Running head: NEUROFEEDBACK & PTSD 1

Neurofeedback as an Alternative Treatment for Posttraumatic Stress Disorder

Gabrielle McClure

Saint Martin’s University

NEUROFEEDBACK & PTSD 2

Abstract

Neurofeedback has been put through several thousand clinical studies in relation to the diagnosis

and treatment of mental disorders such as ADHD, drug use and abuse, anxiety, depression, OCD,

brain injury, and others. Though PTSD is one of the lesser-researched disorders in relation to

neurofeedback, there are several studies that relate to the positive effects that neurofeedback has

on relieving neurological symptoms of PTSD such as uncontrollable emotional reaction related

to trauma memory recall. Neurofeedback is used on delta, theta, alpha, beta, and gamma

brainwave frequencies that can impede emotional and attentional control in the frontal cortex as

well as overall physical and cognitive relaxation. Sessions of neurofeedback range from 20 to 30

minutes and significant improvements in cognitive function begin between 5 and 10 sessions, on

average. Neurofeedback has been utilized to measure amygdala regulation in relation to

traumatic memory recalls as well as comparing brain maps of patients with PTSD to those

without in resting states to learn the overall effect that PTSD has on the brains average

functioning. Studies surrounding the implementation of neurofeedback as a diagnostic tool, as

well as an alternative treatment for PTSD, used control groups to determine positive effects on

the patient’s brains, as well as compared overall effectiveness to common medications and

psychotherapies used for the diagnosis. Neurofeedback was found to have substantial effects on

the re-regulation of EEG frequency bands in patients with diagnosed PTSD in areas that control

attention, emotion regulation, and anxiety, among other symptoms.

Keywords: Neurofeedback, PTSD, brainwave, treatment, delta, alpha, theta, beta, gamma
NEUROFEEDBACK & PTSD 3

Neurofeedback as an Alternative Treatment for Posttraumatic Stress Disorder

As of 2016, there have been over 2,000 peer reviewed scientific studies published on the

effectiveness of neurofeedback treatment for many different disorders in the Diagnostic and

Statistical Manual of Mental Disorders (DSM-V) (American Psychiatric Association [APA],

2013; Bessel et al., 2016). Neurofeedback has been around since the 1960’s and has progressed

through many forms of biofeedback into the electroencephalographic (EEG) biofeedback

commonly used today in the diagnosis and treatment of several disorders such as attention-

deficit/hyperactivity disorder (ADHD)- one of the most researched within the field (Hammond,

2011). Neurofeedback continues to develop its scientific basis as it branches into research

involving disorders such as depression, anxiety, and posttraumatic stress disorder (PTSD)

(Hammond, 2011). Research into the diagnostic and treatment capability of neurofeedback in

regards to PTSD began in the 1990’s, and after significant results were discovered demonstrating

its efficacy in utilizing neurofeedback as a tool for treatment of emotional-control related

symptoms, it has only expanded in scientific culpability since (Penniston & Kulkosky, 1991). A

metanalysis of PTSD treatments in 2016 revealed that less than half of patients with PTSD who

seek out treatment find their symptoms notably reduced during the process; the need for a more

effective treatment of PTSD symptoms is an inescapable issue when the disorder impacts up to

3.5% of all American’s with an estimated lifetime risk of 8.7% (APA, 2013; Gapen et al., 2016;

Gerin et al., 2016). As of 2019, a literature analysis of all data relating to the use of

neurofeedback as a treatment and diagnostic tool for clinically diagnoseable PTSD demonstrates

the efficacy of neurofeedback as an alternative treatment option for PTSD symptoms listed in the

DSM-V (APA, 2013; Chiba et al., 2019; Fragedakis & Toriello, 2014; Reiter, Andersen, &

Carlsson, 2016).
NEUROFEEDBACK & PTSD 4

Posttraumatic Stress Disorder

Diagnostic Criteria

The DSM-V states that a diagnosis of PTSD requires an individual to have directly, or

indirectly, been exposed to “actual or threatened death, serious injury, or sexual violence” (APA,

p. 271), have at least one intrusive symptom associated with the traumatic event that surfaces

following the event(s) (APA, 2013), present with avoidance of “stimuli associated with the

traumatic event(s)” (APA, p. 271), have “negative alterations in cognitions and mood associated

with the traumatic event(s)” (APA, p. 271), as well as displaying “marked alterations in arousal

and reactivity associated with the traumatic event(s)” (APA, p. 272) in question. All symptoms

must also be present for the duration of one month, or more (APA, 2013).

Aforementioned criteria can be indicated through an increased arousal of the sympathetic

nervous system, an alteration that can cause difficulty falling or staying asleep, difficulty

concentrating, hyper-vigilance, exaggerated startle response, and outbursts of anger (Wahbeh &

Oken, 2013). In fact, over 70% of patients diagnosed with PTSD report severe sleep disturbances

that generally present as feelings of restlessness as well as nightmares that relate to the traumatic

event(s) (Modarres, Opel, Weymann, & Lim, 2019). Physical symptoms such as increased heart

rate, decreased heart rate variability (HRV), and increased blood pressure may also emerge in

patients with PTSD diagnoses (Modarres et al., 2013). The reason that traumatic event(s)

produce such symptoms is attributable to the intense fear, helplessness, or horror that the patient

emotes during exposure to the traumatic event(s) (Modarres et al., 2013). These symptoms can

cause an overall impacted quality of life in patient’s due to lower life satisfaction, objective

living conditions, and poorer functioning (Modarres et al., 2013). The symptoms of PTSD also
NEUROFEEDBACK & PTSD 5

frequently increase suicidal behaviors such as ideation and suicide attempts (Modarres et al.,

2013).

