Beta Rhythm

Research Papers

Showing 6 of 16

Deep brain electrical neurofeedback allows Parkinson patients to control pathological oscillations and quicken movements

Bichsel, Oliver, Stieglitz, Lennart H., Oertel, Markus F., Baumann, Christian R., Gassert, Roger, Imbach, Lukas L. (2021) · Scientific Reports

Parkinsonian motor symptoms are linked to pathologically increased beta-oscillations in the basal ganglia. While pharmacological treatment and deep brain stimulation (DBS) reduce these pathological oscillations concomitantly with improving motor performance, we set out to explore neurofeedback as an endogenous modulatory method. We implemented real-time processing of pathological subthalamic beta oscillations through implanted DBS electrodes to provide deep brain electrical neurofeedback. Patients volitionally controlled ongoing beta-oscillatory activity by visual neurofeedback within minutes of training. During a single one-hour training session, the reduction of beta-oscillatory activity became gradually stronger and we observed improved motor performance. Lastly, endogenous control over deep brain activity was possible even after removing visual neurofeedback, suggesting that neurofeedback-acquired strategies were retained in the short-term. Moreover, we observed motor improvement when the learnt mental strategies were applied 2 days later without neurofeedback. Further training of deep brain neurofeedback might provide therapeutic benefits for Parkinson patients by improving symptom control using strategies optimized through neurofeedback.

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EEG spectral power, but not theta/beta ratio, is a neuromarker for adult ADHD

Kiiski, Hanni, Bennett, Marc, Rueda-Delgado, Laura M., Farina, Francesca R., Knight, Rachel, Boyle, Rory, Roddy, Darren, Grogan, Katie, Bramham, Jessica, Kelly, Clare, Whelan, Robert (2020) · The European Journal of Neuroscience

Adults with attention-deficit/hyperactivity disorder (ADHD) have been described as having altered resting-state electroencephalographic (EEG) spectral power and theta/beta ratio (TBR). However, a recent review (Pulini et al. 2018) identified methodological errors in neuroimaging, including EEG, ADHD classification studies. Therefore, the specific EEG neuromarkers of adult ADHD remain to be identified, as do the EEG characteristics that mediate between genes and behaviour (mediational endophenotypes). Resting-state eyes-open and eyes-closed EEG was measured from 38 adults with ADHD, 45 first-degree relatives of people with ADHD and 51 unrelated controls. A machine learning classification analysis using penalized logistic regression (Elastic Net) examined if EEG spectral power (1-45 Hz) and TBR could classify participants into ADHD, first-degree relatives and/or control groups. Random-label permutation was used to quantify any bias in the analysis. Eyes-open absolute and relative EEG power distinguished ADHD from control participants (area under receiver operating characteristic = 0.71-0.77). The best predictors of ADHD status were increased power in delta, theta and low-alpha over centro-parietal regions, and in frontal low-beta and parietal mid-beta. TBR did not successfully classify ADHD status. Elevated eyes-open power in delta, theta, low-alpha and low-beta distinguished first-degree relatives from controls (area under receiver operating characteristic = 0.68-0.72), suggesting that these features may be a mediational endophenotype for adult ADHD. Resting-state EEG spectral power may be a neuromarker and mediational endophenotype of adult ADHD. These results did not support TBR as a diagnostic neuromarker for ADHD. It is possible that TBR is a characteristic of childhood ADHD.

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Effects of a single session of SMR neurofeedback training on anxiety and cortisol levels

Gadea, Marien, Aliño, Marta, Hidalgo, Vanesa, Espert, Raul, Salvador, Alicia (2020) · Neurophysiologie Clinique = Clinical Neurophysiology

OBJECTIVES: According to some studies, a putatively calming effect of EEG neurofeedback training could be useful as a therapeutic tool in psychiatric practice. With the aim of elucidating this possibility, we tested the efficacy of a single session of ↑sensorimotor (SMR)/↓theta neurofeedback training for mood improvement in 32 healthy men, taking into account trainability, independence and interpretability of the results. METHODS: A pre-post design, with the following dependent variables, was applied: (i) psychometric measures of mood with regards to anxiety, depression, and anger (Profile of Mood State, POMS, and State Trait Anxiety Inventory, STAI); (ii) biological measures (salivary levels of cortisol); (iii) neurophysiological measures (EEG frequency band power analysis). In accordance with general recommendations for research in neurofeedback, a control group receiving sham neurofeedback was included. RESULTS: Anxiety levels decreased after the real neurofeedback and increased after the sham neurofeedback (P<0.01, size effect 0.9 for comparison between groups). Cortisol decreased after the experiment in both groups, though with significantly more pronounced effects in the desired direction after the real neurofeedback (P<0.04; size effect 0.7). The group receiving real neurofeedback significantly enhanced their SMR band (P<0.004; size effect 0.88), without changes in the theta band. The group receiving sham neurofeedback did not show any EEG changes. CONCLUSIONS: The improvement observed in anxiety was greater in the experimental group than in the sham group, confirmed by both subjective (psychometric) measures and objective (biological) measures. This was demonstrated to be associated with the real neurofeedback, though a nonspecific (placebo) effect likely also contributed.

