery , motor cortex , primary motor cortex , infarction , physical medicine and rehabilitation , cardiology , ischemia , radiology , functional magnetic resonance imaging , surgery , anatomy , dorsum , mechanical engineering , mathematics , combinatorics , stimulation , myocardial infarction , engineering
Motor deficit is common following anterior cerebral artery (ACA) stroke. This study aimed to determine the impact on the motor outcome, given the location of descending corticofugal fiber tracts (from the primary motor cortex [M1], dorsal and ventral premotor area [PMdv], and supplementary motor area [SMA]) and the regional variations in collateral support of the ACA territory. Methods: Patients with ACA vessel occlusion were included. Disruption to corticofugal fibers was inferred by overlap of tracts with a lesion on computed tomography perfusion at the onset and on magnetic resonance imaging (MRI) poststroke. The motor outcome was defined by dichotomized and combined National Institute of Health Stroke Scale (NIHSS) sub-scores for the arm and leg. Multivariate hierarchical partitioning was used to analyze the proportional contribution of the corticofugal fibers to the motor outcome. Results: Forty-seven patients with a median age of 77.5 (interquartile range 68.0–84.5) years were studied. At the stroke onset, 96% of patients showed evidence of motor deficit on the NIHSS, and the proportional contribution of the corticofugal fibers to motor deficit was M1-33%, SMA-33%, and PMdv-33%. By day 7, motor deficit was present in <50% of patients and contribution of M1 fiber tracts to the motor deficit was reduced (M1-10.2%, SMA-61.0%, PMdv-28.8%). We confirmed our findings using publicly available high-resolution templates created from Human Connectome Project data. This also showed a reduction in involvement of M1 fiber tracts on initial perfusion imaging (33%) compared to MRI at a median time of 7 days poststroke (11%). Conclusion: Improvements in the motor outcome seen in ACA stroke may be due to the relative sparing of M1 fiber tracts from infarction. This may occur as a consequence of the posterior location of M1 fiber tracts and the evolving topography of ACA stroke due to the compensatory capacity of leptomeningeal anastomoses.