The Effects of QEEG-Informed Neurofeedback in ADHD: An Open-Label Pilot Study

Disclaimer: The content below was generated with the assistance of AI and then reviewed and edited by BrainMaster Technologies, Inc. It is provided for educational and informational purposes only and does not constitute medical advice.

1. Overview #

This open-label pilot study evaluated whether QEEG-informed neurofeedback, customized according to individual EEG biomarkers, could improve clinical outcomes in individuals with ADHD. The study included 21 participants (children and adults) and assessed changes in inattention (ATT), hyperactivity/impulsivity (HI), depressive symptoms (BDI), EEG power, and ERP components.

2. Study Purpose #

The study aimed to determine whether:

• EEG-based personalization improves neurofeedback outcomes.

• Baseline EEG traits (e.g., iAPF, beta excess, low-voltage EEG) predict treatment response.

• Neurofeedback alters neurophysiological markers such as ERP amplitudes and SMR power.

3. Methods #

3.1 Participants #

• N = 21 ADHD/ADD patients

• 7 children, 14 adults

• Medication use varied (9 medicated)

3.2 Assessments #

• QEEG (26 channels, standardized acquisition)

• ERP oddball task

• Symptoms measured at pre-, mid-, and post-treatment:

  • ATT & HI (DSM-IV ADHD scale)

  • BDI (when depressive symptoms present)

3.3 Personalized Neurofeedback Protocols #

Protocol selection followed five EEG-based rules, including:

• Frontocentral theta/beta training for excess theta

• Alpha downtraining for excess alpha

• Beta downtraining for beta spindling

• SMR training for low-voltage EEG or sleep issues

Most participants received two complementary protocols, often combining SMR/Theta/Beta approaches.

4. Key Results #

4.1 Clinical Outcomes #

• 76% response rate (16/21)

• Significant improvements across all measured domains:

  • Inattention (ATT): p < .001, Effect Size 1.78

  • Hyperactivity/Impulsivity (HI): p = .001, Effect Size 1.22

  • BDI depressive symptoms: p = .003

Figure 1 (page 5) visually shows strong decreases in ATT and HI scores over time.
Figure 2 (page 5) shows reductions in depressive symptoms with a notable correlation to iAPF.

4.2 Predictive Biomarker Findings #

• Anterior iAPF strongly correlated with improvement in depressive symptoms (r = 0.851, p = .002).

• Slow iAPF predicted weaker improvement in comorbid depression.

• No predictive relationship was found between iAPF and ATT or HI outcomes.

4.3 Neurophysiological Changes #

Pre/post neurophysiology was available for a subgroup treated with SMR neurofeedback.

ERP Effects #

• N200 amplitude increased (p = .014)

• P300 amplitude increased (p = .004)

(Shown in Figure 4, page 7—demonstrating marked post-treatment amplitude increases.)

EEG Power Effects #

• SMR (12–15 Hz) power decreased significantly (p = .009)

• No significant changes in alpha or beta bands

(Displayed in Figure 5, page 8, showing selective SMR power reduction for eyes-open and eyes-closed).

5. Interpretation of Findings #

• Personalizing neurofeedback using QEEG-defined biomarkers may enhance improvement in attention symptoms, as effect sizes exceeded prior meta-analytic findings.

• Increased N200 and P300 amplitudes suggest improved stimulus discrimination and attention/memory updating, consistent with known ADHD ERP abnormalities.

• The paradoxical decrease in SMR power supports the idea that neurofeedback may train voluntary control rather than simply upregulating frequency amplitude.

6. Limitations #

• No control or sham group

• Small sample size; ERP/EEG pre-post data limited to responders

• Patients paid out-of-pocket, potentially influencing motivation and effect sizes

• Effect sizes from pilot data should be interpreted cautiously

7. Conclusion #

This pilot study provides preliminary support for QEEG-informed, personalized neurofeedback as a potential approach associated with improvements in:

• Attention

• Hyperactivity/impulsivity

• Comorbid depressive symptoms

• Specific EEG/ERP neurophysiological markers

Replication in larger, controlled trials is required.