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Episode Summary
I joined the panel on NeuroNoodle's open-mic Q&A alongside Jay Gunkelman, Dr. Mari Swingle, Joy Lunt, and several other practitioners for a live session where the audience drove the questions. The conversation ran across dissociation on the EEG, Parkinson's, the salience network, anterior cingulate protocols, and the practical reality of training kids who are scheduled to the minute. Watch the original conversation. What follows is drawn from my own contributions to that discussion, organized so you can use it.
What does dissociation look like on the EEG?
The most striking thing I have watched in a recording chair came years ago, working with a small group of women who had what was then called multiple personality and is now described as dissociative identity disorder. One of them volunteered to let me see her personalities on the EEG. Her social worker knew every trigger, and we went through them one at a time.
When the personalities switched, the entire signal changed. The whole generation of activity reorganized, well beyond a shift in one band. One personality was a four-year-old child, and the EEG looked like a four-year-old child's: slow waves consistent with that developmental stage, the patterns you would expect from a young brain. The person was awake, alert, talking, interacting. The wave characteristics were those of a different age entirely.
Another personality carried the vigilance load. That one had the smallest theta band I have ever recorded, which fits a hypervigilant state. The body in the chair was the same. The brain producing the signal was not.
Most of us keep our EEG fairly stable and predictable because it runs so much of the rest of us. The human EEG is capable of an enormous range. We just rarely see it move that far. I was not running a QEEG on these people, so this is observation, not a quantitative study. Connectivity is hard to read in real time because noise and amplitude changes contaminate it. What I saw was bigger than a connectivity blip. It was a wholesale change in what the brain was doing.
Why is the salience network bigger in depression?
The panel raised an fMRI study reporting the salience network is roughly twice the size in depressed people (Lynch et al., 2024). A caution on the method first: most fMRI studies run small samples, sometimes 23 participants or fewer, and one autism paper had a structural MRI sample of seven. To characterize a single consistent group you want 25 to 30 people. To separate out EEG phenotypes within a heterogeneous group, you need thousands, because you need 25 or so within each subgroup before the effect on any given phenotype shows up.
The salience network's largest contributors are the anterior cingulate and the anterior insula on both sides. Pain medicine calls the same structure the distress network, which makes sense, because nothing is more salient than distress. Machine learning work has tied anterior cingulate activity to depression, and it has since been recast as a broader category called reward deficiency, which Kenneth Blum characterized over twenty years of writing (Blum et al., 2000). Reward deficiency covers addiction as well.
In our own addiction research we found about a third of the addicted population was driven by an anterior cingulate pattern rather than overarousal. Two-thirds were overaroused, and those got Alpha-Theta training based on their QEEG endophenotype, not on the addiction label. The anterior cingulate third got cingulate-targeted work, and what you do there depends on what the failure mode is.
How do you read the anterior cingulate before choosing a protocol?
The anterior cingulate has at least three failure modes, and the protocol has to match the mode. This is where symptomatic prescribing goes wrong.
Take TMS. The standard move is to assume the spot needs excitation, aim the double-cone coil with a 1.5 to 3 Tesla magnet at the cingulate, and drive it. If the failure pattern is alpha, excitation works well. If it is slightly slowed, stimulation helps. If it is theta, it works less reliably. With a beta spindle, exciting it makes the person worse, acutely, right there in the chair.
Look at the EEG before choosing the method. The reward-deficiency network does respond to ketamine and psilocybin-style therapeutic approaches, used as a designed intervention rather than as a daily habit.
Neurofeedback can train the cingulate directly. Work from the Lubar lab first showed you could control theta at the anterior cingulate. That matters because cingulate-theta OCD is the kind medication barely touches. If you wanted to run a fair medication-versus-neurofeedback comparison, pick a group with anterior cingulate theta. That is a pharmacologically intractable group, and we train them all the time. Nail biting, songs stuck in the head, the disinhibited stimulus-seeking flavor of obsessiveness rather than the ritual-driven kind, all tend to show frontal midline excess tonic theta. You can read the QEEG and see it.
Can neurofeedback help Parkinson's?
I have an N of one that turned into something I take seriously. My mother was diagnosed around age 73. I broke my own rules and told her to start every medication the neurologist recommended, then put her in my chair five days a week. Her gait had changed, she was using a cane because walking without it was dangerous, and her hand tremor was significant.