Etiology

The highest rates of PTSD are found in survivors of rape, people involved in military

combat and captivity, individuals contained under genocidal intentions, and those whose career

involves exposure to traumatic events and their aftermath (APA, 2013). Epidemiologic studies

have determined that about 56% of people will experience a mentally traumatic event in their

lifetime, while roughly 7-12% of those individuals will meet the diagnostic criteria for PTSD

following the event(s) (Modarres et al., 2019). While nearly 50% of adults recover from PTSD

symptoms within the first three months following the traumatic event(s), the other half can

sustain their diagnosis for anywhere between 12 months to well over 50 years (APA, 2013;

Wahbeh & Oken, 2013). The DSM-V also lists pre-traumatic factors that may positively affect

the risk and severity of PTSD onset; these factors include previous mental disorders, negative

environmental influences such as racial status, lower socioeconomic status, and exposure to prior

trauma, and finally discuss genetic factors such as gender and age that may affect the level of

emotional reaction to later traumatic events (APA, 2013; Begić, Hotujac, & Jokić-Begić).

Demographics

Within the United States, PTSD is diagnoseable in approximately 7.7 million (3.5%)

Americans and is particularly present in the veteran community (APA, 2013; Wahbeh & Oken,

2013). About 30.9% of Vietnam veterans have reported PTSD symptoms post-service in the past

and currently, as many as 50% of veterans who are screened for PTSD symptoms on return are at

a diagnoseable level (Wahbeh & Oken, 2013). Up to 19% of these U.S. veterans have a lifetime

prevalence of PTSD symptoms (Modarres et al., 2019). People diagnosed with PTSD face a risk
NEUROFEEDBACK & PTSD 6

of developing chronic symptoms, comorbid disorders, and functional impairment which raise the

overall lifetime cost of each individual in the public health fund (Wahbeh & Oken, 2013).

Treatments

Due to the complex psychopathology as well as common comorbid disorders, PTSD is

one of the more difficult disorders to treat; the low retention rate for main-lined treatment plans

are also lower than statistically desired (Wahbeh & Oken, 2013). Current PTSD diagnoses rely

on patient self-report measures as well as assessments done by clinicians- there is currently no

neurological basis of assessing brain function and severity of PTSD symptoms, which are an

important process in determining the severity of necessary treatment(s) as well as the

neurological effects and growth that the treatment may employ (Modarres et al., 2019). This

neurological observance would also air in reducing post-treatment relapses of PTSD symptoms

by understanding their biological basis as well as determining if the client has the mental support

to keep such symptoms carefully controlled and monitored (Modarres et al., 2019). Metanalyses

of current psychological treatments for PTSD reveal that less than half of people who seek

treatment receive significant improvements in symptomology while the majority continue to

have diminished, yet still present, symptoms post-treatment (Gapen et al., 2016; Gerin et al.,

2016). There is also a sizeable number of patients who drop-out of trauma-focused treatment,

while some subgroups of patients show an increased treatment-resistance as well as decreased

treatment-retention following, or during, continued care (Gerin et al., 2016).

The two major treatments for PTSD are psychotherapy and medication, or a combination

of the two. Trauma-focused psychotherapy has some of the most clinically supported evidence

for treating PTSD symptoms within present research and appears to be the most promising

treatment approach overall (Gerin et al., 2016; Wahbeh & Oken, 2013). Pharmaceuticals are also
NEUROFEEDBACK & PTSD 7

a favorable clinical treatment for symptoms of PTSD, though additional research is needed due

to the shortage of evidence suggesting a sustainable loss of PTSD diagnoses and symptoms in

patients (Wahbeh & Oken, 2013; Gapen et al., 2016). Pharmacological treatments have

demonstrated a lesser response in treatment of PTSD and as of 2016, only two medications have

FDA approval for PTSD treatment- both are selective serotonin re-uptake inhibitors (SSRIs)

(Gerin et al., 2016). The military subgroup of patients with PTSD also have demonstrated a

diminished response to these medications as compared to other groups with the diagnosis (Gerin

et al., 2016).

Neurofeedback

History/Origin

According to Hammond (2011), neurofeedback was first discovered in the 1960’s

through an animal-based research program where alpha brainwave activity was altered with the

purpose of increasing relaxation in subjects. There are five main brainwave frequencies, or EEG

bands, named delta (1-3 Hz), theta (3.5-7 Hz), alpha (7.5-13 Hz), beta (13.5-30 Hz), and gamma

(>30 Hz)- from lowest to highest hertz (Hz) (Hammond, 2011; Jokić-Begić & Begić, 2003;

Modarres et al., 2019). Gamma brainwaves are closely associated with focused attention and

information processing, beta waves are linked with intellectual activity as well as outward

concentration, alpha waves are related with relaxation, theta waves are tied to daydream-like

dissociative states of calm, and delta waves are generally seen in deep sleep with a total lack of

awareness (Hammond, 2011). In the case of ADHD, it is common to find excessively slow

waves present in the frontal regions of the brain, making it difficult to control attention, behavior,

and emotions which result in issues with concentration, impulse control, and hyperactivity

among others (Hammond, 2011).

