Neurofeedback Frequently Asked Questions - Part 02
Links: Previous FAQs - Part I
Could the outcome of Neurofeedback 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.
What is the minimum age for Neurofeedback to be effective?
We have worked in our own office with children as young as two and three years of age. One was chronologically three years, but of mental age of six months. When we see the very young children, they are of course also the most compromised--CP, victims of near- drowning, prenatal substance exposure, severe Tourette's, victims of psychological trauma, etc. Yet these very compromised nervous systems are clearly able to respond to the challenge of the training. Other practitioners have trained with children as young as one year old and even younger. The results are persuasive that the cognitive demand for successful training is extremely low. And it may be recalled that Barry Sterman first did this EEG training with cats.
Links: Previous FAQs - Part I
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