🧠 Join the NeuroNoodle Live Q&A! Whether you're a clinician, parent, or simply curious about neurofeedback and mental health, this session is for you! Our panel of experts will answer your questions in real time—you drive the content, and we provide the answers. This live discussion is perfect for anyone interested in brain health, whether you're a professional or just want to learn more about mental wellness. Panelists include: • Anthony Ramos (Lead Host) • Jay Gunkelman • Dr. Andrew Hill • Dr. Mari Swingle • Joy Lunt • John Mekrut • Santiago Brand • And more! This session is open to all: clinicians, end users, moms and dads—anyone is welcome to join! Don’t forget to like, comment, and subscribe for more interactive sessions. Share this stream with your friends, colleagues, and anyone interested in mental health. #NeuroNoodle #Neurofeedback #MentalHealth #LiveQandA #BrainHealth #AskWeAnswer
Episode Summary
This piece is drawn from a live Q&A I joined on the NeuroNoodle panel with Anthony Ramos, Jay Gunkelman, Dr. Mari Swingle, and others. The format was audience-driven, so the questions ranged across stroke recovery, diagnostic inflation, epileptiform activity, and how a layperson should evaluate a neurofeedback provider. You can watch the original conversation. What follows are my own observations and explanations from that discussion.
What happened to John Fetterman's brain after his stroke?
Someone asked about the senator who paused an interview to wait for closed captions to work. The pattern looks like receptive aphasia, probably auditory in origin. My read: a left posterior or mid-temporal stroke that disrupted tissue in the superior temporal gyrus heading into Wernicke's area, where primary auditory input gets converted into language meaning.
Picture a loud cocktail party. The acoustic signal still arrives, but it comes in degraded, and the system that decodes meaning cannot keep up. That is the lived experience of this kind of aphasia.
He appears to have been rerouting. Reading a word anchors meaning faster and more directly than hearing one, so the visual route through the fusiform region into Wernicke's tissue is cheaper and more reliable when the auditory path is damaged. The fact that he could function visually proves the concept of language was intact. He did not lose the architecture of meaning. He lost one input channel and built a workaround, the way a deaf person uses an accommodative device.
This is recovery in motion, not a fixed deficit. His first conversations after the stroke were painful, with words memorized rather than embodied. Production improved over weeks, and the receptive piece followed. Compare that to Bruce Willis, whose frontotemporal dementia degrades anterior frontal and temporal tissue, right where Broca's production area sits on the left. That is tissue loss from degeneration, not a vascular event, which produces a more anterior, production-side aphasia. Localizing the phenomenon to the tissue is the core of how neuropsychology and QEEG work sits next to it.
Are autism and ADHD rates really rising, or is it just diagnosis?
A review noted a large increase in autism spectrum prevalence over recent decades and raised the usual explanation: looser criteria, more conditions swept into one bucket.
I have heard that explanation for the entire 25 to 30 years I have followed autism research. The criteria are not continuously loosening to manufacture a bigger bucket. Something real is happening underneath. The signal is just noisy.
Several correlates track with the rise. The research links parental obesity to higher autism risk, and obesity has climbed across the same decades. Older paternal age carries a measurable contribution (Sandin et al., 2016), and parents have been having children later since the 1960s. None of these is the answer. We are still early in understanding the brain, and the work is largely phenomenological.
Here is what bothers me about the diagnosis itself. The field admits autism is a spectrum, which is to say it is a giant catchall holding genetic variants, cognitive impacts, and a striking amount of epileptiform activity. If a diagnosis does not predict treatment, it is categorization, not medicine.
Why does epileptiform activity show up so often in psychiatric brains?
Jay Gunkelman has read more EEGs than nearly anyone, and the trans-diagnostic pattern is clear. Epileptiform discharges show up across autism, ADHD, and bipolar presentations, often with no seizure history at all. Reported rates run widely depending on the population and recording length. One study using prolonged EEG monitoring found a high incidence of epileptiform activity in autism with no clinical seizures (Chez et al., 2006).
The background rate in people who clear a normative database is low, in the low single-digit percentages. Anxiety presentations run higher, which sounds small until you compare it against that background. Panic, oddly, runs lower.
The consequence matters. Some groups have observed psychiatric patients, not epilepsy patients, with discharges in their EEG and recommended an anticonvulsant be considered. When that was followed through, many showed positive change. Traditional neurology often will not treat these patients because there are no seizures, so they end up on antipsychotics and neuroleptics that can make the dysregulation worse. The temporal lobe discharges link to events of out-of-control rage, and addressing the source rather than the behavior is what the literature suggests moves the needle. I am describing what researchers report here, not making a recommendation about any individual.