NEUROFEEDBACK & PTSD 8

Neurofeedback is implemented through electrodes positioned on the scalp in placements

that are most beneficial to monitoring specific regions while the equipment delivers real-time

feedback about the patient’s brainwave activity with the purpose of providing awareness over a

typically uncontrollable system (Hammond, 2011). Through this brainwave training, patients are

equipped to influence and alter their brainwave patterns, eventually achieving a sustained

neurological improvement from continuous practice, i.e. operant conditioning (Bessel et al.,

2016; Hammond, 2011). Research into neurofeedback suggests that 75 to 80% of the time

significant improvements in activity occur and prevail through relapses just as a torn muscle

might in physical therapy (Hammond, 2011). In this way, neurofeedback is an excellent option

for treating, and recovering from, endogenous disorders where medication was previously the

sole primary treatment available (Hammond, 2011). Significant improvements usually begin to

appear between 5 to 10 sessions and treatment commonly lasts between 15 and 20 sessions but

some individuals can continue through 30 to 50 depending on the severity of the disorder- each

session lasts between 20 and 25 minutes on average (Hammond, 2011).

While the baseline method of neurofeedback revolves around EEG biofeedback, there are

several specialized types of neurofeedback (Hammond, 2011). Slow cortical potentials training

revolves around the “positive or negative polarizations of the EEG in the very slow frequency

range from .3 Hz to usually about 1.5 Hz”; this baseline covers cognitive processing involved in

seizures, migraines, and ADHD symptoms (Hammond, pp. 308-9). The low energy

neurofeedback system (LENS) observes the feedback of non-dominant brainwaves with an

extremely small electromagnetic field and has proven to help anger, anxiety, depression,

fibromyalgia, restless legs syndrome, insomnia, and more (Hammond, 2011). Live z-score

neurofeedback training is similar to the standard EEG biofeedback though it combines observed
NEUROFEEDBACK & PTSD 9

variables from multiple brain functions and compares results to examples of age-appropriate z-

score’s, eventually helping patients adjust neurological functioning towards those goals

(Hammond, 2011). Low resolution electromagnetic tomography (LORETA) provides an

estimation of the locations where problematic EEG frequencies are being generated and though

the process is more labor-intensive, results are more in-depth and hold promise for difficult cases

as well as shortening the overall length of treatment (Hammond, 2011). Finally, functional MRI

neurofeedback (fMRI) is a system that evaluates brain functioning in deep subcortical areas of

the brain though information on it is scarce due to its expensive nature; the fMRI’s ability to

target localized areas of the brain that are unreachable with EEG holds a very promising future of

enhanced neurofeedback practice(s) (Gerin et al., 2016; Hammond, 2011).

When conducting an overall evaluation of an individual’s brainwave functioning using

neurofeedback, the quantitative electroencephalogram (QEEG)- a complete brain map comprised

of 19 or more electrodes placed on the scalp- is a favorable option (Hammond, 2011). The

procedure usually lasts an hour or more and uses EEG information collected to compare overall

functioning to another healthy neurological example that is based on the same age of the patient

to discuss how functioning may significantly differ from the example’s and what that may

predict (Hammond, 2011). There have been considerable studies published surrounding the use

of the QEEG and its accuracy in evaluation of diagnoses and predicting further treatment

interventions in disorders such as ADHD, traumatic brain injury, obsessive/compulsive disorder

(OCD), autism spectrum disorder (ASD), learning disabilities, panic disorder, drug abuse,

anxiety, as well as multiple other conditions (Hammond, 2011).

NEUROFEEDBACK & PTSD 10

Efficacy of Neurofeedback as a Treatment

Anxiety. Numerous studies have been conducted surrounding the efficacy of

neurofeedback as a treatment for anxiety symptoms, many of which achieving largely positive

results (Hammond, 2011). In 1997, Passini, Watson, Dehnel, Herder, and Watkins founded a

study that focused on alcoholics with anxiety symptoms and found significant improvements in

anxiety levels that were sustained through an 18-month follow-up. Another study done in 2003

by Egner and Gruzelier followed musicians with performance anxiety and compared

neurofeedback treatment to that of physical exercise as well as other mental trainings prior to

performance and they noticed that the neurofeedback group was the only set that resulted in

performance enhancement- similar studies conducted in 2005 and 2008 found matching results

(Kleber, Gruzelier, Bensch, & Birbaumer, 2008; Leach, Holmes, Hirst, & Gruzelier, 2008;

Raymond, Sajid, Parkinson, & Gruzelier, 2005). In 2005, a study conducted by Raymond,

Varney, Parkinson, and Gruzelier on medical students discovered that neurofeedback training

can reliably enhance mood states such as confidence levels, feeling composed, or energetic.

ADHD. Since the 1970’s, neurofeedback has been tested, refined, and researched

regarding ADHD and other learning disabilities (Hammond, 2011). A study in 2006 managed to

document positive adjustments in fMRI scans of the brain as well as behavioral alterations in

children with ADHD who were undergoing neurofeedback treatment, helping to prove the

mirroring effect between neurological and behavioral transformations in people with the disorder

(Levesque, Beauregard, & Mensour, 2006). Neurofeedback has been tested and contrasted with

computerized attention skills training in the treatment of ADHD and ADD and observed as being

more effective in the short and long-term (Gevensleben et al., 2009; Gevensleben et al., 2010;

Strehl et al., 2006). A 1995 study conducted by Lubar performed a 10-year follow-up on
NEUROFEEDBACK & PTSD 11

patient’s post-neurofeedback treatment and found that up to 80% of participants had retained the

neurological and behavioral changes produced through neurofeedback training 10 years prior.

