Let me start by answering some FAQ’s I’m getting with respect to neurofeedback.

Does it have to be the Othmer’s system? There are quite a few choices of systems on the market. I am out of date, because I am just starting to reconnect with old friends in the neurofeedback community, or should I say communities. The Othmer’s new system, Cygnet, does what the others do, plus it is able work at the “ultra low frequencies” that Sue is using in her clinic. They also have a tight network of practitioners who share clinical experiences on a private listserve and consult with Sue about particular patients if needed. It allows me, for example to start a patient here and have them follow-up with someone close to them at home who has the same equipment and uses the same protocol, though, as I said before, it is not a one size fits all protocol. Unfortunately. Judgement is required. It’s getting closer and closer though. It’s fun to think about a future with wireless electrodes and one size fits all neurofeedback that anyone can do anywhere, on their iPhone.

BrainMaster used to give the most for the least money. A quick look at their website and it looks like they still do. I also had a little experience with Roshi and LENS, but I consider them to be in a different category, because they use stim to entrain the brain. It is a powerful technique, but I don’t have enough experience with it personally to write about it or advise strangers to try it. There are many testimonials out there for those techniques, however. They fall into the category of things that could help so many people, but will never be studied, because it doesn’t fit into the dominant paradigm and there isn’t enough money to be made, unless people start saying no to drugs.

Can it hurt you? In the hands of the wrong therapist, yes. As I said in the last post, it can further destabilize initially until a protocol that works for that person is found. For a stable epileptic, tolerating meds, it may not be a good idea. For someone on the brink of harming themselves or others, it may not be a good idea, unless done in a controlled setting. For someone who has not tried meds, or wants off of them? For almost anyone with a neuropsychiatric disorder (and for those of you that haven’t read the DSM IV, that’s most of the entire human race), it’s worth a try.

I do think it’s worthy of comment here. There are people who say they are bothered by WiFi and on first glance, it sounds crazy, but one of things the internet and cell phones have done (also flourescent lights) is create an environment where we are constantly bombarded with electromagnetic frequencies which may entrain the brain to some extent towards poorer function and thus cause symptoms.

Now, oxygen reports and answers to some questions. I have heard from two more people reading the blog who experienced a flare of symptoms (herx) from the doses of normobaric oxygen I am using in my practice. I no longer think a herx is a good thing, but a potentially damaging cytokine storm, though I did see people push through it and improve with very high dose HBOT in my last practice. I now think that if that were to happen in my practice, I would back off, to maybe a half an hour every other day, see if that is helpful and go up from there. I would assume that those people would herx with hyperbaric also and it is possible that they could improve enough with lower dose oxygen that they would later tolerate the addition of pressure. All speculative for now. Anyone trying oxygen, please keep me informed. My practice is tiny and this is how I learn, how we are all learning for now.

I’ve gotten some questions which indicate that some don’t know the difference between a concentrator and a chamber. A concentrator puts oxygen directly into the room,  through a tube, which is delivered to the patient in one of several ways- a cannula that goes in the nose, a simple mask, with holes in the side, or non-rebreather mask that has an oxygen reservoir that holds 100% oxygen and has one way valves to prevent inspiration of ambient air and to allow exhalation of exhalation gases. Oxygen can be brought to the home in tanks or in the form of a concentrator, that takes the oxygen out of the air. Tanks are quieter, but at the flows I’m using, need to be replaced frequently. Concentrators are noisy, but more portable and never run out. Concentrators can be portable or ultra-portable, but portables only give 2-4L/min (liters of flow per minute) and are used with a cannula (delivering 24-27% oxygen, instead of the 21% in air). A standard concentrator usually goes to 5 or 6L/min and can be used with a simple mask (delivering up to 35 or 40% oxygen). Some concentrators go to 10L/min and then can be used with a non-rebreather mask (delivering >60% oxygen depending upon fit). A non-rebreather mask should not be used without enough flow to inflate the bag.

10L/min concentrator

Nasal cannula

Simple mask

Non rebreather mask

A chamber is a way to raise the ambient pressure of the patient above that in the room (normobaric pressure). Chambers can be monoplace, the patient goes into a 100% oxygen environment, or multiplace, multiple people go in together and oxygen is delivered by Scott mask or by hood, a bubble around the head with an airtight neckdam (latex or neoprene) to which oxygen is delivered with high enough flow to blow out the exhaled gases. Hard chambers go to pressures, or “depths”, of up to 3 ATA. Hyperbaric technology came from the need to treat divers with the bends. A huge amount of work has been done by the Navy and the commercial diving industry that has helped to elucidate the physiology of exposure to pressure and hyperoxia.

