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Abstract
ABSTRACTBackgroundExaggerated oscillatory activity in the beta frequency band in the subthalamic nucleus has been suggested to be related to bradykinesia in Parkinson's disease (PD). However, studies seeking correlations between such activity in the local field potential and motor performance have been limited to the immediate postoperative period, which may be confounded by a stun effect that leads to the temporary alleviation of PD deficits.MethodsLocal field potentials were recorded simultaneously with motor performance in PD patients several months after neurostimulator implantation. This was enabled by the chronic implantation of a pulse generator with the capacity to record and transmit local field potentials from deep brain stimulation electrodes. Specifically, we investigated oscillatory beta power dynamics and objective measures of bradykinesia during an upper limb alternating pronation and supination task in 9 patients.ResultsAlthough beta power was suppressed during continuously repeated movements, this suppression progressively diminished over time in tandem with a progressive decrement in the frequency and amplitude of movements. The relationship between changes within local field potentials and movement parameters was significant across patients, and not present for theta/alpha frequencies (5‐12 Hz). Change in movement frequency furthermore related to beta power dynamics within patients.ConclusionsChanges in beta power are linked to changes in movement performance and the sequence effect of bradykinesia months after neurostimulator implantation. These findings provide further evidence that beta power may serve as a biomarker for bradykinesia and provide a suitable substrate for feedback control in chronic adaptive deep brain stimulation. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
Highlights
The diagnosis of Parkinson’s disease (PD) is primarily clinical, with bradykinesia being a core diagnostic feature compromising motor function
As expected from studies of separate single movements,[24] beta activity in the subthalamic nucleus (STN) local field potential (LFP) was suppressed during repeated movements
The degree of suppression progressively diminished over time in tandem with a decrement in the frequency and amplitude of repetitive movements. This relationship was absent over theta/alpha band frequencies in line with the inconsistent relationship between such activity in the STN LFP and force generation.[26]
Summary
The diagnosis of Parkinson’s disease (PD) is primarily clinical, with bradykinesia being a core diagnostic feature compromising motor function. The correlations, not significant after corrections for multiple comparisons, were still negative and appreciable (about 20.5 for LFP power over 11-15 Hz and about 20.4 for power over 15-30 Hz), suggesting that increases in beta activity might contribute to bradykinesia Taken together, these studies indicate that the extent to which beta power might serve as a stable biomarker of bradykinesia over time in individual patients remains uncertain. Adaptive DBS must be chronic to be successfully introduced into clinical practice, so it is crucial that beta activity is shown to continue to predict or correlate with objectively recorded bradykinesia a long time after electrode implantation. Such a correlation should be present within (as well as across) patients if betacontrolled adaptive DBS is to be successful. We consider whether changes in beta activity might be related to the progressive reduction in speed and amplitude of repetitive action within a patient—a core component of bradykinesia that we term the sequence effect
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