Several studies have also compared 20-30 sessions of neurofeedback training to prescribed doses

of Ritalin and uncovered significant improvements in attention, concentration, and IQ in the

experimental neurofeedback group (Fuchs, Birbaumer, Lutzenberger, Gruzelier, & Kaiser, 2003;

Rossiter, 2005; Rossiter & LaVaque, 1995). One distinct study conducted in 2002 by V. J.

Monastra, Monastra, and George observed neurofeedback to be more effective than Ritalin,

citing the superiority of neurofeedback through the absence of necessary follow-up post-

treatment as happens with prescribed pharmaceuticals. Finally, a meta-analysis done in 2010 by

Arns, de Ridder, Strehl, Breteler, and Coenen found significant data to declare neurofeedback as

a efficacious treatment for ADHD, a crucial step when compared to the meta-analysis done on

prescription treatments for ADHD in 2001 by Schachter, Pham, King, Langford, and Moher that

disclosed significant side-effects of medications, an existing publication bias within the

literature, poor overall quality of scientific findings, and lacking data surrounding long-term

effects- the last claim being backed by a meta-analysis done in 2005 by the Drug Effectiveness

Review Project that revealed a lack of scientifically-proven physical safety in the long-term use

of ADHD medications. In summary, neurofeedback is lacking side-effects, psychological

invasiveness, and is successful as a long-term treatment option (Hammond, 2011).

ASD. A more recent contender for the study of neurofeedback treatment application is

ASD- research has been gradually developing just as other treatments involving ASD continue to

do each year as more is understood about the disorder (Hammond, 2011). A study conducted in

2010 by L. Thompson, Thompson, and Reid examined 150 autism spectrum patients and

observed that 40 to 60 sessions of neurofeedback lead to significant improvements in auditory

NEUROFEEDBACK & PTSD 12

and visual attention, impulsivity, reading, spelling, EEG measurements, as well as an average

growth of 9 IQ points. In another analysis, it was found that there was a total 42% reduction in

overall ASD symptoms as well as a 55% increase in social interaction and communication in

participants (Coben, Linden, & Myers, 2010). Neurofeedback may not a feasible option to cure

autism spectrum symptoms, but it has been proven to reduce and sooth them to a significant

degree (Hammond, 2011).

Depression. Depression and PTSD have several shared symptoms such as changes in

sleeping habits, mood, concentration, feelings of guilt or sadness, as well as biologically altering

the brain (Singh & Gerdes, 2009). Specifically with depression, production of serotonin suggests

involvement of the hippocampus which also controls memory function- something that is

correlated to the cognitive decline often observed in patients with the diagnosis (Singh & Gerdes,

2009). Symptoms of depression were witnessed in multiple studies as being significantly

improved when neurofeedback was used to regulate EEG frequency bands and results were

compared with other treatment control groups to evaluate significance (Choi et al., 2011;

Paquette, Beauregard, & Beaulieu-Prevost, 2009).

Substance use. Past EEG recordings of alcoholics and their genetic children have

displayed a divergence from the standard in their lower alpha and theta bands, as well as larger

beta band activity, which illustrates how prolonged substance use can alter brain chemistry

permanently (Hammond, 2011). Or alternatively, does the altered brain chemistry cause the

addiction? These brainwave alterations make relaxing more difficult than it would normally and

since it has been learned that alcohol intake increases alpha and theta band activity, alcohol is an

easily attainable method of self-medication than provides relaxation in the mind and body

(Hammond, 2011). There have also been studies that have approached the connection between
NEUROFEEDBACK & PTSD 13

excessive beta activity and a heightened threat of relapse in both alcoholics as well as cocaine

addicts (Hammond, 2011).

One particular study led in 1989 by Peniston and Kulkosky used neurofeedback treatment

on a group of chronic alcoholics, as well as a second control group with similar situations who

would receive traditional treatment, and recorded that the original neurofeedback group had an

80% retention rate four years later whereas only 20% of the traditionally treated person’s stayed

sober until that point- similar results were reported on studies done in 1995 and 1997 (Saxby &

Peniston, 1995; Kelly, 1997). Another experiment ran in 2005 by Scott, Kaiser, Othmer, and

Sideroff added neurofeedback to the regimen of 121 substance abuse inpatients and, in a yearly

follow-up, recorded that 77% of the neurofeedback group had continued their therapy regimen

for a significantly longer amount of time and were currently sober, whereas only 44% of the

control group without neurofeedback held their sobriety. Many of these studies also found that

more than just sobriety was affected- mood and overall mental health were also raised on

multiple subscales (Hammond, 2011). A similar study followed 270 homeless cocaine addicts

and recognized that the addition of neurofeedback in regular treatment practices nearly tripled

patients’ length of stay at the recovery center(s), and a yearly follow-up revealed that 53.2%

were both alcohol and drug free whereas 23.4% had used less than three times within the year

(Burkett, Cummins, Dickson, & Skolnick, 2005). They also found that 95.7% of patients had

acquired, and were maintaining, residency, 93.6% were either employed or in school, and 88.3%

had not been arrested in the past year. Neurofeedback helps with more than just addictive

tendencies but also with obsessing, psychosis, aggression, hypochondriasis, interpersonal

sensitivity, and the mental and physical desire to use dangerous substances (Hammond, 2011).
NEUROFEEDBACK & PTSD 14

Neurofeedback has the potential to not only aid standard treatment outcomes, but also reverse the

effect that addictive behaviors and genetics have on brain chemistry (Hammond, 2011).

