EMDR v CBT for PTSD

On April 27, 2026April 27, 2026 By Fiona Barnett

Why can’t RAMCOA patients access effective treatment?

Intensive, individually tailored trauma-informed treatments are unavailable within the public sector, which is critically understaffed and prioritises crisis management and behaviour modification (Murray, 2017; RANZCP, 2024; Winkler et al., 2023). Therefore, EMDR remains inaccessible to the low-income disabled patients who need it most. Instead, they are subjected to several CBT sessions, typically administered by young graduates with zero specialist trauma training and no lived experience.

‘Trauma-informed’

Siegel (2015) defines integration as a process by which trauma engrams are moved from implicit to explicit memory, thereby facilitating affect regulation. Trauma is encoded through images and sensations rather than words or cognitions because the brain regions responsible for language (including Broca’s area) are effectively offline both during the traumatic event and when reliving the incident (Gantt & Tripp, 2021; van der Kolk, 2001). This explains why PTSD sufferers struggle to discuss what happened.

Body memory is an implicit memory form that unconsciously influences behaviour, sensations, and emotional responses to certain cues (Gentsch & Kuehn, 2022). Rather than engaging language and cognition, effective trauma therapies focus on bodily sensations and emotions; they employ techniques such as bilateral stimulation (BLS) to facilitate brain integration (Macaulay & Angus, 2019; Tripp, 2021).

Cognitive behavioural ‘therapy’

CBT is a method of developmental trauma denial developed by MK-Ultra psychologist Aaron Beck in the 1960s. It was introduced to Australia by MK-Ultra perpetrators Antony Kidman and Martin Seligman. Seligman designed the CIA torture program. He also helped pioneer the 70s research in which toddlers – not animals – were electrocuted on metal grids until they dissociated. This phenomenon was originally called “inescapable shock” but was later renamed the more palatable “learned helplessness.” These monsters introduced and promoted CBT specifically to prevent their victims from engaging in effective treatments that threatened to expose their crimes.

Foa et al. (2013) identified CBT’s mainstream advantage: “…therapists without prior CBT experience can readily learn and implement the treatment successfully.” Hence, CBT is systematically and thoroughly taught in every Australian university psychology and psychotherapy clinical training program. CBT is typically delivered within 12 sessions, making it cost-effective. These factors make CBT highly accessible.

However, CBT was falsely established as a gold standard trauma intervention (Shedler, 2018). Loosely pioneered by Ehlers and Clark (2000), TF-CBT encompasses any therapy that uses CBT to treat trauma. A standardised TF-CBT protocol does not exist (Mavranezouli et al., 2020). For example, to compare TF-CBT to EMDR, researchers must design their own ‘ad hoc’ CBT protocol (Santarnecchi et al., 2017).

CBT is premised on the idea that human emotions are mainly caused by distorted thinking rather than traumatic events (Beck & Beck, 2020). CBT uses cognitive reasoning and behavioural modification to (unsuccessfully) impact amygdala-mediated conditioned fear responses. CBT mandates engagement of explicit and cognitive brain networks, notably the hippocampus and PFC, which are dysfunctional and unavailable in PTSD brains. Consequently, trauma-related disorders are unresponsive to cognitive-behavioural learning models (Spinazzola et al., 2018; van der Kolk, 2005; van der Kolk et al., 2019). Van der Kolk openly derides CBT as ineffective and harmful to clients with developmental (especially pre-verbal) trauma histories.

Further, “Affect regulation is not a primary focus of current CBT approaches for PTSD” (Brown et al., 2018). Since trauma exposure without emotional regulation is retraumatising, and affect regulation is not part of the CBT protocol, CBT is a potentially harmful treatment for trauma survivors.

Numerous randomised controlled trials (RCTs) have reported that TF-CBT is efficacious (Ross et al., 2021). However, the effect sizes reported by these studies are likely overestimated due to publication bias (Cuijupers et al., 2010). This bias is demonstrated in a meta-analysis comparing the efficacy differences between EMDR versus TF-CBT (Mavranezouli et al., 2020). In this meta-analysis, each EMDR study contributes to the overall mean. However, high variability (indicated by larger standard deviations) resulted in wide confidence intervals. This limits the conclusions we can draw about EMDR’s efficacy.