Sea level is defined as 1 ATA (measure of atmospheric pressure equivalent to 760mm Hg). 2 ATA is equivalent to the pressure at 33 FSW (feet of sea water), the way divers think of pressure. Depth and pressure can be measured in many ways; some common conversions are 1 atmosphere (atm or ATA) = 33 feet of seawater (fsw) = 10 meters of sea water (msw) = 14.7 pounds per square inch (psi) = 1.01 bar. The protocol generally used for treating brain injury is 1.3-1.5 ATA with 24-100% oxygen.

Monoplace chamber

Multiplace chamber

There is ongoing debate in the hyperbaric community as to whether the addition of pressure adds anything to a treatment that you could deliver without it. For example, there have been studies done showing that autistic kids respond to very mild hyperbaric treatments, 1.3 ATA and 24% O2. PaO2 = partial pressure of oxygen in arterial blood is between 75 mmHg and 100 mmHg at sea level (765 mmHg) on room air. A 1.3 ATA treatment with an FiO2 (fraction of inspired oxygen) of 24% will produce a paO2, or partial pressure of oxygen in the plasma of around 300mm Hg; you can get that with a mask and a concentrator, without a chamber (400mm Hg +). But my guess is, yes, it’s better with pressure. And our trail blazer K’s experience, a few blogs back, suggests that will turn out to be the case. A few references below re: possible independent pressure effects.

The breakthrough for hyperbaric treatment that allows it to be safe and simple enough for home use has actually happened since I left my last practice, in the form of the soft chamber. Gamow bags were developed to treat mountain climbers who develop altitude sickness. For this purpose, they are used without oxygen, simply adding pressure to increase the pO2 a little, and this works. It works by compressing the air so that the lung tissue is exposed to a greater number of O2 molecules in the same volume. In the early ’00’s I was worried about the possibility of an explosive decompression, which can be fatal, because the soft chambers sold are not rated for hundreds of duty cycles. But in practice, over quite a number of years now in home settings, it hasn’t happened. They do develop leaks on occasion, but slowly, and then they can be repaired. I see on the internet, there are quite a few newer companies selling cheap chambers, also some from China. I’d advise refraining from a bargain without a track record. To help with cost, I’ve heard of groups who live near each other sharing a chamber.

Soft chamber

Soft chamber inflated

The chambers can be used with or without oxygen, though it says right on them that they are not supposed to be used with oxygen. Nevertheless, they provide a port to hook up your concentrator:). Oxygen should not be delivered directly into the open chamber, but through a mask, just as with a concentrator alone.

Oxygen saturation in blood, or O2 Sat, is measurable by pulse oximetry on the finger and expressed as a percentage. It tells you how much oxygen is getting through the lung into the blood. Since we don’t have trouble saturating hemoglobin, this number is often cited as the reason that we don’t need oxygen. However, it is possible to hyperoxygenate the plasma and we do have cellular hypoxia, meaning not enough oxygen is making it into the cell, or mitochondria (and/or it isn’t being metabolized properly). My guess is that there is an issue with oxygen getting across the mitochondrial membrane. Viral product from activated virus in mtDNA? Elevated anticardiolipin antibodies (and other autoimmune markers) are seen fairly commonly in the patient group. Cardiolipins are located on the inside of the mitochondrial membrane. Oxygen gets into the mitochondria by diffusion across a pressure gradient. Without enough oxygen, the cell can’t make ATP. If you raise the diffusion pressure, more goes in.

