The field of neurofeedback has found itself subject to conflicting forces over the past decades, and it may be helpful to articulate some of the key factors that are driving our evolution as a discipline. On the one hand, we are subject to the constraints of a health care practitioner guild, and on the other we find ourselves in the much more uncertain terrain of frontier science. The demands of both are in essential conflict. The practitioner guild must represent to the world that a coherent system of practice exists, one grounded hopefully on a coherent model that is subscribed to by all of the practitioners. Guidelines and standards of practice likely follow to clarify for practitioners the choices that have been made for the sake of a credibly defensible public posture.

On the other side we have the practical realities of frontier science, acknowledging that we are just beginning to understand the very powerful tool that we have at our disposal. The original hope (which I shared at the outset) was that a simple set of protocols derived from the original Sterman/Lubar research would serve our collective purposes. These simply needed to be pushed forward into general practice, while being subject merely to some subtle refinements. Our original NeuroCybernetics system was designed with very little flexibility because we did not see a need for it. This simple world view has had to be jettisoned.

Instead what has emerged is a broad variety of methods that are based in turn on several distinct operating principles. The fundamental divide, which has been too little articulated, is whether targeting in neurofeedback is to be driven by the objective of enhancing function or whether it is to be guided by the particulars of dysfunction. At its origins, the field started out exclusively with mechanisms-based training, and all the early research soundly established its principles. It was only with the emergence of readily accessible QEEG measures that the field turned in the direction of making dysfunction, insofar as it revealed itself in the EEG, the target of training.

The uninitiated reader might at this point ask why there needed to be a divide along these lines at all. Why not simply adopt the most useful approaches from both perspectives? After all, mechanisms-based training also incorporates inhibits as a matter of course, and much QEEG-based training also incorporates standard reward-based training. One must conclude that the drive in the direction of deficit-targeting was largely politically based, in that it seemed obvious that herein lay the prospect for a “scientifically respectable” neurofeedback. Anything that took us in the direction of a more quantitative approach to targeting was intrinsically preferable—-if the issue is garnering acceptance from the scientific mainstream. But if this new approach was to meet the demands of the guild, then it had to be universally acknowledged within the field.

The resulting campaign to enforce a kind of uniformity of approach across the whole discipline was necessarily in opposition to the naturalistic emergence of new approaches out of the rich soil of clinical practice, and in the spirit of frontier science. The field is now at a place of greater diversity of approach than ever before, with a greater diversity of perspectives emerging from them. Meanwhile, those who believe that a uniformity of vision is essential to mainstream acceptance are becoming increasingly strident in their opposition, as such uniformity is slipping ineluctably from their grasp. Unsurprisingly, the actualities of frontier science are overwhelming the aspirations of the guild leadership toward uniformity of practice.

Looking back over our history, one can trace the development of this unfortunate divide to an environment defined primarily by our critics. The result is that we collectively became outward-focused and adopted defensive postures. This is inimical to frontier science, which then had to be shielded from view. The existence of the basic divide within the field between the path of enforced uniformity of practice versus the path of welcoming diversity also forced new developments under cover even within the field, where the reaction to new initiatives became increasingly toxic. Frontier science does not flourish under duress, or even under premature critical scrutiny. It needs latitude for the investigation of new initiatives.

Recently the journal Science News showed a network of e-mail interchanges illustrating the typical graph for a legitimate project at Enron, and compared that to a comparable graph for one of its illicit projects. In the latter, the e-mail network was much tighter, and showed very few links outside of the in-group. A similar graph holds for the new developments in our field, but for a very different reason. In our case, connections outside of the inner core are rebuffed, and so the networks remain largely disconnected from the rest of the community. This process is well illustrated in micrography showing neurons sending tendrils out to make connections. A network quickly develops, unless the environment is even slightly toxic, at which point the tendrils withdraw.

This reflexive hostility to new ideas places significant constraints on the pace of development within the field, and to the emergence of a comprehensive model for what we do. To illustrate the centrality of information exchange, I cite the following example from our own history. We had a chance to work with an autistic child in the late eighties, and we found that our beta training was not helpful. We immediately backed off, and from that time forward put a fence around autism because we had no assurance that we could be helpful. The same happened to us with Parkinson’s.In the absence of further work with either condition, there was no reason for that posture to ever change. It took external input from our network practitioners to re-open these issues for us some years later.

