Guest guest Posted May 19, 2012 Report Share Posted May 19, 2012 Hi Mark, You asked my thoughts about " theta left frontal to posterior synchrony " as the underlying mechanism of alpha-theta training. You cited Gruzelier [1]. Gruzelier cited von Stein [2] and Aftanas [3]. Let me know if you need those articles. I apologize in advance for my errors in interpreting the literature. I don't think this is the mechanism behind typical alpha theta effects, since that tradition involves only posterior electrodes and may train theta and alpha amplitudes individually. That is why in theta-alpha amplitude training the hallmark feature is the alpha-theta amplitude crossover. This is an indicator of drowsiness or hypnagogic state. , et al [4] found no correlation between the TA crossover and production of imagery. In traditional alpha-theta amplitude training there is no built in flexibility for the fact that one is changing the amplitudes of frequency bands (theta and alpha) that normally take much of their cues from phase shifts at lower frequencies. This AM-PM (amplitude modulation - phase modulation) relationship is a characteristic of 1/f power law systems such as neuronal assemblies. In contrast to amplitude training, synchrony training can be configured to use theta phase shifts to drive alpha or gamma amplitude shifts. The hallmark of this approach is not the T-A amplitude crossover, but rather is the theta-alpha phase reset with its relationship to intelligence and valid perception. Another characteristic of T-A amplitude training is that it is done eyes closed and with relaxing sounds (both the sound and the flow of water exhibit a type of 1/f feature described as " pink noise " ). However, I have found TAG synchrony to be best performed eyes open, although, depending upon network targets, one may want to avoid using central foveal vision because it is anti-correlated with the default mode network. Since I conceive of T-A synchrony training as different than T-A amplitude training, I do not hold that the goal of synchrony is also the hypnagogic state accompanying T-A crossover, so I usually do not try to reward with hypnagogic sounds. My preferred reward for adults (that rarely works with troubled children) is to have theta synchrony reward by turning off a loud hum, and to reward alpha synchrony by turning off pink noise. If the client can avoid excess beta activity (e.g., spindling) then a loud alert sound can be avoided as well. I simply point out the 3 types of noise and ask the client to make them all go away. Thus the reward and encouragement for being in this state is to sit in utter quiet paying attention to the mental states, however they might be perceived. I believe this is an important goal since much of infant affect management is learned by the mother withdrawing stimulation when appropriate and allowing the infant to self-regulate in quiet when possible. Theta alpha synchrony, primarily in the anterior-posterior communications, is required for valid perception according to Varela [5], et al. In his studies of meditation [6] Aftanas (Russian Academy of Medical Sciences) documented the particular importance of theta and alpha synchrony between the left frontal cortex (e.g., F3) and the parietal areas (P3, Pz & P4). Like Klimesch he breaks the alpha clinical band into 3 sub-bands: Low alpha (6-8 Hz), Mid alpha (8-10 Hz) and hi alpha (10-12 Hz). Desynchronization in these 3 bands is associated with 1) alertness and vigilance (Lo Alpha), 2) expectancy (Mid Alpha), and 3) cognitive processing (Hi Alpha). The particular NFB alpha parameters used for a session can thus have individual significance for the client. Because of the effects of theta and alpha phase modulation on gamma amplitude (a consequence of the 1/f power law), it is interesting to look at different gamma patterns in meditators as well. Last month in Israel Berkovich-Ohana et all published a study [7]. Frontal and midline gamma is associated with default mode network functions (self-referential) and, of course, is decreased with attentional demands. However the lateral and posterior gamma is increased in attention and especially in meditators. Lehmann [8] showed that a skilled meditator could change gamma distribution at will by altering the meditation technique: increased right posterior occipital gamma activity in image visualization, increased left central-temporal area in mantra verbalizers. Those practicing emptiness meditation and reconstitution of the self produced increased gamma activity in the right superior frontal and right temporal-parietal sites - areas linked to altered sense of self [9]. Interestingly they also showed that very early in the practice of mindfulness meditation neural plasticity is increased in the self-referential networks (DMN) as well as the attentional networks. I like to paraphrase Siegel's definitions of mindfulness meditation: being aware of the modifications of the mind accompanied by the attitudes of curiosity, openness, acceptance and appreciation. In my opinion this is a useful definition for neurofeedback training as well. If so, then the data of meditation studies may have special relatedness to