Neurofeedback For Posttraumatic stress disorder

Dr Beverley Steffert,
Chartered Psychologist, Neuropsychologist,
British Psychological Society,
Email: b.steffert at
Email: DrSteffert at

Bev is member of the European Society for Post Traumatic Stress and has presented neurofeedback as a therapy for trauma at their annuel conference in Vilnius, Lithuania in 2015.

We run workshops on Neurofeedback For Posttraumatic stress disorder

Connecting the fragmented self with neurofeedback

Normal brain activity shows a dynamic excitation and inhibition which connects functional areas by phase, frequency and timing.
Repeated intense activation of the brain network for fear makes it vulnerable to developing hypersensitivity. The neural signalling activated by fearful experiences - a process that also is involved in learning and in memory formation -- begins when the neurotransmitter glutamate activates a receptor called NMDA, resulting in overwhelming distress, hyper-arousal, intrusive unbidden memories and dissociative symptoms, detachment, numbing, depersonalisation, freezing, distancing of self from experience. Neuronal circuits respond too readily or too strongly to weak inputs and brain systems become unstable. Bremmer suggests that these symptoms are actually two subtypes of PTSD. The prefrontal cortex inhibits the emotional (limbic) system but when this fails, limbic reactivity is too high and is associated with the re-experiencing and hyper-arousal - a form of emotional disregulation - or cortical bypass. Neurofeedback training can improve self-regulation. This instability or thalamocortical disregulation can lead to pain, migraine, seizures, panic attacks, rage, bipolar mood swings and PTSD.
In general brain based studies have shown that the PTSD brain becomes disorganised, lacks coherence, is smaller in gray matter volume in the hippocampus (affecting memory), has a smaller corpus callosum affecting how much the two sides of the brain can work together (lateralisation). The prefrontal cortex which is responsible for inhibiting dangerous impulses, planning, insight and attention, has fewer GABA biding sites in the amygdala, which means less ability to recruit necessary inhibitory processes, poorer myelination in the left arcuate fasciculus which connects the speech and comprehension areas, and weaker connections to the cingulate, fornix and left fusiform gyrus. At the same time there is decreased activity in the orbito-frontal gyrus and medial prefrontal, leading to temporal lobe disruptions and even brainstem deficits.
Thus trauma symptoms in the brain start with limbic system over-arousal with under-arousal in the cortex for at least the majority of victims (70%) but for the 30% left the situation is exactly the opposite. This cortico-limbic inhibition theory suggests that once a threshold of anxiety and hyper-arousal is reached the medical prefrontal cortex inhibits emotional processing in limbic structures including the amygdala, leading to a significant dampening of sympathetic output and reduced emotional experiencing, resulting in the secondary dissociative symptoms. Increased activation of medial prefrontal structures is in effect a hyper-inhibition of the limbic areas, leading to a pathological downgrading of emotion. Thus Cortico-limbic inhibition (excessive or failure of) is one of the underlying responses to trauma. The Medial prefrontal cortex has dense connections to the Amygdala and lower areas which are mostly inhibitory. Lack of inhibition leads to impulsivity, tics, OCD, rage and PTSD, since subcortical impulses are released.
Hollander (1992) found increased low frequency (theta) in the EEG in the left temporal lobe of primary dissociative (or over-aroused) sufferers which is not the case in the EEG's of normal individual's. Low activity in any brain area means less blood flow and less ability to fulfil the function associated with that area. This is where neurofeedback can provide specific intervention.
Trauma is also associated with a wide range of memory deficits, which can be conceived of post-traumatic brain damage. Declarative memory (i.e. of facts or lists) is mediated by the hippocampus in the temporal lobe and is smaller in PTSD depending on the severity and length of abuse experienced. Nondeclarative memory (like riding a bike, conditioned responses) is also affected and there is a significant increase in perseverative errors attributed to frontal lobe dysfunctionning. Gaps in memory (dissociative amnesia) are typical and of course affect recall of abuse.
International 10-20 electrode placement system.
Neurofeedback attempts to stabilize the left and right hemisphere by training at C3 C4 (see the 10/20 system) which affects thalamus generators and bipolar training C3-Fz and C4-Pz - for regulating amplitude and phase - i.e. timing. Thus arousal, stabilisation and control of brainwaves is encouraged. This is generally thought to be achieved by training 12-15 Hertz at Fp1 - Fp2 for inhibition, frontal sites for calming the fear network. Lower and higher frequencies are always inhibited (not rewarded) 2-8 Hz and 21 plus hertz. Some therapists adjust Hertz by Hertz until the client improves but not all clients can recognise or report changes towards agitation or relaxation, so therapists monitor progress with a symptoms list.
Once the brain is more stabilized neurofeedback therapists change their neurofeedback protocols to Alpha-Theta where the brain is conditioned to bring the alpha brainwaves down to crossover with theta amplitude. This is held to promote deep state change and has been shown to affect the default mode network (Ros, 2013). Because dissociation is an adaptive coping mechanism for abused and traumatized people and seems to be associated with excessive amplitude of Alpha, the training down of the Alpha rhythms needs highly experienced trauma counsellors. Abreactions must be expected but this is the time when counsellors have at last their client in a state that enables them to listen, link their past experience to present behaviour and finally come to terms with it.
Areas of the brain that are not developed mean that self-reflection, self-care and self-understanding are minimal while the areas of the brain mediating alertness, anger, fear are overdeveloped. So the brain is disorganised and PTSD victim can't think clearly, express themselves rationally or relate to people - all they experience is fear and shame. So the pathway from lowering arousal moves to recovering themselves, coming to terms with the past and developing an identity that is at peace with itself. Van der Kolk (1996) and others suspect that the Default Mode Network is that final stage.