Much can be gained by allowing network connectivity to establish itself among the various distinct approaches that have emerged in neurofeedback. Broadly these cover both the stimulation and the reinforcement approaches, and cover the range from near DC to high EEG frequencies. At high frequencies the most efficient approaches appeal to coherence relationships in feedback or challenge the phase at particular frequencies with stimulation. At very low frequencies we have episodic SCP-training and continuous infra-low frequency training on the reinforcement side, and tDCS and CES on the stimulation side.

To allow cross-fertilization of ideas and perhaps even some combination of approaches to emerge, we must jettison the siege mentality that still exists within the field, and the susceptibility to outside criticism that still weighs on our affairs. A look back at our history supports this view. The technology has matured despite the adverse climate, while at the same time we don’t have much to show for our effort to assuage the critics. This pattern is likely to continue, because historically critics have demonstrated amazing tenacity in the face of contrary evidence. They should simply be left alone. (“What do scientists do when a paradigm fails? They act as if nothing happened.” –Elaine Morgan.)

My first exposure to scientific dogmatism was in connection with the Kon-Tiki expedition. An anthropologist visiting us in the early fifties was simply apoplectic about Thor Heyerdahl’s effrontery in contradicting prevailing wisdom. She had not read the book about the expedition, and was not about to pollute her mind with such obvious nonsense. It has been sixty years, and we now find in the Journal Science the following: “…the idea of prehistoric contact between Polynesians and South Americans has gone mainstream.” Heyerdahl’s ghost probably slowed the acceptance of this insight rather than accelerating it, simply because it energized the critics along the way, which tilted the playing field. There are some useful analogies here to our own condition. The early scientific research in neurofeedback was thought to have been rejected (whereas in fact it was mostly just ignored); there was the “premature” popularization of alpha training to live down; and we now have the prominent involvement of non-scientists in pushing the frontier.

There are three principal reasons for the ongoing animation of the critics of neurofeedback. The most obvious is Paradigm Paralysis, the categorical assertion that neurofeedback is not possible. This position is almost impervious to data because it is belief-based, so it is best left alone. The second is Panacea Paranoia, the idea that any therapy that promises benefits across the whole domain of mental health cannot be real, and hence must be nothing more than a placebo effect. Interestingly, the only entity that is allowed to be a panacea is the placebo itself. This is merely a case of misplaced concreteness. The panacea lies in the scope of brain plasticity, which we are just beginning to explore with neurofeedback. The neurofeedback itself is a trivially simple tool to elicit and mobilize brain plasticity. It is a humble servant, and should not be assigned substantial agency. The power of the placebo is lodged in the same place. There is no substantial agency there either.

We come then, finally, to the ultimate barrier to acceptance, Placebo Paralogism. What we have here is the appearance of a sound scientific counter-hypothesis when in fact it is nothing of the kind. Whereas the drug researcher can lump non-specific effects into the placebo bin and proceed at will with a controlled design, we cannot do the same. For us this would represent a category error. The argument proceeds as follows: If the placebo model is to explain neurofeedback, then it has to explain all of it. No exceptions. If there are exceptions, then we start having a very different discussion. This means that the placebo model also has to explain the hard cases, not just the easy ones. Let us go then to some of the hard cases.

We know that most cases of minor traumatic brain injury and of PTSD recover on their own. There is also no question that such recovery can be quite non-trivial, and is not explainable in terms of obvious factors such as the subsidence of edema. If such cases had been included in a formal controlled research design, such recovery would have been labeled ‘placebo response.’ But this would have been just a label for the natural process of self-recovery, aided perhaps by some expectancy factors. We now have good evidence to believe that the mechanism of such self-recovery is the gradual re-ordering of neural network functioning. Evidence for this was adduced years ago at UCLA, where imaging data showed persistent changes in the placebo group of depressives, changes which differed from those who responded to medication.

We now also know that the operative mechanism in neurofeedback is the re-ordering of neural network relations. So we have an aspirational approach for the systematic retraining of neural network functioning that is placed in juxtaposition with spontaneous recovery mechanisms. Telling the difference in the moment is impossible, just as it is impossible to tell whether a photon emitted from an atom did so via spontaneous or stimulated emission. But we have other ways of puncturing the placebo bubble that by hypothesis contains all of neurofeedback.

The most immaculate experiment ever done in neurofeedback was that of Barry Sterman with the cats that were injected with monomethylhydrazine. This was for the best of reasons, namely that neither Sterman nor the cats were aware at the time of the grander experiment in which they were playing a role. Hence neither was in a position to put a spin on events: no placebo response on the part of the cats; and no intention on the part of the researcher to end up with divergent results. This early experiment already punctured the placebo balloon, and it did so for all time.

