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

Page 3 of 13

Brain Plasticity
If we are intent on maintaining the structure/function dichotomy, we are ineluctably in a semantic swamp. This is at least in part because the neurosciences are in the process of coming to terms with mounting evidence for what is collectively called "brain plasticity", and the old dualist terminology no longer serves us well. In its most general formulation, EEG biofeedback can be seen as the deliberate exploitation of 'functional brain plasticity'. More specifically, it depends upon plasticity in our neuromodulator systems. However, this concept is at best ambiguous, and a moving target. Simply put, brain plasticity refers to long- term alteration in brain systems that were historically thought to be static. Hence, the word tends to have a historical contextual reference, much like the word 'alternative health': once an intervention becomes mainstream, it is no longer "alternative". Similarly, once plasticity becomes accepted as an attribute of a particular brain system, the term tends to be discarded and future references may simply be to brain function. Hence the term brain plasticity tends to have only a transient utility, and to serve only where the case for plasticity is still being made. However, making the case for EEG biofeedback on a model of brain plasticity may be the most accessible Ansatz.

To make the term maximally useful for our purposes, a review is in order. A remarkably prescient view of the model of brain plasticity is to be found in Brodal (1981, p. 259):

"Although our knowledge about the 'plasticity' of the nervous system is still in its beginnings, there is reason to believe that this plasticity is a general property of the central nervous system, and that it is a prerequisite for the capacity to learn (in general, be it motor patterns or pure intellectual capacities). Restitution after damage to the central nervous system may therefore in essence be likened to a learning process. Practical experience is in agreement with this."

A more modern view is summarized by Oliver Sacks in the popular book, An Anthropologist on Mars. (The views of neuroscientists are often more boldly expressed in their popular writings as opposed to their scientific ones, where they are compelled to be more reserved and circumspect.)

"Work in the last decade has shown how plastic the cerebral cortex is, and how the cerebral 'mapping' of body image, for example, may be drastically reorganized and revised, not only following injuries or immobilizations, but in consequence of the special use or disuse of individual parts. We know, for instance, that the constant use of one finger in Braille leads to a huge hypertrophy of that finger's representation in the cortex." (Sacks,1995, p.41)

Here the focus is on the long-term dendritic re-programming and/or regrowth, which has been shown to occur. However, there has still been little recognition of the obvious ability of the brain to accomplish significant reorganization on time scales much shorter than that of dendritic regrowth, which requires simply changes of state, and of regulatory function, that is, of functional rather than structural reorganization. This is now changing:

"Reorganization of somatic sensory receptive fields can appear within the dorsal column nuclei, the thalamus, and the cortex, within seconds of a peripheral manipulation. Similarly, motor cortical maps show dramatic shifts within hours of a peripheral nerve lesion or [within] minutes of a shift in arm configuration." (Donoghue, 1995)

When considering the reassignment of cortical neuronal resources within a time constant of seconds, one wonders if "plasticity" is the appropriate descriptor for the phenomenon. This is another case in point of the use of the term to describe as mutable something thought to be more permanently stable. If cortical resources can be so readily reassigned, then the mechanisms involved in stabilization must lie principally in the functional rather than structural realm. That is, there is less hard wiring than was thought! Thus we are likely to see the language of structure replaced over time by the language of function, and eventually we will see the disappearance of the term "plasticity" altogether in this connection.

With this in mind the term functional plasticity may be used to refer to all those processes by which brain functions thought to be relatively stable can be altered on a timescale short compared to that of dendritic regrowth, or the formation of new synaptic boutons. Functional plasticity is undoubtedly mediated, inter alia, via alteration of synaptic coupling strengths through the generation or attrition of receptor sites, and the alteration of neurotransmitter chemistry through changes in neuronal gene expression. The present interest will focus specifically on the neuromodulator systems and their regulation. Here the observed "functional plasticity" can have time constants short compared even to the above-postulated processes. For example, when we are frightened, we are capable of changing our state of arousal within fractions of a second. The functional plasticity of neuromodulator systems clearly exists on all behaviorally relevant timescales. The claim of EEG biofeedback is that the dynamic range of neuromodulator system plasticity (flexibility) can be increased where it is deficient, and stabilized when it is unstable, by operant conditioning techniques.

Functional Plasticity: Implications of Recent Research
A number of developments over the past several years have prepared the ground for the claims we are now making for EEG biofeedback. First of all, the findings from functional magnetic resonance imaging (fMRI) are refocusing attention on collective neuronal activity; its time course, temporal interrelationships, and change as learning and habituation take place. Inevitably, these findings will raise questions about how such neuronal populations are organized and managed by the brain. Secondly, there is the ongoing research into the thalamocortical generation of rhythmic activity in the EEG by Mircea Steriade, David McCormick, and others. (Steriade, 1984; McCormick, 1990) Thirdly, there is the emerging interest in the binding problem, the mechanism for how the brain retains as a coherent phenomenon something that is parallel-processed at multiple neuronal sites (a visual image, for example, or a phoneme.) (von der Malsburg, 1995). We shall return to this critical theme below.

At another level, it may be said that much of psychopharmacology implicitly makes the case for the kind of functional plasticity required to explain the presumptive efficacy of EEG biofeedback. Quick-acting medications like stimulants can only operate by shifting the functional state of neuromodulator systems; there is no time for significant structural adaptation. The short-term effects of EEG biofeedback can be explained by similar shifts. The longer- acting medications such as anti-depressants and anti- psychotics work on the same timescale as the cumulative effects shown in many of the recoveries claimed for EEG biofeedback. The effect of Prozac administration, for example, can be discerned in the cerebrospinal fluid within hours, just as with stimulants, and yet its anti-depressant effects may take days or weeks to manifest. Such medications may work by means of longer-term adaptations that involve both functional and structural change. But it is not a large leap to argue that such changes can be induced over time by the challenge to the nervous system imposed by operant conditioning of the EEG. Both EEG biofeedback and pharmacological intervention can even be seen as a disequilibration of nervous system functioning to which the brain responds by long-term adaptation. In this view, their mode of action is seen to be uncannily similar. Regardless of whether or not this concept can survive further scrutiny, it is clear that the claims of EEG biofeedback are consistent with, and certainly not antithetical to, the implications of pharmacology.

Efficacy of pharmacology for a variety of psychiatric disorders is often taken to imply that such chemical intervention is absolutely required for remediation, by analogy to the provision of insulin in the case of Type I diabetes. That this is not the case is demonstrated by the efficacy of electro-convulsive shock therapy for depression. Here the remediation may be long-term even absent any long- term pharmacological support. Additionally, spontaneous recovery from episodes of both mania and deep depression is the rule, not the exception, in even mature cases of bipolar disorder. Clearly, these brains have quite functional states within their inventory. The question of efficacy of EEG biofeedback (for the vast majority of applications) is then reduced to the relatively minor issue of whether a change in functional state can be induced, or at least promoted, by operant conditioning of the EEG, and the second issue of whether such a training can have lasting effects.

In the case of pharmacology, the challenge to the nervous system is provided by neurochemicals or their metabolic precursors, or other metabolic agents, or factors which modulate receptor site sensitivity or ion channel permeability. In the case of EEG biofeedback, the challenge is to the means by which brain function is organized and maintained in the time domain, which is reflected in the EEG. It will be argued in the following that neuromodulator systems function to organize both general organismic arousal and more localized activation of collective neuronal activity by modulation of rhythmicity. The EEG is preferentially sensitive to such collective, periodic, activity.