Research and publications
Neurofeedback brain training for Parkinson's
Neurofeedback and physical balance in Parkinson's patients
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Neurofeedback training is effective on the dynamic balance of Parkinson's patients.
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Neurofeedback training can modify the static balance of Parkinson's patients.
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Effect of neurofeedback on static and dynamic balances was similar.
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PD patients could enhance their beta1 and reduce selectively their theta activity.
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Bereitschaftspotential augmentation by neuro-feedback training in Parkinson’s disease
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Parkinson’s disease (PD) patients could restore decreased early component of Bereitschaftspotential (BP) by means of neuro-feedback (NFB) to control negative slow cortical potentials (SCPs).
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Studies demonstrate that decreased pre-movement cortical activity can be restored by endogenous, subject’s own effort, without externally driven modulatory stimuli or medication.
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Good NFB performance of negative SCPs shifts (negativation) most likely increases excitatory field potentials of pyramidal cells in the supplementary motor area.
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Neural Networks and Neurofeedback in Parkinson’s Disease
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Thalamocortical circuits has been implicated in the pathophysiology of Parkinson’s disease.
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Manipulating these abnormal activation patterns may therefore offer a novel avenue for treating this disabling condition.
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A potential avenue for the modulation of specific neural activation patterns is neurofeedback. This noninvasive technique entails providing a continuous update of one’s neural activity so that volitional control of selected brain regions, networks, or rhythms can be learned.
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This could be accompanied by specific therapeutic changes in behavior and clinical symptomatology in disease, according to the neural circuits that are modulated.
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Most neurofeedback research has used electroencephalography (EEG) but recently neurovascular signals measured with functional magnetic resonance imaging (fMRI) have been targeted as well.
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In this paper, we discuss the evidence implicating certain rhythms, particularly the beta (10–35 Hz) oscillation, in Parkinson’s disease. We also perform a systematic review evaluating the therapeutic efficacy of neurofeedback in Parkinson’s disease and make suggestions for future research.
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Biofeedback for Movement Disorders (Dystonia with Parkinson's Disease): Theory and Preliminary Results
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This paper presents a theoretical framework for using a combination of EEG biofeedback plus regular biofeedback with clients who have movement disorders.
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Training was associated with significant reduction in dystonic movements. Additionally, the client became able to use diaphragmatic breathing to cue herself to turn on a mental state associated with increased SMR production and thus control incidents of freezing, a common problem in advanced Parkinson's disease.
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With twelve more sessions over the next 18 months, the improved quality of life has been maintained.
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This work is reported to put forth a theoretical model of why neurofeedback plus biofeedback is helpful in movement disorders and to encourage research in this area.
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Further reading
Neurofeedback for PTSD
Sensorimotor rhythm neurofeedback as adjunct therapy for Parkinson's disease
Neurofeedback may enhance compensatory brain mechanisms. EEG‐based sensorimotor rhythm neurofeedback training was suggested to be beneficial in Parkinson's disease. In a placebo‐controlled study in parkinsonian nonhuman primates we here show that sensorimotor rhythm neurofeedback training reduces parkinsonian symptoms and both ON and OFF scores during classical L‐DOPA treatment. Our findings encourage further development of sensorimotor rhythm neurofeedback training as adjunct therapy for Parkinson's disease which might help reduce L‐DOPA‐induced side effects.
Neurofeedback for PTSD
Real-Time Neurofeedback to Modulate β-Band Power in the Subthalamic Nucleus in Parkinson’s Disease Patients
The β-band oscillation in the subthalamic nucleus (STN) is a therapeutic target for Parkinson’s disease. Previous studies demonstrated that l-DOPA decreases the β-band (13–30 Hz) oscillations with improvement of motor symptoms. However, it has not been elucidated whether patients with Parkinson’s disease are able to control the β-band oscillation voluntarily.
Here, we hypothesized that neurofeedback training to control the β-band power in the STN induces plastic changes in the STN of individuals with Parkinson’s disease. We recorded the signals from STN deep-brain stimulation electrodes during operations to replace implantable pulse generators in eight human patients (3 male) with bilateral electrodes. Four patients were induced to decrease the β-band power during the feedback training (down-training condition), whereas the other patients were induced to increase (up-training condition).
All patients were blinded to their assigned condition. Adjacent contacts that showed the highest β-band power were selected for the feedback. During the 10 min training, patients were shown a circle whose diameter was controlled by the β-band power of the selected contacts. Powers in the β-band during 5 min resting sessions recorded before and after the feedback were compared.
In the down-training condition, the β-band power of the selected contacts decreased significantly after feedback in all four patients (p < 0.05). In contrast, the β-band power significantly increased after feedback in two of four patients in the up-training condition. Overall, the patients could voluntarily control the β-band power in STN in the instructed direction (p < 0.05) through neurofeedback