One reason that formal research on neurofeedback by people in the academic community hasn’t generally matched what is being accomplished clinically is surely that researchers tended to take the operant conditioning model seriously. Plainly, the rigorous instantiation of a ‘purist’ operant conditioning design of the original SMR-beta protocols leads to a rather inefficient training procedure. This can also be said of the original work of Sterman and Lubar, as they were doing their utmost to stay true to B.F. Skinner’s experimental design. Their work sufficed to provide the method a rigorous and sound foundation, but in the clinical realm such an inefficient method of brain training would be dead on arrival.

To illustrate the extremes to which this fealty to the Skinner model was taken, there is no better example than Lubar’s training of mentally impaired young children. To serve as a reward, Lubar arranged for sugar-laden dollops of water to be delivered to the children’s mouths through a flexible tube. Unsurprisingly, that research failed utterly and the project was abandoned. On the basis of this work, Lubar concluded that young children were not trainable.

BF Skinner himself had demonstrated just how easy it is to reinforce even infant behavior. Sitting with an infant on his lap, he would flick a table lamp on every time the infant moved his arm. In short order, the infant would be waving its arm to make the light turn on. Engagement of the child had made the difference, but of course the method is restricted to the domain of voluntary motor behavior. Training brain behavior presents a very different challenge.

We had a chance to work with several cases of near-drowning in young children early in our neurofeedback career, the early nineties. One case is particularly instructive. An infant girl of about 1.5 years was brought by her parents from Orange County. She had screamed all the way, and was still doing so as electrodes were placed. Her eyes weren’t tracking, so she was not looking at the screen. She was only hearing the auditory beeps that signaled the discrete rewards. She stopped screaming before twenty minutes had passed, and her nervous system had clearly calmed. The parents enjoyed a peaceful ride home.

Skip forward three decades, and we have the following report:

“This was a very colicky baby, with severe constipation and poor sleep, who would cry inconsolably for hours, from 7 PM to midnight. She calmed down in her very first session and stopped crying 18 minutes into it. She then slept through the night. Sleep improved and constipation resolved with additional sessions. She was three weeks old when we started the training.”

In both cases, all that was required was to engage the infant brain. It was not necessary to engage the infant. Such quick results cannot be explained within the scope of an operant conditioning model. And yet the first case above involved nothing more than the discrete rewards of an operant conditioning design, Barry Sterman’s specifically. Of course, there is no question here of learning having taken place in such a short time. All that occurred here was a rapid shift to a calmer state. But by what mechanism was this state change induced?

In the second case above, the training signal was derived exclusively from the infra-low frequency domain, so there were no discrete rewards at all. Here it is easy to argue that the information from the low-frequency domain sufficed to guide the brain to calmer states in short order, which is now routine in our work. It is not unusual for trainees to notice significant state shifts in six to ten minutes in such training.

It is tempting to use the second case to shed light on the first. Perhaps the gradual ebb and flow of beep incidence served as a cue to the slow fluctuations in cortical activation that guided the infant nervous system to calmer states. In support of this conjecture, we observe that the reward incidence had been increased in this protocol, to the point where the beeps were no longer being perceived as isolated events. The continuity between events could be readily discerned, and thus recognized as indexing the contour of the time course of cortical activation.

In the first case described above, the brain had made more use of the signal than had been intended. That of course had to be preceded by an act of recognition by the infant brain that this unusual beeping signal, unprecedented in the infant’s experience, held meaning for itself. The fact that this happened so quickly—and in an infant that was significantly neurologically impaired—testifies to the proposition that the brain is naturally in a perpetual state of anticipation of correlations in the outside world with respect to its own intentional activities. It is perpetually in a state of provisional hypothesis-testing with respect to such correlations.

We cannot rule out the likelihood that the brain is benefiting in ways other than what we had intended and designed for in some generality. After all, single-session effects are now commonplace in the field, and that essentially rules out the standard operant conditioning model as the operative mechanism. Whenever a continuous signal reflecting the brain’s intrinsic activity is being displayed, the brain has a chance to engage with its own dynamics, and thus effect state change. This exercises the relevant control mechanisms, which then have a chance to move toward homeodynamic equilibrium. We have long witnessed that this process can be very efficient.

All this is reminiscent of the role assigned to the placebo in pharmacology research. Here the placebo refers not only to the nebulous action of mind on matter in the aid of recovery. It also encompasses any other physiological mechanism that may be operative outside of the specific drug impact that is being studied but has simply not yet been recognized. The term placebo is used here in that larger, more encompassing sense.

The brain engaging in some extra-curricular self-help during the course of conventional neurofeedback, and operating outside of our awareness, falls within this larger scope of our definition of a placebo. Of course, that designation lasts only until the mechanism is identified, at which point it gets a label that takes it out of the placebo bin. We have called the operative mechanism in the above two cases ‘endogenous neuromodulation’–the brain simply engaging with its own signal–and it undoubtedly has played a role in many a neurofeedback design over the years.

Taking endogenous neuromodulation out of the placebo bin may not leave it devoid of active mechanisms. We must leave the question open. Sometimes training effects are seen so quickly that one wonders how that is possible when working with low-frequency signals. And this can occur even upon a trainee’s first acquaintance with the method. The brain can find its way rather quickly. That keeps us vigilant with respect to the possibility of yet other ‘active ingredients’ in the placebo bin that remain to be recognized.

One additional item in the placebo bin is the relationship between the mother and the infant during the training process. In both of the above cases, mothers were holding the infant. So as the process of calming began to have a beachhead with the infants, quite likely the mothers’ nervous systems calmed as well, and going forward there may well have been co-regulatory activity in which both nervous systems de-escalated jointly to calmer states. We’ve seen this mechanism operative between a feisty fetus and its mother. So, it is even more likely in play at some level in the above cases as well.

This brings us then to the issue of co-regulatory activity between the clinician and the client in the general case. Sue almost always stayed with the client during the session, even if the session was unlikely to yield drama. I have always tended to be very mindful of the presence of the clinician during my own sessions, even if there wasn’t a lot of discussion. Surely the multi-faceted role of the clinician in ILF NF is a significant factor in the success of the clinical journey with ILF NF, and yet it remains consigned to the placebo bin.

It is yet another factor that distinguishes the clinical work from what is being done in formal research. But just because placebo factors are at work in neurofeedback doesn’t mean that the method is reducible to a placebo. They are compounding factors, not confounding ones. They are ever-present force multipliers, but there has to be a multiplicand in first instance…

 
 

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