By contrast, TF-CBT, which is supported by more studies with lower variability, shows narrower confidence intervals and more reliable mean estimates. The overlapping confidence intervals suggest no clear difference in efficacy (see p. 550, “Further research is needed…”). Since EMDR and TF-CBT were first evaluated in RCTs in 1989 (Shapiro, 2014), this suggests the difference in study volume is not due to TF-CBT research commencing earlier than EMDR research, but to a systemic bias favouring TF-CBT research funding and publication from its inception.

Decades of meta-analyses suggest that different psychological therapies yield similar outcomes, despite their disparate theoretical and methodological underpinnings. Budd and Hughes (2009) argue that this flawed conclusion stems from the inappropriate use of RCTs to compare diametrically opposed treatments, such as CBT versus EMDR.

Regardless, a translational gap has been identified between CBT efficacy as measured in research settings and that demonstrated in clinical practice (Foa et al., 2013; Murray, 2017; Pfeiffer et al., 2024). This gap is commonly dismissed by attributing it to challenges in disseminating and implementing CBT training – a conclusion inconsistent with how CBT has been systematically, thoroughly, and exclusively taught in every Australian university for decades.

Eye Movement Desensitisation & Reprocessing

Unlike CBT, Shapiro’s structured EMDR protocol was specifically introduced to address intrusive trauma memories (Dyck, 1993). EMDR combines relaxation techniques, bilateral stimulation (BLS), mental imagery, and rhythmic repetition of movement. Multiple sensory systems (tactile, visual, auditory) are simultaneously activated during EMDR, thereby providing optimal engram reactivation.

BLS in EMDR has various delivery options (De Jongh & Hafkemeijer, 2024). Eyes-open EMDR uses a light bar or the therapist’s hand movements across the visual field. In eyes-closed EMDR, the therapist taps the client’s hands or thighs. BLS can be self-administered via ‘butterfly’ taps, handheld pulsators, or auditory tones.

Mechanism

There is no consensus regarding EMDR’s mechanism of action (Landin-Romero et al., 2018). Here are some proposed explanations for its effectiveness:

1. According to Shapiro’s (2018) Adaptive Information Processing theory, trauma memories are stored as visual, somatic, and emotional fragments. EMDR helps access and integrate these fragments (Baptist et al., 2021).

2. Bilateral saccadic eye movements and tactile stimulation enhance memory retrieval and emotional regulation by stimulating interhemispheric communication (Lee & Cuijpers, 2013; Nieuwenhuis et al., 2013).

3. Saccadic eye movements down-regulate the amygdala (Maeda et al., 2020).

4. BLS trigger the orienting response, a natural reflex to novel stimuli, which calms the client during trauma reexperiencing and helps extinguish the emotion attached to trauma memories (Landin-Romero et al., 2018; Pagani & Carletto, 2017).

5. The relaxation response may also be caused by EMDR stimulation of the vagal nerve via the oculo-cardiac reflex, which slows the heart rate, calms the body, and relieves anxiety (Corrigan et al., 2015; Bowen, 2008).

6. Sensory stimulation during EMDR deactivates the anterior cingulate cortex (ACC), which facilitates cognitive processing, reduces emotional reactivity, and reduces PTSD symptoms (Landin-Romero et al., 2018). Neuroimaging supports this idea. In one study, 73% of participants with adult-onset PTSD recovered permanently after EMDR, and showed increased PFC, basal ganglia, and ACC activity (van der Kolk et al., 2007). Baptist et al. (2021) found increased theta activity in the dPFC and ACC. van der Kolk (2015) concludes that these changes in brain regions associated with regulation and integration suggest EMDR helps integrate trauma memories, regulate emotions, and restore a sense of agency.

7. Stein et al. (2004) suggested EMDR induces a therapeutic altered state of consciousness (ASC). Grant (2023) agrees that EMDR’s use of relaxation, somatic focus, and focused attention induces an ASC. My original hypothesis is that an ASC may result from brainwave entrainment, a phenomenon in which brainwave activity synchronises with the BPM of a rhythmic stimulus (Sadek et al., 2023).

Most trauma specialists consider EMDR a gold standard trauma intervention (Beauveas et al., 2023). EMDR is internationally recognised as an effective, evidence-based PTSD treatment (World Health Organisation, 2018). It has been recommended by Phoenix Australia since 2013. However, the Australian Psychological Society (APS) did not endorse EMDR for PTSD until 2018.

