EEG Spectrum International - EEG Biofeedback: A Generalized Approach to Neuroregulation

EEG Biofeedback: A Generalized Approach to Neuroregulation

By Siegfried Othmer, Susan F. Othmer, and David A. Kaiser

To appear in "APPLIED NEUROPHYSIOLOGY
& BRAIN BIOFEEDBACK"
Edited by Rob Kall, Joe Kamiya, and Gary Schwartz

The Placebo Argument
Does EEG biofeedback, with all its instruments, bells and whistles, include a huge "placebo" component (for which we are not entitled to claim credit)? The placebo argument sometimes serves as a talisman which the scientist, comfortable in his paradigm, may use to ward off disagreeable new claims. However, the placebo effect is no more than the body's means of mobilizing self-recovery. The placebo effect is not a cause. It is not itself a mechanism of recovery, but it does imply a mechanism'though one which may seem featureless and devoid of testable properties when looked at through the prevailing structuralist paradigm. Hence, it can provide no help to our understanding. But EEG biofeedback is by its very nature self-remediation. The part we are entitled to take credit for cannot be experimentally distinguished from "other" aspects of the self-healing process.

For researchers attempting to prove the efficacy of medication, self-recovery represents the counter-hypothesis, which is wrapped up in the concept of "placebo effect" and need not be further discussed. It is not of interest to the designer of drugs. When the discussion is about self-induced recovery (such as EEG biofeedback) and the mechanisms thereof, then we must openly address the placebo effect and ask whether its self-healing properties are any different from what we are claiming. It is a moot point. The existence of the placebo effect proves the existence of self-remediation. Self- remediation cannot then be disproved by invocation of the placebo effect. The existence of a robust placebo effect in medical and mental health disciplines supports the claims of EEG biofeedback. It does not undermine them.

Still, if one cannot in the individual case determine what part of recovery is due to the specific effects of EEG biofeedback training and what part is attributable to non- specific effects, can one be sure that the effects aren't all in the latter category? The normal resolution to this question is by means of statistics. In the case of EEG biofeedback, however, we are not constrained to rely exclusively on statistics (although the statistical argument is favorable as well), as there are other proofs of its efficacy.

The placebo effect, seen here as stalking horse for nonspecific effects of the EEG biofeedback process, is not the explanation for the efficacy claimed for the following reasons:

1. The effects of the training are highly specific to electrode placement and to training frequency band.

2. Training protocols exist which can commonly elicit effects opposite to those desired.

3. The effects of training with one protocol can be reversed with another.

4. The effect of the training is cumulative, rather than fading with time, as is common with placebos. If EEG biofeedback were to be explained in terms of placebo phenomena, it would be the first time that placebos are dose- dependent (i.e., cumulative).

5. Training effects are in line with research from neuropsychology regarding localization of function.

6. Populations can be moved to levels of performance which exceed those of na‹ve populations

7. The effects of the training often lie outside the range of expectations for spontaneous recovery or placebo effects, not only with respect to the magnitude of the changes elicited but also with respect to the consistency with which they are produced, and the timescale over which they occur. (Curiously, the more striking and unusual the claims for EEG biofeedback, the more strenuously is the placebo hypothesis invoked by critics!)

8. EEG biofeedback was discovered in connection with animal research. It may be assumed that the test animals were not subject to the placebo effect. Moreover, the researcher was blind, since the discovery was by way of serendipitous connection to an unrelated experiment (Sterman, 1976).

The spatial and frequency specificity of the EEG training, as well as its reversibility, allow every subject to be their own control in the training. This is not to say that conventional controlled studies are entirely superfluous. We are just at the beginning of the scientific inquiry into this technique, much of which will require controlled paradigms. Rather, we are asserting that the epistemological assumptions operative in the clinical setting are already sufficient to demonstrate efficacy in the case of EEG biofeedback because of the above-enumerated features of the training. In view of the above, then, the recoveries, remediations, and performance enhancements claimed for EEG biofeedback may be regarded on their own merits, and cannot be gainsaid either by placebo factors or by the argument that they are not individually supported by blinded controlled studies.

Another prevailing perception must be examined before proceeding with review of the protocols and the clinical data. It is often asserted that the EEG biofeedback "trainee" is actually training his own behavior, and that the changed EEG is simply a manifestation of that altered behavior. Behavioral state and the EEG are clearly coupled, and a conscious redirection of one's physiological state can obviously be helpful in achieving the objectives of the training in the moment. This is the dominant theme in conventional biofeedback, which is dependent upon a great deal of deliberate engagement in the process by the subject. This is not a necessary condition for EEG biofeedback training to succeed, and in this sense it departs fundamentally from conventional, peripheral biofeedback.

The successful training of cats, of very young children, and even of people in mild vegetative states, demonstrates that the training can proceed without the subject being particularly aware of their behavioral state, or intent upon altering it, or indeed very conscious about what is going on at all. The training in this case consists in operant conditioning of the EEG, neither more nor less. For example, in the use of EEG biofeedback for the remediation of epilepsy and stroke, it is not "behavior" in any conventional sense that is being trained. In fact, we have observed that people can respond quite counter to their own desires, expectations, and motivations; with the expected effects (and even some that weren't expected by either the client or the therapist) arising out of the particular protocol selected. The resulting behavioral state may be concordant with the protocol selected, and quite at odds with the participant's conscious goals. Finally, there is the compelling observation that sleep EEG is changed subsequent to EEG training in the waking state. (Sterman, 1970) All these observations are evidence for the proposition that it is 'brain behavior" that is being trained directly. And brain behavior may be non-specific with respect to overt organismic behavior.

