Dr. John Davis on the Alpha Rebound Protocol for PTSD

Dr. John Davis reviews an exciting advance in neurofeedback for post-traumatic stress disorder (PTSD) published by Nicholson et al. (2023). Dr. Davis reviews the study's scientific strengths and limitations, its counterintuitive findings, and considerations for offering NFB for PTSD.

What is PTSD?

Post-Traumatic Stress Disorder (PTSD) is a psychiatric condition that can develop in individuals exposed to actual or threatened death, serious injury, or sexual violence. This exposure may occur through direct experience, witnessing the event, learning that it occurred to a close associate, or repeated exposure to aversive details of trauma (e.g., first responders) (American Psychiatric Association, 2022).

Diagnostic Criteria

PTSD is characterized by persistent, trauma-specific symptoms that begin after the traumatic exposure, though onset may be delayed. Core symptom domains include: (1) intrusion (e.g., involuntary distressing memories, nightmares, flashbacks); (2) avoidance of reminders; (3) negative alterations in cognition and mood (e.g., guilt, estrangement, diminished interest); and (4) marked alterations in arousal and reactivity (e.g., hypervigilance, exaggerated startle response, irritability). These symptoms persist for more than one month, cause clinically significant distress or impairment, and are not better explained by substance use, medical illness, or other psychiatric disorders.

PTSD Neurobiology

Neurobiologically, PTSD has been associated with functional and structural dysregulation in several brain networks, including hyperactivation of the amygdala, reduced medial prefrontal cortex engagement, and altered connectivity within the default mode network (DMN) and salience network (SN) (Fenster et al., 2018; Nicholson et al., 2020). The DMN is a brain network primarily active during rest and internally focused states. It supports self-referential processing, autobiographical memory, theory of mind, and mental simulation. Key regions include the medial prefrontal cortex, posterior cingulate cortex, and precuneus. Three canonical networks graphic courtesy of Schimmelpfennig and colleagues (2023).

The SN detects and filters behaviorally relevant stimuli, mediating dynamic switching between the DMN and executive control networks. It plays a central role in attention, interoception, and the regulation of autonomic and emotional responses. Core regions include the anterior insula and dorsal anterior cingulate cortex. Abnormalities in stress hormone regulation (e.g., HPA axis dysregulation), heightened autonomic arousal, and disruptions in memory encoding and retrieval are also implicated in this condition.

Demographics

Epidemiological data indicate that the lifetime prevalence of PTSD among U.S. adults is approximately 6.1%, with 12-month prevalence around 3.6%, though rates vary significantly based on population and trauma type (Kilpatrick et al., 2013; Goldstein et al., 2016). Higher rates are found among military veterans, first responders, and survivors of interpersonal violence.

PTSD EEG Biomarkers

PTSD is associated with reduced power in the alpha band. This is observed in hubs of the DMN, such as the medial prefrontal cortex (mPFC, medial portions of BAs 32 and adjacent medial aspects of BAs 8, 9, 10, 11, 12, 24 and 25) and posterior cingulate cortex (PCC, BAs 23 and 31; Lanius et al., 2015).

Among healthy individuals, higher alpha rhythm power is thought to represent resting wakefulness and cortical inhibition (reduced excitation). It is positively correlated with DMN activity (Clancy et al., 2020). Those with PTSD, therefore, are likely to have overly excited brain activity, given their reduced alpha production.

An elevated beta rhythm is a PTSD biomarker (Jokic-Begić & Begić, 2003). Functional connectivity abnormalities within the DMN and the salience network (SN) have also been seen in PTSD, with successful treatment leading to changes in these networks (summarized in Nicholson et al., 2023), and alpha rhythms are a significant predictor of PTSD symptoms (Zhang et al., 2020).

Reduced alpha rhythms in PTSD are thought to be involved in poor excitatory/inhibitory balance in the brain.