We did about 25 to 30 sessions of unfancy work. Before she left for a month in Florida, she started forgetting her cane. That is one of the best signs I see. When people stop reaching for an assistive device, they are needing it less. Her tremor was gone and her gait had improved. The medication dose had not changed. The variable was the neurofeedback.
She came back from a month away with the tremor and the cane back, even though she had kept taking her pills on a timer. We set up one of my first remote training systems to keep her going from Florida. About ten years later, in her early eighties, with no dose increases, a physical therapist assessed her and refused to believe she had been diagnosed a decade earlier, because she would have been far more advanced.
Across the people I have worked with who have parkinsonian features, roughly 80 percent show strong change and about 20 percent show none. This is observation, not a trial. In the responders, the biggest effect is that the medications work better and keep working. Many can sleep through the night without waking to dose, because the tremor and rigidity stop flaring. It appears to slow progression, especially in younger people. Once someone is far progressed with strong tremor and strong attentional dysregulation, classic neurofeedback gets hard. Lisa Tataryn has a case series that is more systematic than a single anecdote, and the Thompsons have shared work with SMR and Parkinson's.
Not every tremor is parkinsonism. Misdiagnosing parkinsonism in someone with a head injury is common. Dementia pugilistica, the boxer's brain, mimics it. With one-third of retired NFL players believing they have CTE, the self-report is shaky in both directions. It is probably an undercount because of survivorship bias: the athletes with the worst outcomes hit their mid-forties and check out. Post-traumatic encephalopathy can mimic almost any psychiatric presentation, which is unsurprising when a psychiatric diagnosis is a cluster of behaviors with no biomarker behind it.
Use the QEEG prognostically, not diagnostically. Figuring out how to move forward and make things work better is exactly what it is for.
What is the right way to think about the alpha rebound effect?
A practitioner asked whether persistent eyes-open alpha should be trained through. I do not train through anything. A rebound, the way I think about it, means: if a protocol I taught produces a negative effect, something is wrong with what I taught. The expected outcomes are no effect or a positive effect. A negative effect means the protocol was wrong.
You can succeed at teaching the brain to do exactly what you want, over and over, until it sticks. If a particular state is the one you want to establish, train it and persist. There is more than one way to train down eyes-open alpha, so if one approach keeps producing a rebound, change the approach.
Why do GLP-1 drugs and appetite live partly in the brain?
The assumption that obesity is a food addiction is wrong for most people. Metabolic rate, lifestyle, and eating patterns all contribute, and for some people the brain's reward circuitry is the driver, for others it is not.
The mechanism is mostly gut. The drug slows the digestive system. Food sits in the stomach longer and moves through the tract more slowly, so fullness lasts longer and appetite drops. The brain influences digestion, but the primary action is slowing the gut. Secondary studies are starting to hint at cognitive effects, muscle-mass changes, and possible absorption changes, which is why I get nervous when one molecule is sold as a cure for everything.
There is a brain angle worth naming. If you target a drug addiction at the anterior cingulate without fixing the cingulate, you get symptom substitution, and the addiction finds something else. For eating and feeding phenomena, the right insula is the relevant target. You can run a protocol across the right insula, but you have to get behind the ear, because there is other tissue on top of it. A bipolar pair like FP1 to M2 activates the right insula. I prefer catching it from CZ to the temporal, because that pair shows insula content well in the raw EEG as a phase reversal, with nothing happening at C3 while CZ and T7 are out of phase. MEG and sLORETA can localize the deep source and use it for feedback. I would stay away from z-score approaches here.
What keeps you awake: orexin or rumination?
Insomnia is not one thing. We published on beta spindles at CZ, which predict insomnia driven by the orexin wakefulness system. If you see CZ beta as a problem, you can predict the insomnia. Running that backward and assuming every insomniac has CZ beta produces wrong protocols.
Anterior cingulate rumination keeps people awake too, and that generator is separate from the orexin drive. Songs cycling through the head and non-negative thoughts that loop both tend to be a theta failure mode at the cingulate. Look at the QEEG before assuming the mechanism. The symptom does not tell you the spot.
Why does the same protocol work for one practitioner and not another?
This field shares generously. At conferences we trade protocols constantly: I found this at this site, I found that. Then someone tries it and reports it does not work. The disagreement usually hides in the details.
