Exploring the Complexity of Theta Waves

I'm going to show your screen. We don't see your screen yet. Thank you. Okay. There we go. A Tale of Two Thetas. Ooh, it sounds like a book. Yeah. Well, Niedermeyer, back in the 90s, finally convinced people with his research that there were actually two alphas, a higher faster frequency alpha and a lower frequency alpha. We've been seeing it in the brain maps for years and have been telling people about it. And when his research came out, it wasn't that much after we were seeing it, but nobody saw his research. And finally, early 2000s, people saying, oh, look, well, Niedermeyer says there's two. And they started looking and pretty soon everybody agreed there's two alphas. What's been going on since 2002, 2003 is that the same thing has happened with Theta, but most people have not been paying attention in our field to that fact. although I've been talking about it since 2004, 2005, when I was digging into this stuff, but it still hasn't really caught on in a sense. People really aren't really understanding this. When you say two thetas, people think of good theta and bad theta. That's not the theta I'm talking about. In fact, just like the two alphas come from... different processes. The two thetas come from different processes in the brain. So, you know, let's talk about theta. It's a very complex subject. Theta has turned out to be way more complex in terms of what it does in the brain than anybody previously imagined, especially in the field of neurofeedback. It was just something you got rid of because kids with attention deficit had too much of it. But the story is way bigger now. You know, you all know that theta is critical for connecting up with the cortex and generating your thinking process, your thought processes. So we'll talk about that later on, too. I'm just going to start off kind of at the myth level because there's always tons of that in our field. And so is the confusion. So if you don't get a lot of what I'm saying, don't feel like you should have gotten it because a lot of it's very. confusing and complex and I'm just going to be presenting a lot of the information, some of it very cutting edge, some of it actually pretty old, about theta just to give you a new perspective on the topic. But this will be posted up on the internet in a few days and you'll be able to review it several times if you like. The theta myths are that attention problems are caused by too much theta. Like if you have too much theta, that... therefore causes attention problems. And that's too simplistic. I mean, it's okay to kind of think that way for convenience sake, but they're correlated. There's not a causal relationship. They're correlated. Something happens in the brain, you end up with a lot of theta, and it tends at the same time that people have attentional issues. But as you know, the brain is a system and it's a very complex relationship that causes this. Another one is that the theta to beta ratio is the best way to tell if there's too much bad theta. Because there was good theta and bad theta. You know, theta is okay, but if you have a lot of it, it's bad. You know, there are different theories about it. The theta-beta ratio is not the best way to tell if there's too much theta, bad theta, and too much of a problem with attention deficit. And we'll show you that in a minute. And then there's the other myth that... theta should never be trained up. Well if you have low theta, if you don't train it up or get it up, you're gonna have a lot of problems with memory and emotion possibly too. So let's look at this map. Here we have a map showing you power or magnitude, you know roughly the same thing, and this person was diagnosed officially by a psychiatrist with attention deficit hyperactivity disorder. So where's the theta here? Where's the low beta here? I mean, not only do we not have high theta, we don't have low beta, so we don't have any theta to beta issue. When we actually look at the raw morphology on this map, what we find is a lot of beta spindling. So it's not a theta issue, it's a beta issue, it's beta spindling, and it's one of the phenotypes Jay Gunkelman recognizes. being associated with complaints of attention problems and actually oppositional behavior problems too. So that just blows that myth right out of the water. So if we're having problems and myths with this, let's kind of drill down a little deeper and see where's theta coming from. What's it doing? So this will make your eyes cross, but this is Coulomb 2005. So it's pretty well established at this point. And what you're seeing here is the hippocampus up here, right, and the hypothalamus over here. And in the middle is this structure called the septum. And I've always said, and we frequently talk about research saying that the septal hippocampal oscillators are what cause theta. Well, this is showing why we say that. And you can see that there's activating neurotransmitters, acetylcholine, and inhibiting neurotransmitters. And the activity of these networks, these little networks, generate oscillator that produces theta. And... There's a lot of arguments about, well, does the septum produce or initiate the oscillations? Is it the hippocampus that initiates because it takes two to play? Who's starting the dance? And then other people say, well, wait a second, maybe it's the hypothalamus. So there's a lot of unresolved issues here that are going on. The septum is a relay between the hippocampus and the hypothalamus. Like the hippocampal formation, the septal area has been implicated in the control functions. normally attributed to hypothalamus, such as aggression, rage, and autonomic functions, and self-stimulation, and drinking behavior. So as it turns out, theta drives the hypothalamus. The septum is driving the hypothalamus more than anybody realized. So a lot of these attributes that the hypothalamus supposedly was in control of turns out to be a function of theta. Just like activation of 15 to 20 hertz in the cortex is related to theta. So as we look into it, theta is a very central rhythm and a very old one in the brain and is a part of our mammalian past. And other animals lower on the echelon... that are mammals, have a lot more theta than we do and it dominates their EEG like alpha and beta dominates ours. The other thing is that it links to what we call the supramamillary nucleus. That connects to the ascending reticular system. So this rhythm is connecting the endocrine system and the electrophysiological system. So it is central to communicating to the body and from the brain and from body back to the brain. Theta is critical for communicating information to both the endocrine system and the electrophysiological system. As it turns out, theta seems to have dual functions in this process, memory and emotion. And if you think about memory and how it relates to emotion, it makes sense that those two functions would have to be together because how you feel about what happens helps you determine how much you remember of it, how long you remember it, and how long it stays available. So different component frequencies of theta enable the hippocampus to potentially select and entrain different resonant loops at different neocortical loci. So saying the hippocampus resonates with the cortex. gray matter in an important way. Its correlated or phase-locked activity may then result in strengthening of synapses in the selected loop by Hebbian mechanism, and this becomes what we call learning memory. Now there's also theta-modulated processing in the hippocampus that may be integrated with theta activity in the frontal or the temporal lobes. So it's not just involved with the cortex in terms of learning. but it has a dual pathway, both to the frontal and the temporal regions of the neocortex between these loops. So if we look at what Kirk and McKay, who were focusing on this for years, their conclusions in 2003, was that there's this 3 and 4 hertz pathway, which today is being called the recurrent pathway. which is dominantly emotional but not exclusively. Nothing ever seems to be exclusive in the brain. And then there's the 5 Hz and 7 Hz pathways, which is more. related to memory but not exclusively. And so that's the ascending pathway. And they have two pictures here of the pathways and you can study those from the internet if you want. I could spend an hour just on this topic right here. But, you know, pulling together different pieces of research, the more recent ones are showing us recurrent theta, 3 to 4 hertz. tends to dominate P3, PZ, P4. And what area is that? That's the default mode network. And you've probably heard at this point that theta is strongest in the default mode network and key to its functioning and processing. And you can see the pathways right here. It goes right through the association cortex into the cingulate region. And it's recurrent and recursive. It keeps... Going through this process, this is where we get rumination from. This is where the default mode system keeps feeding back on those memories and emotions to process, you know, ideas when you're thinking in your mind, eye about things. But it's a very emotional-related process. Knyazov calls it implicit early-stage emotional process. Then we have septal theta or the ascending system which is 5 to 7 Hz and that tends to get up more in the dorsolateral and the midline and FZ. And this is more related to acquisition in terms of directing the external attention system. It helps direct it towards stimuli of interest. It works in conjunction with frontal delta and it's related to working memory quite a bit. And so that's more a part of the central executive. So the recurrent was more related to the default mode system and the more emotional. And then we have the ascending, which is more memory related and more related to the central executive. So we have this pathway and that pathway, the two stages. And Knyazev would call this the explicit late stage emotional process. So you notice. He's noticing that there's an early stage which is very emotional