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Neurofeedback-Linked Suppression of Cortical β Bursts Speeds Up Movement Initiation in Healthy Motor Control: A Double-Blind Sham-Controlled Study

He, Shenghong, Everest-Phillips, Claudia, Clouter, Andrew, Brown, Peter, Tan, Huiling (2020) · The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

Abnormally increased β bursts in cortical-basal ganglia-thalamic circuits are associated with rigidity and bradykinesia in patients with Parkinson's disease. Increased β bursts detected in the motor cortex have also been associated with longer reaction times (RTs) in healthy participants. Here we further hypothesize that suppressing β bursts through neurofeedback training can improve motor performance in healthy subjects. We conducted a double-blind sham-controlled study on 20 human volunteers (10 females) using a sequential neurofeedback-behavior task with the neurofeedback reflecting the occurrence of β bursts over sensorimotor cortex quantified in real time. The results show that neurofeedback training helps healthy participants learn to volitionally suppress β bursts in the sensorimotor cortex, with training being accompanied by reduced RT in subsequent cued movements. These changes were only significant in the real feedback group but not in the sham group, confirming the effect of neurofeedback training over simple motor imagery. In addition, RTs correlated with the rate and accumulated duration of β bursts in the contralateral motor cortex before the go-cue, but not with averaged β power. The reduced RTs induced by neurofeedback training positively correlated with reduced β bursts across all tested hemispheres. These results strengthen the link between the occurrence of β bursts in the sensorimotor cortex before the go-cue and slowed movement initiation in healthy motor control. The results also highlight the potential benefit of neurofeedback training in facilitating voluntary suppression of β bursts to speed up movement initiation.SIGNIFICANCE STATEMENT This double-blind sham-controlled study suggested that neurofeedback training can facilitate volitional suppression of β bursts in sensorimotor cortex in healthy motor control better than sham feedback. The training was accompanied by reduced reaction time (RT) in subsequent cued movements, and the reduced RT positively correlated with the level of reduction in cortical β bursts before the go-cue, but not with average β power. These results provide further evidence of a causal link between sensorimotor β bursts and movement initiation and suggest that neurofeedback training could potentially be used to train participants to speed up movement initiation.

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Subthalamic beta-targeted neurofeedback speeds up movement initiation but increases tremor in Parkinsonian patients

He, Shenghong, Mostofi, Abteen, Syed, Emilie, Torrecillos, Flavie, Tinkhauser, Gerd, Fischer, Petra, Pogosyan, Alek, Hasegawa, Harutomo, Li, Yuanqing, Ashkan, Keyoumars, Pereira, Erlick, Brown, Peter, Tan, Huiling (2020) · eLife

Previous studies have explored neurofeedback training for Parkinsonian patients to suppress beta oscillations in the subthalamic nucleus (STN). However, its impacts on movements and Parkinsonian tremor are unclear. We developed a neurofeedback paradigm targeting STN beta bursts and investigated whether neurofeedback training could improve motor initiation in Parkinson's disease compared to passive observation. Our task additionally allowed us to test which endogenous changes in oscillatory STN activities are associated with trial-to-trial motor performance. Neurofeedback training reduced beta synchrony and increased gamma activity within the STN, and reduced beta band coupling between the STN and motor cortex. These changes were accompanied by reduced reaction times in subsequently cued movements. However, in Parkinsonian patients with pre-existing symptoms of tremor, successful volitional beta suppression was associated with an amplification of tremor which correlated with theta band activity in STN local field potentials, suggesting an additional cross-frequency interaction between STN beta and theta activities.

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Beta wave enhancement neurofeedback improves cognitive functions in patients with mild cognitive impairment: A preliminary pilot study

Jang, Jung-Hee, Kim, Jieun, Park, Gunhyuk, Kim, Haesook, Jung, Eun-Sun, Cha, Ji-Yun, Kim, Chan-Young, Kim, Siyeon, Lee, Jun-Hwan, Yoo, Horyong (2019) · Medicine

BACKGROUND: Mild cognitive impairment (MCI) is a symptom characterizing cognitive decline and a transitional state between normal aging and dementia; however, there is no definitive diagnosis and treatment for MCI. Neurofeedback (NF), which is a training mechanism that employs operant conditioning to regulate brain activity, has been increasingly investigated concerning its beneficial effects for dementia and MCI. METHODS: This study investigated cognitive improvement and hemodynamic changes in the prefrontal cortex (PFC) following NF training in patients with MCI. Five patients with MCI received NF training for enhanced beta band activity in the dorsolateral PFC-16 sessions for 8 weeks-with each session divided into 9 5-minute trials. The primary outcome measure was a cognitive assessment tool: the Korean version of the Montreal Cognitive Assessment. The secondary outcome measures were the Central Nervous System Vital Signs for neurocognitive testing, hemodynamic changes using functional near-infrared spectroscopy in the PFC during a working-memory task, and Beck Depression Inventory scores. RESULTS: After completing the training, patients' cognitive function significantly improved in domains such as composite memory, cognitive flexibility, complex attention, reaction time, and executive function. Increased electroencephalogram beta power was observed over NF training sessions (Spearman rank correlation test: r = 0.746, P = .001). The threshold value for gaining positive feedback from pre-NF baseline on beta power significantly increased (Spearman rank correlation test: r = 0.805, P = .001). Hemodynamic response in PFC changed after NF training, and individual differences were identified. Specifically, hypoactivation of the hemodynamic response by emotional distraction recovered following NF training. CONCLUSION: We suggest that patients' cognitive processing efficiency was improved by the NF training. These beneficial results suggest that NF training may have potential therapeutic applications to prevent the progression from MCI to dementia. TRIAL REGISTRATION NUMBER: Clinical Research Information Service (KCT0003433).

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