neurofeedback training. Here is another interesting thing about 8.5-12.5 Hz periodicity. Now I am not talking about the posterior dominant (alpha) rhythm, but I am talking about discrete state changes in the brain which occur in this frequency range and involved the entire cortex. These are called microstates. They have nothing to do with the brain state technology company. Most people chronically display 4 or 5 characteristic states. They occur in different sequences and last varying times. These microstates have been found to correlate to 4 of the resting state networks (not including the DMN), [10] and their sequencing is disordered in common conditions such as depression, dementia and schizophrenia. This may be one reason that 10 Hz light flicker improves recognition memory in older people [11]. This may be one of the reasons that alpha training (also in the 8.5-12.5 Hz range) is also important in brain state regulation. One important point to remember as we study brain microstates, is that we are used to thinking of the 1/f EEG in terms of the frequency domain, i.e., the power and coherence in the different clinical frequency bands. We have not looked completely yet at the time domain itself. As you will see from the literature, monitoring brain microstates, each lasting 80-120 ms, is very different than watching frequency bins change. When I started neurofeedback in 2008 I was fortunate to learn about the resting state networks. They have been well documented as disordered in a wide range of difficult clinical conditions including addiction, Alzheimer's disease, anxiety, autism, ADD, bipolar disorder, chronic depression, chronic pain, fibromyalgia, Parkinson's disease, PTSD, schizophrenia, etc. [12] The default mode network has anterior connectivity hubs involving the med prefrontal cortex and anterior cingulate, and a posterior connectivity hub at the precuneus and posterior cingulate area. When I was first exposed to alpha-theta training for PTSD I was surprised the training was all posterior. I was commonly met with skepticism about the safety or suitability of up-training frontal theta. Two facts made me persist. One is that although the presence of polymorphic theta (as in ADHD) is associated with inflammation and cytokine imbalance, the type of theta trained is, by the nature of the Fourier transform, may be rhythmic theta. Rhythmic theta is sometimes known as the Cigánek rhythm or frontal midline theta. Its presence is associated with improved self-regulation. Another reason I persisted and started trying theta alpha gamma synchrony in the midline is because the anterior cingulate and the insula are part of the salience network that directs resting state network changes. In my opinion it begs to be included in the neurofeedback. And in order for the salience network to have valid input, there must be long distance alpha-theta synchrony. Although I need to be discrete with the details for a few weeks, a group I am working with has shown that SMR neurofeedback for ADHD strengthens default mode network functionality! A common question I hear is how can SMR training at Cz strengthen resting state functional connectivity (rsFC) across the cortex? This may be because one of the microstates, " D " , has activity centered around the combined Fz-Cz area. And as we now know, brain microstate management has a direct link to resting state activity. This is, of course, in addition to the other benefits that come from learning to self-regulate corticothalamic loop timing. I find it interesting that heart rate variability training often involves about 6 breaths per minute. The frequency of 6 per minute (6 per 60 seconds) is exactly the same as the frequency of 1 per 10 seconds (1/10s) and is the same as 0.01/1 second = 0.01 Hz. Since the resonant frequency of the default mode network is 0.013 Hz and that of the anti-correlated attentional network is 0.016 Hz (both very close to 0.01 Hz, it is very possible that resonant breathing at the same frequency pumps these networks. This may be the basis for Takahashi et al's 2005 suggestion [13] that deviation from the normal power spectrum of the heart rate variability interfered with appropriate modulation of alpha and theta in naive meditators. Here again we see a little into the nature of the 1/f power laws that model reality. Phase modulation of low frequencies (such as 0.01 Hz or even 10 Hz) feeds amplitude modulation of higher bands such as beta and gamma. Monto, et al (2008) said very clearly that " infraslow fluctuations reflect the excitability dynamics of cortical networks. This is as clear and believable explanation for both the positive effects of infra-slow frequency training and also the adverse reactions. This 1/f characteristic of " feeding of high frequency amplitude shifts by low frequency phase shifts " is probably the main reason why neurofeedback can be dangerous. Both infra-low frequency NFB and synchrony NFB can encourage beta spindling. Beta spindling, when observable, usually appears as a fairly isolated peak of beta activity in a very narrow range, such as 20-22 Hz. It may best be considered a sign of irritated or kindled cortex. If your " inhibit