But there is more. Consider the survey on epilepsy research published by Sterman in the EEG Journal in 2000. Essentially all those studies involved medically refractory epileptics. Significant improvement was shown with respect to medication alone. Since all epileptic drugs had already been shown to be better than placebo, there is no question that a study of medication plus neurofeedback would be better than placebo as well. Hence there is no point in even doing the study. It is not necessary for neurofeedback to be better than anti-convulsant medication in a head-to-head comparison. It is sufficient that it be additive. That already places it in the category of an active mechanism.

The results recently published by Jonathan Walker make the same case even more strongly. Adding neurofeedback to medication for migraine had a much better effect than the medication alone. It wasn’t even close. No placebo-controlled study is needed here either. The same goes for ADHD. The studies by Rossiter and LaVaque showed neurofeedback matching the medication response, which again obviates a placebo design. The case for neurofeedback as contributing actively to a self-regulation remedy for epilepsy, migraine, and ADHD can be made on logical self-consistency arguments alone, without any additional placebo-controlled study.

One can also spike the placebo bubble with a collection of individual cases. If placebo explains all of neurofeedback, then we can also line up all of neurofeedback on the other side. Consider the following reports from neurofeedback clinicians: A therapist in Ireland reports working with a client with Multiple Personality Disorder. Whenever he changed reinforcement frequencies he would trigger a transition to another alter. A therapist in Colombia working with a person in Persistent Vegetative State reported the simultaneous emergence of a regularized sleep pattern, regularized menstrual period, and the subsidence of constipation upon the initiation of neurofeedback. A therapist in Key West reports that a woman tried neurofeedback for fifteen minutes at an open house, and came back three days later to say that her hot flashes had declined by 50%. She set up additional sessions for after her vacation. When she returned, she reported that her hot flashes had entirely disappeared in the interim.

Or consider the report on a court-referred Vietnam era veteran with schizophrenia of long standing. At the end of the first session, he reported that he did not feel like smoking any more. At session five, he said that he had not smoked since the previous session, a period of nineteen days. He had not been trying to quit. One may even conjecture that the training affected the underlying condition of schizophrenia, which allowed him to discontinue the dosing with nicotine. But time will tell.

Finally, consider the report on a woman who had been under the care of two psychiatrists for decades for her unrelenting anxiety, one managing her meds and the other doing psychotherapy. The woman was essentially housebound with her pet dog. After some number of neurofeedback sessions, she reported that her anxiety had suddenly disappeared. She had already made travel plans to see her family, an event that came off without a hitch.

The above cases make it difficult to invoke expectancy factors as explanatory. And once the part of the placebo response that is relevant to neurofeedback has been reframed as a “spontaneous” reordering of neural network functioning, the comparison of neurofeedback to placebo loses its saliency. It is neurofeedback that helps us understand the robust placebo response, not the other way around. To treat it as an adversary like a drug researcher is to shoot into our own foxhole. When it comes to deciding whether to wait for autonomous recovery or to intervene actively, there is no debate. With our modern methods we now routinely observe robust single-session effects that settle the question rather quickly as to whether neurofeedback training is going to be worthwhile.

Given this state of affairs, we should not indulge the research community in their zeal for placebo-controlled designs. Rather, we should urge the reframing of hypotheses to something that is relevant to the current state of the art. It would be particularly inappropriate for neurofeedback practitioners to be involved with placebo-controlled studies because that would mean a tacit admission that such studies are answering a question that still needs to be asked. And once the placebo spell has been broken, it must also be acknowledged that the placebo hypothesis cannot be used to dismiss the emerging technological initiatives any more than it can dispose of neurofeedback as a whole.

It is part of the maturation of our field that we should define for ourselves the terms of discussion and the research agenda going forward. Specifically, placebo-controlled studies should have no place in that schema. More of an inward focus on our own priorities would also mean acceptance of our existence on the frontier of neuroscience, and a positive embrace of the technological progeny and procedural variety that the field has produced. We have an advantage possessed by no other part of the neuroscience community. We operate with a tool of great subtlety with immediate feedback on what we do. That keeps us on track, and that makes all the difference.

Siegfried Othmer, PhD
drothmer.com

This entry was posted on Thursday, February 2nd, 2012 at 10:44 pm and is filed under Application of Neurofeedback, Biofeedback, Clinical Methods, Neurofeedback, Professional Issues. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.