and primitive and a more later stage which is more cognitive. The middle temporal lobes are critical factors in what we call the salience network. And so I'm just showing you here from some of the research how the temporal lobe ties together the parietal and occipital cortex, the what and where pathways that we talked about, the dorsal and lateral pathways, and links them to the hippocampus. and the memory function and those all converge through the insular and the ascending pathways, the insular cortex and the ascending pathways, and also involves the vagal system. And this is super mammillary regulated. It's very interesting. So the theta is connecting the brain through these pathways with the body, with the endocrine system. And with the electrophysiology of the body, it's a two-way street. And this, in turn, responds to shifts in symmetry. The front-to-back shifts are related to left-and-right shifts. The front-and-back shifts are much more driven by default mode versus central executive, whereas left-right is much more driven by positive and negative emotions. So these two play off of each other, which is why in the New Mind training, you have... Activation versus symmetry. Activation is front to back, symmetry is left to right. And here's the subcortical pathways for the ascending systems and you can see how involved they are. And if you're interested in this, I've done presentations on the ascending system and asymmetry, and it links into what I'm talking about now. And you can see if you look at the theta generators, how much of the brain they affect. and interact with. You can see the amygdala, the striatum, the motor system, the olfactory system, anterior ventral thalamic nucleus, related more to frontal lobe processing, and then the more septum and the areas that are more limbic and emotional. So it links all of these things together. When we get to the frontal system and we get away from that recurrent system, We have some research showing that frontal midline 6 Hz generates sinusoidal spindles in 1 to 10 second bursts. And that this insight in frontal midline theta is involved in the detection of novelty, of conflict, or things that don't work. We're an error detection system. It's where punishment, you feel negative if something bad happens, and when there's conflict, and when there's error. So the system is looking at... Emotional response to novelty and whether everything's good or a negative system. And that's the external attention system we're always talking about. Now that posterior system that's recurrent, that tends to show up when people get drowsy. So if you're looking at people as they're getting drowsy, you'll see maybe alpha going down. Sometimes some people it tends to go up a little bit at first and then it drops out. And then the delta starts increasing and then theta increases as well. So here we have a map of somebody starting to get drowsy. You can see the alpha starting to drop out and the theta starting to increase. And then if you keep going, the alpha drops out significantly and the theta increases a lot. This is what happens in alpha-theta training. So when we're doing alpha-theta training, we're dropping back to that recurrent system that's driven by the default mode system. So you're shifting in and out of consciousness, but you're tending to focus it on the default mode system in alpha-theta training, which is one of the ways we integrate emotion and trauma is through that system. And, of course, you've heard a lot about that recently. Another aspect of theta is not just emotion and memory, but also glycogen reduction. So theta increases as perfusion decreases. So we get reductions in oxygen or glucose. In other words, if somebody's not getting enough oxygen or they're not getting enough glucose, they're type 1, type 2 diabetic and their blood sugar's dropping, you'll start to get more theta. So here's an example of the alphas dropping out as the theta increases and the delta starts to increase. And then stage 3 in glycogen reduction is you get delta and theta increasing. So you can have theta. As a consequence, not just processing emotion and memory, but it can be an indication that you're getting reduced perfusion or reduced glucose or reduced oxygen in the brain. The emotional recurrent theta is very interesting and it has a relationship that's... That stimulates the ascending system and gets people worrying and ruminating. So I'm just showing you that there's previous research going back quite a ways to the fact that emotional attention was recognized as being related to 5 to 6 hertz theta. And then in the 90s, the frontal parietal research showed that it's very hard for them to distinguish between... what was being reported by some researchers as just frontal exclusive theta or theta relating to the frontal midline. And here's an example of this emotional theta. This was a pre-training screen of an emotional abuse case. This was a child who was in school, who was doing poorly, had a good family, good diet. Nobody could figure out why. We found out that there was an emotionally abusive teacher who was making this kid's life miserable, and he couldn't study, and he was being singled out. And the other kids were starting to bully him because the teacher's attitudes toward him kind of reflected modern political activity. And so after we found that out and got him out of the class, notice this theta here in blue, is that about... 20 microvolts. You can see delta is quite high. It's not getting enough sleep. I mean, in the past, people would just say, well, this is bad stuff. There's too much. Let's just train it down. But once we straightened out the emotional situation, look at what the theta did. This came in like a week after we were training for weeks. This is all we got. After we took them out of the classroom, that's what we got, an actual normal range of activity. So his sleep improved, his emotional life improved. So when you see... elevated theta, particularly in kids, you know, they're calling it attention deficit, but here's an example of it, maybe emotional abuse. Okay, and we saw in the original work with Judy Lubar that when there was a problem in the family and emotions ran high, the kids training in their clinic started to do terrible with theta suppression. This is about getting beyond just looking at the EEG and trying to understand what the physiological causes and social causes are behind it, rather than just blindly training things. Now, some people got a little off kilter because we introduced a new protocol into the system, whereas if you had very little delta eyes closed, but you opened your eyes on your map and you had a lot of delta, the map would say train 2 to 12 down. Well, you know, after we looked at things for a couple of years, we realized, you know, we learned from running statistics and talking to everybody that that's a situation where somebody's not getting enough sleep. And just training delta down is not, you know, with our eyes open, is not necessarily going to fix the sleep problem. So that's why we often encourage people instead of doing that now to do alpha theta training. Now, there's other ways you could do SMR with eyes open. And we've talked about that on other Lunch and Learns. We could. discuss it more, but I don't want to get too bogged down into it. But again, these things are all connected. One of the things that we talk about sometimes, too, is that the digital filters can be fooled by slowed alpha and give you, well, it's false theta, actually. So, you know, you might say, oh, look at this theta in power or magnitude here. The person has a lot of posterior theta. When if you go down to dominant frequency, you can see. that the alpha has slowed way down. We don't really have often very much in the way of fast theta. That's not a typical thing you find. So what you're really seeing, if you actually look at the raw EEG, is alpha that's going as slow as seven cycles a second, and it's being picked up by the digital filters, and it's looking like it's theta in magnitude, and it's not. So you can have a reduction in perfusion. that causes that. You could have reduction in blood sugar, kids with blood sugar problems that cause that. You could have a thyroid or liver issues that cause that. So these are the underlying physiological things that can cause slow alpha that give you false theta. And you could be interpreting it incorrectly. You need to be careful about just making up simple rules about what theta means. Here's an example of how Problems in theta and alpha and beta correspond to increases in communication in the cortex. Here you notice the frontal temporal theta showing elevations, and look at the connectivity. It is compensating. Alpha, frontal and posterior, compensating. Beta, global, almost global compensation. So you can see that theta. just like alpha and beta, tends to increase in communication interhemispherically when there is abnormalities in the magnitude. This is the brain trying to increase communication to compensate for problems. Let's say that your blood sugar is dropping, or that you haven't had enough sleep, or some other thing that's not getting enough oxygen. asthmatic. And what's going to happen is that when that alpha slows and you get frontal theta, maybe you're reducing perfusion here, the brain is going to try to increase communication to offset those problems, trying to compensate for the loss of function. We talked about the fact that theta tells the cortex what to do in terms of beta. Well, it's not quite that simple. There's a feedback loop between the two. But when you go and focus on a salient stimulus in the external world, and your central executive system starts to speed up and pulls you out of the default mode, and you go out to look out to see what's happening over there, that theta will start to resonate with gamma in the cortex, and the gamma will stimulate 15 to 20 hertz beta, which is... Again, stimulating thinking or worrying or ruminating, all of those things. And this came out of Meehan and Bresler's