Misbranding
by Siegfried Othmer | May 10th, 2006The Food and Drug Administration uses the term “misbranding” to finger any piece of medical equipment for which specific claims are being made that have not been validated in research. When we now survey the field of neurofeedback and consider the various “claims” that we believe to be reasonable to make for neurofeedback, it is seems much closer to the truth that it is the disorders that have been misbranded, not the neurofeedback claims.
Any condition for which neurofeedback is highly effective is probably not what practitioners say it is. We can start this argument with Attention Deficit Disorder. This “disorder” keeps metamorphosing from one description to another, yet whatever model is currently in vogue is represented as sacrosanct. Apparent throughout this evolution in thinking is that ADHD is not a unitary condition; it is not stable over time within a subject; it is situationally dependent; the boundary between the well and the impaired is not unambiguous; and it is not independent of other defined disorders. To give the impression that this disorder is something discrete on which various professionals actually agree is visiting a kind of fraud upon the public.
Or take depression. It is not a unitary condition; it is not stable over time within an individual; the boundary between the well and the ill is not well-defined; and it is not independent of other defined disorders. In the attempt to fit depression into a disease model we have here another fraud upon the public. We could make the same argument with respect to anxiety. Jointly with these three categories we have covered the majority of cases referred for mental health services.
So, given the choice of regarding neurofeedback claims as instances of “misbranding”, on the one hand, and of regarding the principal mental disorders as instances of misbranding, on the other, only the latter fits the facts. Efficacy for neurofeedback for clinical complaints in the attentional and anxiety/depression domains is by now well beyond dispute among knowledgeable professionals. On the other hand, proving this efficacy to be specific for the vague and mutable constructs of psychiatric diagnosis is difficult at best. That’s because these constructs do not line up with the way nature actually behaves. The enterprise is so fruitless because it is flawed in its premise. Neurofeedback does not target ADHD, depression, or anxiety with any specificity. Its target is disregulation. Such disregulation can, in turn, manifest in a variety of ways that become clinically apparent. The remediation of clinical complaints is indeed a signpost of useful progress in neurofeedback. It is not evidence that the specific condition has been targeted with a specific remedy. Hence, the intimation of specificity is just another case of misbranding.
Given the current framework of understanding of the psychopathologies, the cards are stacked against neurofeedback. Further, any attempt to prove neurofeedback efficacy within that framework just further distorts the science, and ultimately the practical implementation of the science as well.
The logical flow is therefore as follows: The target of neurofeedback is the disregulation of cerebral network relations in the timing and frequency domains. Such disregulation may eventuate in clinical manifestations in the domains of arousal regulation, attentional regulation, affect regulation, autonomic regulation, motor control, specific cognitive function, working memory, etc. And beneath these categories, one may say even more generally that neurofeedback targets the stability of regulatory systems, the activation/relaxation dynamics of cerebral regulatory networks, and the dynamic response under a challenge.
Addressing the condition of disregulation by means of reinforcement and conditioning techniques may effect a resolution of the particular clinical complaints. These become matters of clinical observation, and such clinical observations can even be submitted to statistical evaluation. But irrespective of how solid these data become, they do not rise to the level of a claim. To claim efficacy for a specific diagnosis is to accept the concreteness and validity of that diagnosis. If the claim is to be meaningful, then something that is demonstrable within the formal diagnosis must be falsifiable outside of it. We do not find that to be the case. By contrast, recognizing our quite considerable clinical effectiveness for attentional and affective complaints allows us to reduce the affected clinical categories to little more than epiphenomena of the status of disregulation. These then have all the features of variability over time and complexity in clinical presentation that characterizes such disregulation.
The case is best illustrated perhaps for premenstrual syndrome, a condition that does not quite rise to the level of being recognized in the Diagnostic Statistical Manual (DSM), most likely for largely political reasons. But we know it when we see it. Here we have a condition that manifests in a variety of symptoms; it is variable within any one individual; and it is diverse in presentation among individuals. Nearly every symptom of disregulation known to woman may be correlated with the regular hormonal shifts. PMS largely resolves with neurofeedback, and usually does so quite quickly, irrespective of symptom presentation. This marks it as a quintessential Disorder of Disregulation. “There is no there there,” outside of mere disregulation. PMS could almost be seen as the defining issue for the Disorders of Disregulation. If the bounds of good taste and political correctness did not require us to be so circumspect in talking about this subject, PMS might well be our marquee issue, even more so than ADHD. There is just no need at all for women’s lives to be compromised by either PMS, menopausal symptoms, or for that matter, migraine.
With the singular and entirely anomalous exception of PMS, then, it is the Disorders of Disregulation that are currently being misbranded by the professions, not neurofeedback. (And, truth be told, even PMS has entered the DSM through the more forbidding term of “Late Luteal Phase Dysphoric Disorder,” which appears in the Appendix. So it is not really an exception, after all.) In the coming years, this dissonance with reality will come to be more universally perceived. It is important as a practical matter to have clarity on this subject, lest our efforts as a discipline be misdirected. As long as the current diagnostic regime is in place, neurofeedback cannot succeed as readily in gaining acceptance.
