A brief history
Pioneer work in neurofeedback began with Sterman1,2 and Lubar.3 In Sterman’s work, cats were connected to an EEG during operant conditioning. During traditional operant conditioning, a cat learned to push a lever when it was hungry. Then, a new element, a tone, was introduced. The cat learned to wait until the tone stopped to press the lever to receive the reward. Sterman noticed that while the cat was waiting for the tone to stop, a specific frequency rhythm of 12-15 Hz was observed. Moreover, the cat could produce the sensorimotor frequency without the tone to get the reward. Sterman called this rhythm the sensorimotor frequency (SMR).
Lubar was the first to use sensorimotor frequency training on a hyperkinetic child in 1976 by placing 2 electrodes at C3 and C4. The child learned to increase the beta rhythm of 12-14 Hz until the theta (4-8 Hz) rhythm was no longer seen. The result was an increase in attention and a decrease in hyperactivity.4 In 1991, Lubar5 used QEEG to match neurofeedback treatment (EEG biofeedback) to theta-beta ratio (TBR) abnormalities only in individuals with ADHD who were identified with a high TBR. QEEG treatment matching is used to match the abnormal EEG biomarker with the impairing symptom, thereby allowing neurofeedback protocols tailored to the individual.
Slow cortical potential (SCP) neurofeedback measures slow activity (<1 Hz). An upward shift of the negative amplitude improves attention. Rockstroh and colleagues6 used SCP in 1993 for drug-refractory seizures; Heinrich and colleagues7 were the first to use SCP for ADHD in 2004.
The evidence for neurofeedback in ADHD
In a meta-analysis of studies using TBR, SMR, or SCP, the within-subject effect size (ES) for hyperactivity was 0.71, for attention it was 1.0, and for impulsivity it was 0.94.8 In randomized, controlled studies, the ES was 0.80 for attention, 0.39 for hyperactivity, and 0.68 for impulsivity. However, some of the controlled studies used a semi-active control, such as cognitive training, which may account for the lower ES for impulsivity and hyperactivity. None of the included studies used QEEG to identify who would benefit most. Although most of the studies were small, the results suggest some promising aspects of neurofeedback.
Not all children with ADHD demonstrate a high TBR; therefore, it is imperative to identify the correct EEG biomarker to target during neurofeedback using QEEG. When QEEG was used to determine the most suitable protocol for neurofeedback, the ES increased substantially.9 In a study by Arns and colleagues10 of youths with ADHD, neurofeedback protocols were based on QEEG (Table). The ES for attention was 1.78 and for hyperactivity it was 1.22.
A meta-analysis of effects of stimulant medications in ADHD by Faraone and Buitelaar11 showed an ES of 0.84 for methylphenidate for attention and 1.01 for hyperactivity/impulsivity. Other findings indicate that neurofeedback and stimulant medication may be comparable.12-14
Follow-up findings of parent ratings revealed that not only did the effects of neurofeedback not fade over time, but attention and particularly impulsivity and hyperactivity continued to diminish.7,15-17 In a study by Gani and colleagues,18 50% of the children with ADHD who received neurofeedback no longer met criteria for ADHD 2 years post-treatment.
Dr. Simkin is Clinical Assistant Professor, Department of Psychiatry, Emory University School of Medicine, Atlanta, GA. Dr. Lubar is Professor Emeritus, Department of Psychology, University of Tennessee, Knoxville, TN; and Affiliate Scientist for the Center of Complex Systems and Brain Sciences, Charles E. Schmidt College of Science, Florida Atlantic University, Boca Raton, FL.
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