1300 Distinctive Spatial Distributions of Motor Cortex Oscillatory Dynamics After Subthalamic Nucleus Deep Brain Stimulation in Parkinson’s Disease

INTRODUCTION: Subthalamic Nucleus Deep Brain Stimulation (STN-DBS) in Parkinson’s Disease (PD) involves disruption of motor cortex-STN synchrony of beta-band oscillations. However, precise neural substrates within the motor cortex where such oscillatory fluctuations and their interactions occur are still unknown. Understanding spatial-temporal dynamics shared across cortex and basal ganglia would be crucial for improving DBS surgical targeting strategies. METHODS: In a PD patient undergoing STN-DBS electrode implantation, the right STN was stimulated with different amplitudes, and respective volumes of tissue activation (VTA) were modeled. The degree of motor STN subregion stimulated (%) from VTA was calculated. In parallel, 1024-contact electrocorticography (ECoG) array was placed on the ipsilateral M1 during STN stimulation. Relative to DBS-OFF condition, changes in ECoG spectral power across five canonical frequency bands (alpha, low-beta, high-beta, gamma) were evaluated. Finally, changes in ECoG power and the degree of motor STN stimulated were correlated, and their correlation-coefficient was mapped across the array channels. RESULTS: With more motor STN subregion stimulated, the mean power in M1 gamma-band oscillations increased (r=0.61,p=0.04), and a nonsignificant trend of decreased beta-band oscillations was observed (r=-0.19, p=0.56 for low beta, r=-0.29, p=0.36 for high beta). Across the entire cortical array, increased STN stimulation was associated with decreased low beta-band power in the medial portion of M1, but in the lateral portion of M1 for high beta-band power. A global increase in gamma-band power was observed across the entire medial-lateral axis of M1. CONCLUSIONS: Our findings suggest that STN-DBS yields distinctive spatial dynamics of low and high beta-band power. These fluctuations are inverted and varied across the medial-lateral axis of M1. Parcellating the cortical response to STN-DBS can elucidate the precise mechanisms of STN-DBS to augment its clinical efficacy.