Health Professionals

What is EEG Biofeedback (Neurofeedback)?

EEG Biofeedback is operant conditioning on EEG parameters. Typically the training reinforces specific EEG frequencies and inhibits others. However, training has also been done successfully with evoked potentials, as well as with individual unit activity of motorneurons.

What is EEG Biofeedback used for?

The most common application of EEG biofeedback is currently to the attention, learning, and behavior problems of children. However, other common applications are directed toward mood disorders, epilepsy, traumatic brain injury, sleep disorders, and the more severe developmental disorders of children.

More recently, EEG biofeedback has found application to alcoholism and other addictions, as well as to Post-traumatic Stress Disorder. The field divides into two domains: A domain of high-frequency training (12-19Hz) and a domain of low frequency training (4-12 Hz). The former is commonly referred to as SMR-beta training, and is directed mainly to physiological normalization. The latter is referred to as Alpha-theta training, and is used primarily for psychological resolution and integration.

The field has also been extended to non-clinical applications, as it has been found that normal, functional brains can benefit from these training regimens as well. In these “mental fitness”, or “optimum performance” applications, both the high and low frequency domains have been found to be beneficial.

How long does the EEG Biofeedback training take?

The EEG training may require some twenty to forty sessions typically for attention, learning, and behavior problems, in order for consolidation of learning to take place. In some cases, particularly if there is organic injury involved, such as in epilepsy or traumatic brain injury, the training may need to be extended to a hundred or more sessions, and some benefit may continue to be observed as the training is continued indefinitely.

In optimum performance applications, the training may be continued at some level for as long as optimum function remains an issue, by analogy to physical fitness training.

What is the history of this treatment modality?

Human EEG biofeedback was first attempted in the 1960s by Joe Kamiya at the University of Chicago. Early investigations focused on operant conditioning of alpha brain waves primarily to facilitate deep relaxation and meditation.

SMR/beta biofeedback developed from operant conditioning of cats’ EEG. Barry Sterman of UCLA serendipitiously discovered that when cats were exposed to toxic chemicals that usually induce epileptic seizures, those who had been trained in the middle to high frequency range (12-20 Hz) from a previous unrelated experiment had greater latency to seizure onset, and a higher threshold for seizure onset, than untrained cats. These results were replicated in monkeys and humans. The results with humans were subsequently replicated in some twelve research centers, comprising some twenty studies.

After several years of treating patients with intractable seizures with SMR biofeedback, it was noted that the hyperactive children not only had decreased seizure activity, but their behavior improved as well. In the mid 70’s, Joel Lubar at the University of Tennessee examined the effect of neurofeedback on hyperactivity absent any seizure history.

Additional research took place during the 1980’s.In 1989, Eugene Peniston of the Fort Lyon (CO) VA Medical Center undertook a groundbreaking study of alcoholics who received alpha-theta neurofeedback training in addition to the program normally provided by the facility. Five years after treatment, 70% of the participants were still abstinent.

Continuing through the present day, a number of researchers have worked to move the field forward.

For more information on Neurofeedback and it’s history, read A Symphony in the Brain: The Evolution of the New Brain Wave Biofeedback by Jim Robbins.

Could the outcome of EEG Biofeedback training be due to a placebo effect?

No, and here are the reasons why:
1.
The effects of EEG biofeedback 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.
5.
If EEG biofeedback were to be explained in terms of placebo phenomena, it would be a first time that placebos are dose-dependent.
6.
Training effects are in line with expectations from neuropsychology regarding localization of function.
7.
Populations can be moved to levels of performance which exceed those of naïve populations
8.
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.
9.
EEG biofeedback was discovered in connection with animal research. It may be assumed that the test animals were not subject to the placebo effect operating. Moreover, the researcher was blind, since the discovery was by way of a confound of an unrelated experiment (Sterman,1976).

What is the mechanism underlying EEG Biofeedback efficacy?

The original Sterman protocol for seizures was deemed to be training motor system excitability, and thus was thought to be applicable mainly to seizures with a motor symptomatology. There was site specificity for the training (sensorimotor strip), and a frequency domain specificity (12-19Hz). Over time, it became apparent that the training was also effective for what used to be called temporal lobe seizures, and are now called complex-partial seizures (Lantz and Sterman). This meant that the training promoted CNS stability in more generality.

The work by Lubar et al on attention problems with the same protocol also implied a more general validity of the training. It was already apparent from Lubar’s work that when one quiets the motorsystem one ineluctably quiets (controls) input function (attention, etc.). Subsequent work with mood disorders and disorders of arousal meant that the training had very broad applicability indeed, requiring even further generalization of the original model.

There is as yet no generally accepted model under which efficacy for all these conditions can be subsumed. It is our view that the Sterman model remains valid, but simply needs to be generalized beyond the motor system. It appears that the activation/deactivation cycle with respect to a variety of CNS functions is managed by the degree of rhythmicity in key EEG frequencies. EEG rhythms have been shown to originate in thalamocortical circuits (Sterman). These can range from a highly rhythmic bursting mode to a relatively desynchronized tonic firing mode (Steriade, McCormick). The entire range of rythmicity between these extremes is believed to be behaviorally relevant, and to manage the activation of neural circuits subserving physiological arousal, autonomic nervous system balance, attention, and affective state.

The enormous range of clinical conditions which are addressed with a simple set of protocols is strongly supportive of the model that EEG rhythmicity plays a key role in neuroregulation in the time domain. It is clear that some such mechanisms need to be operative, and it is also apparent that the current neurochemical models of neuroregulation (i.e., neuromodulation) are of no help to us at all in addressing the complementary mechanisms operative in the time domain, and in the bioelectrical domain.

Is this treatment procedure nonspecific?

The training is certainly not “non-specific” in the usual sense of the critics of the field (the placebo argument). It is specific with regard to the underlying thalamocortical rhythmic activity that sets levels of activation with respect to numerous functions, including attention, arousal, and affect. It is clearly non-specific with respect to clinical disorders. And it is non- specific with respect to QEEG manifestations of disregulation. The challenge of EEG biofeedback is an appeal to what functions in the brain, not to what isn’t functioning.

Research in this field goes back to the early 1970s – why are we only hearing about it now?

There were indeed systematic replications of Sterman’s findings by other groups, and confirming controlled studies by Sterman’s group into the late 80’s.

Funding dried up in this area because the NIH shifted in the mid-eighties from a behavioral focus to a fundamental molecular biochemistry focus for further advances in neurophysiology.

There was a second basic problem, and it relates to the underlying theoretical model. Sterman’s work was rejected not because of the paucity of the data, nor from the lack of replication, but rather from the absence of a consistent model explaining the EEG phenomenology. The models of the time could not explain how remediation could be decoupled from explicit EEG changes consonant with the training protocol. Thus, reinforcement of EEG rhythms at a particular frequency was expected to lead to a systematic finding of higher EEG amplitudes at that frequency in the steady state. In actual fact, of course, the EEG in real life is far too dynamic for that. Nonlinear dynamical models have become available in the last few years which can explain this apparent inconsistency.

 

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