Abstract

Introduction Local field potential (LFP) recordings from implanted deep brain stimulator (DBS) leads can provide insight into the pathogenesis of the Parkinson’s disease (PD) specifically by looking at some of the local network properties at the location of the electrode. We recorded LFP activity from DBE leads implanted in the subthalamic nucleus (STN) and performed subsequent data analysis on PD patients undergoing DBS surgery in the off state both at rest and during continuous movement of the contralateral hand in order to identify any reproducible pathophysiological signatures of the disease. Methods LFPs were recorded in 8 patients with PD who underwent bilateral DBS lead implantation within the STN. Following DBS lead placement, bipolar (0–1, 1–2, 2–3) recordings were performed for 2 min at rest and another 2 min with contralateral repetitive hand grasp movements. All recordings were performed in the off state with at least 12 h of since their last medication and prior to macrostimulation testing in the nucleus. The raw LFP recordings were transformed to the frequency domain via the fast fourier transform and then a power spectral was generated from that data with a frequency resolution of 1.3 Hz. Beta-band spectral peaks were located and compared between the two testing states. Results In all patients, predominance of both low and high beta band frequencies (13–20 and 20–35 Hz respectively) were observed both at rest and during movement at the DBS contact where stimulation was deemed to be most therapeutic. Paradoxically, stronger beta peak energy was noted during movement as opposed to the rest state in all patients. Conclusion In patients with PD, excess beta band coupling that paradoxically synchronizes with movement may be a signature of the off state. This excess beta band activity appears to also correlate with the most active DBS lead contact. This increase in energy, or synchronization, during the movement phase is in contrast to what happens in the cortex during similar EEG analysis. This increase in the abnormal beta energy, in PD patients, may help explain the abnormal movements, such as rigidity and bradykinesia, seen in these patients. Further investigations may to help to identify and provide stimulation in situations where excess beta band activity is prevalent at the active contact.

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