Neurofeedback & PTSD

Neurofeedback as a Diagnostic tool for PTSD

Since 1941, it has been theorized that PTSD symptoms have a biological basis,

something that can be aided through medication and, theoretically, neurofeedback intervention of

the brain (Peniston, Marrinan, Deming, & Kulkosky, 1993; Singh & Gerdes, 2009). Several

brain-imaging studies have linked the source of PTSD symptoms to altered activity in the

ventromedial prefrontal cortex, amygdala, hippocampus, and the insula (Modarres et al., 2019).

These modified connections also disturb certain brain regions, such as the parietal, temporal, and

central regions of the prefrontal cortex, and prolonged observations of such activities may

eventually lead to ascertaining the severity of PTSD symptoms in patients based on region

variations (Modarres et al., 2019). Though, extreme emotional states can also alter the brainwave

frequencies being observed, especially when correlated with states of arousal- something that is

commonly noted in PTSD patients (Khalily, Clarke, & Jahangir, 2009). Research since the 40’s

has only solidified the theory that PTSD, like numerous other disorders, causes biological

fluctuations and is thus more susceptible to the influence of biologically based treatments

(Modarres et al., 2019).

Regulating the amygdala. Research into the biological factors related to PTSD

symptoms has proposed that symptoms may be caused by a dysfunction of the amygdala (Begić

et al., 2001). Aforementioned symptoms are represented by increased heart rate, blood pressure,

sweating, and facial electromyographic responses (Begić et al., 2001). Data from these studies

also suggests the presence of additional biological symptoms in patients with PTSD such as
NEUROFEEDBACK & PTSD 15

decreased hippocampal volume as well as variances in amygdala functioning (Jokić-Begić &

Begić, 2003). One study conducted by Nicholson et al. (2018) followed the downregulation of

the amygdala and how heightened control may affect emotional processing during reactions to

trauma memories and/or triggers. Their study followed 14 patients with PTSD diagnoses who

underwent three sessions of neurofeedback, focusing on amygdala downregulation while actively

reacting to trauma memory(s). Research discovered that fMRI neurofeedback training focused on

the amygdala was significantly helpful in attaining greater emotional control throughout the

intrinsic connectivity networks (ICN). An older study conducted on similar research also found

successful downregulation of the amygdala to be positively correlated with an increase in

prefrontal emotional regulation control (Nicholson et al., 2016).

Electrical tomographic analysis. The low-resolution electrical tomographic analysis

(LORETA) is a version of EEG software analysis that measures the “voltage potential over the

scalp (raw EEG data)” and uses the information observed to determine the origins of each

specific EEG signal being assessed (Todder et al., p. 49). Overall, LORETA observes the global

EEG output of the brain and uses those measurements, as well as the measurements emanating

from each section of the brain, to calculate the relative contributions of each neuroanatomical

structure (Todder et al., 2012). In a study done by Todder et al, 10 participants with PTSD

diagnoses were asked to sit in a comfortable position for three minutes with closed eyes while

EEG activity was recorded- particularly theta band activity because of its involvement in the

limbic system where particular PTSD symptoms are originated. Through EEG readings no

significant differences between the two groups theta bands were found, but when put through the

LORETA analysis, it was uncovered that the PTSD group held certain distinct patterns in EEG

operations. The LORETA analyses revealed a statistically relevant diminished level of activity in
NEUROFEEDBACK & PTSD 16

the lower theta band (4-5 Hz), especially within the temporal lobe. The higher theta band (6-7

Hz) displayed lower activity on both left and right frontal lobes. These findings suggest that the

LORETA analysis may bring about additional important data pertaining to how PTSD affects the

brain’s operations in patients.

Biofeedback. Neurofeedback is biofeedback technology used on the brain, while

biofeedback itself is focused on bodily measurements such as breathing, heartrate, and

temperature (Wahbeh & Oken, 2013). In one study conducted on 86 participants- 59 veterans

with PTSD and 27 without- involving HRV, it was discovered that the PTSD group held lower

high-frequency (HF) HRV peak frequencies when incorporating respiration analysis as a

covariate (Wahbeh & Oken, 2013). The HF peak of the HRV spectrum is biologically produced

by respiration and though both experimental and control groups held similar respiration rates, the

experimental group’s peak HRV was lower overall in comparison. HF HRV peak frequencies are

also a biological indicator of parasympathetic activity and therefore, a lower peak HF HRV leads

to less parasympathetic activity which can boost sympathetic activity as well as symptoms of

hyper-arousal.

qEEG. Though the qEEG is most frequently applied with schizophrenia and depression,

Begić et al. (2001) was the first to apply it in research concerning PTSD due to its scientific

effectiveness, as well as the high percentage of patients with PTSD they had encountered in their

prior work. This study monitored the qEEG’s of 18 veterans with PTSD as well as 20 healthy

non-veterans for 10 minutes each while patients sat in the supine position with eyes closed.

