Amplitude and frequency modulation of subthalamic beta oscillations as biomarkers of the dopaminergic state in Parkinson’s disease

ABSTRACTBackgroundMotor and cognitive dysfunction has been linked in patients with Parkinson’s disease (PD). EEG theta and beta rhythms are reliably associated with cognitive and motor functions, respectively. We tested the hypothesis that PD patients with lower-limb abnormalities would exhibit abnormal beta and theta rhythms in the mid-frontal region during action initiation.MethodsWe recruited thirty-nine subjects, including PD patients with FOG (PDFOG+; n=13) and without FOG (PDFOG−; n=13), and demographically-matched healthy subjects (n=13). Scalp electroencephalogram (EEG) signals were collected during a lower-limb pedaling motor task, which required intentional initiation and stopping of a motor movement.ResultsFOG scores were correlated with disease severity and cognition. PDFOG+ patients pedaled with reduced speed and decreased acceleration compared to PDFOG− patients and to controls. PDFOG+ patients exhibited attenuated theta-band (4-8 Hz) power and increased beta-band (13-30 Hz) power at mid-frontal electrode Cz during pedaling. Frontal theta- and beta-band oscillations also correlated with lower-limb movement in PD patients.ConclusionsFrontal theta and beta oscillations are predictors of lower-limb motor symptoms in PD. These data provide insight into the mechanism of lower-limb dysfunction in PD, and could be used to design neuromodulation for PD-related lower-limb abnormalities.

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Neurofeedback linked suppression of subthalamic beta oscillations speeds up movement initialisation in Parkinsonian Patients

10.1101/687582 ◽

2019 ◽

Cited By ~ 1

Author(s):

Shenghong He ◽

Abteen Mostofi ◽

Emilie Syed ◽

Flavie Torrecillos ◽

Gerd Tinkhauser ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Reaction Time ◽

Brain Stimulation ◽

Average Power ◽

Field Potential ◽

Beta Activity ◽

Neurofeedback Training ◽

Beta Oscillations ◽

Time Dynamics

AbstractEnhanced beta oscillations (13-30 Hz) in the subthalamic nucleus (STN) have been associated with clinical impairment in Parkinson’s disease (PD), such as rigidity and slowing of movement, with the suppression of STN beta activity through medication or deep brain stimulation correlating with improvement in these symptoms. Recent studies have also emphasized the importance of the time dynamics of the STN beta oscillations in the pathology of PD. An increased probability of prolonged beta bursts, defined as periods when beta band power exceeds a certain threshold, was more closely related to motor symptoms than average power; and the occurrence of beta bursts just before a go cue slows cued movements. Here we adopted a sequential neurofeedback-behaviour task paradigm to investigate whether patients with PD can learn to suppress pathological beta oscillations recorded from STN with neurofeedback training and whether the training improves the motor performance. Results from twelve patients showed that, compared with the control condition, the neurofeedback training led to reduced incidence and duration of beta bursts in the STN local field potential (LFP) and also reduced the synchrony between the STN LFP and cortical activities measured through EEG in the beta frequency band. The changes were accompanied by a reduced reaction time in cued movements. These results suggest that volitional suppression of beta bursts facilitated by neurofeedback training could help improve movement initialisation in Parkinson’s disease.Significance StatementOur study suggests that a neurofeedback paradigm which focuses on the time dynamics of the target neural signal can facilitate volitional suppression of pathological beta oscillations in the STN in Parkinson’s disease. Neurofeedback training was accompanied by reduced reaction time in cued movements, but associated with increased tremor in tremulous patients. The results strengthen the link between subthalamic beta oscillations and motor impairment, and also suggest that different symptom-specific neural signals could be targeted to improve neuromodulation strategies, either through brain stimulation or neurofeedback training, for patients with tremor and bradykinesia-rigidity.

