The problem with narcissism is, “what exactly IS it?” A quick run through Google indicates it is “An excessive preoccupation with one’s own personal importance, or with achieving one’s own chosen goals rather than bonding with others, or with associating only with others whom one chooses.” So what is excessive here? An excessive lack of preoccupation with one’s own personal importance or preoccupation with bonding with others at the expense of self is lack of boundaries or perhaps co-dependency. The problem, as always for me, with these diagnoses is that they are extremely difficult to define. “I can’t tell you what it is, but I know it when I see it”. I assume most wagon train leaders, most inventors and many entrepreneurs would meet these criteria.
So I would ask you, as I do in the assessment process, to skip the naming game and go all the way back to the behavioral issues. What exactly are the problems “this” person is demonstrating that lead people to decide he/she is “narcissistic”? With those, we can perhaps pin down what some expected brain activation patterns might look like.
Obsessions and Compulsions
The OCD patterns in your clients are tertiary–they’re defenses against emotional drive issues. In NF we would focus on resolving the emotional drive, then the OCD may melt away or be easier to train away.
Obsessive thought and compulsive behaviors are often used as a way of covering over either anxiety or depression, so you need to be sure to deal with what is underneath the defense before you just go in and blast it away–if the brain LETS you blast it away. The TQ is a great way to start, because you’ll get a better idea if you are looking at depression or anxiety as well as what the pattern is that is related to the O/C behaviors. Some clients will show a hot cingulate (shows up at Fz or Cz); others will have high fast-wave coherences.
Start training what is underneath first, and the intellectual defenses will usually recede before you even start messing with the symptoms. Then the O/C material is much easier to train.
The brain is not actually “wired” like a toaster. It forms and terminates connections constantly, so the idea that there is “faulty” wiring or circuitry is probably not terribly helpful. The brain learns responses/strategies for dealing with challenges, and these do show up in the activation patterns of brain energy, where they tend to be quite stable. However, to suggest that OCD, which is generally a strategy adopted by a specific brain to block excessive depressive or anxious feelings, is anything other than an increasingly dysfunctional strategy has no real basis of which I’m aware. It is already an overly frontal-lobe oriented attempt to intellectualize experience to avoid feeling it. Hence the anterior cingulate, which performs the function (among others) of serving as the spigot which determines how much or how little emotional material from the limbic system gets to the prefrontal cortex (pfc) to be integrated into the decision-making process, is already over-working. That’s why it gets “hot” with excessive fastwave activity–and later “burned out”.
The idea of brain training is that one can identify the places where the excess limbic energy is showing up cortically and train to reduce those levels, which reduces the “pressure” of emotional drive and allows the cingulate to perform in a more functional way. Since another function of the cingulate/basal ganglia/orbitofrontal cortex loop is to send messages to the pfc when a task has been completed, the previously overworked cingulate now has more capacity available to handle this task and the “skipping” which characterizes OCD–not recognizing when something is done so the PFC can move on.
Wolf packs are remarkably stable in their roles, with the alpha male and female maintaining tight control. It is interesting to note that experiments looking at brain activation found that the alpha males at least produced dramatically higher alpha levels than the other wolves in the pack and, in fact, there appeared to be a direct correlation between alpha levels and pack rank. When the alpha male was temporarily disabled (tying one leg or putting it in a cast or something), and another male took over, alpha levels rose in the new leader of the pack and fell in the old one. (I don’t know who thinks up this stuff or how they do it, but it’s interesting.)
Children in a family are like the young wolves in a pack. As long as there is a clear hierarchy, they tend to sustain stable roles (positive or not). However when, due to death, divorce, changes in works schedule or whatever, the alpha male in the family is absent, there is often a competition for that role. Especially when the family is left with a single mother, who must now try to cover both the nurturer and enforcer roles–and who may be feeling guilty or depressed or exhausted at the same time this nearly impossible demand falls on her–there is a strong motivation to “go for it”. It is not only the males who do this, but most of the male children seem to get involved.