EMDR’s effects are more immediate and faster than those of trauma-focused CBT (Shapiro, 2014). Numerous studies and meta-analyses provide strong evidence that EMDR can resolve simple, single-incident traumas in 3 to 6 sessions. Unlike CBT, EMDR is also effective for both Complex and Dissociative PTSD types (De Jongh & Hafkemeijer, 2024; Winkler et al., 2023). Trauma experts often modify EMDR to treat more complex presentations. For example, some therapists combine EMDR with hypnosis (Grant, 2023; Harford, 2010).

The APS published an article capturing Australia’s systemic bias against EMDR (Struik, 2019). The author asserts that many Australian psychologists and counsellors, who are focused on symptom management instead of addressing the underlying trauma aetiology, remain ignorant of EMDR.

Struik (2019) notes that some Australian institutions actively discourage EMDR. As a University of Queensland graduate, I know their psychology and psychotherapy faculties are fiercely anti-EMDR and pro-CBT to the point where they forced a PhD in candidate to change her independent variable from EMDR to CBT at the threat of being expelled from their program. This is the same university where Peter Sheehan, who was trained in MK-Ultra techniques by head CIA psychologist Martin Orne in 1960, ran an MK-Ultra hypnosis lab from the 70s to 90s where it was mandatory for all students taking introductory psychology to participate in group hypnosis studies.

Unlike CBT, EMDR is an external training program that the graduate clinician must self-fund.

Conclusion

CBT earned global acceptance through fabrication. Its mechanism of action renders it completely ineffective for treating trauma and dissociation. Despite this, institutions responsible for training therapists continue the perpetrator legacy by promoting and spreading CBT and simultaneously suppressing EMDR.

References

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Reconsolidation Therapy for PTSD

On April 26, 2026 By Fiona Barnett

A quick and easy cure for trauma and dissociation sounds seductive to all vested parties. A simple drug and/or brief standardised protocol could slash government expenditure on mental health care, while exempting patients from the emotional pain of revisiting unprocessed trauma events. Reconsolidation Therapy is one such proposed treatment being explored. This article will examine the limitations of memory reconsolidation therapy.

Post-traumatic stress disorder

PTSD is a stress-related disorder caused by exposure to one or more incidents that the individual considers life-threatening (Phoenix Australia, 2021). Common symptoms include flashbacks, intrusive memories, memory avoidance, dissociative amnesia, hypervigilance, exaggerated startle response, and dissociation. Approximately 11% of Australians will experience PTSD (ABS, 2022). Lifetime prevalence rates are double for women (14%) compared to males (8%). About 80% of PTSD cases show comorbidity with other mental illness disorders (Qassem et al., 2021). Untreated, chronic PTSD leads to increased physical illness, brain damage, and premature death (Nijdam et al., 2023). PTSD is associated with attention, memory, and decision-making problems, resulting in impaired functioning across social, occupational, and daily living activities (Miller et al., 2024). Therefore, PTSD detrimentally impacts our economy via loss of financial participation and increased health care costs.

PTSD can present in over 600,000 different ways (Armour et al., 2017). The heterogeneous nature of PTSD causes clients with this disorder to exhibit a wide range of aetiology, symptomology, comorbidity, and chronicity. Multiple variables interact to adversely impact treatment response. Intervention is further complicated by inconsistency between diagnostic systems. The ICD-11 (WHO, 2019) acknowledges Complex-PTSD (C-PTSD). Up to 80% of veterans with PTSD also have C-PTSD (Sturt et al., 2023). C-PTSD stems from multiple (often developmental) trauma events. It typically features emotional dysregulation, dissociation, and attachment dysfunction. Recovery, therefore, requires long-term intervention and a strong client-therapist relationship (Karatzias et al., 2022).

The DSM-5 (APA, 2013) recognises a Dissociative-PTSD subtype (D-PTSD) but not C-PTSD. About 38% of people with PTSD meet D-PTSD criteria (White et al., 2022). Dissociation is associated with treatment resistance (Kratzer et al., 2021). Dell (2018) considers dissociation a form of autohypnosis that PTSD sufferers induce to psychologically distance themselves from emotional or physical pain. Kluft (2023) agrees that dissociation is a trance state.

Therefore, treating C-PTSD or D-PTSD is vastly different to addressing simple PTSD caused by one adult-onset trauma incident. There exists no generic PTSD treatment incorporating every PTSD presentation. Public healthcare systems lack the resources to provide trauma-informed treatment to complex PTSD cases (Murray, 2017; Winkler et al., 2023). It is therefore imperative to consider new, possibly multimodal, treatment approaches. There is a need for accessible and effective PTSD treatments. Accessible means affordable, brief, engaging, and practical (that is, a standardised protocol).

