Efficacy Discussion

Abstract /

  Introduction

  Method
  Results
  Discussion
  References

METHOD

Efficacy of SMR-Beta Neurofeedback for Attentional Processes

David A. Kaiser and Siegfried Othmer
EEG Spectrum, Inc. Encino, CA
November 1997

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DISCUSSION
The present study demonstrated the efficacy of SMR-beta neurofeedback in treating attentional deficiencies using an outcome study. Significant improvement was found for measures of inattention, impulse control, and consistency of response after approximately 20 training sessions. There was a systematic tendency toward improvement in attention, with the most significant improvements occurring where the pre-treatment test scores are in most severe deficit. More than three-quarters of all subjects in deficit improved on one or more measures, a response rate comparable with psychostimulant therapy for ADHD. Impulse control improved from a borderline functional level (a score of 85.5) prior to training to the population norm (98.9). When only those individuals with severe pre-treatment deficits in a measure were analyzed, significant improvement was seen in all measures. Inattention scores improved nearly two standard deviations in response to treatment. For those individuals who chose to continue treatment until 40 sessions (n=72), impulse control and response consistency continued to improve after 20 sessions.

Malone, Kershner, and Swanson (1994) proposed a neurochemical model to explain medical effects on ADHD, a model which holds promise for understanding the efficacy of EEG biofeedback according to the present protocols. Malone et al. (1994) elaborate a bi-hemispheric model of regulation of attention and arousal by Tucker and Williamson (1984). In this model, the dopaminergic system, linked to left hemisphere function, is involved in maintenance of tonic activation, of sustained attentional activity, sequencing, and motor planning; whereas the norepinephrine system, linked to right hemisphere function, is involved in phasic arousal, orientation to novelty, alertness, and shifts of attention in general. ADHD is postulated to result from dysregulation in this asymmetric neural control system for attention and arousal. This may consist of a failure of bihemispheric coordination of attentional processes, in particular due to lack of left hemisphere inhibitory control over the right hemisphere. ADHD is seen as generally characterized by dopamine-mediated under-activation at the left frontal cortical region, concurrent with norepinephrine-mediated overarousal at the right parietal region. Stimulant medication such as with methylphenidate is seen as impacting on both the dopamine and norepinephrine systems so as to restore them to regulatory balance.

The present study does not explicitly confirm the validity of this model, since the data were not derived by random assignment, and since subjects were not treated with only a single protocol. Moreover, the presence of comorbidities such as Tourette Syndrome, minor traumatic brain injury, Conduct Disorder, anxiety or depression, in our sample population has their own implications for protocol selection and thus the outcome for TOVA measures were often mixed, as shown in Figure 1. Declines in impulsivity measures were obtained in several instances. However, EEG biofeedback is the only intervention for ADHD which involves explicit hemispheric localization, and thus is specially suited for evaluating the Malone model. Future research on the specificity of EEG biofeedback protocols should shed further light on the mechanisms involved.

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