One study showed an extremely high incidence of “ODD” behavior (perhaps better called “auditioning for dominance”) suddenly appearing in families where such a dislocation had occurred. Given an understanding of this phenomenon, perhaps the correlation with “RAD” clients, who have suffered pretty significant dislocations, makes sense. And, of course, the co-existence with anxiety (“I don’t really know if I SHOULD be the alpha male, since I’m only 6!”) may also make sense.
When a new parent joined the family, there was also frequently a disruption in the homeostasis and, especially where one of the male children had assumed the alpha male role and was “running the show”, the entry of another male often correlated with lots of “ODD” behavior.
Russell Barkley (hate to quote the guy, but) refers to some pretty impressive research that indicates ODD is very often a “trained” response produced by parents. In the Atlanta practice, we often did a 3-session ODD workshop for both parents (if possible) in a group setting. We motivated them with data about what happens to kids who reach age 14 without having dealt with ODD issues. We demonstrated the well-known “If you don’t stop that right now, I’m going to…” game in two levels, usually generating knowing or guilty smiles on the parts of the parents. We asked if they had seen the common pattern of a. it only happens with one parent, then b. now he does it with both of us, and finally c. now he’s doing it at school too. Then we taught them a very simple limit-setting technique and got their commitment to use it together. A week later, when we met again for reports and updates, it was astonishing how many of the ODD kids were “cured”! There’s interesting work been done on the correlation between onset of ODD behavior and divorce, remarriage, death of a parent, etc. and the behavior of young male wolves in a pack. This is not to say that I don’t believe that certain brains are more disposed to this type of behavior (just as most Filtering kids have an incredible capacity to split parents and/or teachers). We can certainly work with that right prefrontal shortfall; but in a huge percentage of the cases we worked with over a decade, changing the parenting changed the “disorder”.
Look for areas of high beta or high hibeta activation (especially in the relative/percent levels and especially on the right side–particularly frontal). I’d try training these down at a specific site if you find them. You might want to do the sub-assessment of the frontals as well (run 3 minutes with Fp1 and Fp2, at F7 and F8 replacing F3 and F4) to see if you find anything in the very high or very low frequencies, especially on the right side.
Try training either 2-5 Hz down or 15-23 (or 15-35 Hz) down if you find anything significant in a monopolar one-channel protocol and see where you get results.
Often chronic fatigue, chronic pain and fibromyalgia are very wound-up Tone issues. There is a major sub-cortical drive related to long periods of unremitting stress, but the brain responds to it by wrapping itself in cotton (alpha) to anesthetize. The client doesn’t “feel” the emotional material, but it often becomes somaticized, and physical symptoms become major issues. This kind of alpha also is often low in frequency and blocks poorly with eyes open.
I’d probably stay away from SMR with a person with chronic pain: it makes you more connected to your body, which may not be a good thing.
Chronic pain/fibromyalgia types of pain systems often include a lot of frontal slow alpha that blocks poorly, if at all, with eyes open, and I think HEG could be very helpful with that pattern.
Alpha intrusions (or alpha delta sleep) are common in fibromyalgia, chronic pain or fatigue. It simply means that a brain that is using slow alpha as an emotional anesthetic when waking, also begins to use it when sleeping as well. Stage 3 or 4 sleep, deep delta sleep, is the physically-restorative part of sleep. But a brain that can’t stop producing slow alpha (often a common finding in fibromyalgia) produces it even in delta sleep, so the sleep is constantly being interrupted by intrusions of semi-awareness.
You can imporive the fibromyalgia/pain/fatigue,anxiety/depression stuff that is likely a part of this client’s life. And yeah, they’ll probably sleep better too.
