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Episode Summary
This conversation originally aired on the NeuroNoodle expert panel. You can watch the original conversation. What follows are my own observations from that discussion, written up here in long form, with the host's questions and the other panelists' material left out except where attribution helps the point land.
What does it actually mean to do neurofeedback "remotely"?
Most of the people I work with never set foot in one of our offices. We have physical locations in New York, St. Louis, Los Angeles, Orange County, London, and Stockholm, and the bulk of our clients train from home. This morning alone I troubleshot a USB amp cable for someone in Dubai, then took a call from Portugal, then one from Oman. If you have a brain and you have equipment, you can train it.
People ask me during pre-sales whether you get better results in the office. You get better results from home. The reason is engagement. People train more often when the equipment lives on their desk. They pay closer attention. They are a captive audience for the check-ins, and they have a private communication channel staffed twelve hours a day. We see far more round-trip, real-time feedback from a home trainer than we ever did from someone driving in twice a week.
The biggest point of failure in neurofeedback is getting people to tell you how the training felt afterward. We are insistent about it. We guarantee it, we check in, and we write everything down. Anyone doing this work seriously has to control the subjective data as carefully as the EEG. If you want the longer version of how home training works, I cover it in the remote neurofeedback guide.
Why do remote clients train so much longer?
Because I am a scientist teaching you about your own brain rather than a clinician fixing a diagnosis, people tend to stay in training far longer and self-select very long programs. I have clients up around 700 and 800 session counts. By that point they are skilled trainers themselves, and my role is mostly confirmation: that is a good protocol, run it twice more, good job. Giving someone agency over their own brain training changes the whole relationship with the EEG.
What goes wrong on a remote setup?
My first high-tech boss had a line that still holds: nine times out of ten the answer is on the screen, the tenth time it is not plugged in. A lot of remote support is exactly that. We use EEGer, which crashes if you unplug and replug the amp mid-session, so we built documentation and a cheat sheet for finding head locations, and we run a shared desktop to jump in when someone hits trouble. People move from handheld guided work, to photographing their head and screens so we can check the setup, to deep independent training over a few weeks.
The other honest data point: we lose one QEEG amplifier a year. About half of those arrive back as an empty box because the shipping carrier loses the contents. That is around $6,000 a year down the drain.
What is a "hot cingulate" and what does it actually do?
A hot cingulate shows up on a brain map as elevated high beta and beta activity over the cingulate region. It is associated with cognitive rigidity, rumination, an insistence on being right, and the kind of drive that does not let go.
A hot cingulate is a two-sided coin. The same signature drives elite athletes, successful entrepreneurs, and the people who write books in six months. Nothing stops them from a goal. The problem is direction, not the trait itself. If the goal is harming someone, you have a problem. If the goal is catching a criminal, you have a police dog who will jump over a waterfall to do it.
Statistically, this is a population-level signature: roughly a third of people carry some version of it. In women, the high beta to beta ratio tends to rise with age, and you find real powerhouses in more mature women partly for that reason.
Can you "fix" a hot cingulate, and is it genetic?
A viewer asked whether a hot cingulate is genetic, since both he and his rigid sister seem to have it. There is likely a familial component, but be very careful with the logic. All cats have four legs; that does not mean every four-legged animal is a cat. Rigidity has many sources. Sensory reintegration difficulties make people rigid. So do dozens of other patterns. You cannot pull up a single brain region and declare it the cause, and you certainly cannot match an electrode to a complaint without matching the person to their own QEEG first.
When you do work with the cingulate, you are softening rigidity and shifting the trajectory of a life. The older work in this area, including studies in Canadian prisons by Doug Quirk, reported large drops in one-year reincarceration rates after a single course of neurofeedback in violent offenders. Treat that as historical clinical observation rather than a modern controlled trial, but the direction of the effect is consistent with what the cortico-striatal rigidity circuit does when you train it down.
Is the hot cingulate the same as OCD-linked hypersexuality?
A viewer asked whether the hot cingulate connects to sexual paraphilias, given the OCD link. My read, and I am biased by what I have seen in the brain maps: yes, but not directly. The connectivity runs through the anterior temporal lobe and the structures behind the insula, plus the right temporoparietal junction. Classic cases like KlΓΌver-Bucy syndrome, where you lose the anterior temporal tips and get disinhibited, orally focused hypersexuality, point to that tissue as the driver (KlΓΌver & Bucy, 1939). The cingulate is often where you see the signal on a map. The driver is more likely temporoparietal.
How do norepinephrine and the adrenals shape the EEG?
This came up around a question about adrenal insufficiency. Norepinephrine is generated in the brainstem and acts as a systemic chemical. It helps set your alpha frequency. Too much norepinephrine drives gross over-arousal, makes beta, and speeds alpha up. Too little leaves your alpha too slow. The cortex has some influence on alpha tuning, but it is minor compared with the brainstem and the thalamus.
The thalamic nuclei, including the reticular nucleus, set your background rhythm (Steriade et al., 1990). Think of it like a sampling rate. Slow background rhythm gives you low resolution, and your semantic and declarative memory does not work well. Faster, and everything clicks. A large part of what we do in neurofeedback is tuning that alpha and getting it out of the locations it should not be in. If you want the deeper mechanism, see decoding alpha waves.