Relative contraindications to hyperbarics are seizure disorder, inability to clear ears for pressurization, though this should be able to be handled in almost all cases, without barotrauma, but takes patience on the part of the chamber operator, as well as good communication with the patient. Severe COPD with CO2 retention, is another relative contraindication, although in practice CO2 narcosis only happens in the setting of acute decompensation. Asthma is a concern, because wheezing can cause air trapping and a wheezing patient shouldn’t be decompressed as trapped gases will expand and cause barotrauma. Asthmatic patients should be pretreated. Hereditary spherocytosis because of red cell fragility. Pregnancy and cancer are considered relative contraindications because of the unknown, although there are hints that HBOT may in fact be helpful for cancer. Certain prior ear surgeries are a concern and should be discussed with an otolaryngologist. Also some eye problems should be carefully considered. Hyperbarics may accelerate the maturation of existing cataracts, though if this is true, it takes a lot; HBOT does not cause cataracts de novo, according to the literature. An exam by an ophthalmologist is a good idea prior to embarking on hyperbaric treatment. There have been cases of optic neuritis that worsened with hyperbaric treatments. Implanted devices should be checked prior to treatment with the manufacturer as to whether they are hyperbaric safe. The only absolute contraindictions to hyperbarics are the presence of an untreated pneumothorax (collapsed lung) and recent prior or concurrent treatment with doxyrubicin, cisplatinum, Sulfamylon or disulfiram (Antabuse).

Hyperbaric safety amounts to common sense. Don’t create sparks in the chamber as oxygen is an accelerant. It sounds like a simple thing, but there have been some terrible accidents, all due to human error. Only cotton should be worn in the chamber. Reading material is permitted, but not newsprint. Always make sure you have nothing in your pockets when entering a chamber.

There is a review on MedScape (here’s the link for those who can get in) from 2010 that lays out the party line, which is that only patients with certain very circumscribed indications should do it, but when you look into it further, it’s pretty clear that that is all about what insurance will and won’t pay for. Hospitals charge exorbitant per session prices and will only treat the indications that insurance covers. It is a global treatment. It affects every cell in the body and its potential uses are very broad. Risks low. The article also says that soft chambers are becoming popular (gasp) and that they can go to 1.5 or 1.7 ATA. DO NOT TRY THIS AT HOME. The soft chambers come with a pressure relief valve that prevents going above 1.3 ATA (aka 4 PSI). These can be disabled to allow higher pressures. The only accident I have heard about through the rumor mill involved someone who altered a chamber to go to 1.5 ATA. It doesn’t sound like much of a difference, but I’m sure there is an engineer out there reading who can put it in perspective for us. Amusingly, the Undersea and Hyperbaric Medicine Society defines a hyperbaric treatment as above 1.5 ATA.

A little interesting history of hyperbarics from the MedScape article:

Hyperbaric oxygen therapy (HBOT) is breathing 100% oxygen while under increased atmospheric pressure. HBOT is a treatment that can be traced back to the 1600s. The first well-known chamber was built and run by a British clergyman named Henshaw. He built a structure called the domicilium that was used to treat a multitude of diseases. The chamber was pressurized with air or unpressurized using bellows. The idea of treating patients under increased pressure was continued by the French surgeon Fontaine, who built a pressurized, mobile operating room in 1879. Dr. Orville Cunningham, a professor of anesthesia, ran what was known as the “Steel Ball Hospital.” The structure, erected in 1928, was 6 stories high and 64 feet in diameter. The hospital could reach 3 atmospheres of pressure. The hospital was closed in 1930 because of the lack of scientific evidence indicating that such treatment alleviated disease. It was deconstructed during World War II for scrap.

The military continued work with hyperbaric oxygen. The work of Paul Bert, who demonstrated the toxic effects of oxygen (producing grand mal seizures), as well as the work of J. Lorrain-Smith, who demonstrated pulmonary oxygen toxicity, were used with Navy divers. Exposure times to oxygen at different depths of water (and, hence, different levels of pressure) were quantified and tested based on time to convulsions.

This last work mentioned may be the source of the fear of oxygen. However, the Navy worked out the doses long ago. They have been using Nitrox, or oxygen enriched air, to prevent the complications of prolonged and repeated exposure to nitrogen bubbles produced during depressurization. Over time, hundreds of dives on air cause cognitive decline and joint disease. If you are diving with a mask in a multiplace or soft chamber, please make sure to wear your oxygen on the way up. There is huge experience from the diving industry that oxygen enriched air exposure, during exercise, is safe over many, many exposures. And that’s with pressure.

From this same MedScape article, which was written by detractors of alternative uses of HBOT:

Additionally, evidence is growing that HBOT alters the levels of proinflammatory mediators and may blunt the inflammatory cascade. More studies are needed to further elucidate this complex interaction.