In my experience, when a person experiences pain (or anxiety, or depression or fear, etc.) that is fairly constant and doesn’t seem to respond to what they try to do to manage it, it’s nearly impossible NOT to experience a sense of loss of control. How I feel seems to me to be one of the most basic and fundamental levels of control I have over myself, and when I lose the ability to manage that, it undermines my entire sense of control in my life. That’s not a fault, it’s a reality. And people who have suffered with that reality for decades often have a very difficult time letting go of their loss of control, simply because it’s woven into their entire experience at a pretty basic level. That’s also not a fault. But a trainer who hopes to help someone with fibromyalgia or any of these other chronic issues will be well advised to be aware of those “secondary gain” issues that may block the client from actually doing what they most want to do.
Complex Regional Pain Syndrome, also known as Reflex Sympathetic Dystrophy
RSD is generally a Tone problem–excessive activation of the autonomic nervous system. There can be a number of different cortical patterns related to the underlying stress response. I would suggest that you do an assessment and see what you find. Base your training on that. Oftentimes pain issues relate to problems with alpha, but it will be important to address not just the symptoms in this case but also the underlying stress drive.
Alpha problems (slow peak, very high amplitudes, poor blocking, frontal alpha) are often the things that unwind the pain. I don’t know what protocol you are using, but identifying the main tone strategies and training to quiet the temporals, shift the balance of alpha and beta side-to-side or front-to-back are the keys to releasing the emotional material underneath it all.
Parkinsons is related to death of dopamine-producing cells in the substantia nigra. That’s not the same as the apparent issues in essential tremors; those appear to involve the basal ganglia and cerebellum (and GABA, not dopamine).
I have used Fz/A1/g/Cz/A2 with linked ears, training a standard SMR protocol with some success in symptom reduction in 6 or 7 cases of individuals with Parkinson’s. It appears the problem with Parkinsonians is deterioration of the dopamine producing system. Dopamine is a major neurotransmitter in the prefrontal cortex, where it arrives via the medial forebrain bundle, a set of passages that run under the midline. Training up SMR has always seemed to me to have the effect of increasing dopamine.
Increasing SMR at Cz could have a positive effect on the basal ganglia. There is anecdotal evidence that training below O1 and O2 (bipolar one-channel montage) to squash all frequencies and increase 12-15 has had effects with problems of gait and balance (sometimes also present with ET). These would involve training on either side of the cerebellum. Theoretically it can’t work, because there aren’t pyramidal (EEG producing) cells in the cerebellum, so it should be “invisible” on the EEG, but there are those pesky reports of it working.
Parkinsons is a degenerative process, and you really can’t stop the dopamine producing neurons from dying. I’ve had some very good responses in terms of minimizing and even turning back symptoms and slowing down the rate of decline (according to the client’s physician). It is something that requires regular training–and daily is best if possible. I generally got people to set up their own systems so they could train at home.
I’ve had good luck training along the frontal midline, reducing all frequencies (there may be fast activity, but there is nearly always lots of slow) and uptraining SMR. FCz/A1-A2 or Fz/A1/g/Cz/A2 (L) would work.
Tremors are often related to an imbalance in dopamine and norepinephrine, which would likely be exacerbated by stress and/or anxiety. Depending on the assessment, some alpha training in the back, some SMR at C4 or Cz or even at Fz/Pz might help stimulate the dopamine system. The effects should be reduced or gone tremors, improved ability to experience positive feelings and perhaps improved ability to fall asleep.
There is a valid point about “peak performance” training that says that ALL neurofeedback is just that. Unless you happen upon a perfect brain, whatever that might look like, everyone, even high performers, have issues of anxiety or low energy or obsessiveness or lapses of attention of impulsive behavior or whatever. If you start by looking at the client’s brain and determining what is KEEPING him from performing even better, then training that, you will often make your greatest gains in performance right there.
Athletes and Peak Performance
In my work with athletes, we have always discussed the process of performance in three interconnected areas:
The Plan: the golfer looking over a putt, reading the green, planning the line of the putt; the hitter deciding what pitch he’s looking for in this situation from this pitcher and how he’ll recognize it, etc.
The Visualization: the golfer visualizing in detail herself standing over the ball, the stroke, seeing the ball follow the line and drop into the cup; the hitter seeing the pitch he’s looking for and seeing/feeling himself driving it where he wants it to go.