o In the first stage of treatment (stabilization), Ruth Lanius (2005) says focus on enhancing emotional awareness and enhancing capacity for emotion regulation helps victims set boundaries so they can feel safe within their body.

o By the end of that phase of treatment, the individual now has words for their feelings, knows what they're feeling, has some skills to regulate their feelings, is more self-compassionate towards themselves and can be mindful of the moment - not pulled into the past or future, but that they can be in the present. As a result of all this, they should be able to have more constructive and safer interpersonal relationships.

o Once the therapist has established that form of safety, they focus on the traumatic memories; help people put these memories into the past so they are no longer flooded by them through exposure-based techniques - either in vivo exposure or in narrative storytelling by writing about their traumatic experience as well as Alpha-Theta neurofeedback.

Sequence of neurofeedback therapy for PTSD

1) Stabilisation of arousal to a "window of tolerance". This may require Biofeedback or heart rate variability (HRV) training, first - so an assessment of arousal is important

2) For neurofeedback balancing the brain rhythms - C3-C4, then frontal sites to calm down the fear network, FP1-Fp2 (stopping and thinking) F3-F4 (motor initiation/sequencing) verbal expression (F7-F8) all as necessary.

3) Cz (cingulate - monitors discrepancies between current state and desired state and initiates behaviour to improve state

4) Then going beyond to reconnect to self - Alpha/Theta

The great advantage of Neurofeedback over other forms of therapy is that it avoids the re-traumatization and helps suffers who cannot or will not talk about their experience. When many people with untreated PTSD talk about it they are re-traumatized. Much of their present reality is filtered through their past experience. Talk therapy lacks effectiveness with this population because they can't talk about it without re-experiencing it. The limbic suppressors will even deny it, or pretend they're over it, so as not to be re-traumatized. Busy therapists may also shrink from the terrible experiences (torture) and agree, they are cured! So Neurotherapy, having no expectations of talking is ideal for them. The therapist just monitors - gives guided visualisations and the client, seeded with the visualisations experiences what they need to erode their symptoms. Their subconscious knows their limits and doesn't overload them. Often they may have dreams the evening after their neurofeedback session which they can be prepared for, and can also be examined, talked about and "put to bed" in the next session.