Dysfunctional DMN and SN activity are supposed to relate, respectively, to negative self-referential thinking, social cognition, bodily self-consciousness, and autobiographical memory (DMN) and hyperarousal, hypervigilance, avoidance, and interoception problems (SN).

Conventional PTSD Treatments

The primary treatments for PTSD are types of cognitive-behavior therapy (CBT), including prolonged exposure, cognitive processing therapy, and eye movement desensitization and reprocessing (EMDR; Department of Veterans Affairs and Department of Defense, 2023). Medications such as SSRI and SNRI antidepressants can also help. However, not all individuals who receive treatment experience a significant reduction in symptoms (Varker et al., 2020), and treatments often have high dropout rates (Imel et al., 2013).

Therefore, in keeping with an evidence-based healthcare model, it is important to identify a portfolio of evidence-based treatments from which to select based on patient preference, predictions of best patient-treatment matching, treatment effectiveness, side-effect profile, clinician expertise, and accessibility so that alternative interventions can be offered either as the primary choice, or as a back-up if the patient fails to respond to their first choice (Djulbegovic & Guyatt, 2017).

Neurofeedback for PTSD

Neurofeedback for PTSD has a long history, including protocols to increase both alpha and theta power (Peniston & Kulkosky, 1991). Subsequent NFB studies have increased high alpha power (Vander Kolk et al., 2016) and used individualized LORETA z-score NFB (Bell et al., 2019), infra-low frequency training (Winkeler et al., 2022), and rt-fMRI neurofeedback (Zotev et al., 2018).

Especially with EEG NFB studies, a moderate effect size (i.e., an important real-world improvement) on reduced symptoms of PTSD is seen in randomized controlled investigations (Choi et al., 2023), with changes in neurophysiological measures (EEG, BOLD signal) also appearing in most studies that measured those parameters (Askovic et al., 2023).

Randomized controlled designs have largely supported the rationale and scientific evidence for the benefits of NFB for PTSD. Moss, Shaffer, and Watkins (2023) assigned a level-4 rating of efficacious to biofeedback (BF) and NFB for PTSD based on RCTs and quasi-experimental designs. They concluded:

... most studies have shown that HRV BFB training or NF interventions have produced significant reductions in PTSD symptoms, as measured by reliable psychometric measures, in some case with magnitudes in symptom reduction or effect sizes rivaling the best RCTs for psychotherapy and pharmacotherapy.

This intervention requires additional study. For example, the field needs larger samples, double-blind controls, sham controls, replication by independent research groups, and concurrent measurement of clinical, EEG, and MRI variables.

Nicholson and Colleagues' Novel Protocol

Andrew Nicholson and a group of prominent PTSD researchers have undertaken a years-long program of research to investigate brain function and PTSD. This has led to a series of studies of the basic science related to NFB and NFB for PTSD using experimental designs that provide a high level of scientific evidence.

Nicholson et al.'s (2023) study is a recent example of a scientifically very well-executed study of NFB for PTSD that randomized about 20 participants rigorously diagnosed with PTSD to NFB and sham-control groups. This small sample size limited generalizability. Strict inclusion and exclusion criteria were used for PTSD subjects, as well as for a third group of neurotypically healthy subjects. The researchers matched participants in all groups on age and sex, with the two PTSD groups also showing no pre-treatment differences on measures of PTSD, such as the Clinician-Administered PTSD Scale-5 (CAPS-5).

How was their study novel? Given findings of reduced alpha power among PTSD subjects, Nicholson et al. (2023) counterintuitively used NFB to reduce alpha power, despite previous research from other studies that uptrained alpha with success and earlier findings of reduced alpha in PTSD.

Nicholson and his team treated patients with alpha downtraining based on their earlier program of research, which showed what they called an alpha rebound effect (Ros et al., 2016), where alpha power rebounds to a higher-than-baseline level after downtraining of alpha power with NFB.

The authors hypothesized that the alpha rebound effect occurs because of brain homeostasis self-tuning mechanisms that regulate the balance of cortical excitability and inhibition.

