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Waveform changes with the evolution of beta bursts in the human subthalamic nucleus.

ABSTRACT: OBJECTIVE:Phasic bursts of beta band synchronisation have been linked to motor impairment in Parkinson's disease (PD). However, little is known about what terminates bursts. METHODS:We used the Hilbert-Huang transform to investigate beta bursts in the local field potential recorded from the subthalamic nucleus in nine patients with PD on and off levodopa. RESULTS:The sharpness of the beta waveform extrema fell as burst amplitude dropped. Conversely, an index of phase slips between waveform extrema, and the power of concurrent theta activity increased as burst amplitude fell. Theta activity was also increased on levodopa when beta bursts were attenuated. These phenomena were associated with reduction in coupling between beta phase and high gamma activity amplitude. We discuss how these findings may suggest that beta burst termination is associated with relative desynchronization of the beta drive, increase in competing theta activity and increased phase slips in the beta activity. CONCLUSIONS:We characterise the dynamical nature of beta bursts, thereby permitting inferences about underlying activities and, in particular, about why bursts terminate. SIGNIFICANCE:Understanding the dynamical nature of beta bursts may help point to interventions that can cause their termination and potentially treat motor impairment in PD.

SUBMITTER: Yeh CH

PROVIDER: S-EPMC7115847 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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Waveform changes with the evolution of beta bursts in the human subthalamic nucleus.

Yeh Chien-Hung CH Al-Fatly Bassam B Kühn Andrea A AA Meidahl Anders C AC Tinkhauser Gerd G Tan Huiling H Brown Peter P

Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology 20200629 9

<h4>Objective</h4>Phasic bursts of beta band synchronisation have been linked to motor impairment in Parkinson's disease (PD). However, little is known about what terminates bursts.<h4>Methods</h4>We used the Hilbert-Huang transform to investigate beta bursts in the local field potential recorded from the subthalamic nucleus in nine patients with PD on and off levodopa.<h4>Results</h4>The sharpness of the beta waveform extrema fell as burst amplitude dropped. Conversely, an index of phase slips ...[more]

PMID: 32682236

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Project description:No biomarker of Parkinson's disease exists that allows clinicians to adjust chronic therapy, either medication or deep brain stimulation, with real-time feedback. Consequently, clinicians rely on time-intensive, empirical, and subjective clinical assessments of motor behaviour and adverse events to adjust therapies. Accumulating evidence suggests that hypokinetic aspects of Parkinson's disease and their improvement with therapy are related to pathological neural activity in the beta band (beta oscillopathy) in the subthalamic nucleus. Additionally, effectiveness of deep brain stimulation may depend on modulation of the dorsolateral sensorimotor region of the subthalamic nucleus, which is the primary site of this beta oscillopathy. Despite the feasibility of utilizing this information to provide integrated, biomarker-driven precise deep brain stimulation, these measures have not been brought together in awake freely moving individuals. We sought to directly test whether stimulation-related improvements in bradykinesia were contingent on reduction of beta power and burst durations, and/or the volume of the sensorimotor subthalamic nucleus that was modulated. We recorded synchronized local field potentials and kinematic data in 16 subthalamic nuclei of individuals with Parkinson's disease chronically implanted with neurostimulators during a repetitive wrist-flexion extension task, while administering randomized different intensities of high frequency stimulation. Increased intensities of deep brain stimulation improved movement velocity and were associated with an intensity-dependent reduction in beta power and mean burst duration, measured during movement. The degree of reduction in this beta oscillopathy was associated with the improvement in movement velocity. Moreover, the reduction in beta power and beta burst durations was dependent on the theoretical degree of tissue modulated in the sensorimotor region of the subthalamic nucleus. Finally, the degree of attenuation of both beta power and beta burst durations, together with the degree of overlap of stimulation with the sensorimotor subthalamic nucleus significantly explained the stimulation-related improvement in movement velocity. The above results provide direct evidence that subthalamic nucleus deep brain stimulation-related improvements in bradykinesia are related to the reduction in beta oscillopathy within the sensorimotor region. With the advent of sensing neurostimulators, this beta oscillopathy combined with lead location could be used as a marker for real-time feedback to adjust clinical settings or to drive closed-loop deep brain stimulation in freely moving individuals with Parkinson's disease.

Dataset Information

Waveform changes with the evolution of beta bursts in the human subthalamic nucleus.

Publications

Waveform changes with the evolution of beta bursts in the human subthalamic nucleus.

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