instruments " are set to auto-threshold then beta in a narrow range, say 20-22 Hz can increase significantly, and your auto-threshold will merely elevate in order to accommodate the increased amplitude. Forty percent of frontal lobe epilepsy is not apparent on routine EEG even with provocation. If you see any change in beta spindling that is accompanied by any behavioral sign, such as sudden restless legs or change in demeanor, you may be dealing with paroxysmal kindled cortex - seizure by definition. Ultimately attempting to change frontal metabolism with neurofeedback may lead to problems if the client has imbalance in glutathione and glutamate. One of the first questions I ask clients is whether or not there is any bipolar disorder or schizophrenia in the family. If so, there is likely a 20-40% reduction in frontal glutathione. This is actually a very common condition. In my " theory of synaptic recidivism " (www.cortexercise.com) I summarize some of the literature showing that all of the disorders that are so common and difficult to treat (such as the list I gave above and [12]) are characterized by disordered excitation (glutamate poorly moderated by the reduced levels of glutathione). Because all learning (and neuroplasticity in general) requires significant inflammation for synaptic remodeling, and since the anti-inflammatory glutathione is in short supply in chronic illness, and since the average American diet contains possibly 20 times more excitotoxins (such as MSG) than it did 15 years ago when MSG was relabeled " natural spices " , change is difficult or impossible for some clients. N-acetyl-cysteine (NAC) is a generally safe dietary amino acid that provides the cysteine that is rate limiting in glutathione synthesis. Perhaps that is why the journal Biological Psychiatry has just pre-published results of a study showing effectiveness of NAC in treating autistic children [15]. Other problems find significant benefit from NAC, e.g., bipolar disorder, schizophrenia, trichotillomania, gambling, addiction. When attempting to optimize any sort of neurofeedback it may be important realize that there is already an imbalance in excitation, and microstate management will be difficult without neuroprotection. I have seen over-arousal occur with tDCS as well, and it is often relieved by NAC (best accompanied by other nutraceuticals). Neuroprotection and neuroplasticity are largely related to the infra-slow frequencies characteristic of resting state networks [16]. These lower frequencies are the Archimedean lever that raises the higher clinical EEG bands. Thank you for the question, Mark. I find it thought provoking. Perhaps others could chime in here. Best wishes, Dailey Near San Francisco CA [1] Gruzelier J (2008) - A theory of alpha-theta neurofeedback, creative performance enhancement, long distance functional connectivity and psychological integration. Cognitive Processes. Published online 11 Dec 2008. [2] von Stein A, et al (2000) - Different frequencies for different scales of cortical integration - From local gamma to long range alpha-theta synchronization. International Journal of Psychophysiology 38 2000. 301-313 [3] Aftanas LI, et al (2001) - Human anterior and frontal midline theta and lower alpha reflect emotionally positive state and internalized attention - EEG investigation of meditation. Neuroscience Letters 310(2001);57-60, [4] JP, et al (2000) - Comparison of alpha-theta, alpha and EMG neurofeedback in production of alpha-theta crossover and occurrence of visualizations. Journal of Neurotherapy, Vol. 4(1) 2000 [5] Varela F, et al (2001) - The brainweb - Phase synchronization and large-scale integration. Nature Reviews Neuroscience, Volume 2 April 2001 p 229. [6] Aftanas LI, et al (2001) - Human anterior and frontal midline theta and lower alpha reflect emotionally positive state and internalized attention - EEG investigation of meditation. Neuroscience Letters 310(2001);57-60, [7] Berkovich-Ohana A, et al (2012) - Mindfulness-induced changes in gamma band activity – Implications for the default mode network, self-reference and attention. Clinical Neurophysiology 123(2012);700-710. [8] Lehmann D, et al (2001) - Brain sources of EEG gamma frequency during volitionally meditation-induced, altered states of consciousness, and experience of the self. Psychiatry Res 2001;108:111–21. [9] BL, et al )2001) - Neuroanatomy of the self: evidence from patients with frontotemporal dementia. Neurology 2001;57:817–21. [10] Britz J, et al (2010) - BOLD correlates of EEG topography reveal rapid resting-state network dynamics. NeuroImage 52 (2010) 1162–1170 [11] J, et al (2006) - 10 Hz flicker improves recognition memory in older people. BMC Neuroscience 2006, 7:21 [12] Broyd SJ, et al (2009) - Default-mode brain dysfunction in mental disorders - A systematic review. Neuroscience and Biobehavioral Reviews 33 (2009) 279–296 [13] Takahashi T, et al (2005) - Changes in EEG and autonomic nervous activity during meditation and their association with personality traits. International Journal of Psychophysiology 55 (2005) 199– 207. [14] Monto S, et al (2008) - Very slow EEG fluctuations predict the dynamics of stimulus