meta-analysis as far back as 2012, which is five years. That's a long time in research, but in terms of the street, most of this has never even hit the street. Most people don't even know much about this kind of stuff. So we have cross-frequency coupling that involves theta frequencies interacting with dit. distant regions through phase coherence while coupling with gamma freeze frequencies to drive cortical activities in the 15 to 20 hertz range. And you can see here's your gamma, right, and here's your theta, and they nest. They're nested, and this is an example of how they nest together. And this nesting sequence, the phase relationship, and of course we don't have time to go into it here. Again, I've discussed it in network. related presentations. This nested gamma here is what stimulates cortical activity to get these metastable networks going, which represent you processing information. Let's talk about theta and the spectral distribution. In the frequency domain, if you look at here's The eyes open on the left in A and eyes closed in B, and you can see that familiar bump up at 10 Hz in alpha when the eyes are closed. And notice it's dominating on the right, not just what I talk about. This shows up consistently in research on symmetry, but even people just looking, what's the distribution of the EEG? You can see alpha's highest on the right side with eyes closed. It's elevated. We look at theta. Theta is... Here we got, they're looking at 6 hertz here. We can see that it's higher than alpha with eyes open, and it tends, frontal and midline tends to be highest with eyes open. But when you close your eyes, notice that the theta tends to be central, more balanced, and it tends to be more towards the posterior. And that's because the default mode network, when your eyes are closed, should have the highest theta. This was predicted by our... our brain map algorithm. I was predicting that before anybody did any of this research because when we ran the algorithm that's what it predicted and we weren't hearing from anybody else about that and you know that's one of the reasons that our database system is different from others. It's based on an algorithm and not just on a statistical descriptive processing. In terms of spatial distribution of theta, more recent research, 2013, is telling us it's highest at PZ, again, default mode. T3, T4, T5, T6, this is a classic default mode pattern. So there's your frontal midline theta, there's your posterior theta. These are the two theta networks. There's your ascending, and there's your recurrent, back here. Default mode and the ascending. becomes critical in the central executive processing when the eyes open. The salience network in the middle temporal lobe switches back and forth between a more dominating frontal ascending system or a more dominating posterior system, and that's related to the salience switch. When we're in optimal twilight state, theta is dominating. and alpha is low. So we're pretty much in a liminal state in the default mode system integrating processing there. And these crossovers were noted in early alpha theta training and you know eventually evolved into major studies on using this unique feature of theta to help people integrate. Alpha synchronization and desynchronization, which we talk about in peak performance, all the time is related to theta. Theta salience shifts move you into the central executive, and that reduces alpha activity, or into the more default mode, which produces more alpha activity. So you shift back and forth with this middle temporal activity. responding both to stimuli coming in and to, you know, in terms of the perceptual processing, but also the body's response to the stimuli coming in, you know, and the discussion between the amygdala and the early emergency detecting system and the heart and the lungs and the rest of the body. Now all of these have their own linked system connected with the vagal system and the whole body responds to input, salient input. and it goes up the ascending system and it tells the septal hippocampal region, oh, you know, we've got something of interest. What do we do? What do we tell the endocrine and physiological system to do from this point on? So you see it's very complex, and we're just still learning about that in neuroimaging. And one of the emergent theories, which has strong basis in the electrophysiology, is that psychopathology is very related to salience, and that when the salience network's not working well, or if somebody's deeply stressed, they may withdraw into the default mode system more and have trouble activating the central and frontal systems, central executive and the frontal regions, dorsolaterals. So this problem... with processing is a characteristic of a lot of disorders. People are kind of stuck in their default mode network. And if you're not getting enough sleep, you're also going to have trouble activating your central executive. You're going to be stuck in your default mode network. So papers have been written saying, you know, maybe this is one of our best measures of disorder. How flexibly can people shift from internal default mode network processing to external processing? And is there a balance between the two in both states? Or are people more extreme external and more extreme internal? It's a whole area of research which could be very promising. And again, this SN that's causing the shift here is related to theta and to stimulus detection. So let's jump over and talk a little bit about theta artifacts. Theta can show up in maps, and it could be just artifact from eye blink, also from body and head moving. And if you have an electrode that's cracked that you're using or defective, you could get theta as well. It's not real theta. So we have to keep an eye out for false theta from eye blinks and eye saccades. You have to watch people's eyes when you're mapping them and training them, and watch your raw EEG to see if it's this kind of artifact theta. Again, there's a whole presentation on artifacts, and this goes into more detail on that presentation up on the Internet. Here's an artifact that we talk about in that presentation of this person's normal theta, and then an ear clip that keeps getting whacked by hair or a collar on a coat. It might be wintertime, and they don't want to take their jacket off because the core temperature is low, even though they're in a comfortable room, and then they keep hitting their ear clip on the high coat collar. So this is the kind of false theta you get, and delta, when it's really down here. So there was work done. Back in 2001, when we were all looking at attention deficit and wondering why theta seemed to dominate in it, people weren't looking at low beta so much as they were looking at high theta. Confirmation bias there, you know. And this research showed that prefrontal blood flow dysregulation in children with attention deficit that weren't taking drugs. And they didn't have structural abnormalities. What they found was, in fact, elevated theta, especially friendly, often indicated reduced perfusion. So that goes back to the beginning of our discussion when I said, well, you know, theta could be a consequence of reduced glucose or reduced oxygen or both in terms of reduced perfusion. So when you look at a brain map and you see theta below I mean, high frontally, that could be very easily a perfusion issue. Whereas if it's global, you know. It could be related to inflammation. If delta is high, it could be related to degradation of the brain and the temporal regions like in dementia. So elevated theta is not just a simple case. You have to look at what else is high and what else is low. We talk about that all the time. So the theta-beta ratio mythology. is put to bed by the co-registration studies. Beta, theta to beta ratio fails to take into account delta magnitude, as well as theta and delta locations, since it's taken only from CZ. This is a problem. You know, theta is at different levels frontally and posteriorly, and may be higher or lower for various different reasons. And also, if you're not accounting for delta being elevated, you're not going to get an accurate level of brain activation. Because if we look at blood flow and perfusion, theta is one good measure of it, but it's not enough by itself. So Rosa et al. in 2009, they tried to figure out what's the relationship between electrical activity and blood flow in the brain, and could you make electrical activity a proxy measure of blood flow? And they found that, yes, indeed you could. could and that's one of the whole concepts behind our what we do at New Mind and with the database system and how we interpret the database system which makes us somewhat different from a lot of the way a lot of other people are looking at it and we find it's much more accurate when it comes to getting at the source of the problem but then our perspective doesn't rely solely on neurofeedback our system says you have to take a biopsychosocial approach to resolving problems. In this piece of research with Rosa et al., you can see they had to include delta to get a correlation that looked like that. So here's the BOLD signal, blood flow, activation, glycogen, and here's their heuristic, their EEG heuristic, the way they calculated it, which is very complex and beyond the scope of what we're doing here. But basically they're looking at both delta and theta and relating it to fast wave activity and looking at that ratio. And so you have to include delta to really get an accurate sense of perfusion maximally. All of this over the years has led us to the stages of oxidative stress perspective. I'm not going to go into too much detail. There's whole presentations on the internet. I've written papers. I've posted research on InMind Journal. I've done presentations at ISNR. Those are all out there and available. And I'm getting a lot of support from a lot of directions on this. But you can see the brain starts out pretty green and slowly gets red as it becomes overactive. And then over time, it starts to get pretty red