Though contrasts between the two groups revealed no significant differences in alpha and delta

activity, there were substantial (p < 0.01) differences in beta and theta waves. While theta

activity was increased over central regions of the brain in patients with PTSD, beta activity was
NEUROFEEDBACK & PTSD 17

increased over central, frontal, and left occipital regions of the brain. The explanation for

increased theta activity over central regions may be attributed to regular alterations of the

amygdala and hippocampus in patients with PTSD- such as shrinking or lessened overall

activity. An increase in theta activity over central, frontal, and left occipital lobes might be

influenced by “global cortical hyperexcitability, prolonged wakefulness, or attention

disturbances in PTSD patients” (Begić et al., p. 171).

A follow-up study was done with a group of 116 combat veterans- 79 with diagnosed

PTSD and 37 without PTSD symptoms (Jokić-Begić & Begić, 2003). EEG recording’s in this

experiment failed to present any significant differences between the groups in delta or theta

frequencies, though there were considerable changes in alpha and beta frequencies. In the

veteran group, alpha frequencies were decreased over frontal, central, and occipital regions of the

brain, while beta frequencies were increased over frontal and central regions. Suppressed alpha

frequencies may point to a disturbance of the thalamus in PTSD patients that generally results in

sensory dysregulation symptoms, while the decrease may also point to a deficit in focused

attention (Jokić-Begić & Begić, 2003). An increase in beta activity has been observed in patients

with mania; the increased activity in the people observed in this study may have been attributed

to sleep disturbances, instabilities in attention, cortical hyperexcitability, impaired alertness, or

hyperarousal (Jokić-Begić & Begić, 2003). Following this, increased beta frequencies have also

been proven to positively correlate with restlessness, anxiety, focused attention, and emotional

activation (Jokić-Begić & Begić, 2003).

A separate study conducted by Wahbeh and Oken (2013) measured the EEG of

participants and recorded higher peak alpha frequencies in patients with PTSD, with the right

side of the brain harboring a heightened frequency compared to the left. Using an ANOVA
NEUROFEEDBACK & PTSD 18

analysis, the study discovered that peak alpha frequency was strongly associated with symptoms

of PTSD such as hyper-arousal, numbing or avoidance, and uncontrollable re-experiencing of

traumatic events. Peak alpha frequencies regulate awareness and cognitive vigilance while the

lower brackets cause global relaxation; although, peak alpha frequencies did not vary

significantly when contrasted with all symptoms of PTSD and thus may not be a reliable

measure when determining the overall amount and severity of PTSD symptoms in patients. No

relationship was found between other EEG frequencies in this study.

Resting EEG evaluation. A study conducted by Kluestsch et al. (2014) looked at the

effects on neural connectivity during an individual’s resting state when decreasing the alpha

band within the default mode network (DMN) and the salience network (SN) while also

collecting anxiety and arousal self-report measures before and after neurofeedback training.

Desynchronization of the alpha band has been tied to improved cognitive processing and directed

attention through past research, and it has been validated that a single neurofeedback session of

30 minutes is adequate to plastically alter the functional connectivity of the DMN and SN

(Kluestsch et al., 2014).

Though the t-test’s ran prior and post-training did not present any significant divergence

in feelings of anxiety in subjects, there was a surge in calmness following neurofeedback training

in patients (Kluestsch et al., 2014). In the alpha band’s case, patients were able to greatly reduce

their own alpha frequencies during training, though this was something that resulted in an

opposing increase in alpha band amplitude during resting-state while the second EEG baseline

was being observed. An fMRI scan conducted before and after the neurofeedback training also

revealed improved functional connectivity in the SN in all sections as well as an increase in the

DMN functionality in all sections, except for the right middle temporal gyrus and the posterior
NEUROFEEDBACK & PTSD 19

cingulate cortex (PCC) where connectivity was significantly decreased. In a contrasting study

performed with healthy individuals, it was discovered that there was no correlation between

alpha band desynchronization and a following rebound in resting-state alpha amplitude but

rather, healthy individuals lacked the rebound and retained the lowered alpha frequency. There is

the possibility that increased alpha amplitude base rates may be attributed to the feelings of

relaxation and calmness that generally follow neurofeedback trainings and the disparities in

anxiety states between PTSD and healthy individuals may be the rational for such discrepancies.

Sleeping EEG evaluation. There is a curiosity over the disruptive sleeping tendencies

that individuals with PTSD frequently endure which has spurred numerous studies analyzing the

sleep of patients with diagnosed PTSD and those without; research has produced mixed results

concerning the parallels between sleep efficacy as well as the rapid eye movement (REM)

density in patients (Begić, Hotujac, & Jokić-Begić, 2001). Sleep disturbances of multiple levels

are often reported as a symptom of PTSD and studies done on patients with PTSD often find

sleep disturbances to be closely related with the severity of standard PTSD symptoms (Modarres

et al., 2019). In fact, these studies concluded that the onset of sleep disturbances are typically

within one month following a traumatic event and thus may be a way to predict a later diagnosis

of PTSD (Modarres et al., 2019).

Research conducted by Modarres et al. in 2019 recruited 38 veterans with PTSD and 38

veterans without the diagnosis who were invited to sleep overnight inside the lab where EEG

bands were recorded using the Polysomnography (PSG) method. This study observed precisely

targeted areas of the brain labeled as PTSD-sensitive neuromarkers that were recorded during

both awake and sleeping states and noticed that recordings accurately represented the severity of

PTSD diagnoses when compared with written scales that participants filled out before-hand. The
NEUROFEEDBACK & PTSD 20

analysis surveyed the overall calculation of EEG signals from specified neuromarkers in the

brain to calculate the Brain Coherence Markers (BCM) for each participant; these numbers were

then related to control group scores and it was discovered that those with PTSD diagnoses had

larger BCM markers than controls, something that carried true through both awake and sleep

states.

