Characterization of electrocorticogram high-gamma signal in response to varying upper extremity movement velocity

The mechanism by which the human primary motor cortex (M1) encodes upper extremity movement kinematics is not fully understood. For example, human electrocorticogram (ECoG) signals have been shown to modulate with upper extremity movements; however, this relationship has not been explicitly characterized. To address this issue, we recorded high-density ECoG signals from patients undergoing epilepsy surgery evaluation as they performed elementary upper extremity movements while systematically varying movement speed and duration. Specifically, subjects performed intermittent pincer grasp/release, elbow flexion/extension, and shoulder flexion/extension at slow, moderate, and fast speeds. In all movements, bursts of power in the high-$$\gamma $$γ band (80–160 Hz) were observed in M1. In addition, the amplitude of these power bursts and the area of M1 with elevated high-$$\gamma $$γ activity were directly proportional to the movement speed. Likewise, the duration of elevated high-$$\gamma $$γ activity increased with movement duration. Based on linear regression, M1 high-$$\gamma $$γ power amplitude and duration covaried with movement speed and duration, respectively, with an average $$r^2$$r2 of $$0.75 \pm 0.10$$0.75±0.10 and $$0.68 \pm 0.21$$0.68±0.21. These findings indicate that the encoding of upper extremity movement speed by M1 high-$$\gamma $$γ activity is primarily linear. Also, the fact that this activity remained elevated throughout a movement suggests that M1 does not merely generate transient instructions for a specific movement duration, but instead is responsible for the entirety of the movement. Finally, the spatial distribution of high-$$\gamma $$γ activity suggests the presence of a recruitment phenomenon in which higher speeds or increased muscle activity involve activation of larger M1 areas.