The Zone: no thought, no trying, just absolute presence in time and place, letting muscle memory take over and performing the task at absolute best.
A few sales people I’ve worked with found this model to be useful as well. Planning what they want from a contact, “reading” a client or knowing from history and research what the “line” of the contact might be; visualizing themselves in the situation (or perhaps several different potential ones), asking good questions, listening for key points, connecting with the client, answering objections, etc.; and then actually going into the situation and staying loose and present, riding where it goes.
The first state I would usually train with beta/smr vs theta/delta, often at the C3 and C4 sites. Of course, if the assessment identifies other activation issues that I would consider more basic (temporal reactivity, disconnect, reversals, blocking, etc.), then those will block successful outcomes and should be trained first.
The second state I would usually train with 7Hz percent uptraining, probably at P4 or O1, while actually having the client practice visualizing in detail. The trick here is to get into the state quickly (you can’t stand over a putt for 20 minutes while you drift down to alpha/theta crossover), so triggering and anchoring techniques are often useful. You can see these at work in the rituals of free-throw shooters in the NCAA tournament.
The third state I would train with alpha coherence, probably at P3/A1 and P4/A2.
Coherent Alpha and Performance
Zen meditators and B2 bomber top gun pilots I guess would qualify as peak performers. Both produce lots of coherent alpha.
In order to do so, neurons in the cortex need to “loosen up” and allow themselves to “go with the flow” from the thalamus. That’s how you get coherence in alpha. People who can’t release cortical neurons when they aren’t processing waste a lot of energy, hence they are unlikely to be able to perform late into the “game” in stressful situations.
Try Cz/A1 IN 2-38 and REW 12-16 (SMR training) for the physical relation states.
One of the things that most trainers have to run head-on into a few times before they recognize it is that clients report their subjective experience, and that is generally measured against their standard state experience. It is amazing the first time you have someone with massive beta who wants to be able to relax and work more efficiently–and they successfully change states and HATE it! Can’t focus, can’t concentrate, can’t get anything done. Compared to where they traditionally have been for many years, the more centered state does indeed feel TOO relaxed. It takes some working through and practice for the motivated ones to recognize that they are able to produce as well as ever, just without all the fuss and noise.
Cz or C4 SMR up (I like training it up as a percentage of the EEG) could be very helpful for restless leg. This would be especially true if there are sleep onset issues as well.
Racing thoughts are often an indication of hot temporals, but they can also be consistent with high levels of beta and high-beta in various areas of the brain.
Working with seizures is probably trickier than meets the eye. There may be some possibility of triggering seizures in people who have had a history of them. I would think twice about working with such a person without a fair amount of experience or tight supervision by a well-experienced person.
Seizure activity is normally related to extremely slow areas of the brain–as are ADHD and language-based learning problems. In the neurofeedback world, below the level of diagnoses, they’re all pretty much the same thing, just with differences in symptoms. One of the earliest uses of NF published by Barry Sterman in the 60s was work with seizure disorders (with excellent results). The studies were so good, so well done by a UCLA neuropsychologist, and published in quality journals that one would assume neurologists would know about them, though of course nearly none actually do.
Slow frequencies are often strongly dominant in seizure prone brains, but the spike pattern (which is very fast) is also an indicator. Seizures themselves are often a kindling fast-wave pattern. Training down slow activity is a good way to help protect the brain. Pushing it into certain fast speeds is a good way to trigger a seizure in one who is prone to them. It is the pushing of light/sound driving technologies which is the problem.
One of the classic EEG trainings–perhaps the first to be used and published–was Sterman’s work with seizures, training C3/C4 one-channel bipolar, reducing slow activity and fast activity and increasing SMR. The Othmers also did a lot of this training in the 90s using T3/T4, same protocol. You can try each for a couple sessions and then, if both seem to be positive, combine them using the 2C Seizure protocol in the 2Specialty folder in the brain-trainer designs.