in the low frequencies as it becomes underactive because it's exhausted itself by too much activity, what we call excitotoxicity. One of the things when you down-train theta, you often get a systemic response. We often note that when we down-train delta or theta things, the whole system gets lower, and people go like, oh, my God, we're over-training. That was an old concept from the late 90s. It doesn't make any sense physiologically. Somebody kind of pulled it out of a hat. They really weren't thinking through things physiologically. But then again, in fairness, we didn't have quite as much information back then. And really what we understand now is that when you're resolving inflammation, okay, the perfusion activity increases. So theta drops out when the delta drops down, when the inflammation drops down. And what's happening is you're starting to see the real skyline, the real distribution of the person. This is a distribution. that is driven, inflated by delta and theta, by lack of perfusion and too much inflammation. When we start to remove those factors through nutrition and counseling and exercise and neurofeedback, we start to see, oh, this person's system is pretty exhausted. Their native MAP is actually quite low. And if we keep training, this delta comes down. We'll probably even see this theta dropping to blue. Now, it doesn't stay this way. If you can get the... profusion increased and the inflammation down, you may have a lot lower than average power. But over time, as you take care of your system, the power will globally come up across the board. But this doesn't happen that often in just, you know, a few months. A lot of times this process can take a year or two. I mean, people don't get into this trouble in just a few months usually. So down training results here. We're down training. Power is decreasing again in this particular map. It's a different one. Note that the change is in. low frequency, and we're getting a 35% change. That's good. The brain's responding well to the neurofeedback. Very good reorganization. Unusually high normalization. They're both at 50-50. Usually reorganization's at 60 and normalization's at 40. So this is a good solid change that we would expect. Everything's going low, and now slowly everything will start to return to normal power, but in the right distribution. When we train up, sometimes we get some interesting changes. Here, this person had low delta, and what we found is when we trained the delta up, their sleep improved. Well, now there's research showing that if you train delta down, sleep gets worse. So you don't want to train delta down when it's already normal. Not a good idea because that would make people sleep worse. And so, you know, we adjust our protocols in the system bit by bit as we learn this stuff. We're not just going to keep everything static. I know it kind of moves your cheese and rattles your cage a little bit, but think about the fact that what we're doing is actually gradually learning and improving the system so your clients do better. In this case, the delta was trained up. You can see the post-map shows a lot of extra green, great change. Notice that the alpha in the pre dropped down. This person is getting more sleep. The beta is dropping down. They're less anxious. The theta is increasing. Why is frontal theta increasing? We don't always know the answer to all these questions. It's a very complex process. But what's very likely is this person could be having a brief period of intense emotional processing and having insights frontally. That is consistent with seeing what we've showed you in terms of frontal midline theta and insight and increased activity when people are having insight. So, I mean, that's a theoretical improvisation, but it's grounded in very good theory and clinical observation. And again, that brings us back to alpha theta training. Theta will increase when we're having insight. It will also, more frontally, it will tend to increase in the back. When we're integrating, both those pathways need to be worked. This client has theta already high, like a crossover, but it's not frontal. It's more in the back that is high. So that means they may be drowsy. You notice that the delta is starting to go up. They may be not getting enough sleep. If this is eyes closed, there's a little bit of inflammation in the back. We have a lot of excess activity in the emotional realm there in the back. This is like that kid that we showed you before was having problems with the teacher. Something else that's shown up that's interesting recently, training theta with photic stimulation. And we've posted this, I think, on the Internet. But what they found is they actually found improvements. in memory by training with theta photic stimulation. This is a new hot topic in research and using MRI to research the benefits of theta for memory. As you imagine with so many older people having problems with memory, increasing theta can enhance memory, especially if you have low theta. So stimulating people at... 5.5 Hz actually helped. This is 2016. The beneficial effects of stimulation in theta range are not limited to cognitive processes. For example, low-frequency stimulation has been shown to be beneficial after an acute spinal cord contusion or an 8 Hz stimulation of the Ralf nucleus. Improved motor coordination, sensory processing, increasing white matter integrity, and reducing astrocytosis. This is slow at alpha, actually. It shows that lower frequencies, you know, close to the theta range, also have benefits physiologically. Kirk and McKay, who I started out this study, were the ones who were, I mean, this presentation, were the ones who first made notice of the fact that there seemed to be two thetas. And they went on to say, we further suggest that it's possible that noninvasive neocortical recording of theta EEG activity, what we do with QEG, from the scalp in humans may provide a window through which to... is the integrity of limbic theta-related processing. And it's from that insight that we started looking at the maps and places like O102, sequential processing, P3P4, short-term memory, F3F4, working memory, T3T4, semantic memory. They're hubs. They all work together. But if any hub is out, you have a problem. And if you're not getting enough theta input, then likely there's something wrong with your memory and emotion processing. So Kirk and McKay inspired us to interpret maps differently. Here's a classic attention deficit pattern. Notice again, frontal theta excessive. Is this a perfusion issue or an emotional processing issue? Well, you won't know unless you investigate. Do a good... clinical interview and look at all your data because that's what's required to make that distinction sometimes. Here's theta in Parkinson's and notice the reduced beta activity. This is inflammation, reduced perfusion, and reduced resources for activation of the higher frequency beta. You see dominant frequency alpha is slowed but theta is not read so we've got Slowed alpha, that's elevated. We've got real theta, reduced perfusion, and real delta inflammation. And then here's theta and dementia. Notice that delta and theta are dominating. This person was clearly diagnosed as having dementia by a neuropsychologist, and that's the map. Interestingly enough, their beta is not blue yet. Everybody's a little different. The stages are a little different. People respond to disorders in the same way, differentially as they respond to medication or neural feedback. This is what makes it so challenging to do this. But that should give you a good overview of theta, TBI, damage to structures in the temporal lobes. We have problems with hippocampal response to septal oscillations, so memory is dysregulated. Phase timing is off, so we can't integrate with our thinking brain, and projection of cortical regions becomes disruptive. If we look at the computerized performance testing with the new mind system, here's a good example of theta and delta being low in the posterior. Input to sequential and short-term memory is reduced, and what's showing up is sequential memory is most affected. Again, people are differential in their responses. Here's sequential memory and excess theta. So not only is low theta a problem, but too much theta can be overwhelming. And again, sequential memory is a problem. You can see that 0102 is disrupted there, again, for sequential memory. And then working memory, low theta frontally at F3, F4, and delta. Delta is critical to working memory, particularly in the frontal region. And notice that we have working memory is not working, and sequential memory is being affected as well. So there's 0 and 02 in the back. And we can see that we should get some issues with short-term. Short-term memory is a little low, but not that bad. So you see that the correlations line up when you start looking at all this stuff. Again, another working memory. And... Lastly, when we go to train, we can't always train in the area that anatomically makes the most sense. So if I have somebody who has a problem with word retrieval, and we know T3, T4 is the hub for word retrieval, it won't always get you the results you want. In many cases, it didn't work for us. We trained at FP1, FP2, particularly FP1 in the left frontal region. And we went from a pre-test of 35 percentile to post-test of 85 percentile in two weeks, training the frontal area. because our problem was really in the frontal area more than the temporal region. And you can see the temporal region is out there, but again, if I trained coherence here, it wouldn't have improved things as much as if I trained FP1, FP2. And lastly, we have what OxyContin and Klonopin combined can do. Notice we have elevated frontal beta from the Klonopin, and slowed alpha and reduced perfusion from the OxyContin. This person's like asleep with her eyes open. So that's what that does. Okay, so I got through it and that's going to be our presentation on the two thetas. I hope that helped give you some insight into the complexity and a lot of the ideas here.