Neurofeedback as a Treatment for PTSD

Neurofeedback has been demonstrated to positively regulate sleep, mood, memory,

cognition, affect regulation, and sustained attention through the stabilization of EEG activity

(Bessel et al., 2016). Improving affect regulation in clients with PTSD has shown to reduce

symptom severity, decrease risk-taking behaviors, and benefit the effectiveness of future

exposure therapy (Bessel et al., 2016). Common EEG markers of disordered arousal involved in

PTSD are an increased alpha/theta ratio as well as increased cortical activation- both of which

stem from reduced alpha activity (Bessel et al., 2016). Both attentional processes and working

memory are impaired in people with PTSD and both can be attributed to disturbed alpha and

theta brainwaves (Bessel et al., 2016). Treatment has also proven to possess the capability in

increasing functional connectivity across the alertness and salience networks (Gapen et al.,

2016). Neurofeedback focuses on the stabilization of neural regulations rather than the

processing of trauma-related memories that most mainline treatments strive for; thus,

neurofeedback is a procedure that can aid in the regulation of emotional processing and attention

centers of the brain activated throughout trauma-related treatments in a way that supplements

overall effectiveness (Bessel et al., 2016).

BSC. A study done by Singh & Gerdes in 2009 provided eight participants with Brain

State Conditioning (BSC)- a style of EEG neurofeedback- for 4-6 sessions of 90 minutes over 2-
NEUROFEEDBACK & PTSD 21

5 days’ time. Subjects were recruited so that four participants had diagnosed PTSD while the

other four had diagnosed depression. Each group had goals of diminishing symptoms of PTSD as

well as depression symptoms, some of which were identical across groups such as worsened

sleeping habits and poor cognitive performance. Prior to BSC, subjects were given a brain map

as well as distributed opposing PTSD and depression questionnaires to determine mental and

neurological symptoms as well as their severity. Within the PTSD group, all four subjects

reported a reduced PTSD score of 41%, 55%, 64%, and 75% in PTSD symptom severity.

Subjects with depression reported decreased scores between 43% and 95% in their depressive

symptoms as well as a 54% to 100% reduction of anxiety symptom severity. Such a significant

reduction in anxiety scores specifically, as seen in the second group, is a good sign regarding the

reduction of anxiety symptoms that plague PTSD victims.

EEG. The second study ever conducted utilizing biofeedback- or in this case,

neurofeedback- on patients with PTSD was done in 1991 by Penniston & Kulkosky. Utilizing

EEG measurement tools, 29 Vietnam veterans with a history of 12-15 years of chronic PTSD

were selected to have alpha, theta, and beta rhythms trained for thirty 30-minute sessions, five

days a week. This research also utilized multiple versions of biofeedback, such as body

temperature. During sessions, patients were requested to think about past traumatic events during

combat and subsequently instructed on imagining themselves falling into a calm state while

listening and observing audio and visual feedback linked with desired EEG levels. Prior and

post-neurofeedback, both the control and experimental groups were asked to complete the

Minnesota Multiphasic Personality Inventory, and it was revealed that the experimental

treatment group had a significant reduction in scores as well as a larger variation of results from

before and after treatment (Hathaway & Meehl, 1951; Penniston & Kulkosky, 1991). In a
NEUROFEEDBACK & PTSD 22

follow-up study done 30 months later, all 14 of the control group patients had a relapse of

previously lessened PTSD symptoms while only 3 of the 15 in the experimental group had any

rebounding symptoms post-treatment (Penniston & Kulkosky, 1991). This study recorded a

shrinkage of anxiety-provoking traumatic and reoccurring nightmares, and flashbacks, as well as

a lessened use of medication post-treatment.

A second study done two years later by Penniston, Marrinan, Deming, and Kulkosky

(1993) was conducted on 20 Vietnam veterans who had between 12-15 years of chronic PTSD as

well as comorbid alcoholism. Patients were administered similar alpha-theta neurofeedback

treatment over thirty 30-minute session, similar to that done in past studies but now focused on

the synchronicity of brainwaves- the dominance of a specific brainwave frequency band

throughout the brain. In this case, alpha and theta waves were trained to lower frequencies during

sessions as a way of enhancing the learning of psychological skills presented in psychotherapy;

beta waves were also monitored but not the basis of training. Subjects, similar to the previous

study, were asked to think about traumatic events from their time in the military and then

instructed, throughout the neurofeedback session, to alter brainwaves into a relaxed state.

Participants were also provided simultaneous biofeedback training involving the temperature of

their body due to the research theory that such training can increase theta brainwave frequencies

(Hall, 1997; Penniston et al., 1993). This study managed to produce a substantial rise in the

synchronicity of the frontal and parietal occipital lobes as well as increasing theta and beta

waves- alpha frequency adjustments were unsuccessful (Penniston et al., 1993). Though, there

was a reliable interaction between theta and alpha waves where the increase of theta waves

caused a gradual decrease of alpha band frequency. A 26-month follow-up was conducted and

only 4 of the 16 participants who agreed to the follow-up reported a relapse in PTSD symptoms.
NEUROFEEDBACK & PTSD 23

These results indicate the probability that increased theta and beta brainwaves can enable easier

access to traumatic memories and images associated with highly emotional states through the

synchronization across both hemispheres and the limbic system. This enables the patient with the

capacity to easily access traumatic memories as well as actively continue the processing of the

emotions tied to those images and experiences.

