For Posttraumatic stress disorder
Dr Beverley Steffert,
Chartered Psychologist, Neuropsychologist,
British Psychological Society,
Email: b.steffert at mail.bbk.ac.uk
Email: DrSteffert at learningrecovery.co.uk
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.
run workshops on Neurofeedback For Posttraumatic stress
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
|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.
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
|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
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
|Sequence of neurofeedback therapy for
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
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
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.
Polyvagal Theory" by Steve Porges
Healthy Relationships" with Dr. John Gottman and Deborah
|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
|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
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.
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
|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.
OBJECTIVE: 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
OBJECTIVE: 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
|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
|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
|Alpha-Theta Brainwave Neuro-Feedback for Vietnam
Veterans with Combat Related Post-Traumatic Stress
|Peniston EG, Kulkosky PJ.
|Medical PsychorIherapy 1991, Volume 4,
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):
|Alcoholic personality and alpha-theta brainwave
|EG Peniston, PJ Kulkosky
|Medical Psychotherapy, 3, 37-55. 1990
|EEG brainwave training as a bio-behavior intervention
for Vietnam combat-related PTSD.
|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;
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,
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  and Kuskowski et al  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
|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.
|Holist Nurs Pract. 2013 Jul-Aug;27(4):246-50.
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.
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.