And possibly pertinent to our patient group, although frank congestive heart failure is not typical of our illness…

As HBOT is known to decrease heart rate while maintaining stroke volume, it has the potential to decrease cardiac output. At the same time, through systemic vasoconstriction, HBOT increases afterload. This combined effect can exacerbate congestive heart failure in patients with severe disease; however, clinically significant worsening of congestive heart failure is rare.

I am weaning patients off fentanyl patches with oxygen concentrators and getting mail from all over the world from very sick people about how much it is helping them and thanking me. Oxygen is the best thing I’ve got to offer, not all by itself, but in synergy with other things. Of course not everyone benefits, but lots of people do and no one is harmed if used sensibly. If I could only do one thing for the sickest people, it would be to give them a concentrator to try daily for a while and during their worst moments. CFS doctors have bad mouthed oxygen for decades due to a logical fallacy, that because there is already oxidative stress, and oxygen produces temporary oxidative stress, during administration, that that is all it does, so therefore it is bad for us. As a result, patients have had to suffer more than necessary for a very long time. But no worries, soon those same doctors, who said oxygen was too dangerous to try, will be able to make lots of money giving everybody Ampligen and Rituxan.

Please read this wonderful paper:

Hyperbaric oxygen therapy promotes neurogenesis: where do we stand?

Numerous in vivo and in vitro studies confirm that HBOT induces neurogenesis however, underlying mechanisms remain unknown. Activation of several signaling pathways and transcription factors have been suggested to play an important role in HBOT induced neurogenesis, including Wnt, hypoxia-inducible factors (HIFs) and cAMP response element-binding (CREB)…

On HBOT and oxidative stress: HBOT enhances the production of reactive oxygen species (ROS) and causes oxidative stress in body tissues. Excessive accumulation of oxidative stress may contribute to neurodegenerative processes and cell death in the brain, as seen in diseases like Alzheimer’s disease (AD) and Parkinson’s disease (PD). Since HBOT-induced oxidative stress is directly proportional to both exposure pressure and duration, the benefits of HBOT, may outweigh the side effects due to the phenomenon of hormesis. Hormesis is a process that results in a functional improvement of cellular stress resistance, survival, and longevity in response to sub-lethal levels of stress. We suggest that this process might be beneficial in the treatment of oxidative stress associated neurodegenerative diseases like AD and PD.

Hyperbaric oxygen therapy protects against mitochondrial dysfunction and delays onset of motor neuron disease in Wobbler mice

Our data suggest that HBOT significantly ameliorates mitochondrial dysfunction in the motor cortex and spinal cord and greatly delays the onset of the disease in an animal model of motor neuron disease.

Dr. Rossignol believes that there is an independent pressure effect that induces mitochondrial biogenesis: This prior blog has links to some of Dr. Rossignol’s papers as well as slides from a lecture last year, and other oxygen references. The Next Step For Us. Here is one with an especially pertinent quote: The effects of hyperbaric oxygen therapy on oxidative stress, inflammation, and symptoms in children with autism: an open-label pilot study

This prospective open-label pilot study in children with autism indicates, as measured by changes in plasma GSSG, that HBOT ranging from 1.3 to 1.5 atm and 24% to 100% oxygen was not significantly associated with increased intracellular oxidative stress. The use of therapies to raise glutathione levels and lower oxidative stress before beginning HBOT in individuals with autism appears prudent. Among children with high initial CRP, hyperbaric therapy led to a large improvement in CRP levels; this suggests that inflammation in these children improved with treatment. Improvements in clinical outcomes as measured by several scales were observed at both 1.3 atm and 1.5 atm.

Here are some interesting random recent references:

Hyperbaric oxygen treatment for inflammatory bowel disease: a systematic review and analysis

Conclusions: HBOT lowered markers of inflammation and oxidative stress and ameliorated IBD (inflammatory bowel disease) in both human and animal studies. Most treated patients were refractory to standard medical treatments. Additional studies are warranted to investigate the effects of HBOT on biomarkers of oxidative stress and inflammation as well as clinical outcomes in individuals with IBD.

Hyperbaric oxygenation therapy alleviates chronic constrictive injury-induced neuropathic pain and reduces tumor necrosis factor-alpha production.