On the endocrine side, your adrenals modulate cortisol based on stress, and you can burn them out with chronic high arousal or with chemicals used to push yourself too hard for too long. Cortisol has a bad reputation it does not deserve. It modulates your immune system. Without enough of it, your immune system can do real damage. Balance matters more than minimizing cortisol output.
How should you track whether neurofeedback is doing anything?
I ask for reports every day, twice a day, whether or not someone trained that day. I want to watch states, traits, and goals shift over time, and I do not assume every change comes from the neurofeedback. Sometimes you can tell: if a fast beta protocol left you wired and you cleaned your whole house at midnight, the frequency was probably too fast. Usually it is a gradual trend across the arc.
The sampling matters. This is the Nyquist theorem applied to people. You have to survey someone's experience at least twice as often as their experience actually changes, or you will miss what is happening. Twice-daily logging gives me that resolution. Other excellent practitioners who see clients three times a week in person get the same resolution a different way, by being in the room.
What questions are worth asking at check-in?
Beyond sleep, the questions get set during assessment. One of my last intake questions is: what would you notice that would tell you the neurofeedback is doing something? What would feel different? I want the client to build that list, match it against what I see in the EEG, and keep it to three top priorities at a time. More than three and things get convoluted, and you lose the ability to track what is actually shifting. When the top priority resolves, item four becomes the new item one.
I also hold conclusions at bay. When someone arrives convinced a session caused them distress, I believe their experience completely while staying agnostic about the cause. People generate a lot of theories about their own brains. My job is to back them out of a bad state quickly, not to win an argument about why they got there.
Do more EEG channels mean better neurofeedback?
More channels is more math, not more training. You are still training a signal you solved for at the scalp. You are not reaching cortically or subcortically with whole-head approaches, Loretta, or z-score in the way people imagine. You train the scalp signal.
There is a real gap in the field between people working with one to four channels and people invested in full-head training. Both can be done well. Both can be done completely wrong. Channel count does not make the neurofeedback work. Knowing what your equipment is doing makes it work. I see more confusion with more channels. With fewer channels you are forced to know the head you are training, and you catch a problem faster because the moves are more discreet.
The danger sits with systems that promise magic: automatic artifact handling, automatic protocol selection, protocols pulled off a complaint checklist. When those work, great. When they fail, the operator has no idea what to do, and if you are even slightly atypical, weird things happen.
How common are side effects, and what do they mean?
Across roughly 10,000 people over more than 30 years, I have seen a serious, sticky adverse reaction once or twice. It is genuinely rare. Side effects almost never show up after one or two sessions. With traditional, discreet, one- or two-channel training, you have to work at creating an effect that lasts beyond the transient. Where you do see trouble is full-head training run aggressively, 75 parameters at once.
When a client arrives every month convinced neurofeedback caused profound anxiety or depersonalization, I take the experience seriously. Sometimes the trigger was a scowl from a poor provider rather than the training itself. A side effect is still an effect, which is part of why the people who think neurofeedback does nothing change their mind the first time something goes the wrong direction. The work is iterative. A science practitioner uses acquired knowledge, explains the risks and the benefits, and iterates toward your goals based on your own reports. For the anxiety-specific evidence, see neurofeedback for anxiety.
What is SMR training and why does tuning matter?
SMR, the sensorimotor rhythm coined by Barry Sterman, runs 12 to 15 times per second, recorded over the motor strip at C3 or C4, not at CZ, and you compare it against theta to track the ratio (Sterman & Friar, 1972). The location and the comparison matter as much as the frequency band.
There was a useful disagreement on the panel. Joy Lunt cautioned that uptraining 12 to 15 Hz is not universally well tolerated and can send someone home miserable if you misjudge the head. I find SMR very well tolerated, and the reason is tuning. I do not just slap 12 Hz on a scalp. I think about anxiety, aging, and infirmity, then tune the frequency, often in quarter-hertz increments rather than full-hertz jumps. If someone reports feeling wired at 12 Hz, that is information; I lower the frequency. The disagreement is smaller than it looks. We are both saying the same thing from two directions: tune to the individual head, take a baseline, watch the SMR-to-theta ratio, and the side effects mostly disappear. When they show up, use them. For the training mechanics, see SMR neurofeedback.
How I teach across very different audiences
Whether I am on my own live stream, a branded podcast, or a guest appearance, I never sell neurofeedback or a particular technique. I drop back to the neuroscience and break complicated topics into simple ideas about the brain, again and again. That is also how I run the training itself. I do not adhere strictly to DSM categories. I look at brain resources and drop below the diagnostic buckets when I can.
I stay out of the diagnostic, confirmational role. One of my jokes captures the split: doctors have to be right, so go to them for answers. Come to scientists for questions. A science practitioner works from accumulated knowledge, communicates the risks and benefits, and adjusts toward your goals as your own reports come in.
If you want to start understanding your own patterns before you train anything, the QEEG brain mapping guide is the right first stop. From there, decide what kind of program fits your life. Some people want a personal trainer and a short intensive. Others want to train from home over a long arc. Both work. The variable that matters is whether the person guiding you knows what the equipment is doing and can read the raw signal.
References
- Steriade (1990). Substantia nigra pars reticulata projects to the reticular thalamic nucleus of the cat: a morphological and electrophysiological study. doi:10.1016/0006-8993(90)91832-2
- Sterman (1972). Suppression of seizures in an epileptic following sensorimotor EEG feedback training. doi:10.1016/0013-4694(72)90028-4