期刊
STROKE
卷 46, 期 4, 页码 1045-1051出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/STROKEAHA.114.007044
关键词
cerebral infarction; diffusion tensor imaging; functional neuroimaging; magnetic resonance imaging; motor cortex; neuronal plasticity
资金
- National Basic Research Program of China (973 program) [2011CB707804]
- Natural Science Foundation of China [81425013, 91332113, 81271564]
- Natural Science Foundation of Tianjin [12JCZDJC23800]
Background and Purpose-Motor recovery after stroke has been shown to be correlated with both the fractional anisotropy (FA) of the affected corticospinal tract (CST) and the interhemispheric resting-state functional connectivity (rsFC) of the primary motor cortex (M1). However, the role of the restoration or enhancement of the M1-M1 rsFC in motor recovery remains largely unknown. We aimed to clarify this issue by investigating the correlations between the M1-M1 rsFC and the integrity of the M1-M1 anatomic connection and the affected CST in chronic subcortical stroke patients with good motor outcomes. Methods-Twenty patients and 16 healthy controls underwent multimodal magnetic resonance imaging examinations. Diffusion tensor imaging was used to reconstruct the M1-M1 anatomic connection and bilateral CSTs. White matter integrity of these tracts was assessed using FA. Resting-state functional magnetic resonance imaging was used to calculate M1-M1 rsFC. Group differences in these measures were compared. Correlations between M1-M1 rsFC and FA of the M1-M1 anatomic connection and the affected CST were analyzed in patients with stroke. Results-Compared with healthy controls, patients with stroke exhibited significantly reduced FA in the affected CST and the M1-M1 anatomic connection and a significantly increased M1-M1 rsFC. The FA values of the affected CST were positively correlated with the M1-M1 anatomic connection, and these FA values were negatively correlated with the M1-M1 rsFC in these patients. Conclusions-Our findings suggest that the M1-M1 anatomic connection impairment is secondary to CST damage, and the M1-M1 rsFC enhancement may reflect compensatory or reactive neural plasticity in stroke patients with CST impairment.
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