And I found what looks to be a well done YouTube video where I could copy some bonaural beats: youtu.be/eqKQACO4HAk
But I have not figured out if I want Gamma, Beta, or Theta waves (or any waves). For now I am listening to that YouTube one until I figure out what I want to try.
Since I have not figured it out, I am just dumping all my notes here for anybody to pick through:
☐ Pure tones of 420 Hz and 460 Hz presented to the left and right ear, respectively, were perceived as a 40-Hz BB with a 440 Hz fundamental tone. Pure tones of 431.85 Hz and 448.15 Hz were used to produce the 16-Hz BB with the same fundamental tone. Sound files of 15 min duration were created with Matlab and presented continuously in the background during the RSVP experiment.
☐ In conclusion, listening to 15Hz binaural beats during a visuospatial working memory task can not only increase the response accuracy but also change the properties of the the cortical networks supporting task performance. A 3% increase in Δ Accuracy, over the 5 minutes, was found in participants who listened to the 15Hz binaural beat. All other acoustic stimulation conditions produced a negative change.
☐ Plastic changes in the auditory cortex induced by intensive frequency discrimination training brainmusic.org/EducationalA...
☐ The slow auditory evoked (wave N1m) and mismatch field (MMF) elicited by sequences of pure tones of 1000 Hz and deviant tones of 1050, 1010 and 1005 Hz were measured before, during and 3 weeks after subjects were trained at frequency discrimination for 15 sessions (over 3 weeks) using an odd-ball procedure. The task of the subject was to detect deviants differing by progressively smaller frequency shifts from the standard stimulus. Frequency discrimination improved rapidly in the first week and was followed by small but constant improvements thereafter. N1m and MMF responses to the deviant stimuli increased in amplitude during training. This enhancement persisted until training was finished, but decreased 3 weeks later. The results suggest a plastic reorganization of the cortical representation for the trained frequencies.
☐ This one is not using binaural beats, but is using pure tones and having participants identify the pure or altered tones.
The brain's neuron's discharge in groups which create measurable oscillations (EEGs). From what I've read, the healthy brain has different oscillations in different regions that fluctuate. In the PD brain, all the different regions synch and oscillate at about 20 Hz. BNB in theory, can entrain brain oscillations and break up the harmful synchronization of oscillations believed to cause some symptoms of PD.
☐ Parkinsonian Beta Oscillations in the External Globus Pallidus and Their Relationship with Subthalamic Nucleus Activity ncbi.nlm.nih.gov/labs/pmc/a...
☐" Synchronized neuronal oscillations in the brain have been correlated with distinct behavioral or brain states, suggesting a functional link (Singer, 1999; Buzsáki and Draguhn, 2004). Moreover, it has been proposed that synchronized oscillations provide a mechanism for dynamic, optimal communication and computation within and between dispersed neuronal networks (Engel et al., 2001). If synchronized oscillations are indeed important for normal brain function, then abnormal or uncontrolled synchronization could be disadvantageous or even pathological (Schnitzler and Gross, 2005; Uhlhaas and Singer, 2006). This idea is supported by studies in idiopathic Parkinson's disease (PD) and its animal models, in which loss of midbrain dopamine neurons induces excessive synchronization of (oscillatory) activity in the basal ganglia (BG) and associated circuits (Nini et al., 1995; Bergman et al., 1998; Boraud et al., 2005; Gatev et al., 2006). In PD patients, synchronization of the oscillatory activities of single neurons and/or neuronal populations in cortex, subthalamic nucleus (STN) and internal pallidum preferentially occurs at beta (β) frequencies (15–30 Hz) (Brown, 2006; Hammond et al., 2007). These exaggerated β oscillations are reduced during voluntary movements (Kühn et al., 2005; Williams et al., 2005), and are attenuated, together with motor symptoms, by therapeutic interventions (Brown et al., 2001; Levy et al., 2002; Williams et al., 2002). Altogether, these clinical studies suggest that, by inappropriately coordinating neuronal activities, exaggerated β oscillations play pathological “antikinetic” roles in PD (Brown, 2006)."
anti- + kinetic. AdjectiveEdit. antikinetic (not comparable). That decreases motility of the gastrointestinal tract.