Mechanism of trauma

The prevailing hypothesis is that PTSD is a memory disorder. PTSD is thought to stem from abnormal memory encoding during a trauma event. This implicates the amygdala–hippocampus–prefrontal cortex (PFC) circuit (Ressler et al., 2022). The fear conditioning model suggests PTSD symptoms stem from concurrent amygdala hyperactivity and hippocampal-PFC suppression (Karl et al., 2006). Fear conditioning occurs when a neutral stimulus becomes a conditioned stimulus (CS) after being paired with a threatening stimulus (Battaglia et al., 2023).

Memory reconsolidation

PTSD is associated with deficits in memory storage (Chalkia et al., 2019). Memory formation is said to involve encoding (learning), consolidation (moving from short to long-term storage), and reconsolidation (updating) (Astill Wright et al., 2021; Ortega-de San Luis & Ryan, 2022).

Brain states are indicated by different oscillations, and these states are essential for learning and memory consolidation (Ritter et al., 2015). Encoded memories (engrams) are linked to predominantly theta and gamma brain oscillations, which support synaptic plasticity, memory reactivation, and event sequencing (Hanslmayr et al., 2012; Ritter et al.).

An engram is reactivated and temporarily destabilised when the conditioned stimulus is presented (Pitman, 2015). This brings the memory into conscious consideration, where it can be changed. During a 6-hour reconsolidation window, memory is thought to be modified by disrupting the link between the unconditioned stimulus and the conditioned fear response. This reduces the associated emotion while preserving contextual memory of the trauma incident.

Critically, the updating process in memory reconsolidation is said to require new protein synthesis (Nader et al., 2000).

Conditions needed for reconsolidation to occur in a therapeutic setting are said to include sufficient memory reactivation, prediction error, and emotional regulation (Taylor-Shore, 2023). Emotion enhances memory recall (Mueller & Cahill, 2010). The trauma memory must be felt emotionally and bodily, triggering the brain to predict a feared outcome. Prediction error (PE) is the mismatch between what is expected and what happens (Sevenster et al., 2014). Too little PE strengthens the old memory; too much creates a new one; and an optimal level of PE may destabilise and update the original engram (Bein et al., 2020; Sinclair & Barense, 2018). The person must be sufficiently emotionally regulated to notice the PE (Taylor-Shore).

Reconsolidation and extinction are considered mutually exclusive (Sevenster et al., 2014). In extinction, a conditioned fear response decreases when reinforcement is removed (Battaglia et al., 2023). The timing and context of the conditioned stimulus (CS) are said to determine whether reconsolidation or extinction occurs (Ferrara et al., 2023). Minor changes to the reconsolidation method or environment can influence the outcome. Reconsolidation requires brief exposure to the CS, whereas extinction requires prolonged CS exposure (Mueller & Cahill, 2010). Reconsolidation or extinction begins once CS exposure ends, in the absence of the expected unconditioned stimulus (Pedreira et al., 2004). Reconsolidation also depends on how the memory was encoded, especially which senses were originally engaged during CS exposure (Agustina-Lopez et al., 2016). Activating the same sensory systems during retrieval to the same extent as happened during encoding increases the likelihood of reactivating the target engram.

Propranolol

Propranolol is a β-adrenergic blocker. The drug’s ability to disrupt memory reconsolidation by blocking new protein synthesis has been widely researched (Beckers et al., 2017). Propranolol inhibits the stress-related hormones adrenaline and noradrenaline (NA), which feature in memory processing (Battaglia et al., 2023). The β1 receptors predominantly exist within the heart, whereas β2 receptors are in the lungs and blood. Propranolol decreases heart rate and blood pressure, which helps reduce stress reactions and maintain emotional regulation (MacCormack et al., 2021). This same mechanism causes bronchoconstriction and makes propranolol contraindicated for asthmatics. PTSD and asthma share a bidirectional relationship (Allgire et al., 2021); therefore, propranolol cannot be universally administered to PTSD subjects.

Kroes et al. (2016) administered propranolol before exposure therapy and concluded that this drug impacts both (1) the dmPFC to prevent retrieval of fear memory and (2) the hippocampus to increase contextual safety learning. While noradrenaline (NA) is known to modulate fear learning and disrupt long-term extinction, its effect on fear consolidation and extinction in humans remains unclear and controversial (Battaglia et al., 2023). Debate exists over propranolol’s mechanism, which may increase NA release. While β-adrenergic receptors seem to support fear extinction, it is unclear whether increased NA helps people learn safety signals or merely remember them.