I'm going to show your screen. We don't see your screen yet. Thank you.

Okay. There we go. A Tale of Two Thetas. Ooh, it sounds like a book.

Yeah. Well, Niedermeyer, back in the 90s, finally convinced people with his research that there were actually two alphas, a higher faster frequency alpha and a lower frequency alpha. We've been seeing it in the brain maps for years and have been telling people about it.

And when his research came out, it wasn't that much after we were seeing it, but nobody saw his research. And finally, early 2000s, people saying, oh, look, well, Niedermeyer says there's two. And they started looking and pretty soon everybody agreed there's two alphas.

What's been going on since 2002, 2003 is that the same thing has happened with Theta, but most people have not been paying attention in our field to that fact. although I've been talking about it since 2004, 2005, when I was digging into this stuff, but it still hasn't really caught on in a sense. People really aren't really understanding this.

When you say two thetas, people think of good theta and bad theta. That's not the theta I'm talking about. In fact, just like the two alphas come from...

different processes. The two thetas come from different processes in the brain. So, you know, let's talk about theta. It's a very complex subject.

Theta has turned out to be way more complex in terms of what it does in the brain than anybody previously imagined, especially in the field of neurofeedback. It was just something you got rid of because kids with attention deficit had too much of it. But the story is way bigger now.

You know, you all know that theta is critical for connecting up with the cortex and generating your thinking process, your thought processes. So we'll talk about that later on, too. I'm just going to start off kind of at the myth level because there's always tons of that in our field. And so is the confusion. So if you don't get a lot of what I'm saying, don't feel like you should have gotten it because a lot of it's very.

confusing and complex and I'm just going to be presenting a lot of the information, some of it very cutting edge, some of it actually pretty old, about theta just to give you a new perspective on the topic. But this will be posted up on the internet in a few days and you'll be able to review it several times if you like. The theta myths are that attention problems are caused by too much theta. Like if you have too much theta, that... therefore causes attention problems.

And that's too simplistic. I mean, it's okay to kind of think that way for convenience sake, but they're correlated. There's not a causal relationship.

They're correlated. Something happens in the brain, you end up with a lot of theta, and it tends at the same time that people have attentional issues. But as you know, the brain is a system and it's a very complex relationship that causes this. Another one is that the theta to beta ratio is the best way to tell if there's too much bad theta.

Because there was good theta and bad theta. You know, theta is okay, but if you have a lot of it, it's bad. You know, there are different theories about it.

The theta-beta ratio is not the best way to tell if there's too much theta, bad theta, and too much of a problem with attention deficit. And we'll show you that in a minute. And then there's the other myth that... theta should never be trained up. Well if you have low theta, if you don't train it up or get it up, you're gonna have a lot of problems with memory and emotion possibly too.

So let's look at this map. Here we have a map showing you power or magnitude, you know roughly the same thing, and this person was diagnosed officially by a psychiatrist with attention deficit hyperactivity disorder. So where's the theta here? Where's the low beta here?

I mean, not only do we not have high theta, we don't have low beta, so we don't have any theta to beta issue. When we actually look at the raw morphology on this map, what we find is a lot of beta spindling. So it's not a theta issue, it's a beta issue, it's beta spindling, and it's one of the phenotypes Jay Gunkelman recognizes.

being associated with complaints of attention problems and actually oppositional behavior problems too. So that just blows that myth right out of the water. So if we're having problems and myths with this, let's kind of drill down a little deeper and see where's theta coming from. What's it doing? So this will make your eyes cross, but this is Coulomb 2005. So it's pretty well established at this point.

And what you're seeing here is the hippocampus up here, right, and the hypothalamus over here. And in the middle is this structure called the septum. And I've always said, and we frequently talk about research saying that the septal hippocampal oscillators are what cause theta.

Well, this is showing why we say that. And you can see that there's activating neurotransmitters, acetylcholine, and inhibiting neurotransmitters. And the activity of these networks, these little networks, generate oscillator that produces theta. And...

There's a lot of arguments about, well, does the septum produce or initiate the oscillations? Is it the hippocampus that initiates because it takes two to play? Who's starting the dance? And then other people say, well, wait a second, maybe it's the hypothalamus. So there's a lot of unresolved issues here that are going on.

The septum is a relay between the hippocampus and the hypothalamus. Like the hippocampal formation, the septal area has been implicated in the control functions. normally attributed to hypothalamus, such as aggression, rage, and autonomic functions, and self-stimulation, and drinking behavior.

So as it turns out, theta drives the hypothalamus. The septum is driving the hypothalamus more than anybody realized. So a lot of these attributes that the hypothalamus supposedly was in control of turns out to be a function of theta. Just like activation of 15 to 20 hertz in the cortex is related to theta.

So as we look into it, theta is a very central rhythm and a very old one in the brain and is a part of our mammalian past. And other animals lower on the echelon... that are mammals, have a lot more theta than we do and it dominates their EEG like alpha and beta dominates ours. The other thing is that it links to what we call the supramamillary nucleus. That connects to the ascending reticular system.

So this rhythm is connecting the endocrine system and the electrophysiological system. So it is central to communicating to the body and from the brain and from body back to the brain. Theta is critical for communicating information to both the endocrine system and the electrophysiological system. As it turns out, theta seems to have dual functions in this process, memory and emotion.

And if you think about memory and how it relates to emotion, it makes sense that those two functions would have to be together because how you feel about what happens helps you determine how much you remember of it, how long you remember it, and how long it stays available. So different component frequencies of theta enable the hippocampus to potentially select and entrain different resonant loops at different neocortical loci. So saying the hippocampus resonates with the cortex. gray matter in an important way. Its correlated or phase-locked activity may then result in strengthening of synapses in the selected loop by Hebbian mechanism, and this becomes what we call learning memory.

Now there's also theta-modulated processing in the hippocampus that may be integrated with theta activity in the frontal or the temporal lobes. So it's not just involved with the cortex in terms of learning. but it has a dual pathway, both to the frontal and the temporal regions of the neocortex between these loops.

So if we look at what Kirk and McKay, who were focusing on this for years, their conclusions in 2003, was that there's this 3 and 4 hertz pathway, which today is being called the recurrent pathway. which is dominantly emotional but not exclusively. Nothing ever seems to be exclusive in the brain. And then there's the 5 Hz and 7 Hz pathways, which is more.

related to memory but not exclusively. And so that's the ascending pathway. And they have two pictures here of the pathways and you can study those from the internet if you want. I could spend an hour just on this topic right here.

But, you know, pulling together different pieces of research, the more recent ones are showing us recurrent theta, 3 to 4 hertz. tends to dominate P3, PZ, P4. And what area is that?

That's the default mode network. And you've probably heard at this point that theta is strongest in the default mode network and key to its functioning and processing. And you can see the pathways right here. It goes right through the association cortex into the cingulate region. And it's recurrent and recursive.

It keeps... Going through this process, this is where we get rumination from. This is where the default mode system keeps feeding back on those memories and emotions to process, you know, ideas when you're thinking in your mind, eye about things.

But it's a very emotional-related process. Knyazov calls it implicit early-stage emotional process. Then we have septal theta or the ascending system which is 5 to 7 Hz and that tends to get up more in the dorsolateral and the midline and FZ.

And this is more related to acquisition in terms of directing the external attention system. It helps direct it towards stimuli of interest. It works in conjunction with frontal delta and it's related to working memory quite a bit.

And so that's more a part of the central executive. So the recurrent was more related to the default mode system and the more emotional. And then we have the ascending, which is more memory related and more related to the central executive. So we have this pathway and that pathway, the two stages.

And Knyazev would call this the explicit late stage emotional process. So you notice. He's noticing that there's an early stage which is very emotional and primitive and a more later stage which is more cognitive.