As with most training, it makes little sense to force the client to stop taking something that is working in order to try doing something else that might work. As stability improves with training, you can start trying to back down the dose of the meds and slowly work off them (with the support of you physician) as the brain can operate without them
Seizures are often responses by an unstable brain to excessive slowing in the EEG–the brain overdoes it trying to speed up and locks into hypercoherence in fast activity.
I would recommend against as simplistic a strategy as simply training at C4. Dr. John Hughes, the EEG/’QEEG specialist who heads the Epilepsy unit at University of Illinois taught me (as did Margaret Ayers) about a mirror phenomenon. For instance, let’s say you did 0bipolar training at T4-C4 to reduce seizures–the seizure focus may after while shift to homologous sites in the opposite hemisphere. Therefore, a better strategy can be to train at the same sites in each hemisphere for 15 minutes each.
Entrainment and Seizures
Ever hear the story of the Japanese cartoon that caused lots of kids in Japan (and reportedly other places as well) to have seizures while watching TV? May be an urban legend or may be true. However, the idea of “driving” the brain with light/sound stimulation (there were flashing lights in the cartoon) at 17Hz or higher is related to potential for triggering seizure activity. Kindling beta, large bursts that spread out from a focal point, is related to seizure activity, and in one prone to seizures anything that stimulates activity in that range has the potential to be dangerous. Don’t, as a general rule, use any driving–especially light–with potentially seizure-prone clients to avoid stimulating seizure activity.
Seizures in EEG
There are a variety of patterns on an EEG that are considered epileptiform. One question would be whether what was seen was actually seizure activity–that is the brain was in the seizure state–or was indicative of the potential for seizure. Excessive slow wave activity is sort of the bed from which seizures spring, but the seizures themselves are usually very fast activity that “kindles” out from a central point and locks up an area of the brain with highly coherent fast activity. One description I’ve always liked is that the brain is always sliding back and forth in a fairly narrow band between coma (excessive slow activity) and seizure (excessive fast). Most brains perform this balancing act without much trouble, but when a brain has areas of instability, where it is less able to stay on the high-wire, when if feels itself starting to tumble toward coma, the brain tries to go in the opposite direction and may tumble into seizure.
Although many trainers prefer training for seizures in the sensory-motor cortex, that’s not necessarily where the seizure focus is. It can be anywhere–often in the temporal lobes. What IS in the sensory-motor cortex is sensorimotor rhythm (SMR). Training SMR, since the early work done by Sterman in the 60’s, has been one of the most effective ways of improving seizure activity and making a brain proof against them. However there are other trainings popular as well, including T3/T4 bipolar.
Some people, if they know where the focus of the seizures is, prefer to train to activate that area, to make it more stable on the high-wire, and to train up SMR as well.
Sensory inputs are supposed to be screened through the thalamus, which, in concert with the pre-frontal cortex, filters what is sent to the cortex to be processed, and blocks material that is not considered necessary. When this function fails, or is too weak to do its job in situations of greater sensory load, the client’s sensory integration and association areas can be overloaded by chaotic inputs, resulting in what we see from the outside is extreme sensitivity. This could appear in the EEG as excessive slowwave activity in the prefrontal areas, and/or it can appear as low levels of sensorimotor rhythm (SMR) relative to theta in the sensorimotor cortex (C3, Cz, C4). Neurons in the sensorimotor cortex (SMC) receive inputs from rhythm generating sets of nucleii in the thalamus, some of which produce 4-6 Hz theta, some 8-10 or 10-12 Hz alpha and some 12-15 Hz SMR. It appears that when the SMC neurons are linked to the slower generators, they are not as activated and don’t do their job as well. When they are dancing to the rhythm of the faster generators, the thalamus is more active in its screening function. Hence we often train in the SMC to increase SMR and decrease theta activity to wake it up.