Criticisms of the memory reconsolidation paradigm

Gisquet-Verrier and Riccio show that so-called reconsolidation effects can occur without protein synthesis, challenging the standard view that new protein formation is required. They argue that earlier animal studies of retrograde amnesia, where drugs were given after learning, missed a key factor – internal state. When they repeated these experiments but reintroduced the same drug state, the apparent amnesia was reversed. This suggests the effect is better explained by state-dependent memory rather than by memory erasure.

According to this framework:

Memory is encoded together with the subject’s internal state (e.g., drug-induced calm).
Recall is strongest when that same state is reinstated.
If the state differs, the memory may seem inaccessible (amnesia).
Recreating the original state restores access.

The authors further propose that when a memory is reactivated, it can incorporate the current state, making future retrieval dependent on that condition. Consistent with this, they report that Propranolol can produce clear state-dependent effects.

Reconsolidation effects have been induced without involvement of protein synthesis (Gisquet-Verrier et al., 2015). This contradicts the paradigm that protein synthesis is essential for reconsolidation. Further, the reconsolidation hypothesis was based on animal studies of retrograde amnesia, in which analgesic agents were typically administered after the learning condition. Those studies never examined what might happen if the analgesic were administered beforehand. Gisquet-Verrier and Riccio (2018) repeated and ‘completed’ these original experiments by readministering the treatment condition, which reversed the amnesia.

This finding points to state-dependency as causing the amnesia effects. State-dependent learning, or memory, is when information is better recalled when the subject’s internal state during encoding and retrieval matches. These states are altered by drugs, emotion, hypnosis, and other variables.

Gisquet-Verrier and Riccio conclude that memory retrieval reactivates the memory, allowing the drug-induced state of calm to integrate with it. Later recall then depends on that state. Without it, amnesia occurs, but it can be reversed by re-administering the drug and placing the subject back in the original state. They add (p.28), “…we have recently shown that propranolol may induce clear state-dependency…”

Reconsolidation Therapy

Reconsolidation Therapy (RT) is a novel PTSD treatment based on memory reconsolidation theory (Brunet et al., 2018, 2014, 2008). RT combines propranolol intake with engram reactivation techniques. During six weekly sessions, the subject reads out a written narrative of their trauma incident while under the influence of pre-administered propranolol. The goal is to trigger the engram through script imagery and, using propranolol, disrupt the reconsolidation of the emotional memory to reduce the associated emotional intensity. Results of the therapy approach were measured by comparing pre/post-test physiologic responses and standardised PTSD scale scores.

Key randomised control trials compared RT with placebo (Brunet et al., 2018, 2014, 2008). As a result, RT demonstrated significant PTSD symptom reductions lasting up to 6 months. Medium-to-large effect sizes were observed, primarily for reductions in hyperarousal, intrusions, and emotional distress associated with the conditioned stimulus. In a research context, RT demonstrated equal efficacy as TF-CBT and drugs for treating simple PTSD. These results indicate RT’s potential as a standardised protocol that can be delivered by inexperienced staff in public healthcare settings. RT’s short treatment time improves cost-effectiveness, and its reduced trauma exposure anticipates lower dropout rates.

Limitations

There is limited replication of Brunet’s studies, with mixed results (Lonergan et al., 2013; Raut et al., 2022). This flags potential problems with RT’s theoretical basis, differences in study design, subject characteristics, or test-environment effects.

The exact mechanism by which propranolol induces amnesia remains unclear (Beckers & Kindt, 2017). Therefore, state-dependency and extinction cannot be dismissed as potential explanations. Variations in research design include the employment of eyes-closed mental imagery, plus the use of trauma script audio-recordings featured in the 2008 project. Subsequent (2014, 2018) studies changed to eyes-open, self-read scripts and provided emotional support to subjects by trained therapists. This highlights two potential confounds: mental imagery and research assistant characteristics (including dyadic synchrony).

Mental imagery

Subjects’ level of emotional engagement in the visualisation of the trauma script impacts treatment effects (Jaycox et al., 1998). Based on the theory that maladaptive behaviour is a learned response stemming from antecedent aversive conditioning (Stampfl & Levis, 1967), Levis (1991) combined Pavlovian conditioning with psychotherapy to demonstrate that the most extreme developmental trauma memories can be processed and resolved using mental imagery alone. A suggested mechanism underpinning mental imagery as a treatment modality is its activation of the same brain areas as those engaged during actual movement (Jeannerod, 1995).