"The Polyvagal Theory" by Steve Porges
"Creating Healthy Relationships" with Dr. John Gottman and Deborah Rozman
Bremmer J.D., (1999) "Acute and chronic responses to psychological trauma: where do we go from here", American Journal of Psychiatry, 156(3), 349-351 (suggests that Primary dissociation is the re-experieicing hyperarousal commonly assocatiated with flashbacks, nightmares, unbidden recollections while secondary dissociation is the numbness, amnesia, detachment states, deperonalisation, deralisation, freezing, analgesic responses which are distancing oneself from emotional experience).
Ros T, Théberge J, Frewen PA, Kluetsch R, Densmore M, Calhoun VD, (2013), "Mind over chatter: Plastic up-regulation of the fMRI salience network directly after EEG neurofeedback", Neuroimage. 2013 Jan 15;65:324-35.
Van der Kolk B.A. Pelcovitz D, Roth S, (1996). "Dissociation, somatization, and affect regulation: the complexity of adaptation to trauma", American Journal of Psychiatry, 153, 83-93
Lanius R.A. Williamson PC Bluhm, (2005), "Functional connectivity of dissociative responses in PTSD: a functional magnetic resonance imaging investigation", Biological Psychiatry, 57, 873-884
Hollander E., Carrasco J Mullen L et al (1992) "Left hemisphere activation in Depersoalisation Disorder; A case report" Biological Psychiatry, 31, 1157 - 1162
Hopper JW, Frewen PA van der Kolk BA (2007), "Neural correlates of re-experieincing, avoidance, and dissociation in PTSD. Symptom dimensions and emotional dysregualtion in responses to script driven trauma imagery", Journal of Trauma and Stress, 20, 713-725
Pentagon’s Brain-Powered Videogames Might Treat PTSD
Is PTSD A Product of War, or Of Our Times?
How long has PTSD been around? Is the response to trauma outlined in our current PTSD diagnosis something that has long happened to a subset of people facing trauma? Or did our current concept of PTSD rise from cultural and medical concerns and definitions peculiar to a particular time in history?


Tuning pathological brain oscillations with neurofeedback: a systems neuroscience framework.
Ros T, J Baars B, Lanius RA, Vuilleumier P.
Front Hum Neurosci. 2014 Dec 18;8:1008. doi: 10.3389/fnhum.2014.01008. eCollection 2014.
Neurofeedback (NFB) is emerging as a promising technique that enables self-regulation of ongoing brain oscillations. However, despite a rise in empirical evidence attesting to its clinical benefits, a solid theoretical basis is still lacking on the manner in which NFB is able to achieve these outcomes. The present work attempts to bring together various concepts from neurobiology, engineering, and dynamical systems so as to propose a contemporary theoretical framework for the mechanistic effects of NFB. The objective is to provide a firmly neurophysiological account of NFB, which goes beyond traditional behaviorist interpretations that attempt to explain psychological processes solely from a descriptive standpoint whilst treating the brain as a "black box". To this end, we interlink evidence from experimental findings that encompass a broad range of intrinsic brain phenomena: starting from "bottom-up" mechanisms of neural synchronization, followed by "top-down" regulation of internal brain states, moving to dynamical systems plus control-theoretic principles, and concluding with activity-dependent as well as homeostatic forms of brain plasticity. In support of our framework, we examine the effects of NFB in several brain disorders, including attention-deficit hyperactivity (ADHD) and post-traumatic stress disorder (PTSD). In sum, it is argued that pathological oscillations emerge from an abnormal formation of brain-state attractor landscape(s). The central thesis put forward is that NFB tunes brain oscillations toward a homeostatic set-point which affords an optimal balance between network flexibility and stability (i.e., self-organised criticality (SOC)).