High levels of coherence, especially in faster frequencies like 12-15 Hz, 15-18 Hz or above, can also show up as sensory sensitivity when they appear in the temporals, parietals, SMC or occipitals–essentially toward the back of the brain, where sensory information is processed. For example, when a person is having a migraine and experiencing light sensitivity, we will often see high fastwave coherence in the occipital lobes. In these cases, the pools of neurons which should be working independently tend to get locked together so they are all doing the same thing at the same time and an overload results.
A listening integration program would be more likely to affect the areas left and right between P3/T3/T5 and P4/T4/T6, where sensory integration takes place. Also, any training you were doing away from T3 or T4 was probably not having a lot of affect on the amygdala. The amygdala can’t be seen on the EEG (it’s not made of the right kind of neurons to show up), but you can see its effects often in the anterior temporal lobes. The prefrontal cortex has the “off” switch for the hypothalamus, to turn off the sympathetic (fight/flight/freeze) response that they amygdala turns on whenever it perceives potential danger. So calming the alarm response is part of the idea, but activating those frontal controllers is another potential training approach. And waking up the underpowered parasympathetic branch of the autonomic system is also an important part of successful training.
The amount of sleep you require seems to be related to your ability to get into and process through 5 REM cycles per night. The more high beta, the less beta, or the more alpha intrusions, etc. you have, the harder it is to complete this, so the brain doesn’t get to do its psychological restoration and long-term memory storage and it doesn’t feel rested and ready to get up.
Stages of Sleep
When we are awake, the brain should be producing alpha and beta frequencies. That would be stage 0 sleep.
When we get ready to sleep, we move into Stage 1 sleep: eyes-closed, relaxing, ready to fall asleep. We see the EEG slow down from alpha and beta to theta frequencies—alpha drops and theta rises. What characterizes the changes from Stage 1 sleep (alpha down/theta up–as in alpha theta) and stage 2 sleep is bursts of 12-15 Hz “sleep spindles” in the sensory-motor cortex and K-complexes.
Stage 2 sleep is when you actually go unconscious. In the EEG we see what are called “sleep spindles” (bursts of SMR) and K-complexes, both of which are involved with relaxing and calming the body.
After some time in a relatively light Stage2 theta sleep, we drift down into Stage 3, where the theta slows down into delta and we enter a deep and profound sleep, much like a coma. This is when physical restoration occurs.
Five-six times a night most brains rise from this deep state into Stage 4, or REM, sleep, where we produce rapid eye movements and dream–the psychologically-restorative sleep. In REM, the EEG produces lots of alpha a beta, such that it’s often very difficult to tell from the EEG whether the client is awake or asleep.
From REM, the brain returns to Stage2 and starts the process again.
As to the delta sleep states, the numbering systems differ, but there are generally two delta states described. The first is often Level 3, which is theta dropping, delta rising. The second goes away with aging–normally in the early 20s or earlier. It generally occurs only in the first couple sleep cycles of the night in children and adolescents, and it disappears (except in those who do heavy physical exercise) quite early in life. Both delta sleeps are related to physical restoration; the second seems to be related to release of human growth hormone and more significant repairs (related to growing bodies).
The best thing to do for sleep is an assessment to see what patterns are related to whatever you want to change, then train those. In some sense you could say that, as all neurofeedback is peak performance training (since it tends to improve function in multiple areas), all brain training should have a positive effect on sleep.
There are several forms of sleep difficulties that training can focus on and resolve early:
Sleep-Onset Insomnia (not falling asleep)
Terminal Insomnia (waking up and not being able to sleep again)
Restless sleep (moving around in sleep; muscle tension)
Interrupted sleep (waking multiple times during the night)
Non-restorative sleep (cannot wake up)
Sleep Onset Insomnia
Sleep onset problems result in a person lying in bed unable to fall asleep–or staying up till all hours until he is so exhausted that he falls asleep. People with either inability to produce SMR (sleep spindles) when they lie down to go to sleep, or some anxious people with hot right-rear quadrants will have sleep-onset insomnia and have difficulty falling asleep, though they often sleep well when they do go to sleep and awaken rested.