The middle temporal lobes are critical factors in what we call the salience network. And so I'm just showing you here from some of the research how the temporal lobe ties together the parietal and occipital cortex, the what and where pathways that we talked about, the dorsal and lateral pathways, and links them to the hippocampus. and the memory function and those all converge through the insular and the ascending pathways, the insular cortex and the ascending pathways, and also involves the vagal system.

And this is super mammillary regulated. It's very interesting. So the theta is connecting the brain through these pathways with the body, with the endocrine system.

And with the electrophysiology of the body, it's a two-way street. And this, in turn, responds to shifts in symmetry. The front-to-back shifts are related to left-and-right shifts. The front-and-back shifts are much more driven by default mode versus central executive, whereas left-right is much more driven by positive and negative emotions.

So these two play off of each other, which is why in the New Mind training, you have... Activation versus symmetry. Activation is front to back, symmetry is left to right. And here's the subcortical pathways for the ascending systems and you can see how involved they are. And if you're interested in this, I've done presentations on the ascending system and asymmetry, and it links into what I'm talking about now.

And you can see if you look at the theta generators, how much of the brain they affect. and interact with. You can see the amygdala, the striatum, the motor system, the olfactory system, anterior ventral thalamic nucleus, related more to frontal lobe processing, and then the more septum and the areas that are more limbic and emotional.

So it links all of these things together. When we get to the frontal system and we get away from that recurrent system, We have some research showing that frontal midline 6 Hz generates sinusoidal spindles in 1 to 10 second bursts. And that this insight in frontal midline theta is involved in the detection of novelty, of conflict, or things that don't work.

We're an error detection system. It's where punishment, you feel negative if something bad happens, and when there's conflict, and when there's error. So the system is looking at...

Emotional response to novelty and whether everything's good or a negative system. And that's the external attention system we're always talking about. Now that posterior system that's recurrent, that tends to show up when people get drowsy. So if you're looking at people as they're getting drowsy, you'll see maybe alpha going down. Sometimes some people it tends to go up a little bit at first and then it drops out.

And then the delta starts increasing and then theta increases as well. So here we have a map of somebody starting to get drowsy. You can see the alpha starting to drop out and the theta starting to increase. And then if you keep going, the alpha drops out significantly and the theta increases a lot.

This is what happens in alpha-theta training. So when we're doing alpha-theta training, we're dropping back to that recurrent system that's driven by the default mode system. So you're shifting in and out of consciousness, but you're tending to focus it on the default mode system in alpha-theta training, which is one of the ways we integrate emotion and trauma is through that system.

And, of course, you've heard a lot about that recently. Another aspect of theta is not just emotion and memory, but also glycogen reduction. So theta increases as perfusion decreases.

So we get reductions in oxygen or glucose. In other words, if somebody's not getting enough oxygen or they're not getting enough glucose, they're type 1, type 2 diabetic and their blood sugar's dropping, you'll start to get more theta. So here's an example of the alphas dropping out as the theta increases and the delta starts to increase.

And then stage 3 in glycogen reduction is you get delta and theta increasing. So you can have theta. As a consequence, not just processing emotion and memory, but it can be an indication that you're getting reduced perfusion or reduced glucose or reduced oxygen in the brain.

The emotional recurrent theta is very interesting and it has a relationship that's... That stimulates the ascending system and gets people worrying and ruminating. So I'm just showing you that there's previous research going back quite a ways to the fact that emotional attention was recognized as being related to 5 to 6 hertz theta.

And then in the 90s, the frontal parietal research showed that it's very hard for them to distinguish between... what was being reported by some researchers as just frontal exclusive theta or theta relating to the frontal midline. And here's an example of this emotional theta. This was a pre-training screen of an emotional abuse case. This was a child who was in school, who was doing poorly, had a good family, good diet.

Nobody could figure out why. We found out that there was an emotionally abusive teacher who was making this kid's life miserable, and he couldn't study, and he was being singled out. And the other kids were starting to bully him because the teacher's attitudes toward him kind of reflected modern political activity.

And so after we found that out and got him out of the class, notice this theta here in blue, is that about... 20 microvolts. You can see delta is quite high. It's not getting enough sleep.

I mean, in the past, people would just say, well, this is bad stuff. There's too much. Let's just train it down. But once we straightened out the emotional situation, look at what the theta did. This came in like a week after we were training for weeks.

This is all we got. After we took them out of the classroom, that's what we got, an actual normal range of activity. So his sleep improved, his emotional life improved.

So when you see... elevated theta, particularly in kids, you know, they're calling it attention deficit, but here's an example of it, maybe emotional abuse. Okay, and we saw in the original work with Judy Lubar that when there was a problem in the family and emotions ran high, the kids training in their clinic started to do terrible with theta suppression.

This is about getting beyond just looking at the EEG and trying to understand what the physiological causes and social causes are behind it, rather than just blindly training things. Now, some people got a little off kilter because we introduced a new protocol into the system, whereas if you had very little delta eyes closed, but you opened your eyes on your map and you had a lot of delta, the map would say train 2 to 12 down. Well, you know, after we looked at things for a couple of years, we realized, you know, we learned from running statistics and talking to everybody that that's a situation where somebody's not getting enough sleep.

And just training delta down is not, you know, with our eyes open, is not necessarily going to fix the sleep problem. So that's why we often encourage people instead of doing that now to do alpha theta training. Now, there's other ways you could do SMR with eyes open. And we've talked about that on other Lunch and Learns. We could.

discuss it more, but I don't want to get too bogged down into it. But again, these things are all connected. One of the things that we talk about sometimes, too, is that the digital filters can be fooled by slowed alpha and give you, well, it's false theta, actually. So, you know, you might say, oh, look at this theta in power or magnitude here.

The person has a lot of posterior theta. When if you go down to dominant frequency, you can see. that the alpha has slowed way down.

We don't really have often very much in the way of fast theta. That's not a typical thing you find. So what you're really seeing, if you actually look at the raw EEG, is alpha that's going as slow as seven cycles a second, and it's being picked up by the digital filters, and it's looking like it's theta in magnitude, and it's not. So you can have a reduction in perfusion.

that causes that. You could have reduction in blood sugar, kids with blood sugar problems that cause that. You could have a thyroid or liver issues that cause that. So these are the underlying physiological things that can cause slow alpha that give you false theta.

And you could be interpreting it incorrectly. You need to be careful about just making up simple rules about what theta means. Here's an example of how Problems in theta and alpha and beta correspond to increases in communication in the cortex.

Here you notice the frontal temporal theta showing elevations, and look at the connectivity. It is compensating. Alpha, frontal and posterior, compensating. Beta, global, almost global compensation.

So you can see that theta. just like alpha and beta, tends to increase in communication interhemispherically when there is abnormalities in the magnitude. This is the brain trying to increase communication to compensate for problems.

Let's say that your blood sugar is dropping, or that you haven't had enough sleep, or some other thing that's not getting enough oxygen. asthmatic. And what's going to happen is that when that alpha slows and you get frontal theta, maybe you're reducing perfusion here, the brain is going to try to increase communication to offset those problems, trying to compensate for the loss of function. We talked about the fact that theta tells the cortex what to do in terms of beta. Well, it's not quite that simple.

There's a feedback loop between the two. But when you go and focus on a salient stimulus in the external world, and your central executive system starts to speed up and pulls you out of the default mode, and you go out to look out to see what's happening over there, that theta will start to resonate with gamma in the cortex, and the gamma will stimulate 15 to 20 hertz beta, which is... Again, stimulating thinking or worrying or ruminating, all of those things.

And this came out of Meehan and Bresler's meta-analysis as far back as 2012, which is five years. That's a long time in research, but in terms of the street, most of this has never even hit the street. Most people don't even know much about this kind of stuff.