Plastic modulation of PTSD resting-state networks and subjective wellbeing by EEG neurofeedback.
Kluetsch RC, Ros T, Théberge J, Frewen PA, Calhoun VD, Schmahl C, Jetly R, Lanius RA.
Acta Psychiatr Scand. 2014 Aug;130(2):123-36. doi: 10.1111/acps.12229. Epub 2013 Nov 25.
Electroencephalographic (EEG) neurofeedback training has been shown to produce plastic modulations in salience network and default mode network functional connectivity in healthy individuals. In this study, we investigated whether a single session of neurofeedback training aimed at the voluntary reduction of alpha rhythm (8-12 Hz) amplitude would be related to differences in EEG network oscillations, functional MRI (fMRI) connectivity, and subjective measures of state anxiety and arousal in a group of individuals with post-traumatic stress disorder (PTSD).
METHOD: Twenty-one individuals with PTSD related to childhood abuse underwent 30 min of EEG neurofeedback training preceded and followed by a resting-state fMRI scan.
RESULTS: Alpha desynchronizing neurofeedback was associated with decreased alpha amplitude during training, followed by a significant increase ('rebound') in resting-state alpha synchronization. This rebound was linked to increased calmness, greater salience network connectivity with the right insula, and enhanced default mode network connectivity with bilateral posterior cingulate, right middle frontal gyrus, and left medial prefrontal cortex.
CONCLUSION: Our study represents a first step in elucidating the potential neurobehavioural mechanisms mediating the effects of neurofeedback treatment on regulatory systems in PTSD. Moreover, it documents for the first time a spontaneous EEG 'rebound' after neurofeedback, pointing to homeostatic/compensatory mechanisms operating in the brain.

Distinct intrinsic network connectivity patterns of post-traumatic stress disorder symptom clusters.
Tursich M, Ros T, Frewen PA, Kluetsch RC, Calhoun VD, Lanius RA.
Acta Psychiatr Scand. 2015 Jan 9. doi: 10.1111/acps.12387
Post-traumatic stress disorder (PTSD) is considered a multidimensional disorder, with distinct symptom clusters including re-experiencing, avoidance/numbing, hyperarousal, and most recently depersonalization/derealization. However, the extent of differing intrinsic network connectivity underlying these symptoms has not been fully investigated. We therefore investigated the degree of association between resting connectivity of the salience (SN), default mode (DMN), and central executive (CEN) networks and PTSD symptom severity.
METHOD: Using resting-state functional MRI data from PTSD participants (n = 21), we conducted multivariate analyses to test whether connectivity of extracted independent components varied as a function of re-experiencing, avoidance/numbing, hyperarousal, and depersonalization/derealization.
RESULTS: Hyperarousal symptoms were associated with reduced connectivity of posterior insula/superior temporal gyrus within SN [peak Montréal Neurological Institute (MNI): -44, -8, 0, t = -4.2512, k = 40]. Depersonalization/derealization severity was associated with decreased connectivity of perigenual anterior cingulate/ventromedial prefrontal cortex within ventral anterior DMN (peak MNI: 8, 40, -4; t = -3.8501; k = 15) and altered synchrony between two DMN components and between DMN and CEN.
CONCLUSION: Our results are consistent with prior research showing intrinsic network disruptions in PTSD and imply heterogeneous connectivity patterns underlying PTSD symptom dimensions. These findings suggest possible biomarkers for PTSD and its dissociative subtype.

Alpha-theta brainwave neurofeedback training: an effective treatment for male and female alcoholics with depressive symptoms.
Saxby E, Peniston EG.
J Clin Psychol. 1995 Sep;51(5):685-93.
This was an experimental study of 14 alcoholic outpatients using the Peniston and Kulkosky (1989, 1991) brainwave treatment protocol for alcohol abuse. After temperature biofeedback pretraining, experimental subjects completed 20 40-minute sessions of alpha-theta brainwave neurofeedback training (BWNT). Experimentally treated alcoholics with depressive syndrome showed sharp reductions in self-assessed depression (Beck's Depression Inventory). On the Millon Clinical Multiaxial Inventory-I, the experimental subjects showed significant decreases on the BR scores: schizoid, avoidant, dependent, histrionic, passive-aggression, schizotypal, borderline, anxiety, somatoform, hypomanic, dysthmic, alcohol abuse, drug abuse, psychotic thinking, and psychotic depression. Twenty-one-month follow-up data indicated sustained prevention of relapse in alcoholics who completed BWNT.