This is generally related to one of two patterns:
1. Sleep onset problems are often related to levels of SMR at C4 below 10%. Low levels of SMR (12-15Hz) in the eyes-open EEG at C4 or Cz usually indicate a brain that is unable to move from stage 1 (eyes closed, relaxed, ready to go to sleep) to stage 2 (asleep). Sleep spindles and K-complexes both relate to sustained relaxation of the muscles, which appears to be an important element in this transition. People with low SMR also often show lots of movement in bed when sleeping, restless leg, bruxism, etc. Training to reduce overall activity and increase SMR can be helpful (side note: SMR frequency in children may not be 12-15Hz, based on what the peak alpha frequency in the parietals/occipitals is).
2. A “hot” right-posterior quadrant (P4, T6, O2) with low levels of delta/theta relative to the amount of beta/high-beta. When beta levels are higher on the right than left in homologous sites and/or higher in the back than the front, this often relates to anxiety and (when alpha is low) sleep-onset insomnia. I often train 2 channels at P4/A2 and Oz/A2, inhibiting 19-38 or 23-38 and rewarding 6-13 or 9-13 depending on how much 6-8 Hz activity is attenuated. Movement is not so much an issue here as anxiety. For those who have a beta problem, the SMR training is not likely to be successful.
Terminal Insomnia is usually related to hot right-posterior quadrant of the brain. People who have fast right-rear quadrants tend to fall asleep easily, then awaken after several hours and not be able to return to sleep after perhaps one REM cycle, so they often don’t feel rested.
Look at beta and high beta levels at P4, O2, Oz or T6 relative to those levels in the left frontal and right frontal areas.
Alpha uptraining in the parietal sites or beta down (if there’s already enough alpha) can help for anxious clients who fall asleep okay then wake up and can’t fall asleep again. It is common for sleep to improve with increased alpha PF.
Cz or C4 SMR up (I like training it up as a percentage of the EEG) training could be very helpful for restless sleep/restless leg issues. This would be especially true if there are sleep onset issues as well.
I usually see multiple awakenings during the night with high levels of beta/high-beta with eyes closed. The brain moves down through stages 1 and 2 into stage 3 (delta), then starts up into REM, where it is producing an EEG almost exactly like a full waking EEG. However, excessive beta can pop the brain out of the sleep state. Many clients can return to sleep fairly quickly–or barely recall that they woke up–but they don’t get the psychologically restorative benefit of full REM cycles and are often tired. They may or may not remember dreams.
Often beta reversals front/back (more beta in P and O sites than in the F sites) result in waking up sometime after initial sleep onset and then being unable to return to sleep due to rumination, worry, etc. If there is sufficient alpha, you can train down beta in the back; otherwise, train up alpha.
Often people who sleep heavily all night and don’t awaken rested have difficulty producing fastwave activity, so they don’t get into the REM cycle–they stay all night in delta (coma) sleep, so they never get psychologically restored. This can also happen with people who have excessive fast activity—especially high beta–when awake. They experience awakening multiple times during the night, pretty much every time they try to go up into REM.
This can also be related to extremely slow brain activity with little capacity to produce beta. The client goes down into stage 3 sleep and is unable to cycle up into REM. Some clients experience that they wake up multiple times during the night and fall back to sleep quickly, because they have a bit more beta. Bed-wetting is often related to this pattern.
Speeding up the brain often resolves these issues.
Robust ability to shift into beta speeds seems to help increase REM sleep. Clients who have EEG’s dominated by slow frequencies during waking states often sleep heavily but not restfully, because they either can’t get into or stay in REM (which has lots of fast-wave activity in it).
Alpha intrusions, or alpha-delta sleep, mean that alpha—often slow alpha—is appearing in bursts during what is supposed to be delta sleep, the deepest state of unconsciousness. Delta sleep is supposed to be physically restorative, and with alpha intrusions, it is not. It sometimes also intrudes into REM, so the client doesn’t get enough REM sleep and wakes always feeling tired from not enough psychologically restorative sleep.