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Lactiplantibacillus plantarum PS128 Alleviates Exaggerated Cortical Beta Oscillations and Motor Deficits in the 6-Hydroxydopamine Rat Model of Parkinson’s Disease

Probiotics and Antimicrobial Proteins ◽

10.1007/s12602-021-09828-x ◽

2021 ◽

Author(s):

Yi-Fan Ma ◽

Yi-An Lin ◽

Chin-Lin Huang ◽

Chih-Chieh Hsu ◽

Sabrina Wang ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Rat Model ◽

Motor Deficits ◽

Beta Oscillations ◽

6 Hydroxydopamine

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Emergence of Beta Oscillations of a Resonance Model for Parkinson’s Disease

Neural Plasticity ◽

10.1155/2020/8824760 ◽

2020 ◽

Vol 2020 ◽

pp. 1-15

Author(s):

Yaqian Chen ◽

Junsong Wang ◽

Yanmei Kang ◽

Muhammad Bilal Ghori

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Hopf Bifurcation ◽

Center Manifold ◽

Beta Oscillations ◽

Resonance Model ◽

Form Analysis ◽

Center Manifold Theorem ◽

Analysis Center ◽

Insight Into

In Parkinson’s disease, the excess of beta oscillations in cortical-basal ganglia (BG) circuits has been correlated with normal movement suppression. In this paper, a physiologically based resonance model, generalizing an earlier model of the STN-GPe circuit, is employed to analyze critical dynamics of the occurrence of beta oscillations, which correspond to Hopf bifurcation. With the experimentally measured parameters, conditions for the occurrence of Hopf bifurcation with time delay are deduced by means of linear stability analysis, center manifold theorem, and normal form analysis. It is found that beta oscillations can be induced by increasing synaptic transmission delay. Furthermore, it is revealed that the oscillations originate from interaction among different synaptic connections. Our analytical results are consistent with the previous experimental and simulating findings, thus may provide a more systematic insight into the mechanisms underlying the transient beta bursts.

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Pallidal Deep-Brain Stimulation Disrupts Pallidal Beta Oscillations and Coherence with Primary Motor Cortex in Parkinson's Disease

Journal of Neuroscience ◽

10.1523/jneurosci.0431-18.2018 ◽

2018 ◽

Vol 38 (19) ◽

pp. 4556-4568 ◽

Cited By ~ 36

Author(s):

Doris D. Wang ◽

Coralie de Hemptinne ◽

Svjetlana Miocinovic ◽

Jill L. Ostrem ◽

Nicholas B. Galifianakis ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Deep Brain Stimulation ◽

Motor Cortex ◽

Brain Stimulation ◽

Primary Motor Cortex ◽

Beta Oscillations ◽

Pallidal Deep Brain Stimulation ◽

Deep Brain

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Nonsinusoidal oscillations underlie pathological phase-amplitude coupling in the motor cortex in Parkinson’s disease

10.1101/049304 ◽

2016 ◽

Cited By ~ 6

Author(s):

Scott R. Cole ◽

Erik J. Peterson ◽

Roemer van der Meij ◽

Coralie de Hemptinne ◽

Philip A. Starr ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Basal Ganglia ◽

Motor Cortex ◽

Field Potential ◽

Synaptic Activity ◽

Motor Deficit ◽

Beta Oscillations ◽

High Gamma ◽

Phase Amplitude

AbstractParkinson’s disease (PD) is associated with abnormal beta oscillations (13-30 Hz) in the basal ganglia and motor cortex (M1). Recent reports show that M1 beta-high gamma (50-200 Hz) phase-amplitude coupling (PAC) is exaggerated in PD and is reduced following acute deep brain stimulation (DBS). Here we analyze invasive M1 electrocorticography recordings in PD patients on and off DBS, and in isolated cervical dystonia patients, and show that M1 beta oscillations are nonsinusoidal, having sharp and asymmetric features. These sharp oscillatory beta features underlie the previously reported PAC, providing an alternative to the standard interpretation of PAC as an interaction between two distinct frequency components. Specifically, the ratio between peak and trough sharpness is nearly perfectly correlated with beta-high gamma PAC (r = 0.96) and predicts PD-related motor deficit. Using a simulation of the local field potential, we demonstrate that sharp oscillatory waves can arise from synchronous synaptic activity. We propose that exaggerated beta-high gamma PAC may actually reflect such synchronous synaptic activity, manifesting as sharp beta oscillations that are “smoothed out” with DBS. These results support the “desynchronization” hypothesis of DBS wherein DBS counteracts pathological synchronization throughout the basal ganglia-thalamocortical loop. We argue that PAC can be influenced by more than one mechanism. In this case synaptic synchrony, rather than the often assumed spike-field coherence, may underlie exaggerated PAC. These often overlooked temporal features of the oscillatory waveform carry critical physiological information about neural processes and dynamics that may lead to better understanding of underlying neuropathology.

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