These data show that HBOT alleviates CCI-induced neuropathic pain and inhibits endoneuronal TNF-α production, but not IL-1β in CCI-induced neuropathic pain. Reduced TNF-α production may, at least in part, contribute to the beneficial effect of HBOT.

Hyperbaric oxygen therapy in the management of paroxysmal sympathetic hyperactivity after severe traumatic brain injury: a report of 6 cases.

Thus, HBOT may present an option for the management of PSH (paroxysmal sympathetic activity) in addition to pharmacologic therapy. Potential mechanisms for these effects are discussed.

But whatever the mechanism, the proof is in the pudding. Relief is relief. Patients know it if they feel it. If it doesn’t make them feel better they can turn it off. The patients tell you what they need, if you listen. They tell you they have air hunger and are short of breath. Well, not at all surprisingly, oxygen can relieve it. The disease is characterized by diffuse vascular spasm. Even insurance companies will pay for oxygen for migraines. Unless you have CFS. Then you get nothing.

Our chamber, early 2000, Great Barrington, MA, and my husband, Anthony, at the console.

Today’s song: Black Muddy River

Erratum:  De novo cataract development following a standard course of hyperbaric oxygen therapy. A recent paper reporting a case of de novo cataract formation after 48 HBOT sessions at 2.5 ATA for 90 minutes for chronic refractory osteomyelitis, an enormous dose compared to the doses discussed in this blog (high dose normobaric and mild hyperbaric treatments, all <1.5 ATA with 100% O2). There is a huge amount of wound care that has been done over many, many years now at the doses this patient was treated with and this case was considered reportable as a cautionary statement to suggest that it can occasionally happen at doses less than previously thought. As I said above, it is a good idea to get an eye exam prior to embarking on oxygen treatment and discuss any contraindications you might have. More importantly, if you try it and it works, you might want to involve your ophthalmologist in the decision to continue long term, especially if you have any pre-existing eye conditions.

As soon as Siegfried’s post went up, I was questioned on FaceBook as to how I could promote something as unscientific as neurofeedback. There is science to support its use, but my personal answer to that question is, let’s not get blinded by science. I’m a clinician. Neurofeedback helps sometimes, maybe even oftentimes in some hands, when nothing else has. And here’s some interesting science as well.

• Clinical Neurofeedback: Case Studies, Proposed Mechanism, and Implications for Pediatric Neurology Practice 
• Taking Back the Brain: Could Neurofeedback Training Be Effective for Relieving Distressing Auditory Verbal Hallucinations in Patients With Schizophrenia?
• EEG-based upper alpha neurofeedback training improves working memory performance.
• EEG and behavioral changes following neurofeedback treatment in learning disabled children.
• The Effects of QEEG-Informed Neurofeedback in ADHD: An Open-Label Pilot Study
• Neurofeedback in ADHD: a single-blind randomized controlled trial.

Medicine is an art. Healing, different from curing, happens in the context of relationship. There are many factors at play. I mostly treated untreatable things in my last practice, and now again. I try things that aren’t dangerous, relatively speaking, discard the things that don’t work and keep the things that do, and I look for synergy. When a patient is successful at turning their illness around, it is generally because of a constellation of things. There are always many uncontrollable variables in clinical practice. Science doesn’t do well with multi-factorial treatments. Sometimes anecdote is the best thing we have to go on.

Here are a few cases from my last practice that come immediately to mind. Cases I treated with neurofeedback, on now obsolete equipment.

6 year old boy with greater than 100 seizures a day. Idiopathic onset of grand mal seizures 6 months prior. On 3 anticonvulsant drugs, having many small breakthrough seizures, without loss of postural tone or incontinence, but followed by a period of post-ictal confusion. Very disruptive to his life and that of his family members. The child was a well behaved, very smart, well functioning kid prior to onset of epilepsy. On presentation, his EEG showed generalized slow wave activity with intermittent paroxysmal bursts, also generalized.

We did a few sessions and he responded with fewer seizures, but he lived over an hour from me, could come for treatment only a couple of times per week, and would slide between sessions. After a dozen or so sessions, it was clear that neurofeedback helped him. His mother learned to run his sessions and bought a machine that she used to treat him at home under my direction. He was seizure free in 3 months and drug free in 6 months. Now 14, he continues to train on that same obsolete system, 21 minutes a day. He is an A student and has avoided years of brain deadening drugs. The only time he has seized is when he tried to wean from the neurofeedback and wound up back on drugs for a few months. Is he cured? No, his epilepsy is controlled with neurofeedback, something that helps brain function, without hurting anything.