What counts as "normal" versus dysregulated?
Dr. Mari Swingle raised a concern I share. The window of acceptable natural variation in people keeps narrowing, ironically during an era that celebrates diversity. Plenty of kids who would have been labeled a classroom-management problem went on to full lives. Adolescent angst was once a phase, not a diagnosis of anxiety or depression.
I avoid DSM categorization in my own work because I am a scientist and educator, not a diagnostician. I think in terms of goals, suffering, and dysregulation in the data. Something sticks out in the EEG. Fine. Difference is not the same as a problem. People are weird, and weird is good. The goal is never to drag someone to the middle of a bell curve.
The useful move is to find what sticks out, test whether it maps to the person's actual goals or suffering, and if it does, work on the obvious regulatory features first. I had a conversation with a parent that same day asking whether their 14-year-old's anger was a problem or hormones. Often the honest answer is that it sounds typical. You can do serious transformation without pathologizing it, which is the same reframe I use when parents are getting pulled into yelling matches with an ADHD kid.
Why doesn't TMS and psychiatry look at the EEG first?
In psychiatry, TMS is usually targeted off a DSM label rather than the underlying EEG. A practitioner finds the motor spot that makes the fingers wiggle, then works forward to a depression target. Going off-label into the actual brain data feels like No Man's Land to most of them, and that caution is reasonable given how aggressively these tools can push.
There is more interesting work at the edges. One protocol skips the DSM entirely: find a thalamocortical dysrhythmia, point the TMS at it, and combine it with a psychoactive agent like ketamine or psilocybin. The high-end functional MRI feedback literature, real-time fMRI targeting the anterior cingulate for OCD, opened the door for the broader scientific community to take neuromodulation seriously (deCharms et al., 2005). MEG feedback that modulated the insula for pain control, blinded and placebo-controlled, helped too, because MEG sees subcortical tissue more cleanly.
You do not need any of that to help most people. Thalamocortical dysrhythmia responds to SMR training. The cortico-striatal circuit is the target in OCD work. The basic protocols still earn their place.
Why is there no large definitive neurofeedback study?
Nobody owns neurofeedback enough to fund the study it needs. A proper individualized, placebo-controlled, double-blind trial across six months with sham conditions and an adequate sample is a five-million-dollar undertaking minimum, and no single party has the stake to pay for it.
If I had that five million, it would buy a strong study. You can show the feedback happening in real time as a visible brain process, almost like an ERP. You can do tailored protocols that follow a person's change rather than freezing the intervention. You can run genuine placebo control with software like EEGer, and you can power it for a real effect size. What it would not do is instantly erase 50 years of small-n studies and case reports that require you to read the whole literature before you believe it. Sandra Loo's meta-analytic work out of UCLA, with Martin Arns, shows neurofeedback in a positive light from honest researchers (Arns et al., 2009). Russell Barkley's loud dismissals are where you land if you stop reading at the insurance company position papers. The legitimacy question is worth understanding in full, which I cover in a research overview and the ADHD-specific evidence.
As a layperson, what should I ask a neurofeedback practitioner?
Start with the data. Ask what they see in your EEG. Ask whether they have worked with your particular goal or complaint before, and how long they have been doing this work.
Your starting question shapes the right provider. Coming to neurofeedback for meditation is different from coming with intractable epilepsy or migraine. A provider working in epilepsy needs specialized experience there. Here is my honest position on credentials: a clinical license or a BCIA or QEEG-D certification is not required to do good neurofeedback, and I do not think it should be. No research links any specific neurofeedback credential to better outcomes. A certification is at most a baseline-training signal, never a guarantee of skill, and some of the best practitioners built their skill through years of supervised practice rather than a certification pathway. BCIA certification can also cover pelvic floor biofeedback rather than EEG, so confirm they are EEG-experienced, ideally with QEEG training.
A few signals I weight heavily:
- Do not ask what equipment they use. Ask how they use it. A practitioner over-attached to one system or protocol is a yellow flag. You want broad knowledge and a tool chosen to fit you.
- Do they individualize from your QEEG data, track outcomes with objective measures, and re-map periodically? Good practice means re-reading your data every 20 to 25 sessions and adjusting, not running one-size-fits-all protocols.
- Are they honest about non-response? Non-response in the 15 to 30 percent range is normal. A provider who builds in off-ramps and reassessment is being honest with you. One who sells a high-pressure prepaid package with no reassessment is not.