detection and oscillation amplitudes in humans. The Journal of Neuroscience, August 13, 2008 • 28(33):8268–8272. [15] Hardan AY, et al (2012) - A Randomized Controlled Pilot Trial of Oral N-Acetylcysteine in Children with Autism. Biol Psychiatry in press. [16] Raichel ME (2010) - Two views of brain function. Trends Cogn Sci. 2010 Apr;14(4):180-90. From: [mailto: ] On Behalf Of Mark Baddeley Sent: Saturday, May 19, 2012 12:39 AM Subject: Theta Synchrony Hi I've recently read Gruzelier's theoretical basis for alpha theta training. My take away message was that the underlying mechanism is really theta left frontal to posterior synchrony. I'd be interested in your thoughts. Regards Mark Baddeley ----- Original Message ----- From: Dailey Sent: Saturday, May 19, 2012 4:18 PM Subject: alternative method for training down theta? Hello , I am impressed with the careful attention to detail you have undertaken in this matter. Since you asked for comments, here are mine. Roughly speaking there is good theta and bad theta. Bad theta is polymorphic. This means that the observed periodic phenomena in the EEG occur roughly 4-8 per second but have a varying morphology that is not sinusoidal. " Good " theta is rhythmic and sinusoidal like eyes-closed alpha and is primarily frontal midline. Bad theta is indeed a hallmark of a variety of malfunctions such as ADD. In many cases it is due to maternal immune activation. In other cases it is due to current or on-going stimuli disrupting homeostasis. Neurofeedback uses Fourier transforms to isolate primarily the rhythmic good theta. Normally this is roughly midline. You are correct in assuming that a left frontal concentration of theta (good or bad) is an aberration. It is essential to remember that on occasion localized theta may be a manifestation of focal abnormality (vascular, neoplastic, degenerative, traumatic, inflammatory, etc.) However, you talk like the theta was not only bad but might also be a culpable agent with an agenda. In such a scenario we usually agree to attack the aggressor (the theta amplitude). But there might be another interpretation. Delta to gamma brainwaves are ALL slow waves compared to the 500-1000 Hz waves that are included in the panoply when one looks under the hood. Especially delta, theta and alpha are all bases for long-distance network communication. So if you see theta segregated to an isolated region you know you are dealing with a loss of long-distance integration and synchrony. The goal then is NOT to suppress some local theta (or gamma or whatever) but to reintegrate it so that it can continue its role as a bases for network communication. It is not immediately obvious that excess focal theta can be reduced by increasing global theta synchrony. However this may be the case. You may risk unexpected outcomes by dealing with theta amplitude while ignoring any possible phase changes between the theta waves in various parts of the cortex. The well-documented fact that the EEG exhibits what is called a 1/f (one over F) power law can give us clues that are not immediately available elsewhere. The 1/f power law of the EEG clearly enforces that fact that phase shifts (phase modulation) at low frequencies (e.g., delta and theta) control amplitude modulation at the higher frequencies (beta and gamma). This means that the normal essential fractal dimensionality of the EEG may be violated by certain attempts to control low frequency amplitude (e.g., theta training) without attention to the resultant shift in distribution of higher frequencies (beta and gamma). I propose that this is the basis for many of the adverse outcomes of neurofeedbac. Quite a few researchers (Aftanas, Varela, etc.) have shown that long distance theta and alpha synchrony are essential for valid perception. My experience (unpublished) has shown that focal concentrations of theta can often be relieved by up-training theta alpha and gamma synchrony between the 'problem' area and another remote area. Thus, an apparent " accumulation " of theta in the left frontal region may be relieved by recognizing that theta is a long-distance global synchronization signal. Any focal accumulation signifies focal segregation - not long-distance integration and synchronization. I believe we will be able to show that focal amplitude accumulations can be treated by reintegration by phase synchronization. It also good to remember that if there is schizophrenia or bipolar disorders anywhere in the family line, then there is going to be a 20-40% reduction in frontal glutathione leading to neuronal irritability. Increased left frontal theta may be an adaptation when normal cognitive and historical networks cannot cope for chronic stress. As a result you can often expect increased anxiety as a result of treatment. This is a good sign. The anxiety is usually very primitive and the client was not shown self-regulation. The left frontal slow waves may be a mechanism to cope, but lead with other problems such as depression and attention issues.l Gamma normally is " nested " within theta. Therefore a focal accumulation of theta can alter the ultimate binding activities of gamma. Different mediation techniques (imagery, mantra, emptiness) create different cortical gamma distributions. The 1/f power laws show that patterns of theta phase relationship enforce focal gamma amplitude changes, such as are seen with different meditative approaches. Aftanas, et al, have shown that in mature healthy meditators, left frontal theta (and alpha) is especially strongly phase synchronized with the left parietal cortex (P3), the precuneus region (Pz) and the right parietal cortex (P4). I look forward to learning the results of your continued investigations. Best wishes, Dailey www.growing.com www.cortexercise.com From: [mailto: ] On Behalf Of Zumbach Sent: Friday, May 18, 2012 7:46 AM Subject: Re: alternative method for training down theta? It isn't very hard to see the difference between an errant eye blink and a burst of theta lasting several seconds so I'm not too worried about that. It is important to keep the eyes resting partially closed so that one only needs to blink occasionally, but you already knew that. I would argue that using all four channels is a fine idea on the principle of the fact that more data is generally better and that it gives me the ability to see the bursts of theta as they progress all the way across the left frontal. I would also assume that it would be better to make sure to train the theta down all the way across the left frontal instead of isolating the feedback to one small area. I don't think theta is bad but I'm under the understanding that theta production in the left prefrontal is characteristic of ADD and that the more there is, and the more frequent the bursts, the worse the symptoms are (according to this book: http://tinyurl.com/6qxvtz8). Are we saying that protracted bursts of 4-7hz activity in the left PFC is a desirable thing? I'm also correlating these bursts of theta to breaks in protracted concentration during alpha-synchrony/meditation training. With my latest design I can calculate the exact amount of time I'm in synchrony while meditating and I'm up to an average of 45 minutes out of 60 for most sessions (baring something foolish like caffeine consumption) and I see some strong evidence that these waves of theta washing over the left prefrontal seem to be the cause of my interrupted attention during the remainder. This is the impetus for my action. Thanks for you input Pete, DZ On Thu, May 17, 2012 at 11:32 AM, pvdtlc <pvdtlc@...> wrote: Of course the very first thing to be aware of is that every time you blink or move your eyes, you're very likely to produce a burst of slow activity that looks like theta or delta. If that's what is happening, you may end up training yourself not to blink, but you won't have much effect on brain activity. Second thing is that theta around 7 Hz is actually a GOOD frequency, since it involves connection with the hippocampus or memory center.. Looking at one thing in one place and deciding what to train is probably not the best way to decide on a training plan. What are you noticing as a problem in your performance/mood/etc that you think is related to this theta? Or have you just read that theta is " bad " ? If you are training in a very small area as you are describing, aside from the fact that you have 4 channels and really want to use them all, I can't see any benefit to 4C over 1C. Pete -- Van Deusen pvdtlc@... http://www.brain-trainer.com USA 678 224 5895 BR 47 3346 6235 The Learning Curve, Inc. On Thu, May 17, 2012 at 12:13 PM, Zumbach <zumbach@...> wrote: [Attachment(s) from Zumbach included below] Hey everyone, I realized recently that I have a great deal of theta popping up between FC3 and F3 and decided to start training it down. I have some experience using bipolar montages but have decided that I am against using them. Everywhere I read about bipolar setups (here, the Othmers, quantitative EEG textbook) it seems apparent that no one actually knows what is happening during the training. We may be training the signal up at the active point or down at the active point, down at the reference or up at the reference, changing the phase relationship at either location in one direction or another, but in the end we have literally no idea what is going on other than a vague conception that the electrical activity at one site is now more similar or more different than the activity at the other. For this reason I have created a new design based on, of all things, the alpha-synchrony design that Les Fehmi uses. The logic is that I can put four electrodes between FC3 and FP1 and then sum the theta at these locations. I then set a threshold around 85% and set it to " decrease " so that when, for example, there is a burst of theta in my left frontal region pacman stops moving. I find the inhibit only strategy appealing because once you train theta down the remaining activity will be whatever frequency of beta my brain is most comfortable making, as opposed to trying to get my brain to make a particular frequency of beta. What are people's thoughts on this strategy and my rationale? I would really appreciate any feedback at all. Zumbach Quote Link to comment Share on other sites More sharing options...
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