"Discussion
Excessive β oscillations (15–30 Hz) emerge in corticobasal ganglia circuits involving the STN in PD. Here, we resolve several critical issues surrounding the cellular and network substrates of these pathological oscillations. We demonstrate using large-scale recordings that oscillatory activity in GP neuronal networks also becomes excessively and selectively synchronized at β frequencies in a spatially widespread and brain state-dependent manner after dopamine loss. We also show that GP contains two types of neuron with distinct temporal couplings, firing rates and patterns that are maintained across extreme brain states. Finally, the precisely timed discharges of GP and STN neurons indicate that rhythmic sequences of recurrent excitation and inhibition in the STN-GP network, and lateral inhibition between GP neurons, could support abnormal β oscillations. We propose that GP neurons are critical for orchestrating exaggerated β oscillations in STN and corticobasal ganglia circuits in PD."
"Further functional implications
Dopamine coordinates neuronal activity in the frequency domain (Costa et al., 2006). When controlled by dopamine, dynamic β oscillations in corticobasal ganglia circuits may be important for normal movement (Courtemanche et al., 2003; Rubino et al., 2006). However, after dopamine loss, inappropriate reverberatory interactions within GP, and between GP and STN, may not only support but also actively promote the emergence of excessively synchronized β oscillations at the network level. Indeed, cycles of precisely timed excitatory and inhibitory outputs from STN and GP, respectively, could synchronize their common targets and thus, the excessive rhythms propagate to BG output nuclei (Brown, 2006) and thence, thalamocortical and midbrain circuits. Therefore, GP neurons, by virtue of their widespread innervation of all BG nuclei and feed-back/feed-forward mechanisms, are in a central position to orchestrate the generation and propagation of exaggerated β oscillations in STN and the entire BG. Precisely if and how the altered firing rates/patterns we define here impact on behavior is uncertain. However, dysregulation of corticobasal ganglia network activity in space and time after dopamine loss will profoundly affect information processing therein (Mallet et al., 2008), providing a possible mechanism whereby excessive β oscillations may be pathological in PD (Brown, 2006)."
What I am reading here is that loss of dopamine neurons causes one area of the brain to start oscillating at 20hz, and this 20hz oscillation is pathogenic when it spreads to the rest of the brain
And I highly recommend Happy Light by Verilux to supplement happiness protocol. I don’t “battle depression” nor do I “deal with anxiety.” I lean towards , move towards health , gratitude and contentment and it helps the darkness recede to the shadows. What we focus on grows. 💕
BNB are created by playing a constant tone at a set frequency in 1 ear, for example 100 HZ in say the left ear, while playing a different tone (for example 140 HZ) in the other (right) ear. The brain creates a 3rd tone, the BNB which beats at the difference between, left 100HZ - right 140 or 40HZ. This (40HZ BNB) will entrain brain oscillations to 40 / gamma bands.
Simply meditating trains the brain to utilize brain waves and thereby focus. I have a tape of rain. When I listen I'm calm. With meditation practice I'm calm anyway. So I don't know that the tape does anything more. Maybe if you have trouble getting into calmness--beta waves!--the tape might help. The tape of a soft summer rain. It puts me in mind of sitting a a dock looking at the sea. It sounds like in the distance there are bells ringing, like the warning bells of shallow water. But actually it's gongs ringing.
Motor symptoms of Parkinson’s disease are related to the excessive synchronized oscillatory activity in the beta frequency band (around 20Hz) in the basal ganglia and other parts of the brain. This review explores the dynamics and potential mechanisms of these oscillations employing ideas and methods from nonlinear dynamics. We present extensive experimental documentation of the relevance of synchronized oscillations to motor behavior in Parkinson’s disease, and we discuss the intermittent character of this synchronization. The reader is introduced to novel time-series analysis techniques aimed at the detection of the fine temporal structure of intermittent phase locking observed in the brains of parkinsonian patients. Modeling studies of brain networks are reviewed, which may describe the observed intermittent synchrony, and we discuss what these studies reveal about brain dynamics in Parkinson’s disease. The parkinsonian brain appears to exist on the boundary between phase-locked and nonsynchronous dynamics. Such a situation may be beneficial in the healthy state, as it may allow for easy formation and dissociation of transient patterns of synchronous activity which are required for normal motor behavior. Dopaminergic degeneration in Parkinson’s disease may shift the brain networks closer to this boundary, which would still permit some motor behavior while accounting for the associated motor deficits. Understanding the mechanisms of the intermittent synchrony in Parkinson’s disease is also important for biomedical engineering since efficient control strategies for suppression of pathological synchrony through deep brain stimulation require knowledge of the dynamics of the processes subjected to control.
