Background and Purpose: Behavioral outcome after stroke is the product of both neural injury and neural function. Little is known about how injury to the corticospinal tract (CST) affects the function of motor cortex. The purpose of this study was to understand how subcortical injury to the CST affects function and connectivity of motor cortex.
Methods: Patients with chronic hemiparetic stroke completed (1) a 3-minute resting-state EEG recording using a dense-array (256-lead) system, (2) a structural MRI scan, and (3) behavioral testing. Motor cortex activity was defined as EEG power within the high beta (20-30 Hz) frequency band commonly associated with motor network activity. Motor cortex connectivity was defined as coherence in the same frequency band. CST injury was defined as % lesion overlap with CST.
Results: Of the 39 subjects (56 ± 14 years, 10 females, 15 ± 25 months post-stroke), none had injury to ipsilesional primary motor cortex (M1). Spearman correlation analyses revealed that increased CST injury was significantly related to reduced cortical activity in EEG leads overlying M1 (r= -0.48, p <0.002), dorsal premotor cortex (r= -0.41, p= 0.01), and supplementary motor area (r= -0.41, p= 0.01), but not in any other brain region, bilaterally. However, increased CST injury was not associated with any changes in M1 connectivity. Arm motor status (Fugl-Meyer score) tended to be associated with increased CST injury (r= -0.28, p= 0.08) but had no relationship with M1 connectivity.
Conclusions: Increased CST injury after stroke is associated with decreased activity in those motor areas that issue descending fibers via this tract, a finding consistent with prior reports indicating that axonal injury modulates upstream function of surviving cortical elements. Increased CST injury was not associated with changes in M1 connectivity, suggesting a retained capacity for plasticity in support of behavioral recovery.