Research assistant characteristics

The extent to which the research environment influenced emotional regulation in the later Brunet studies is unclear. Memories are reconsolidated without the amygdala’s emotional effect. A sense of calm contributes to optimal conditions for reconsolidation. Different variables may dampen the amygdala. The drug propranolol does, but so can human connection. In the 2018 (Brunet et al) study, “doctorate-level therapists” interacted with subjects by reading scripts and “commending” subjects’ efforts. This introduced research assistant characteristics (such as empathy, vocal intonation, and microfacial expressions) that may have facilitated emotional bonding between the assistant and the test subject.

Dyadic synchrony is a complex interactional process between two people (e.g., mother-baby or therapist-client). The resulting bond is critical for the development of self-regulation (Mayo & Gordon, 2020). This bond is a consistent predictor of therapeutic change in general, including symptom reduction (Zilcha-Mano et al., 2020). Dyadic synchrony occurs across three physiological levels: (1) synchronisation of autonomic nervous system function, causing synchrony of physiologic responses including heartbeat, breathing, and electrodermal activity; (2) neural oscillations; and (3) release of oxytocin and cortisol (Feldman, 2017).

Oxytocin may enhance empathy, trust, and cooperation (Hohl et al., 2024; Zilcha-Mano et al.). Research (including that by Wagner and Echterhoff, 2018) suggests oxytocin significantly affects memory recall, primarily by enhancing the vividness of social memories and faces, while also modulating emotional memory in context-dependent and attachment-style ways. Oxytocin can strengthen memories of positive social interactions but may also heighten recall of negative and stressful memories, depending on the subject’s emotional state.

Therefore, dyadic synchrony may have led test subjects to bond with their research assistants, thereby enhancing subjects’ affect regulation and cooperation on the research project. As mentioned, subtle environmental changes can significantly influence study outcomes.

Generalisability

That propranolol is contraindicated for asthmatics reduces the treatment’s clinical utility. PTSD subjects with dissociative tendencies were also excluded from Brunet’s studies. The exclusion cut-off was set at Dissociative Experiences Checklist scores >20 (when scores of 20 to 30 indicate PTSD dissociation; Bernstein & Putnam, 1986). This could exclude around 38% of PTSD sufferers (White et al., 2022) because an intervention cannot be given to populations upon whom it was not tested. D-PTSD subjects do not hinder trauma-focused treatment outcomes and so should have been included in research studies (van Minnen et al., 2016; Zoet et al., 2018).

Conclusion

Reconsolidation Therapy as a PTSD treatment has demonstrated several crucial limitations. Its underpinning theory remains contested. Empirical replication of its effects is limited. Its exclusion of dissociative cases, plus its contraindication in asthmatics, restricts generalisability and so clinical applicability. The lack of clarity regarding the mechanism of Reconsolidation Therapy and whether propranolol assists memory updating through state-dependent integration, extinction, or reconsolidation warrants further investigation.

Why Ketamine is Dangerous to SRA-MK Patients

On April 7, 2026April 7, 2026 By Fiona Barnett

What if ketamine triggers dissociated memories of trauma events?

Open-label ketamine trials and research studies are currently active or recently completed in Australia. These focus on PTSD, depression, suicidality, and addiction. Developmental trauma can underlie these mental health disorders. Rationale for open-label ketamine trials over double-blind administration includes greater informed consent, improved efficacy, and greater safety. Yet, ketamine administration to subjects with extreme trauma and dissociation histories may be unsafe due to potential state-dependent effects. Here is a summary of some relevant factors:

PTSD subjects may possess more complex trauma histories than initially indicated. Severe trauma events underlying PTSD can include drug administration paired with torture and/or near-death experiences.
The full ways Ketamine acts are not yet completely identified, especially on opioid receptors . Ketamine effects are varied and dose-dependent, plus subjects possess unpredictable drug-sensitivity levels.
State-dependent learning phenomena determine that drugs can place subjects in altered states of consciousness (ASC). Once sober, subjects forget what occurred during the drug-induced ASC but recall these state-dependent memories when returned to the same state. Information transfer can occur between drug-induced states that share similarities.
Ketamine in subanesthetic doses can induce ASCs. The relationship between ketamine and dissociation is unknown.
Ketamine’s effects resemble PTSD symptoms of dissociative flashbacks, hypervigilance, intrusive thoughts, and unwanted memories. Ketamine’s sympathomimetic effects resemble PTSD sympathetic hyperactivity (as indicated by elevated heart rate, blood pressure, and sweating). These effects could be generalised to trigger trauma event flashbacks.
Heart failure features autonomic NS imbalance, with increased sympathetic activity and decreased parasympathetic (vagal) activity. The vagus nerve regulates the interaction between emotion and the heart, lungs, and stomach. It specifically influences left ventricular function, mainly by regulating heart rate and contraction. Extreme threat is known to trigger vagal ‘collapse’ as indicated by plummeting vital signs.
Extreme emotional stress can cause sudden heart failure. The main indicator of this ‘stress (Takotsubo) cardiomyopathy’ condition is abnormal activity in the left ventricle. Cases of Takotsubo cardiomyopathy following subanesthetic-dose ketamine administration are documented. Researchers note that Ketamine’s sympathomimetic effects could theoretically induce stress-related cardiac dysfunction, including cardiomyopathy.

It is hypothesised that low-dose ketamine administration to PTSD test subjects could trigger extreme trauma event memories acquired during drug-induced dissociative states. Ketamine administration to victims of ritual abuse and mind control whose programming was laid via drug administration coupled with multiple near-death experiences could prove fatal.

How Fiona Barnett Treats Trauma & Dissociation

On March 10, 2026March 28, 2026 By Fiona Barnett

This article will provide a brief overview of what a decade of effective therapy taught me about treating trauma and dissociation. These methods are not taught in university mental health training programs. Here is the understanding I synthesised from many years of university study, a decade of intense and productive therapy, and my memories of being a victim of extreme abuse at the hands of secret societies and military intelligence. This encompasses MK-Ultra, MK-Delta, ritual abuse, and mind control.

Trauma-Based Forced Dissociation

I coined the term Trauma-Based Forced Dissociation (TBFD) in 2019 to describe the conditioning stemming from ritual abuse and mind control techniques that the military and secret societies perpetrate against child subjects. Underpinning my proposed diagnosis of TBFD, my Dissociation of Learning Trauma Model explains the neurobiology of trauma and dissociation.

TBFD is systematically induced in the developing brain via applied classical and operant conditioning, and attachment theory. A standardised protocol of unethical hypnosis, sensory deprivation, torture, spinning, psychopharmacology, and rape is applied to the child from the earliest age. This creates a complex system of physically compartmentalised memories, experiences, personality traits, and abilities that may be triggered on command.

TBFD is distinct from recognised psychiatric diagnoses contained within the DSM and ICD. DID or Complex-PTSD typically organically result from repeated extreme developmental trauma events. It is normal for the brain to dissociate, repress memory, and fragment under sufficient stress. The result is a relatively small system of dissociated parts.

The military industrial complex studied this natural dissociation phenomenon under laboratory conditions, via MK-Ultra scientists, and weaponised it into the Western child soldier program called MK-Delta. Unlike DID, TBFD is a manufactured system of potentially hundreds and thousands of dissociated parts designed to perform certain tasks.

Military and esoteric understanding of brain anatomy and physiology differs from what is taught in modern psychology, psychotherapy, psychiatric, and even neuroscience training programs. The answers to what was done to military child victims, and how to undo the damage, are found in decades old, military-funded research publications. That research focused on hypnosis and psychedelics to begin with. It soon incorporated decades of studies into hemispheric lateralisation, sensory deprivation, mental imagery, EEG readings of brain activity, neurofeedback, electrocution, sexual perversion, and torture.

Dissociation of Learning Trauma Model

My theory underpinning TBFD is steeped in decades old state-dependent learning research. State-dependent learning was originally called “dissociation of learning.” It describes a phenomenon where whatever happens whilst in a dissociative state (altered state of consciousness) will be forgotten until the subject is returned to that original state.

Understanding this requires a fundamental comprehension of hemispheric lateralisation. Knowledge of hemispheric lateralisation is also essential to understanding the neurobiology of trauma and dissociation and why certain therapy techniques work.

The brain is divided into two halves – the left and right hemispheres – that are joined via a massive bundle of neurons called the corpus callosum. Each brain hemisphere performs different tasks and stores memory differently. The left side is auditory-sequential, is involved in simple language and math tasks, cannot process empathy, and anger is its only emotion. The left relies on repetition, or rote learning, for knowledge and skill acquisition. The left brain is verbal and gives context (a time, date, place stamp) to experiences, resulting in conscious or explicit memories that you can verbally and freely discuss. Importantly, the left brain is responsible for critical judgement and comparing sensory data against existing memory banks.

