Introduction
Stroke is one of the major diseases that cause long-term motor deficits of adults (1). However, our poor understanding of the mechanisms underlying motor impairments after stroke limits greatly the development of effective intervention and evaluation methods. In general, motor impairments after stroke are deemed to arise from changes in both neural and muscle properties. Poststroke changes in the neural system have been studied from different points of view such as the decreased excitability of the affected cortex (2, 3) and the increased inhibitory effect from the unaffected hemisphere on the affected hemisphere (4). Spasm and flaccid paresis of muscles are believed to result from the loss of control input from the brain at different phases after stroke. Even though stroke survivors have been demonstrated to have significant descending information flow in the affected side during the chronic period (5), there is evidence that poststroke impairments reflect the reduced central neural drive to muscles. Mima et al. and Fang et al. found that the functional coupling between cortical commands and consequent muscle activities of stroke subjects were weaker than that of healthy controls (6, 7). The conduction time from the central cortical rhythm to peripheral oscillations in the affected side was significantly prolonged compared with that of the unaffected side after stroke (8).
It is believed that stroke interrupts the motor-related neural network and then reduces the neural drive to the muscles. The coherent activities between the motor cortex and the muscles are believed to reflect the synchronized discharge of corticospinal cells (9). It can be estimated by analyzing the frequency domain coherence (10) between electromyography (EMG) and electroencephalography (EEG) signals termed as corticomuscular coherence (CMC). Although previous studies have demonstrated that the CMC strength of poststroke subjects was weaker than that of healthy controls, it is still not clear whether the corticomuscular coupling will enhance along with the motor function recovery to directly reflect the motor function state of paretic limbs after stroke. In the current study, a poststroke patient was recruited to participate in two times of experiments involving an elbow flexion task. The time interval between two times of experiments was determined to guarantee that the patient had obtained an obvious motor function recovery of the affected upper extremity. CMC from two times of experiments was estimated and compared to verify whether motor function recovery can be reflected by the change of corticomuscular coupling strength.
Backgrounds
Experiment and Subject
An elbow flexion task was designed for the stroke patient because only poor rehabilitation outcomes can be generally obtained for hand. The force applied by the elbow flexion was monitored by a strain gage and fed back to the patient visually to help him finish the task with moderate and constant muscle contractions (11), because coherence analyses (12, 13) have demonstrated that the coupling is most pronounced in the beta-band range during steady muscle contractions and the beta-band CMC is assumed to be associated with strategies for controlling submaximal muscle forces (12, 14, 15). The designed motion task and the visual feedback information on screen are illustrated in Figures 1A,B, respectively. A trial was initiated when a circle and a target ring showed on screen and was over when they disappeared. Each trial lasted 11 s and there was a 2-s long interval between adjacent trials. Each run contained 20 trials and each side of upper limbs performed two runs, respectively. The subject practiced before data recording until the target force could be reached within the first 2 s of each trial.
TBI Rehabilitation 