Alpha intrusions can result in reduced release of human growth hormone in younger clients and eventually in chronic fatigue/chronic pain/fibromyalgia symptoms in older clients. It is most commonly seen in those cases where emotional drive material is being “wrapped up” in alpha during waking, usually a predictor that the client will somaticize the emotional issues (which he/she generally doesn’t admit) and begin to have physical pain, fibromyalgia, chronic pain or fatigue.
The pattern appears in the TQ7 as alpha (especially slow) in the frontal area of the head with closed eyes (may continue with open eyes too). There will be lots of red in the maps of 9-10 Hz in front.
Train down the alpha. Train it down with eyes closed. Especially focus on training down the slow alpha. You might also try training alpha down and beta up, especially on the left and toward the front. Anything you can do to get the brain to use alpha more appropriately should have a positive effect on sleep problems (and a bunch of other things the person may not be complaining of).
Greater awareness of dreams can indicate more REM, but it can also suggest that the client is waking up partially (which may indicate a shortage of beta-producing capacity) early in each dream, which would be a good way to remember them.
One thing to be aware of is that many people with lots of slow activity rarely do dream, since they have a hard time getting into or staying in the REM state, so they don’t get the psychological restoration that REM seems to bring. As you improve the brain’s ability to produce faster states and sustain them, you are more likely to dream (and especially in the beginning to remember them).
When someone is severely sleep deprived, they will never make up all the delta sleep (physical restoration) they have lost, but the brain will make up all the REM (psychologically restorative sleep) as quickly as possible. So when a client sleeps and immediately skips through stages 2 and 3 into REM, that’s a pretty good indication of severe sleep deprivation.
In delta sleep, which one is unlikely to enter in an office with feedback being produced, the brain is completely shut off from environmental information. Not so in REM. Anyone who has ever dreamed and integrated some external sound (dog barking, alarm going off, etc.) into a dream can attest to that. So the feedback gets through.
Sleep-deprived brains try to make up their lost REM cycles as quickly as possible. If a client appears to fall asleep, allow it and keep the training going. When the feedback stops, the person will come up by herself. Eventually, the person will be able to train awake.
Very high alpha peak frequencies—at or above 11 Hz—are a much rarer source of sleep onset problems. It is worth trying to train that down toward 10 to see if it helps.
Seniors and Sleep. I think for many older adults the problem of sleep is not so much its duration as its depth. They tend to wake frequently, which is consistent with reductions in fast wave production: each time the brain tries to go into REM, it can’t sustain the beta and the client awakens (very much like slow-wave ADD kids often do). If the brain maintains its speed, I don’t believe this is a built-in part of aging.
Narcoleptics get waking and sleep pretty confused in their brains and they suffer from sleep deprivation. In dreaming, our brains put us in a state called cataplexy, a kind of complete loss of muscle tone which keeps us from actually getting up and acting out our dreams. Narcolepsy also often involves theta hallucinations like nightmares, sleep paralysis and cataplexy during the “waking” state. These are often triggered by strong emotions.
In the EEG, the studies I’ve seen have shown (in eyes-closed readings, not necessarily eyes-open) theta and low-alpha amplitudes are dominant and 10-12 Hz alpha and beta amplitudes are decreased, which is kind of what you would expect. A very common indicator is that the client will enter REM/dream sleep almost immediately upon sleeping–very much like anyone who is sleep deprived and trying to make up the lost “psychologically-restorative” REM. They do enter REM, and have about as many periods during a night as normal sleepers, but where most of us increase the length of REM periods as the night goes on, they remain about the same for narcoleptics.
Neurofeedback can be helpful in speeding up brain function, but the sleep disturbances which are the main basis of narcolepsy haven’t responded as well–at least in cases I’ve worked with or consulted on. Two I worked with had lots of delta spiking, so you may have some success reducing variance in delta and/or theta (2-5 Hz).