Longitudinal Mapping of a Randomized Controlled Trial of EEG Neurofeedback in PTSD: Early Symptom Stabilization and Implications for Adjunctive Therapeutic Potential

• Alpha-desynchronization EEG-NFB produces early and sustained therapeutic response. • PTSD participants downregulate alpha during training with within-session rebound. • Alpha downregulation and rebound attenuate across EEG-NFB sessions. • Therapeutic response is associated with greater alpha suppression and rebound. PTSD is characterized by reduced alpha (8-12 Hz) rhythms, reflecting cortical hyperarousal and disrupted large-scale network dynamics. Across single- and multi-session studies, alpha-desynchronizing EEG neurofeedback (EEG-NFB) restores alpha rhythms toward normative levels (“alpha rebound”) and reduces PTSD symptoms. However, prior research has focused mainly on pre-to-post intervention changes, leaving longitudinal trajectories of therapeutic improvement and neural modulation unclear. We conducted longitudinal mapping of clinical and neural outcomes during a 20-week randomized sham-controlled trial (RCT) of alpha-rhythm EEG-NFB in individuals with PTSD (n = 38). Participants were randomized to an experimental group receiving weekly EEG-NFB targeting alpha downregulation or a sham-control group. PTSD symptoms were assessed biweekly using the PCL-5. Alpha modulation was analyzed between and within sessions using linear mixed-effects models. Active EEG-NFB produced an early and sustained therapeutic response, with the proportion of participants below the probable PTSD threshold stabilizing by approximately week 11. Only the experimental group showed consistent alpha downregulation during training and diminishing within-session alpha rebound across sessions, consistent with a ceiling effect. Greater alpha suppression and more pronounced rebound dynamics were associated with therapeutic response, indicating a direct link between neural modulation and clinical improvement. This study provides the first longitudinal mapping of clinical and neural trajectories in an RCT of EEG-NFB for PTSD, demonstrating early stabilization of response and identifying neural mechanisms associated with symptom improvement. These findings may inform the optimization of EEG-NFB protocols and support its role as an adjunctive, symptom-stabilizing scaffold for psychotherapy.