Alpha-theta brainwave training and beta-endorphin levels in alcoholics.
Peniston EG, Kulkosky PJ.
Alcohol Clin Exp Res. 1989 Apr;13(2):271-9.
An alpha-theta brainwave biofeedfack training program was applied as a novel treatment technique for chronic alcoholics. Following a temperature biofeedback pretraining phase, experimental subjects completed 15 30-min sessions of alpha-theta biofeedback training. Compared to a nonalcoholic control group and a traditionally treated alcoholic control group, alcoholics receiving brainwave training (BWT) showed significant increases in percentages of EEG record in alpha and theta rhythms, and increased alpha rhythm amplitudes. Alcoholics receiving BWT showed a gradual increase in alpha and theta brain rhythms across the 15 experimental sessions. These experimentally treated alcoholics showed sharp reductions in self-assessed depression (Beck's Depression Inventory) compared to the control groups. Alcoholics receiving standard medical treatment (abstinence, group psychotherapy, antidepressants) showed a significant elevation in serum beta-endorphin levels at the conclusion of the experiment. This neuropeptide is an index of stress and a stimulant of caloric (e.g., ethanol) intake. Application of brainwave treatment, a relaxation therapy, appears to counteract the increase in circulating beta-endorphin levels seen in the control group of alcoholics. 13-month follow-up data indicate sustained prevention of relapse in alcoholics that completed alpha-theta brainwave training.

Alpha-Theta Brainwave Neuro-Feedback for Vietnam Veterans with Combat Related Post-Traumatic Stress Disorder
Peniston EG, Kulkosky PJ.
Medical PsychorIherapy 1991, Volume 4, pp. 47-60
An experimental group of 20 male Vietnam combat veterans with a diagnosis of Post Traumatic Stress Disorder (PTSD) and alcohol abuse were treated with alpha-theta Brainwave Neuro-feedhack Therapy (BWNT). A four channel EEG, video screen and ...

EEG alpha-theta brainwave synchronization in Vietnam theater veterans with combat-related post-traumatic stress disorder and alcohol abuse
EG Peniston, DA Marrinan, WA Deming, PJ Kulkosky
Advances in Medical Psychotherapy 6.7 (1993): 37-50.

Alcoholic personality and alpha-theta brainwave training
EG Peniston, PJ Kulkosky
Medical Psychotherapy, 3, 37-55. 1990

EEG brainwave training as a bio-behavior intervention for Vietnam combat-related PTSD.
Peniston EG
The Medical Psychotherapist. 1990, 6(2), Spring.

Regarding the database for the Peniston alpha-theta EEG biofeedback protocol.
Graap K, Freides D.
Appl Psychophysiol Biofeedback. 1998 Dec;23(4):265-72; 273-5.
Five papers by Peniston and colleagues, which constitute the basic literature for alpha-theta EEG biofeedback treatment for alcoholism and posttraumatic stress disorder, are reviewed. As a result, we raise three questions: (a) Are the samples studied independent? (b) What was the clinical status of the participants prior to treatment? (c) What treatment did the participants actually receive? In seeking answers to these questions we aim to strengthen the database for neurofeedback with specific procedural information so that claims of efficacy can be tested and accepted or rejected on an objective basis.

Neurofeedback with anxiety and affective disorders
D. Corydon Hammond
Child and Adolescent Psychiatric Clinics of North America Volume 14, Issue 1, January 2005, Pages 105–123
Compelling evidence exists for a neurophysiologic basis for obsessive-compulsive disorder (OCD). A large number of positron emission tomographic and single photon emission computed tomographic studies have found increased blood flow and metabolism in the mediofrontal, anterior cingulate, right frontal, or orbitofrontal areas [1–14], which implicates a cortico-striato-thalamocortical network. Functional abnormalities also have been documented in a large number of quantitative EEG (qEEG) studies [15–22] and evoked potential studies [23–27]. OCD seems to be somewhat heterogeneous, however, with at least two qEEG subtypes that have been found [17–21]. Prichep et al [20] and Kuskowski et al [15] found a group with excess alpha brain waves throughout most of the head, with frontal excess beta, whereas another subgroup has an excess of theta activity, particularly in frontal and posterior temporal areas. Clinical experience in conducting qEEG assessment with patients with OCD also has shown that excess beta activity is often found along the midline, in cortical areas approximately over the anterior cingulate.

