Separating the aperiodic and periodic components of neural activity in Parkinson's disease.

Most studies on electrophysiology have not separated aperiodic activity from the spectra but have rather evaluated a combined periodic oscillatory component and the aperiodic component. As the understanding of aperiodic activity gradually deepens, its potential physiological significance has acquired increased appreciation. Herein, we investigated the two components in scalp electroencephalogram in 16 healthy controls and 15 patients with Parkinson's disease (PD); the results revealed that aperiodic parameters were approximately symmetrically distributed in topography in patients with PD and were significantly modulated by dopaminergic medication in channels C4, C3, CP5 and FC5. In sum, our findings might provide indicators for evaluating treatment response in PD and highlight the importance of re-evaluating the neuronal power spectra parameterization.

Subthalamic nucleus dynamics track microlesion effect in Parkinson's disease.

Parkinson's Disease (PD) is characterized by the temporary alleviation of motor symptoms following electrode implantation (or nucleus destruction), known as the microlesion effect (MLE). Electrophysiological studies have explored different PD stages, but understanding electrophysiological characteristics during the MLE period remains unclear. The objective was to examine the characteristics of local field potential (LFP) signals in the subthalamic nucleus (STN) during the hyperacute period following implantation (within 2 days) and 1 month post-implantation. 15 patients diagnosed with PD were enrolled in this observational study, with seven simultaneous recordings of bilateral STN-LFP signals using wireless sensing technology from an implantable pulse generator. Recordings were made in both on and off medication states over 1 month after implantation. We used a method to parameterize the neuronal power spectrum to separate periodic oscillatory and aperiodic components effectively. Our results showed that beta power exhibited a significant increase in the off medication state 1 month after implantation, compared to the postoperative hyperacute period. Notably, this elevation was effectively attenuated by levodopa administration. Furthermore, both the exponents and offsets displayed a decrease at 1 month postoperatively when compared to the hyperacute postoperative period. Remarkably, levodopa medication exerted a modulatory effect on these aperiodic parameters, restoring them back to levels observed during the hyperacute period. Our findings suggest that both periodic and aperiodic components partially capture distinct electrophysiological characteristics during the MLE. It is crucial to adequately evaluate such discrepancies when exploring the mechanisms of MLE and optimizing adaptive stimulus protocols.