The recognition of neurofeedback will go hand in hand with a reframing of the central issue in psychopathology as lying in the realm of clinical psychophysiology rather than either in psychopharmacology on the one hand, or in psychodynamic disciplines on the other. The contribution of the traditional approaches is not to be undervalued, of course. But the core of what is to be done in the remediation of mental dysfunctions lies in the realm of restoring good self-regulatory function of the relevant cerebral networks, however that may be brought about. Everything else is secondary.
In competition with psychopharmacology, neurofeedback loses out to the “chemical deficiency” model, and in competition with psychodynamic approaches neurofeedback runs up against the banalities and absurdities of the placebo hypothesis. Consider that the more outrageous the claims for neurofeedback, the more strident is the demand that the claims be backed by placebo-controlled studies. This is done because people are not prepared to credit the findings, not because they really believe that a placebo mechanism is responsible. The absurdity is fully exposed when it is recognized that those who wittingly posit a placebo mechanism have already implicitly acknowledged the central proposition of neurofeedback, namely that a self-regulation remedy is sufficiently availing for the issue at hand.
Once a placebo hypothesis is invoked as the alternative explanation of clinical data, we are just arguing about the details about how the improved self-regulation status actually came about. On the one hand we have an ordered process for improved self-regulation, one with a sound scientific model and forty years of development behind it. On the other, we have the mysterious combination of white coat effect, the power of authority, the power of belief, expectancy effects, the power of the red pill, and a lot of other mumbo-jumbo thrown into the mix that cannot be parsed readily by the scientific method. The result, however, is self-regulation either way. And either way, the outcome will have been mediated by a re-ordering of cerebral regulatory processes.
[It is remarkable that nearly all discussions of the placebo model begin and end with its psychological dimension, when in fact the loop ultimately has to be closed with physiology. We collectively submit to the yoke of the placebo model that harbors a vacuum precisely where intention translates into state change, and state change into improved regulation. It is obviously our cerebral networks that mediate this interaction.]
So the placebo argument ultimately boils down to little more than the assertion that self-regulation of states can come about in a variety of ways, and it does not depend upon a systematic approach. It can happen quite randomly, and it can be induced by a variety of influences. Let us hasten to grant the point, by all means. The bias in nature is certainly in favor of self-regulation if the nervous system is given even half a chance. So now we get to the core of the matter: The placebo is not an argument against the Self-regulation Remedy. It is an argument against the claims of specificity. And in that regard, we can only hasten to add our voice to the chorus: Specificity is not our claim; rather, it is to highlight the power of the Self-regulation Remedy, however it may be brought about. Now if someone actually approaches us for help, then of course we resort to the systematic remedies of which we are aware rather than merely relying on the random ones.
It is those who aspire to make the claim for specific remedies for specific conditions that have to contend with the multi-headed hydra of the placebo. They have made their own bed. Those of us who see things from the vantage point of the Disregulation Model, and who therefore target disregulation wholesale, can muse at some remove from the tantrums in the cloakroom about the compartmentalization and fracturing of evidence that is better seen whole.
Now in this promulgation of a grander vision of neurofeedback, I must hasten to issue a disclaimer. There is in our collective deployment of neurofeedback modalities a considerable degree of tactical specificity, none more so than in what we ourselves teach. But this tactical specificity actually helps to shore up our argument in the end. The specificity of approach into which we are shaped individualizes and particularizes the training, and we observe that the specificity relates much more to the individual than to the diagnosis the person may have brought in the door. This is certainly true with the recent evolution of our mechanisms-based training, and it is equally true of the recent evolution of coherence-based training. The target of the intervention is not likely to be uniquely related to the underlying diagnosis except in narrow circumstances, such as those involving localized cortical injury.
It is this divergence between clinical tactics and clinical diagnosis that now stands as the most compelling indictment of the DSM formulation. Whether we do so through the pathway of EEG phenomenology (QEEG-based feedback) or through dynamic feedback from the experience of the training itself (i.e., mechanisms-driven), we are teasing out the particulars of the disregulation that may be targeted most efficiently. These particulars may bear only the most tenuous relationship to the proffered diagnosis. If there were a connection, then as our techniques are progressively refined the correlation would stand in greater relief as time went on. The very opposite is the case.
Just as the current specificity of the diagnostic categories co-evolved with psychopharmacology over the past few decades, neurofeedback will co-evolve with a new and more appropriate model of the psychopathologies over the next decade or two. But these more integrated models also have independent evidence in their favor, outside of the evidence provided by neurofeedback itself. In the interest of furthering the advance of the field, we should ally ourselves with all such forward-looking developments.
On the flipside, we should not strive to attach ourselves to a model that looks increasingly moribund. Those who tie their fates too closely to the DSM model remind me of those polar bears drifting out to sea on shrinking ice floes. We should simply turn the tables on our critics: Instead of neurofeedback devices being misbranded in the current diagnostic regime, neurofeedback provides the final clinching evidence of the misbranding purveyed by the DSM.