Here’s another: Anna’s Story. Her doctors wanted to remove part of her brain.

I remember a 12 year old boy with NLD, on the autistic spectrum. He had wonderful, proactive parents. He had such severe dysgraphia that he needed a scribe at school. He was too clumbsy for sports. He had no friends. He had an obsessive interest in movies, knew all the names of everyone involved in many, many movies. After, maybe 9 months of neurofeedback, about twice a week?, don’t remember exactly, his handwriting was legible, he was on the basketball team at school, had had a sleep over date at a friend’s house and was writing a movie column for the school paper. I eventually did some hyperbaric with him, but for him, it was the neurofeedback that had the power. Have no long-term follow-up on him. He was a lovely boy. I’d love to know what kind of a man he grew into. I recall that his father had fibromyalgia.

I treated a yoga instructor with life long full blown panic attacks. Appeared out of the blue, without content. They went away after the first treatment. She finished 20 treatments, for luck, but the first treatment appeared to fix them. I had maybe 6 months or a year of follow-up and they didn’t reappear. Like a restart of a computer. This was an extremely rare case and I treated people who weren’t helped at all. But hey, no harm, no foul.

Obviously, these are very memorable cases, but I treated hundreds of people and it is useful, as an adjunctive therapy, for many conditions, especially conditions that involve unstable brain states. I found it especially effective for all kinds of anxiety disorders and it often significantly reduced the need for medication in short order. I used to advise committing to 10 sessions. If it is helping, continue. If nothing has happened by then, quit. The worst reaction is no reaction. I also used to say, if I can move you in the wrong direction, I can move you in the right direction. The diagnoses I worried about with respect to moving someone even temporarily in the wrong direction were epilepsy, depression with suicidal ideation and serious anger management problems. For these conditions, I advise a very experienced therapist.

The history of neurofeedback has a wonderful, serendipitous story behind it. Barry Sterman, PhD at UCLA, a psychologist and sleep researcher, did Pavlov type experiments with cats, where they had to push levers to get food. He monitored their EEGs during testing. Cats have an unusual rhythm that shows up at about 14 Hz, a burst of high amplitude activity, a little higher than the alpha rhythm. The SMR, or sensori-motor rhythm, is associated with stalking behavior in cats, a state of watchful waiting, not resting, but active and in the moment. He decided to use that rhythm as a training device, because it was easy to see and count. He was able to teach the cats to produce these bursts of EEG activity at will to get food. Some time later, he was hired by the Air Force to figure out how much rocket fuel their pilots could be exposed to before they had seizures. He tested on cats, because he had them. After doing the experiments, the data showed two clear groups, with respect to seizure threshold. Barry then realized that the cats with the higher seizure thresholds were the ones that had previous SMR reward training. He went on to try it with people. I am telling this story from memory, so Barry, forgive me if I butchered it.

Various people also started realizing that there was some advantage to down training, or inhibiting, slow waves, for performance enhancement in ADD kids. A lot of work has been done on this. However it is much easier to give children speed than to do this non-invasive treatment that takes time and effort. In fact, neurofeedback costs less than psychostimulants over time, but the drugs have big money behind them to prove that a normal variant is a disease, and to label large numbers of children with it. Ritalin is a performance enhancer for anyone that can tolerate the side effects. If you want your perfectly normal B student to get B+’s, just add some Ritalin. And when they get old enough, they can make extra money selling it to their friends. Or you could try some neurofeedback. Except that it isn’t scientific. Don’t get me going… However, brain damage, MBD, as it was known when I went to medical school, from a structural injury or persistent inflammation, is another story entirely. Neurofeedback helps here too, when no amount of Ritalin will change it.

Here’s how it works. You put electrodes on the scalp, in various locations, depending on what part of the brain you want to exercise or challenge. The electrodes don’t put anything into the patient, but they measure the EEG, the electrical activity produced by the brain and measurable on the scalp. First the area gets prepped with a mildly abrasive substance, the electrode is applied with paste between it and the scalp to reduce the impedance, or how much opposition there is to measuring the signal. The EEG is amplified and fed into a computer where software breaks the signal down into frequency bands, generally 0-40 Hz. One hertz or Hz is one cycle per second of a wave form. The Othmer’s new work is looking at a very slow signal, close to zero. It is pioneering work, and as such, is being met with resistance in the more conventional neurofeedback community, since it is so unscientific, meaning clinically driven.