What Is the Science Supporting Alpha Rebound?

Ros et al. (2016) previously demonstrated that a single session of alpha-down neurofeedback led to increased alpha power during post-training rest in individuals with PTSD, which was interpreted as a homeostatic restoration of cortical inhibition. The rebound in alpha power was also associated with a reduction in hyperarousal symptoms and normalization of functional connectivity within the DMN and salience network.

A similar rebound was reported by Kluetsch et al. (2014), who found that alpha-down training resulted in symptom reduction and plastic shifts in resting-state network dynamics. The authors proposed that this apparent paradox reflects a neurobiological drive toward equilibrium, consistent with homeostatic plasticity mechanisms.

Du Bois et al. (2021) extended this finding to a low-cost wearable EEG system in a PTSD sample from Rwanda, reporting that seven sessions of alpha-down training produced both a rebound in resting alpha and substantial symptom improvement.

In a healthy population, Ros et al. (2013) observed that even across repeated sessions, alpha amplitudes suppressed during training rebounded during subsequent rest, supporting the concept of a homeostatic set point for alpha oscillations. This finding aligns with systems neuroscience models suggesting that the brain actively counterbalances deviations in oscillatory activity to maintain excitatory/inhibitory (E/I) stability (Ros et al., 2014).

Theoretical work further supports this interpretation. In a review of neurofeedback for anxiety and PTSD, Micoulaud-Franchi et al. (2021) highlight alpha rebound as a central neurophysiological mechanism mediating symptom change.

Orendácová and Kvašňák (2021) explain that such effects are expected under homeostatic neuroplasticity principles: perturbing oscillatory activity in one direction (e.g., suppressing alpha) leads to a compensatory rebound in the opposite direction, thereby restoring optimal neural functioning. This phenomenon is not unique to alpha rhythms or PTSD but may represent a general principle of oscillatory regulation in the brain.

The rebound is measurable not only in raw alpha amplitude but also in signal complexity metrics such as long-range temporal correlations (LRTCs), which Ros et al. (2016) showed increased following alpha-down training.

These results, taken together, suggest that paradoxical alpha rebound is a reproducible, mechanistically interpretable, and clinically significant response to neurofeedback protocols targeting alpha suppression.

Rather than reflecting a failure of training, the rebound appears to indicate successful engagement of intrinsic plasticity mechanisms that restore inhibitory tone, particularly in networks disrupted by trauma.

Across experimental and clinical populations, the consistency of this effect underscores its relevance. When viewed through the lens of self-regulating systems, the alpha rebound effect exemplifies how non-invasive neuromodulation can engage deep regulatory processes in the brain. Its implications extend beyond PTSD to broader questions about how the brain maintains functional equilibrium in the face of perturbation, and how neurofeedback can harness these dynamics for therapeutic benefit.

What Did They Do?

Neurofeedback was provided at Pz to downtrain alpha rhythms among the experimental subjects using auditory and visual feedback. Sham-NFB for control subjects was based on feedback provided to yoked experimental subjects, which was also paused when eye blink and muscle artifacts occurred. The investigation employed a double-blind design, in which both experimenters and subjects were blinded to their assigned condition.

A minimum of 15 sessions to a maximum of 20 sessions of NFB were delivered. All subjects completed at least 17 sessions, which included a pre-training baseline followed by six 3-minute and one 2-minute training periods, totaling 20 minutes of training time. Pre-NFB, post-NFB, and 3-month follow-up measures were collected. The measures included resting qEEG, fMRI, CAPS, Structured Clinical Interview for DSM Disorders (SCID), and inventories of childhood trauma and dissociation.

What Did They Find?

Compared to the neurotypical control subjects, PTSD subjects in both groups showed significantly reduced relative alpha power at baseline, with maximal differences in the dorsomedial prefrontal gyrus, especially in the right hemisphere (dmPFC; BAs 8, 9, and 10), and in the cuneus (BA 18). Brodmann area graphic © Big8/Shutterstock.com.