- Experience is a teacher you cannot shortcut. Larry Johnson sent the same edited EEG epoch to many QEEG services. The recommendations came back looking random until he split them by experience. Above five years of practice clustered toward general agreement. Below five years scattered.
- Ask about a mentor. Good supervision over months or years is how this field actually transmits skill.
Keep the training itself boring, especially for anyone with an attention problem. If the screen captures their attention, the session looks great and does not transfer to the environments where their attention actually fails.
Why do some people have a bad reaction to neurofeedback?
A bad reaction is almost always a fit problem, not the method failing. Push too fast and you get brain fatigue. An attentive provider slows down or switches the protocol. Trauma work can produce an abreaction, which is part of the process and different from a true bad reaction.
Persistent side effects build when a protocol is a poor fit and the provider ignores what happens afterward, reinforcing the problem session after session. The brain tolerates an imperfect ask for a while. It stays mostly okay until it is not, until someone is overactivated into anxiety, thrown into disregulated sleep, or pushed until a seizure breaks through. I have seen people who got driven into anxious states by non-adjusting black-box devices and were told to push through. Those effects can stick after 10 or 15 sessions.
There are protocols I would never run more than three in a row, even when the client wants more. You stop, switch, and let the brain settle, because the fourth one can be too much. Prepare the client to report fatigue or a headache, check your notes, check your data, and do not let it get that far. The field reports roughly 80 percent success on soft criteria, and even that is a somewhat coercive question to ask someone who just invested a year. The honest claim is not 100 percent.
Is there a college degree that prepares you for this work?
There are accredited programs with applied psychophysiology orientations, and universities internationally run neurofeedback-oriented training. None of it fully prepares you on its own. You cannot get ready inside a four or five-year bachelor's-to-master's track, because the judgment comes from staring at signals for years before it settles in. MD, psychiatry, and psychology degrees often arrive with no EEG training at all. The two halves go together.
The dangerous combination is a weekend workshop followed by putting electrodes on someone's head. That has happened a great deal over the past few decades. A better path runs through allied health: become a registered EEG tech, get very good at recordings and waveforms, then work alongside a psychologist or psychiatrist and become the hands-on person who knows the physiology they lack. I spent years as a back-lab tech watching half a million EEGs go by, and it served me well.
Can neurofeedback actually scale or make money?
At the individual level, the people charging $300 a session in New York are psychiatrists who bill their hourly rate and use neurofeedback as the tool. Make money with something that already makes money, then deploy neurofeedback inside it.
I think about scale as access rather than franchising. The product we offer is agency: teaching people how their own brains work. If everyone did an attention test and a brain map and understood their own stress, fatigue, and attention, there would be far less suffering, because people would build their own accommodations. Brand-licensing models exist with hundreds of names under one umbrella, but they often amount to unaffiliated doctors sharing a marketing banner. The real risks at scale are brain spas and brain mills that stop reading the individual EEG. Standardization is hard precisely because the individual brain is not standardized, and the headset technology is not yet good enough to guarantee clean signal without someone who knows what they are looking at.
How do you convince a skeptical neurologist or psychiatrist?
One convert at a time. Psychiatrists who never believed in neurofeedback have referred to me after a hard case forced their hand. We get a brain map, I tell them three things they did not tell me, the picture they are tracking improves, and the referrals start. There is nobody as supportive of neurofeedback as a former skeptic.
I have not found neurologists hostile, because I work directly in epilepsy research and QEEG, and they recognize within minutes that you understand what the brain is doing. General MDs and neurologists tend to be easier than PhD-level psychiatrists and talk therapists, who are the most resistant referral group. Master's-level clinicians, the licensed social workers and mental health counselors in the trenches, refer freely. They are skilled, busy, and they see a lot of ADHD and trauma they want handled differently.
The honest framing is complement, not competition. A little counseling pairs well with brain training. Some cases need the physiological intervention to move at all. The discipline that talks with you, reads your data, and chooses tools to fit your goal is the one worth your time.
This was a panel built for entertainment and education, not clinical advice. If you are working through your own EEG or your child's, that data is the start of agency, not a verdict. Bring it to a provider who will read it carefully and check with your primary care physician first.
References
- Charms (2005). Control over brain activation and pain learned by using real-time functional MRI. doi:10.1073/pnas.0505210102
- Arns (2009). Efficacy of Neurofeedback Treatment in ADHD: The Effects on Inattention, Impulsivity and Hyperactivity: A Meta-Analysis. doi:10.1177/155005940904000311