• Jingchun Liu, Wen Qin, Jing Zhang, Xuejun Zhang, and Chunshui Yu.
• From the Departments of Radiology and Tianjin Key Laboratory of Functional Imaging (J.L., W.Q., J.Z., C.Y.), Tianjin Medical University General Hospital, Tianjin, China; and Department of Medical Imaging, School of Medical Imaging, Tianjin Medical University, Tianjin, China (X.Z.).
• Stroke. 2015 Apr 1; 46 (4): 1045-51.

Background And PurposeMotor 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.MethodsTwenty 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.ResultsCompared 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.ConclusionsOur 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.© 2015 American Heart Association, Inc.

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