At baseline compared to neurotypical subjects, PTSD subjects also showed greater relative delta power in the medial frontal gyrus (BA 8) and the cuneus (BAs 17 and 18), greater relative theta power in the posterior cerebellum and reduced relative theta power in the superior frontal gyrus (BAs 6 and 8), and greater beta power globally, especially in the supplemental motor area (BA 6).

Only the PTSD subjects who received NFB showed significant reductions in their CAPS total score from pre- to post-NFB and from pre- to 3-month follow-up NFB that were clinically significant.

Sixty percent of those receiving NFB no longer met diagnostic criteria for PTSD at 3-month follow-up, while this was the case for only 33% of the sham control subjects.

The PTSD remission rate seen in the NFB group was consistent with that seen in gold standard treatments for PTSD (Ehring et al., 2014). There were no dropouts from the NFB group, suggesting its tolerability and safety.

Only the PTSD subjects who received NFB showed relative alpha power increase from pre- to post-NFB, with the increase localized to the medial prefrontal gyrus (BAs 8, 9, and 10; see Nicholson et al.'s Figure 3 below). The NFB group also exhibited relative decreases in beta power in the right anterior cingulate and insula (BAs 13, 33, and 47).

The sham-control group showed a relative reduction in delta power in the left precentral gyrus (Broca's areas 4 and 6). Alpha power that was deficient before training in the dorsomedial prefrontal gyrus (BAs 8, 9, and 10), the anterior hub of the default mode network (DMN), normalized only in the NFB group, specifically in neural circuitry consistently implicated in PTSD.

During the NFB and sham sessions, only the NFB group showed an initial decrease in relative alpha power, which gradually returned to baseline levels. Nicholson et al. (2023) interpret this as a homeostatic rebound in the NFB group. The NFB group demonstrated lower relative alpha power than the sham-control group throughout the series of training sessions.

Future studies may investigate the up- or downtraining of different EEG bands, various electrode placements, and diverse training schedules. Exploring whether other NFB protocols affect similar brain regions is also important.

What Is the Impact?

Alpha downtraining durably affects the brain in regions associated with PTSD. It leads to remission of PTSD at a 3-month follow-up that is comparable to gold-standard psychological treatments. Alpha downtraining results in a rebound normalization of relative alpha power in the anterior hub of the DMN and appears to represent the brain's self-tuning efforts to reestablish homeostasis after the challenge of NFB downtraining of alpha rhythms.

The study by Nicholson et al. (2023) is a scientifically rigorous investigation grounded in a program of basic and applied science. It also replicates earlier findings (Ros et al., 2016).

More speculatively, can the brain be treated in isolation? Are brain-only treatments sufficient for treatment success?

Nicholson and colleagues' study suggests that NFB for PTSD, a treatment only directed to the brain, may be sufficient for the majority (60%) of those with PTSD.

Discussion

Future research should study additional experimental patients, use double-blind designs and sham controls, and concurrently measure clinical, EEG, and MRI measures. Independent research groups should replicate experimental findings. Moss, Shaffer, and Watkins (2023) likewise observed:

There is a need for additional RCTs for both BFB and NF, with a larger sample size, rigorous randomization to controls, careful reporting of pre- and post-treatment physiological measures and symptom checklist scores, and longer follow-ups.

Would NFB provided in a multi-component, holistic biopsychosocial treatment (Thomson, 2025) work more quickly for a higher proportion of patients? Perhaps brain-only treatments jumpstart a process in which the patient initiates psychological changes, whether behavioral or cognitive, leading to environmental changes that create a self-sustaining positive feedback loop, preserving the improvement.

Conclusion

Buzsáki (2019) describes the brain as evolved to explore. NFB may alter the brain's direction of exploration, for instance, away from interactions in environments that sustain inflexible pathology, and toward engagement with interactions whose outcomes lead to flexible and satisfying health.