Neurofeedback and Biofeedback for Mood and Anxiety Disorders: A Review of the Clinical Evidence and Guidelines – An Update [Internet].
Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2014 Aug.
Patients with mental health disorders usually require pharmacological and/or psychological interventions such as cognitive-behavioral therapy. However, patients may not have easy access to such treatments, especially for those living in rural areas, or may not respond well to them. For example, approximately two-thirds of patients with major depressive disorder do not have adequate responses to pharmacological and/or psychological interventions. Biofeedback therapies are non-pharmacological treatments that use non-invasive electrical devices with bio-monitoring system and sensors to measure, amplify and feed back information primarily from nervous system processes such as respiration, heart rate, muscle tension, skin temperature, blood flow and blood pressure, to the individual being monitored, thus promoting awareness of these processes in an individual to assist with gaining voluntary control over body and mind. Neurofeedback is a specific form of biofeedback that monitors central nervous system activity via the measurement and regulation of brainwave activity from electrodes placed on the scalp. Training with neurofeedback aims to enable the individual to modify patterns of cortical activity and normalize brain activity. In general, biofeedback and neurofeedback are designed to increase patients’ coping skills for their current situations, and usually multiple sessions of treatment are required. This report was undertaken to update a previous summary of the evidence on the clinical effectiveness and safety of neurofeedback and biofeedback which was completed in 2012. In that report, findings from preliminary analyses raised the possibility that biofeedback and neurofeedback may have a potential for the treatment of post-traumatic stress disorder (PTSD), generalized anxiety disorder (GAD) or depression.

Neurofeedback: an integrative treatment of substance use disorders.
Ross SM.
Holist Nurs Pract. 2013 Jul-Aug;27(4):246-50. doi: 10.1097/HNP.0b013e3182971b7c.
Substance use disorders are exceedingly complicated as is the treatment. To increase positive outcomes, an understanding of all facets, bio/psycho/social/spiritual,economic, and interdisciplinary aspects, are essential to successful treatment. Neurofeedback has been applied successfully as an integrative treatment of SUDs for more than 30 years. Highlighted research that includes the Peniston Alpha-Theta protocol and Scott-Kaiser modifications of the Peniston protocol has shown that SUD treatment when combined with conventional treatment has the potential to improve measurable parameters and significantly increase positive outcomes.

Peak high-frequency HRV and peak alpha frequency higher in PTSD.
Wahbeh H, Oken BS.
Appl Psychophysiol Biofeedback. 2013 Mar;38(1):57-69. doi: 10.1007/s10484-012-9208-z.
Posttraumatic stress disorder (PTSD) is difficult to treat and current PTSD treatments are not effective for all people. Despite limited evidence for its efficacy, some clinicians have implemented biofeedback for PTSD treatment. As a first step in constructing an effective biofeedback treatment program, we assessed respiration, electroencephalography (EEG) and heart rate variability (HRV) as potential biofeedback parameters for a future clinical trial. This cross-sectional study included 86 veterans; 59 with and 27 without PTSD. Data were collected on EEG measures, HRV, and respiration rate during an attentive resting state. Measures were analyzed to assess sensitivity to PTSD status and the relationship to PTSD symptoms. Peak alpha frequency was higher in the PTSD group (F(1,84) = 6.14, p = 0.01). Peak high-frequency HRV was lower in the PTSD group (F(2,78) = 26.5, p < 0.00005) when adjusting for respiration rate. All other EEG and HRV measures and respiration were not different between groups. Peak high-frequency HRV and peak alpha frequency are sensitive to PTSD status and may be potential biofeedback parameters for future PTSD clinical trials.

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