Research History: Implications for Mechanisms of EEG Biofeedback
If EEG biofeedback training is indeed capable of promoting self-healing, its role is that of facilitating a process of change the capacity for which already exists in the human brain. But how is it that such an apparently simple tool is capable of such wide-ranging effects? What is it about the brain that allows it to be led to more functional states? And how can the operant conditioning process embodied in EEG biofeedback be applied systematically and predictably, to good effect?

The implications of our clinical findings are that the EEG training is not narrowly specific in its clinical effects, but that it impacts very basic regulatory mechanisms, the disregulation of which is responsible for causing or at least maintaining the disorders discussed. In the following, the case will be further made for such a simple underlying model. A connection will be made to current models of brain function, and the central role of rhythmic brain activity will be discussed in explaining the remarkable breadth of efficacy of this emerging modality.

The early model of efficacy proposed by Sterman is that the EEG training at sensorimotor cortex lowers the setpoint of the gamma motor system reactivity (Howe, 1972). As a result, cortical hyperexcitability is reduced. This manifests in higher threshold of onset of seizures, most particularly in the case of motor seizures (Sterman, 1984). Lubar initially worked only with those hyperactive children who were Ritalin- responsive, on the assumption that these were the ones whose hyperactivity was grounded in underarousal (Shouse & Lubar, 1979). So the early work already presaged our current perspective, that the principal mechanism of action of EEG biofeedback is to normalize autonomous management of arousal and to enhance overall nervous system stability. The intimate relationship between seizure susceptibility and arousal makes it plausible that efficacy for seizures is also at least partly attributable to normalization of arousal regulation.
On the basis of the early work, it was close to hand to consider all the conditions being treated in terms of their arousal dimension, and in terms of the stability/instability continuum. Table 1 shows a classification of conditions with respect to the arousal axis, and with respect to the instability axis. In preparation of Table 1 it became obvious that this system of categorization represents an oversimplification, although it does provide a useful perspective. It is, for example, an oversimplification to talk about depression and anxiety as separate and distinct entities. It is a further oversimplification to appear to reduce these to merely arousal disorders. It is perhaps better to identify these as correlations or covariations. Then again, arousal itself is not a unitary concept. Moreover, the arousal dimension is very important in the conditions we have listed as instabilities (as already mentioned for seizures). It is hoped that the Table will prove useful in illustrating the connection between various conditions at the process level, and indeed the mechanisms by which EEG biofeedback can impact them.

Table 1. Classification of Common Disorders in Terms of Arousal and Instability

Underarousal

Endogenous Unipolar or Reactive Depression
Attention Deficit Disorder: Inattentive Subtype
Chronic Pain (Low Pain Threshold)
Insomnia (Frequent Waking)

Overarousal

Anxiety Disorders
Sleep Onset Problems/Nightmares
Hypervigilance
Attention Deficit Disorder: Impulsive Subtype
Anger/Aggression
Agitated Depression
Chronic Nerve Pain
Spasticity

Underarousal/Overarousal

Anxiety and Depression
Attention Deficit Hyperactivity Disorder:
Combined Type

Instabilities

Endogenous Vulnerability

Tics
Obsessive-Compulsive Disorder
Aggressive Behavior
Episodic Rage Disorder
Bruxism
Panic Attacks
Hot Flashes
Bipolar Disorder
Migraine Headaches
Narcolepsy
Epilepsy
Sleep Apnea
Vertigo
Tinnitus
Anorexia/Bulimia
Suicidal ideation and behavior
PMS
Multiple Chemical Sensitivities
Dysglycemia; Diabetes (Type II);
Hypoglycemia
Explosive Behavior

Exogenous Vulnerability

Just as depression has its arousal dimension, it also has its attentional dimension, and its affective dimension. Similarly for the other conditions listed. For present purposes, it is sufficient to argue that these are coupled systems. One of the most obvious implications of the biofeedback work is that it is not possible to intervene unilaterally with the brain. Impinging upon the arousal axis has implications for attention and affect, and vice versa. Moreover, challenging the brain with biofeedback tends to move the brain toward stability. The observation was made decades ago by Elmer Green that biofeedback in general moves the organism toward homeostasis and toward stability. This has been abundantly confirmed in the present work. Having said this, it is also possible to drive the brain toward any instability that may exist, with a powerful technique such as this. Skillful clinical application is still required.

Instabilities can be characterized by the degree to which they arise autonomously within the CNS or require an external trigger for initiation. An internal vulnerability is referred to as endogenous, and an externally triggered vulnerability is referred to as exogenous. The relevant instabilities are distributed along a continuum in this regard, and a case can be made that there is a natural progression for different instabilities from the exogenous domain to the endogenous over the course of a lifetime. This is known as the kindling model, and it is particularly applicable to seizures, Tourette's syndrome, OCD, depression, anxiety and panic, bipolar disorder, and migraines. A crude attempt has been made at an ordering along the exogenous/ endogenous axis in Table 1.