The brain's nature may be to explore the limits or boundaries of the world, of which itself is one part. Fear may impede this exploration and contribute to inflexibility, the antithesis of health. With an appropriate challenge, such as NFB, the brain's homeostatic self-tuning ability may develop greater flexibility and adaptivity, leading to improved health and increased resilience in the individual.

Key Takeaways

1. Neurofeedback for PTSD shows moderate-to-strong efficacy.

2. Meta-analyses (e.g., Choi et al., 2023) report a standardized mean difference of approximately –0.74, which is moderate to large, indicating meaningful symptom relief; effects are most pronounced in individuals with complex trauma histories.

3. Alpha-down neurofeedback induces paradoxical “rebound” effects

   Training aimed at suppressing alpha rhythms yields a robust post-session increase in alpha power, reflecting homeostatic plasticity. This effect has been documented in both PTSD and healthy populations.
   

4. Clinical improvements align with neurophysiological normalization

   In Nicholson et al. (2023), PTSD patients exhibited significant reductions in CAPS scores and 60% remission at 3-month follow-up alongside restored alpha in DMN hubs.
   

5. Rigorous methodological standards are still needed. While the evidence is promising, many neurofeedback studies (including early RCTs) remain small, heterogeneous, and at moderate risk of bias. Larger, multicenter trials with robust controls are essential.

Additional information and articles can be found on the University of Ottawa's Nicholson website.

Glossary

alpha rebound effect: a counterintuitive increase in posterior alpha power following neurofeedback-based down-regulation; interpreted as a neurophysiological homeostatic response to maintain excitatory-inhibitory balance.

beta rhythm: EEG oscillations ~13–30 Hz; elevated beta power is frequently observed in PTSD, associated with increased arousal and hypervigilance.

Clinician‑Administered PTSD Scale (CAPS): a gold-standard clinician-rated instrument measuring PTSD symptom severity and diagnostic status.

default mode network (DMN): a resting-state brain network involved in self-referential thinking and memory, including regions like the medial prefrontal cortex and posterior cingulate cortex.

effect size: a quantitative measure of the magnitude of a phenomenon, indicating the strength of a relationship or the size of a difference, independent of sample size. Common metrics include Cohen’s d (for mean differences) and r (for correlations).

excitatory/inhibitory balance (E/I balance): the neurobiological equilibrium between excitatory and inhibitory signaling in cortical circuits; disruption is implicated in PTSD.

fMRI neurofeedback: a neurofeedback modality using real-time functional MRI signal to train individuals to modulate activity in specific brain regions (e.g., amygdala regulation in PTSD treatment).

homeostatic plasticity: neural regulatory mechanisms that restore physiological setpoints following perturbations, such as rebound increases in alpha after suppression.

intrusion: PTSD symptom domain involving involuntary, distressing memories, nightmares, or flashbacks of a traumatic event.

long-range temporal correlations ( LRTCs): measures of temporal structure in neural oscillations; increased post-NFB, suggesting restored criticality in cortical dynamics.

Pz electrode: the midline parietal electrode site used as the target for alpha neurofeedback protocols.

Post‑Traumatic Stress Disorder (PTSD): a psychiatric disorder arising from exposure to severe trauma, characterized by intrusion, avoidance, cognitive/mood alterations, and arousal/reactivity changes.

salience network (SN): a brain network anchored in the anterior insula and dorsal anterior cingulate cortex that supports threat detection, interoception, and network switching.

sham-control: In neurofeedback RCTs, a control condition in which participants receive non-contingent (“yoked”) feedback rather than their own brain signal.

theta band: EEG oscillations ~4–7 Hz, often associated with memory and emotional processing; may be targeted in different neurofeedback protocols.

References

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About the Author

Dr. John Raymond Davis is an adjunct lecturer in the Department of Psychiatry and Behavioural Neurosciences at McMaster University's Faculty of Health Sciences. His scholarly contributions include research on EEG changes in major depression and case studies on neurological conditions. ​