Parkinson’s disease is one of the medical conditions where the symptoms are apparently related to pathologies of neural synchrony in certain brain regions.
The feedback circuits in basal ganglia [32,33] and the rich membrane properties of basal ganglia neurons [34,35] have been shown to support oscillations. In particular, oscillatory activity in the beta frequency band (loosely defined as activity around 20Hz) is related to motor control and its alterations in the parkinsonian state. Movement attenuates the power of and synchronization between basal ganglia activity and the cortical EEG [36] and attenuates synchronization between subthalamic nucleus (STN) neurons [37]. The strength of beta oscillations in STN local field potential (LFP) is inversely correlated with motor performance [38]. Single-unit STN recordings in PD yield similar results [39]. Note that LFP and single-unit recordings represent two different kinds of neuronal activity. The former is mostly formed by synaptic potentials, while the latter is mostly formed by the somatic and axonal electrical activity. However, both signals exhibit oscillatory dynamics in basal ganglia, apparently because somatic activity is influences by synaptic activity and the oscillatory dynamics is exhibited by multiple basal ganglia – thalamocortical loops, rather than an oscillator confined to a single nuclei.
The action of dopaminergic medication on movement and synchronized oscillations fits this framework. Administration of L-DOPA (a major dopaminergic drug used in Parkinson’s disease management) decreases coherence between STN and GPi in the beta range [40], attenuates beta power in STN LFP [37,41], and leads to similar effects in other parts of the basal ganglia-thalamocortical network [42]. The nonselective dopamine agonist apomorphine suppresses beta-band LFP activity in PD patients [43]; intraoperative injection of apomorphine in STN and pallidum leads to similar effects on spiking [37,43]. Dopaminergic lesions in rodents increased LFP coherence across basal ganglia and cortex in beta-band. Application of apomorphine tends to partially reverse this effect [44]. Beta-band synchronization of the EEG from motor areas correlated with the severity of motor symptoms and decreased as the symptoms were alleviated by dopaminergic medication or DBS [45,46].
The intermittent nature of the synchronous dynamics in Parkinsonian basal ganglia may also have some important ramifications for Parkinson’s disease treatment. At the present time there is no cure for Parkinson’s disease and pharmacological treatment of symptoms usually leads to substantial side-effects in the long run. Thus there is a substantial interest in basal ganglia DBS in Parkinson’s disease. STN DBS is the most frequent surgical procedure in Parkinson’s disease. This “classical” DBS requires delivering large amplitude high-frequency pulses, which are probably so strong that they simply override the pathological beta-band synchronized oscillations. This is sub-optimal procedure and it can have multiple side effects. This leads to interest in adaptive effective control strategies to suppress the pathological rhythmicity. Therefore it is important to understand the nature of the dynamics one wishes to suppress and, in particular, the dynamical nature on these synchronized oscillations.
I've exchanged emails with Dr Tass @ Stanford, I wanted to get into his clinical trial, then COVID hit and everything fell apart. Hopefully things will get back on track soon.
I went with a 40 hz gamma wave and layered it on top of a Librivox recording of Thought Vibrations (part 1). You need headphones to get the effect. I have no idea what this will do. 40 hz gamma wave beats are easy to find, so I don't expect anything terrible
Please let me know if you like it. I plan to make more.
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Vibration to un-sync or sound waves and light TO sync : are these not contradictory? 
Gamma brain wave entrainment using sound and light at 40 Hz
Frequency difference between tremors and dyskinesia
WHY haven't we heard more about PEMF results, like these!!!