So we have cross-frequency coupling that involves theta frequencies interacting with dit. distant regions through phase coherence while coupling with gamma freeze frequencies to drive cortical activities in the 15 to 20 hertz range. And you can see here's your gamma, right, and here's your theta, and they nest. They're nested, and this is an example of how they nest together. And this nesting sequence, the phase relationship, and of course we don't have time to go into it here.

Again, I've discussed it in network. related presentations. This nested gamma here is what stimulates cortical activity to get these metastable networks going, which represent you processing information. Let's talk about theta and the spectral distribution. In the frequency domain, if you look at here's The eyes open on the left in A and eyes closed in B, and you can see that familiar bump up at 10 Hz in alpha when the eyes are closed.

And notice it's dominating on the right, not just what I talk about. This shows up consistently in research on symmetry, but even people just looking, what's the distribution of the EEG? You can see alpha's highest on the right side with eyes closed. It's elevated.

We look at theta. Theta is... Here we got, they're looking at 6 hertz here. We can see that it's higher than alpha with eyes open, and it tends, frontal and midline tends to be highest with eyes open.

But when you close your eyes, notice that the theta tends to be central, more balanced, and it tends to be more towards the posterior. And that's because the default mode network, when your eyes are closed, should have the highest theta. This was predicted by our... our brain map algorithm. I was predicting that before anybody did any of this research because when we ran the algorithm that's what it predicted and we weren't hearing from anybody else about that and you know that's one of the reasons that our database system is different from others.

It's based on an algorithm and not just on a statistical descriptive processing. In terms of spatial distribution of theta, more recent research, 2013, is telling us it's highest at PZ, again, default mode. T3, T4, T5, T6, this is a classic default mode pattern. So there's your frontal midline theta, there's your posterior theta.

These are the two theta networks. There's your ascending, and there's your recurrent, back here. Default mode and the ascending. becomes critical in the central executive processing when the eyes open. The salience network in the middle temporal lobe switches back and forth between a more dominating frontal ascending system or a more dominating posterior system, and that's related to the salience switch.

When we're in optimal twilight state, theta is dominating. and alpha is low. So we're pretty much in a liminal state in the default mode system integrating processing there. And these crossovers were noted in early alpha theta training and you know eventually evolved into major studies on using this unique feature of theta to help people integrate.

Alpha synchronization and desynchronization, which we talk about in peak performance, all the time is related to theta. Theta salience shifts move you into the central executive, and that reduces alpha activity, or into the more default mode, which produces more alpha activity. So you shift back and forth with this middle temporal activity.

responding both to stimuli coming in and to, you know, in terms of the perceptual processing, but also the body's response to the stimuli coming in, you know, and the discussion between the amygdala and the early emergency detecting system and the heart and the lungs and the rest of the body. Now all of these have their own linked system connected with the vagal system and the whole body responds to input, salient input. and it goes up the ascending system and it tells the septal hippocampal region, oh, you know, we've got something of interest. What do we do?

What do we tell the endocrine and physiological system to do from this point on? So you see it's very complex, and we're just still learning about that in neuroimaging. And one of the emergent theories, which has strong basis in the electrophysiology, is that psychopathology is very related to salience, and that when the salience network's not working well, or if somebody's deeply stressed, they may withdraw into the default mode system more and have trouble activating the central and frontal systems, central executive and the frontal regions, dorsolaterals.

So this problem... with processing is a characteristic of a lot of disorders. People are kind of stuck in their default mode network. And if you're not getting enough sleep, you're also going to have trouble activating your central executive.

You're going to be stuck in your default mode network. So papers have been written saying, you know, maybe this is one of our best measures of disorder. How flexibly can people shift from internal default mode network processing to external processing? And is there a balance between the two in both states? Or are people more extreme external and more extreme internal?

It's a whole area of research which could be very promising. And again, this SN that's causing the shift here is related to theta and to stimulus detection. So let's jump over and talk a little bit about theta artifacts. Theta can show up in maps, and it could be just artifact from eye blink, also from body and head moving.

And if you have an electrode that's cracked that you're using or defective, you could get theta as well. It's not real theta. So we have to keep an eye out for false theta from eye blinks and eye saccades. You have to watch people's eyes when you're mapping them and training them, and watch your raw EEG to see if it's this kind of artifact theta. Again, there's a whole presentation on artifacts, and this goes into more detail on that presentation up on the Internet.

Here's an artifact that we talk about in that presentation of this person's normal theta, and then an ear clip that keeps getting whacked by hair or a collar on a coat. It might be wintertime, and they don't want to take their jacket off because the core temperature is low, even though they're in a comfortable room, and then they keep hitting their ear clip on the high coat collar. So this is the kind of false theta you get, and delta, when it's really down here. So there was work done.

Back in 2001, when we were all looking at attention deficit and wondering why theta seemed to dominate in it, people weren't looking at low beta so much as they were looking at high theta. Confirmation bias there, you know. And this research showed that prefrontal blood flow dysregulation in children with attention deficit that weren't taking drugs. And they didn't have structural abnormalities. What they found was, in fact, elevated theta, especially friendly, often indicated reduced perfusion.

So that goes back to the beginning of our discussion when I said, well, you know, theta could be a consequence of reduced glucose or reduced oxygen or both in terms of reduced perfusion. So when you look at a brain map and you see theta below I mean, high frontally, that could be very easily a perfusion issue. Whereas if it's global, you know. It could be related to inflammation. If delta is high, it could be related to degradation of the brain and the temporal regions like in dementia.

So elevated theta is not just a simple case. You have to look at what else is high and what else is low. We talk about that all the time.

So the theta-beta ratio mythology. is put to bed by the co-registration studies. Beta, theta to beta ratio fails to take into account delta magnitude, as well as theta and delta locations, since it's taken only from CZ. This is a problem. You know, theta is at different levels frontally and posteriorly, and may be higher or lower for various different reasons.

And also, if you're not accounting for delta being elevated, you're not going to get an accurate level of brain activation. Because if we look at blood flow and perfusion, theta is one good measure of it, but it's not enough by itself. So Rosa et al. in 2009, they tried to figure out what's the relationship between electrical activity and blood flow in the brain, and could you make electrical activity a proxy measure of blood flow? And they found that, yes, indeed you could. could and that's one of the whole concepts behind our what we do at New Mind and with the database system and how we interpret the database system which makes us somewhat different from a lot of the way a lot of other people are looking at it and we find it's much more accurate when it comes to getting at the source of the problem but then our perspective doesn't rely solely on neurofeedback our system says you have to take a biopsychosocial approach to resolving problems.

In this piece of research with Rosa et al., you can see they had to include delta to get a correlation that looked like that. So here's the BOLD signal, blood flow, activation, glycogen, and here's their heuristic, their EEG heuristic, the way they calculated it, which is very complex and beyond the scope of what we're doing here. But basically they're looking at both delta and theta and relating it to fast wave activity and looking at that ratio. And so you have to include delta to really get an accurate sense of perfusion maximally.

All of this over the years has led us to the stages of oxidative stress perspective. I'm not going to go into too much detail. There's whole presentations on the internet.

I've written papers. I've posted research on InMind Journal. I've done presentations at ISNR. Those are all out there and available. And I'm getting a lot of support from a lot of directions on this.

But you can see the brain starts out pretty green and slowly gets red as it becomes overactive. And then over time, it starts to get pretty red in the low frequencies as it becomes underactive because it's exhausted itself by too much activity, what we call excitotoxicity. One of the things when you down-train theta, you often get a systemic response. We often note that when we down-train delta or theta things, the whole system gets lower, and people go like, oh, my God, we're over-training.

