The effect of L-dopa and DBS on cortical oscillations in Parkinson's disease analyzed by hidden Markov model...

Parkinson's disease (PD) is a movement disorder caused by dopaminergic neurodegeneration. Both Levodopa (L-dopa) and Subthalamic Deep Brain Stimulation (STN-DBS) effectively alleviate symptoms, yet their cerebral effects remain under-explored. Understanding these effects is essential for optimizing treatment strategies and assessing disease severity. Magnetoencephalogram (MEG) data provide a continuous time series signal that reflects the dynamic changes in brain activity. The hidden Markov model (HMM) can capture and model the temporal features and underlying states of the MEG signal to extract potential brain states and monitor dynamic changes. In this study, we employed HMM to investigate the cortical mechanism underlying the treatment of PD patients using MEG recordings.

21 PD patients treated with medication underwent MEG recording in both L-dopa medoff and medon conditions. Additionally, 11 PD patients receiving STN-DBS treatment underwent MEG recording in both dbsoff and dbson conditions. The MEG data were segmented into four states by Time-delay embedded Hidden Markov Model (TDE-HMM) algorithm. The state parameters including Fractional Occupancy (FO), Interval Times (IT), and Life Time (LT) for each state and power spectrum of β band were analyzed to study the effects of L-dopa and STN-DBS treatment respectively.

L-dopa significantly increased the motor state of HMM and power in the motor area of both high β (21-35 Hz) and low β (13-20 Hz); the motor state of high β in medoff were correlated with the Unified Parkinson's Disease Rating Scale III (UPDRS III). Conversely, DBS significantly diminishes the motor state of HMM and power in motor area of high β oscillations. The score changes of tremor and limb rigidity after DBS treatment were significantly correlated with the changes of motor state of high β.

This study demonstrates that L-dopa and STN-DBS exert differing effects on β oscillations in the motor cortex of PD patients, primarily in high β band. Understanding these distinct neurophysiological impacts can provide valuable insights for refining therapeutic approaches in motor control for PD patients.