Neurofeedback and Basic Learning Theory: Implications for Research and Practice

Brain activity assessed by electroencephalography (EEG) has been demonstrated to respond to conditioning techniques. The concept of modulating this activity has been called EEG biofeedback, more recently neurofeedback, and is based on operant learning principles. Technological advancements have significantly enhanced the ease and affordability of recording and analyzing brain activity. Thus, properly trained practitioners can implement these conditioning strategies in their practice. Recent research indicating evidenced-based efficacy has made this technique a more viable option for clinical intervention. The objective of this article is to highlight the learning principles that have provided the fundamentals of this neuromodulatory approach. In addition, it is recommended that future applications in clinical work, research, and development adhere to these principles

Different Spectral Analysis Methods for the Theta/Beta Ratio Calculate Different Ratios But Do Not Distinguish ADHD from Controls

There has been ongoing research on the ratio of theta to beta power (Theta/Beta Ratio, TBR) as an EEG-based test in the diagnosis of ADHD. Earlier studies reported significant TBR differences between patients with ADHD and controls. However, a recent meta-analysis revealed a marked decline of effect size for the difference in TBR between ADHD and controls for studies published in the past decade. Here, we test if differences in EEG processing explain the heterogeneity of findings. We analyzed EEG data from two multi-center clinical studies. Five different EEG signal processing algorithms were applied to calculate the TBR. Differences between resulting TBRs were subsequently assessed for clinical usability in the iSPOT-A dataset. Although there were significant differences in the resulting TBRs, none distinguished between children with and without ADHD, and no consistent associations with ADHD symptoms arose. Different methods for EEG signal processing result in significantly different TBRs. However, none of the methods significantly distinguished between ADHD and healthy controls in our sample. The secular effect size decline for the TBR is most likely explained by factors other than differences in EEG signal processing, e.g. fewer hours of sleep in participants and differences in inclusion criteria for healthy controls

Double-Blind Placebo-Controlled Randomized Clinical Trial of Neurofeedback for Attention-Deficit/Hyperactivity Disorder With 13-Month Follow-up

Objective: To determine whether theta/beta-ratio (TBR) electroencephalographic biofeedback (neurofeedback [NF]) has a specific effect on attention-deficit/hyperactivity disorder (ADHD) beyond nonspecific benefit. Method: In a 2-site double-blind randomized clinical trial, 144 children aged 7 to 10 years with rigorously diagnosed moderate/severe ADHD and theta/beta-ratio (TBR) ≥4.5 were randomized 3:2 to deliberate TBR downtraining versus a control of equal duration, intensity, and appearance. Two early dropouts left 142 children for modified intent-to-treat analysis. The control used prerecorded electroencephalograms with the participant's artifacts superimposed. Treatment was programmed via Internet by an off-site statistician-guided co-investigator. Fidelity was 98.7% by trainers/therapists and 93.2% by NF expert monitor. The primary outcome was parent- and teacher-rated inattention; analysis was mixed-effects regression. Because the expense and effort of NF can be justified only by enduring benefit, follow-ups were integrated. Results: Blinding was excellent. Although both groups showed significant improvement (p <.001, d = 1.5) in parent/teacher-rated inattention from baseline to treatment end and 13-month follow-up, NF was not significantly superior to the control condition at either time point on this primary outcome (d = 0.01, p =.965 at treatment end; d = 0.23, p =.412 at 13-month follow-up). Responders (Clinical Global Impression−Improvement [CGI-I] = 1−2) were 61% of NF and 54% of controls (p =.36). Adverse events were distributed proportionally between treatments. The 13-month follow-up found nonsignificant improvement from treatment end for NF (d = 0.1), with mild deterioration for controls (d = −0.07). NF required significantly less medication at follow-up (p =.012). Conclusion: This study does not support a specific effect of deliberate TBR NF at either treatment end or 13-month follow-up. Participants will be reassessed at 25-month follow-up. Clinical trial registration information: Double-Blind 2-Site Randomized Clinical Trial of Neurofeedback for ADHD; https://clinicaltrials.gov/; NCT02251743