That was an old concept from the late 90s. It doesn't make any sense physiologically. Somebody kind of pulled it out of a hat.

They really weren't thinking through things physiologically. But then again, in fairness, we didn't have quite as much information back then. And really what we understand now is that when you're resolving inflammation, okay, the perfusion activity increases.

So theta drops out when the delta drops down, when the inflammation drops down. And what's happening is you're starting to see the real skyline, the real distribution of the person. This is a distribution. that is driven, inflated by delta and theta, by lack of perfusion and too much inflammation.

When we start to remove those factors through nutrition and counseling and exercise and neurofeedback, we start to see, oh, this person's system is pretty exhausted. Their native MAP is actually quite low. And if we keep training, this delta comes down.

We'll probably even see this theta dropping to blue. Now, it doesn't stay this way. If you can get the... profusion increased and the inflammation down, you may have a lot lower than average power.

But over time, as you take care of your system, the power will globally come up across the board. But this doesn't happen that often in just, you know, a few months. A lot of times this process can take a year or two. I mean, people don't get into this trouble in just a few months usually. So down training results here.

We're down training. Power is decreasing again in this particular map. It's a different one. Note that the change is in. low frequency, and we're getting a 35% change.

That's good. The brain's responding well to the neurofeedback. Very good reorganization.

Unusually high normalization. They're both at 50-50. Usually reorganization's at 60 and normalization's at 40. So this is a good solid change that we would expect. Everything's going low, and now slowly everything will start to return to normal power, but in the right distribution.

When we train up, sometimes we get some interesting changes. Here, this person had low delta, and what we found is when we trained the delta up, their sleep improved. Well, now there's research showing that if you train delta down, sleep gets worse.

So you don't want to train delta down when it's already normal. Not a good idea because that would make people sleep worse. And so, you know, we adjust our protocols in the system bit by bit as we learn this stuff.

We're not just going to keep everything static. I know it kind of moves your cheese and rattles your cage a little bit, but think about the fact that what we're doing is actually gradually learning and improving the system so your clients do better. In this case, the delta was trained up. You can see the post-map shows a lot of extra green, great change.

Notice that the alpha in the pre dropped down. This person is getting more sleep. The beta is dropping down.

They're less anxious. The theta is increasing. Why is frontal theta increasing?

We don't always know the answer to all these questions. It's a very complex process. But what's very likely is this person could be having a brief period of intense emotional processing and having insights frontally. That is consistent with seeing what we've showed you in terms of frontal midline theta and insight and increased activity when people are having insight.

So, I mean, that's a theoretical improvisation, but it's grounded in very good theory and clinical observation. And again, that brings us back to alpha theta training. Theta will increase when we're having insight. It will also, more frontally, it will tend to increase in the back. When we're integrating, both those pathways need to be worked.

This client has theta already high, like a crossover, but it's not frontal. It's more in the back that is high. So that means they may be drowsy. You notice that the delta is starting to go up.

They may be not getting enough sleep. If this is eyes closed, there's a little bit of inflammation in the back. We have a lot of excess activity in the emotional realm there in the back. This is like that kid that we showed you before was having problems with the teacher. Something else that's shown up that's interesting recently, training theta with photic stimulation.

And we've posted this, I think, on the Internet. But what they found is they actually found improvements. in memory by training with theta photic stimulation. This is a new hot topic in research and using MRI to research the benefits of theta for memory.

As you imagine with so many older people having problems with memory, increasing theta can enhance memory, especially if you have low theta. So stimulating people at... 5.5 Hz actually helped. This is 2016. The beneficial effects of stimulation in theta range are not limited to cognitive processes. For example, low-frequency stimulation has been shown to be beneficial after an acute spinal cord contusion or an 8 Hz stimulation of the Ralf nucleus.

Improved motor coordination, sensory processing, increasing white matter integrity, and reducing astrocytosis. This is slow at alpha, actually. It shows that lower frequencies, you know, close to the theta range, also have benefits physiologically.

Kirk and McKay, who I started out this study, were the ones who were, I mean, this presentation, were the ones who first made notice of the fact that there seemed to be two thetas. And they went on to say, we further suggest that it's possible that noninvasive neocortical recording of theta EEG activity, what we do with QEG, from the scalp in humans may provide a window through which to... is the integrity of limbic theta-related processing.

And it's from that insight that we started looking at the maps and places like O102, sequential processing, P3P4, short-term memory, F3F4, working memory, T3T4, semantic memory. They're hubs. They all work together.

But if any hub is out, you have a problem. And if you're not getting enough theta input, then likely there's something wrong with your memory and emotion processing. So Kirk and McKay inspired us to interpret maps differently. Here's a classic attention deficit pattern.

Notice again, frontal theta excessive. Is this a perfusion issue or an emotional processing issue? Well, you won't know unless you investigate. Do a good... clinical interview and look at all your data because that's what's required to make that distinction sometimes.

Here's theta in Parkinson's and notice the reduced beta activity. This is inflammation, reduced perfusion, and reduced resources for activation of the higher frequency beta. You see dominant frequency alpha is slowed but theta is not read so we've got Slowed alpha, that's elevated.

We've got real theta, reduced perfusion, and real delta inflammation. And then here's theta and dementia. Notice that delta and theta are dominating. This person was clearly diagnosed as having dementia by a neuropsychologist, and that's the map.

Interestingly enough, their beta is not blue yet. Everybody's a little different. The stages are a little different.

People respond to disorders in the same way, differentially as they respond to medication or neural feedback. This is what makes it so challenging to do this. But that should give you a good overview of theta, TBI, damage to structures in the temporal lobes.

We have problems with hippocampal response to septal oscillations, so memory is dysregulated. Phase timing is off, so we can't integrate with our thinking brain, and projection of cortical regions becomes disruptive. If we look at the computerized performance testing with the new mind system, here's a good example of theta and delta being low in the posterior. Input to sequential and short-term memory is reduced, and what's showing up is sequential memory is most affected.

Again, people are differential in their responses. Here's sequential memory and excess theta. So not only is low theta a problem, but too much theta can be overwhelming.

And again, sequential memory is a problem. You can see that 0102 is disrupted there, again, for sequential memory. And then working memory, low theta frontally at F3, F4, and delta. Delta is critical to working memory, particularly in the frontal region.

And notice that we have working memory is not working, and sequential memory is being affected as well. So there's 0 and 02 in the back. And we can see that we should get some issues with short-term.

Short-term memory is a little low, but not that bad. So you see that the correlations line up when you start looking at all this stuff. Again, another working memory.

And... Lastly, when we go to train, we can't always train in the area that anatomically makes the most sense. So if I have somebody who has a problem with word retrieval, and we know T3, T4 is the hub for word retrieval, it won't always get you the results you want. In many cases, it didn't work for us.

We trained at FP1, FP2, particularly FP1 in the left frontal region. And we went from a pre-test of 35 percentile to post-test of 85 percentile in two weeks, training the frontal area. because our problem was really in the frontal area more than the temporal region. And you can see the temporal region is out there, but again, if I trained coherence here, it wouldn't have improved things as much as if I trained FP1, FP2.

And lastly, we have what OxyContin and Klonopin combined can do. Notice we have elevated frontal beta from the Klonopin, and slowed alpha and reduced perfusion from the OxyContin. This person's like asleep with her eyes open.

So that's what that does. Okay, so I got through it and that's going to be our presentation on the two thetas. I hope that helped give you some insight into the complexity and a lot of the ideas here.

Transcript for:Exploring the Complexity of Theta Waves

Transcript for:
Exploring the Complexity of Theta Waves