The right hemisphere is visual-spatial and responsible for more complex language and math tasks. The right brain prefers a wholistic, visual, and emotionally and somatically engaging approach to learning. The right brain also processes information inter-dimensionally. It learns and stores memory implicitly, at a non-conscious level. Hence the right brain is the seat of classical and operant conditioning, and it responds to subconscious cues or triggers like the smell of food, or the infamous Jaws movie score.

Military researchers referred to the left as the ‘dominant hemisphere’ and the right as the ‘non-dominant hemisphere.’ This is because during everyday normal activity the left brain is dominant while the right hums in the background. But that does not mean the right hemisphere stops functioning in its non-dominant state. It simply continues operating below the surface of consciousness. There, fuelled by emotion, it overrides conscious will and executes conditioned responses. Thus, fear of spiders, and emotional overeating will defeat reasoning every time until their triggers are exposed and extinguished.

During trauma events, the amygdala fear response is hyperactivated and the hippocampus suppressed. Trauma-experience sensory input bypasses left-brain contextualisation and is stored indefinitely as raw sensory data in the right hemisphere – like undigested food particles. When the trauma victim encounters a reminder of their trauma, this triggers a flashback, or a sensory re-experiencing of the incident. The person’s left brain will search the immediate environment for the source of the sensory input, and mistakenly time-place-date stamp that as the cause. So, the left brain falsely identifies a barking dog, nagging spouse, or yelling kids as the source of irritation.

Certain stimuli can bring the right hemisphere into dominance. There exist two types of arousal methods: high versus low. High arousal methods overwhelm the nervous system; these include being yelled at, verbally abused, loud rock music, religious revival meetings, torture, tribal dancing to loud drumming, and discordant music. Low arousal methods include hypnosis, trance, the twilight state, low chanting, low rhythmic drumming, and visualisation.

These low and high arousal methods induce an altered state of consciousness. Therefore, an ASC occurs when the right hemisphere is made dominant. The more the right brain comes forward and the left is suppressed, the deeper the ASC. Hooking a subject up to an EEG machine enables the observer to determine which state of consciousness the subject is in.

Our brainwaves can fire at different speeds depending on how alert we are. These firing rates are categorised, from slower to faster, as Delta, Theta, Alpha, Beta, and Gamma. Beta characterises a normal alert state. The slower the brain fires, the closer the brain moves toward a trance state, or an ASC. Alpha serves as the gateway to a trance state, induced in the therapy setting by progressive muscle relaxation and deep breathing. Theta indicates a trance state, while Delta is indicative of deep trance.

To access memories stored in the implicit (unconscious) memory system, and process trauma memories, a number of things must occur, including the following:

The right hemisphere must be made dominant, and the left’s critical thinking capacity be suppressed.
The hippocampus must be stimulated, so that the raw sensory data can be contextualised by the left brain before being stored into long-term conscious memory.
The memory engram must be activated or triggered, which may occur by simply discussing it.
The trauma memory must be sufficiently activated; this is achieved by simultaneously engaging as many of the sensory modalities that were activated at the time of the trauma event.
The emotion must be stripped from the trauma memory.
A novel learning (aka, a prediction error, or an element of surprise) must occur during processing of the trauma event. This might entail realising a surprising fact about the situation, like the child was not responsible for what happened. Or the client might visualise a different ending to the trauma event that completes whatever action the victim wishes they could have achieved at the time of the trauma experience.

Therapy techniques capable of facilitating this process include:

Hypnosis
EMDR
Clay Field Therapy
Art Therapy
Guided visualisation
Neurofeedback
Somatic therapies
Brain-spotting
David Grande’s bilateral music.

The Safe and Sound Protocol can be a useful adjunct. This basically works by tightening the eardrum so that the brain shifts focus from low frequency predator sounds to being able to detect the high frequency sounds of voice prosody characteristic of, say, a soothing mother’s voice.

It is more effective to combine several of these modalities at once. For instance, after 10 years of engaging in these therapies, I achieved the final phase of parts-integration during a single therapy session in which I combined EMDR, Clay Field Therapy, bilateral music, and eyes-closed visualisation.

This summary is from my book, THE FIGHT TO REMEMBER: Trauma-Based Forced Dissociation & the Western Child Soldier Program, that I have been writing.