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

2016 ◽  
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.

Correlation between Spike Potential and Field Potential in the Motor Cortex of Rats with Parkinson’s Disease

2018 ◽  
Vol 16 (1) ◽  
Author(s):  
Xiao Zhang ◽  
Xiwen Geng ◽  
Min Li ◽  
Jinlu Xie ◽  
Guangheng Gao ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Cortex ◽  
Field Potential ◽  
Spike Potential

scholarly journals Oscillatory activity in basal ganglia and motor cortex in an awake behaving rodent model of Parkinson's disease

Basal Ganglia ◽  
2014 ◽  
Vol 3 (4) ◽  
pp. 221-227 ◽  
Author(s):  
Claire Delaville ◽  
Ana V. Cruz ◽  
Alex J. McCoy ◽  
Elena Brazhnik ◽  
Irene Avila ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Motor Cortex ◽  
Rodent Model ◽  
Oscillatory Activity

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

2019 ◽  
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.

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

2018 ◽  
Vol 38 (19) ◽  
pp. 4556-4568 ◽  
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

scholarly journals Parkinsonism and vigilance: alteration in neural oscillatory activity and phase-amplitude coupling in the basal ganglia and motor cortex

2017 ◽  
Vol 118 (5) ◽  
pp. 2654-2669 ◽  
Author(s):  
David Escobar Sanabria ◽  
Luke A. Johnson ◽  
Shane D. Nebeck ◽  
Jianyu Zhang ◽  
Matthew D. Johnson ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Neural Activity ◽  
High Frequency ◽  
Closed Loop ◽  
Oscillatory Activity ◽  
Motor Circuit ◽  
Phase Amplitude ◽  
Frequency Power

Oscillatory neural activity in different frequency bands and phase-amplitude coupling (PAC) are hypothesized to be biomarkers of Parkinson’s disease (PD) that could explain dysfunction in the motor circuit and be used for closed-loop deep brain stimulation (DBS). How these putative biomarkers change from the normal to the parkinsonian state across nodes in the motor circuit and within the same subject, however, remains unknown. In this study, we characterized how parkinsonism and vigilance altered oscillatory activity and PAC within the primary motor cortex (M1), subthalamic nucleus (STN), and globus pallidus (GP) in two nonhuman primates. Static and dynamic analyses of local field potential (LFP) recordings indicate that 1) after induction of parkinsonism using the neurotoxin MPTP, low-frequency power (8–30 Hz) increased in the STN and GP in both subjects, but increased in M1 in only one subject; 2) high-frequency power (~330 Hz) was present in the STN in both normal subjects but absent in the parkinsonian condition; 3) elevated PAC measurements emerged in the parkinsonian condition in both animals, but in different sites in each animal (M1 in one subject and GPe in the other); and 4) the state of vigilance significantly impacted how oscillatory activity and PAC were expressed in the motor circuit. These results support the hypothesis that changes in low- and high-frequency oscillatory activity and PAC are features of parkinsonian pathophysiology and provide evidence that closed-loop DBS systems based on these biomarkers may require subject-specific configurations as well as adaptation to changes in vigilance. NEW & NOTEWORTHY Chronically implanted electrodes were used to record neural activity across multiple nodes in the basal ganglia-thalamocortical circuit simultaneously in a nonhuman primate model of Parkinson’s disease, enabling within-subject comparisons of electrophysiological biomarkers between normal and parkinsonian conditions and different vigilance states. This study improves our understanding of the role of oscillatory activity and phase-amplitude coupling in the pathophysiology of Parkinson’s disease and supports the development of more effective DBS therapies based on pathophysiological biomarkers.

scholarly journals Synchrony Drives Motor Cortex Beta Bursting, Waveform Dynamics, and Phase-Amplitude Coupling in Parkinson's Disease

2020 ◽  
Vol 40 (30) ◽  
pp. 5833-5846 ◽  
Author(s):  
Andrew B. O'Keeffe ◽  
Mahsa Malekmohammadi ◽  
Hiro Sparks ◽  
Nader Pouratian
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Cortex ◽  
Phase Amplitude

scholarly journals Subthalamic nucleus activity dynamics and limb movement prediction in Parkinson’s disease

Brain ◽  
2020 ◽  
Vol 143 (2) ◽  
pp. 582-596 ◽  
Author(s):  
Saed Khawaldeh ◽  
Gerd Tinkhauser ◽  
Syed Ahmar Shah ◽  
Katrin Peterman ◽  
Ines Debove ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Subthalamic Nucleus ◽  
Local Field ◽  
Local Field Potential ◽  
Field Potential ◽  
Beta Frequency Band ◽  
Potential Activity ◽  
Beta Frequency

Abstract Whilst exaggerated bursts of beta frequency band oscillatory synchronization in the subthalamic nucleus have been associated with motor impairment in Parkinson’s disease, a plausible mechanism linking the two phenomena has been lacking. Here we test the hypothesis that increased synchronization denoted by beta bursting might compromise information coding capacity in basal ganglia networks. To this end we recorded local field potential activity in the subthalamic nucleus of 18 patients with Parkinson’s disease as they executed cued upper and lower limb movements. We used the accuracy of local field potential-based classification of the limb to be moved on each trial as an index of the information held by the system with respect to intended action. Machine learning using the naïve Bayes conditional probability model was used for classification. Local field potential dynamics allowed accurate prediction of intended movements well ahead of their execution, with an area under the receiver operator characteristic curve of 0.80 ± 0.04 before imperative cues when the demanded action was known ahead of time. The presence of bursts of local field potential activity in the alpha, and even more so, in the beta frequency band significantly compromised the prediction of the limb to be moved. We conclude that low frequency bursts, particularly those in the beta band, restrict the capacity of the basal ganglia system to encode physiologically relevant information about intended actions. The current findings are also important as they suggest that local subthalamic activity may potentially be decoded to enable effector selection, in addition to force control in restorative brain-machine interface applications.

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