The signal is converted by the neurofeedback system into a graphic representation of the information gleaned from the EKG. If the brainwaves change, the picture changes. The graphic reinforces increases in the reward band and tries to inhibit slow wave excursions. The visual feedback can be anything you want, including a movie. Different people respond to different graphics. Auditory feedback used to be beeps, but blessedly, the new software uses music instead of beeps, getting louder to reinforce whatever the therapist has chosen to reinforce. There is also tactile feedback in the form of a vibrating teddy bear, like holding a purring cat.

Unfortunately, clinical results with neurofeedback are highly system and operator dependent. A choice must be made at the start of each session about where and at what frequency to train. Reinforcing the wrong thing over time can even make things worse, though in eight years of practice, I never produced a new symptom that persisted. If the treatment is wrong, it sends the patient in the wrong direction, but generally somewhere familiar, and then the protocol can be changed to address symptoms. Usually, a protocol is found that can be repeated going forward. When that is the case, home training becomes a good option for some people.

Experience has taught that certain locations produce predictable effects in groups of people with common symptoms. Sue Othmer, in particular, has a coherent model for choosing training sites and optimal frequencies to reward that accomodate entire spectrums of neuropsychiatric illness. Without drugs. The downsides? Cost and time.

There are fractious groups within the neurofeedback community. Some are wedded to the more scientific approach of measuring the QEEG, or quantitative analysis of the EEG signal at multiple sites and subjecting the data to comparisons with various normative databases. A number of people have tried to define neuropsychiatric disorders and brain injury according to deviations from statistical norms. Then the idea is to fix those abnormalities. I did QEEG in my last practice and it’s fascinating, but I was never impressed that I was able to fix the QEEG with neurofeedback, even in the face of huge clinical improvements, so in the end, I decided it wasn’t worth the trouble or expense, generally speaking; if there is a structural abnormality, then a QEEG may be helpful, mostly to tell you where not to train. Anecdotally, I had better luck “fixing” the EEG with HBOT than neurofeedback.

My metaphor to explain why neurofeedback works is that it is like a reset, or mini shock treatment, all of the effort on up-training and down-training particular features in the EEG notwithstanding. If you tug on the EEG, cause a perturbation in the system, the brain will take over and order things in a more functional fashion. It has nothing to do with learning, or even training really, though that word is often used, for want of a better word. Here is a baby performing the task. Understanding is not required.

This is a YouTube video of a teenager currently in treatment with Sue Othmer. It is a small introduction, a glimpse into her approach. Many providers do neurofeedback in the context of psychotherapy, but therapy is not needed for efficacy. As a physician, it wasn’t that different from prescribing drugs, except that it worked better.

When I became disabled the first time, in early 1996, I was completely at a loss. I had had insidious onset of sensory neurological symptoms associated with autonomic and vascular instability, as well as anxiety and symptoms of PTSD for a year. I thought I might have MS, but whatever the diagnosis of my then mystery illness, I knew enough to know that conventional medicine had nothing to offer me. Instead I turned to biofeedback. I went to a conference in ?, can’t even remember where anymore, but I met Sue and Siegfried Othmer in an auditorium, after hearing them lecture. I gave Sue a little history and she hooked me up. I did maybe 20 minutes on her machine, went back to my hotel room and had the first good night’s sleep I’d had in years. I bought a system the next morning, then $14,000 (they are much less now). I took their training course, trained myself, then a few friends and was so impressed with the results that I went into practice with it, still in recovery myself. I used their system for 8 years in practice. Their new system and training protocol seem even stronger to me so far this time around, space age compared to my old system. Sue Othmer is a master clinician and anyone within shouting distance should certainly consider training with her. Siegfried has been a mentor to me for many years now. I am excited to introduce him to you. There is too little cross-pollination between the ME/CFS group and other communities. Please note: caregivers can benefit as much as patients. Neurofeedback is peak performance training, starting from wherever you are. So, without further ado, here’s Siegfried…