Saying "train CZ minus T7" is naming a destination, like saying you want to go to France. It says nothing about the frequencies, the direction you are pushing each band, or how you are delivering the information to the brain. Two practitioners at the same location with different populations, different reward and inhibit bands, and different lived experiences in their clients will get different results. Before you tear someone's claim down, look at their data. The variation outside textbook ADHD is enormous, and even within ADHD there are at least five points of variation.
Mechanisms of action are not the same for every person, even at the same site. A consult I ran recently came down to changing how the practitioner was inhibiting a child's theta. The theta was out of whack session after session and not budging, so it had to become the star of the session: more inhibit on theta, less reward and inhibit spread across the other bands.
How should you train children who are scheduled to the minute?
The school-kid wave arrives in January, after the first round of report cards. Around week six parents start questioning, and by January you get the failures and the parent-teacher meetings.
Kids are exhausted. Dance, soccer, music, second-language lessons, family-origin-language lessons, plus the hours on devices and a late bedtime. A lot of these kids show high theta because they are tired and underperforming because they are tired. Pulling a child out of activities to deal with a learning difference or ADHD over a few months is usually the right trade. Calculate how much school they are effectively missing by sitting in class falling behind.
The "no time for neurofeedback" objection has two answers. Adding neurofeedback raises plasticity, so the sport, the weightlifting, and the language all get easier. The training is also mostly involuntary. A child can do homework while wired up, because you do not have to watch the screen or track the feedback consciously. Training while tasking works well. The constraint becomes structuring the time, not finding free time.
For families who genuinely cannot get to a clinic on a clinic's schedule, remote training is the answer. I get better effects from my home clients than from my office clients, because home clients do more sessions. Home training requires a different set of skills and a different support structure than in-office work. I run coaches seven days a week, twelve hours a day, with a live chat for every client. Most practitioners do not want to take that on, because it creates a different kind of relationship. I take an agnostic stance on location. Whether you are a kid with ADHD, a CEO drinking too much, or an athlete recovering from an injury, you have goals, I have techniques, and the coaches handle setup and support.
How do you prioritize with an autistic child?
Treating autism as a single thing is a DSM problem. The label is a pile of different presentations, and the order of operations flows from the specifics of the case. If there are discharges in the temporal lobe, acting-out aggression can be temporal lobe epilepsy. Match the EEG to the behaviors. This is personalized work, not a generalized category.
Sleep is one of the easiest outcomes to measure and one of the first I track, because falling asleep, staying asleep, and cycling through sleep stages are all involuntary signs the training is settling in. Simple CZ work with an autistic child can bring more eye contact and more relational engagement, which are early markers the training is landing.
Sometimes you let the brain decide where to spend the gains. I worked with a nonverbal eight-year-old girl whose first goal was simply staying in the school building, because she kept running out into danger. We hit that. Then the teacher started asking for more focus in class. The bar keeps moving, and priorities shift under their own momentum. Nutrition matters too. If the nutritional platform is poor, neurofeedback fights uphill, so address inflammation and diet alongside the training.
Is hyperfocus the same as flow?
They are opposite neurological states. Hyperfocus is a lack of neuroplasticity. A kid with a terrible attention span can lock onto a Lego build so completely that the house has to stand up and move before they notice anything else. That is stuck attention with no flexibility.
Flow is extreme flexibility, the ability to move attention fluidly while still looking intensely focused from the outside. The two states look similar from across the room and feel similar to the person inside them, while the underlying EEG and the underlying capacity run opposite.
Where this leaves you
Read the brain before you choose the protocol. The anterior cingulate alone has three failure modes, insomnia has at least two distinct generators, and the same site can work through different mechanisms in different people. Use the QEEG to plan forward, track an involuntary outcome like sleep to confirm the training is settling, and match the work to the individual rather than the diagnostic label. If you want to see what a brain map actually shows before training, that is the place to start.
References
- Lynch (2024). Large-scale evaluation of outcomes after a genetic diagnosis in children with severe developmental disorders. doi:10.1016/j.gimo.2024.101864
- Blum (2000). Regenerable immunobiosensor for the chemiluminescent flow injection analysis of the herbicide 2,4-D. doi:10.1016/s0039-9140(99)00298-2