In a study done by Bessel et al. (2016), 52 subjects who met PTSD diagnosis

requirements were split into control groups and experimental groups who each underwent

twenty-four 20-minute neurofeedback training sessions, twice a week, with set EEG Hz

threshold goals that were met each session. These thresholds were altered by one Hz a session if

a patient reported an over or under-arousal during neurofeedback training for two or more

sessions in a row. Each subject had undergone six months of trauma-focused psychotherapy prior

to the experiment, of which they had not responded to with any significant changes in

symptomology during that time. Prior to the start of the study, participants rated average PTSD

testing scores of 75% (control) and 88.9% (experimental), thus meeting full criteria for PTSD

diagnoses. By week 12 (post-treatment), there was a higher (68.2%) number of control

participants than experimental (27.3%) that still met full criteria for PTSD and by the 16th week,

participants still available revealed control groups to have maintained a higher (90%) number of

PTSD diagnoses than the experimental group (42%) to a significant degree. The control group

did not experience any meaningful adjustment of symptoms between prior and post-treatment

phases while the neurofeedback group held a significant one. Not only was the rate of

completion for the neurofeedback group (79%) greater than that reported on exposure-based

treatments (75%), but the neurofeedback group also managed to lower the number of patients
NEUROFEEDBACK & PTSD 24

who met PTSD criteria by 72.7% rather than the 62% reported through a metanalysis of other

treatment studies.

In a study done by Gapen et al. (2016), 23 individuals with chronic PTSD symptoms

underwent 40 sessions of neurofeedback training, twice a week, with Hz thresholds being altered

by one Hz depending on over or under-arousal symptoms being communicated by patients

(under- inattention, nausea, depressive symptoms, decreased alertness or mental clarity, and

fatigue or decreased energy; over- nightmares, sleep difficulties, anger, anxiety, self-harm,

suicidal or homicidal ideation, hyperactivity, and aggressive behaviors). In this experiment,

PTSD symptoms as well as affect dysregulation were monitored and analyses found that both

were significantly decreased throughout the span of the neurofeedback treatment. When

comparing the reduction of PTSD symptoms to the decrease in affect dysregulation, this study

discovered that while the decrease in affect dysregulation did not hold control over the decrease

in PTSD symptoms, the decrease in PTSD symptoms did hold substantial control over the

increase of affect regulation. While this study did not provide a total recovery from PTSD

diagnoses, it did reveal a significant 20 point (14.62%) decrease on the Davidson Trauma Scale

on patients who had received prior therapy of 10 years or more that had failed to produce

significant recovery of symptoms (Davidson et al., 1997; Gapen et al., 2016).

fMRI. Finally, a study by Gerin et al. (2016) utilized fMRI neurofeedback on three

veterans with chronic PTSD, for three 30-minute training sessions, where the amygdala was

targeted with expectations of decreasing hyperarousal and anxiety in patients. Participants were

trained to control emotion-related brain functioning, as regulated by the amygdala, that is

activated during trauma memory recall. Each subject was asked to remember six traumatic life

events that were recorded and edited into 60 second strips and played during fMRI
NEUROFEEDBACK & PTSD 25

neurofeedback training. Each participant was administered the Clinician Administered PTSD

Scale (CAPS) prior to the first neurofeedback session as well as post-treatment. Two of the three

participants had a significant shift in CAPS scores, 47 and 34 points respectively, while the third

participant did not have a substantial enough decrease in scores. Participants were also

administered the military version of the PTSD checklist (PCL-M), and while one patient had a

reliable drop in their score, only two of the subjects had a significant decrease in overall severity.

MRI scans were also completed on patients prior and post-treatment which exposed a constant

increase in connectivity between the amygdala and orbitofrontal cortex (OFC), as well as the

ventral anterior cingulate cortex (vACC), while there was a reduction in communication between

the amygdala and several salience networks. This may relieve multiple PTSD symptoms

surrounding hyperarousal and fear due to their nature in being controlled through subconscious

processes. As this was the first research done using fMRI on PTSD patients, as well as the small

subject size, such data only suggests the need and promise for future research on the subject.

Discussion

Neurofeedback continues to mature as a research-based treatment for multiple disorders,

and for a disorder such as PTSD, a scientifically based treatment that has a reliable 50%-and-

over rate of success is greatly needed in the field (Gapen et al., 2016). Many patients who go

through trauma and are diagnosed with PTSD are unable to find help through medication or

trauma-focused psychotherapy due to the altered biology of their brain that prevents the learning

of emotional regulation as well as coping skills (Wahbeh & Oken, 2013). Patients are being

asked to relive trauma that produces uncontrollable emotional reactions as a method of tiring out

the nervous system as a whole as well as attempts at altering personal cognitions surrounding

traumatic memories. Medication that is prescribed to PTSD patients focuses largely on

NEUROFEEDBACK & PTSD 26

symptoms of depression and anxiety that patients feel and are unable to help with the loss of

subconscious emotional control and regulation that cause flashbacks, anger outbursts, and

distress in normal activities that are unable to be avoided. Neurofeedback provides a way to

rewire the brain through the available plasticity of neurons in ways that can greatly accent the

effectiveness of many mainline treatment options available to PTSD patients (Gapen et al.,

2016). Neurofeedback also delivers a form of self-control in patients’ treatment goals and

activation since neurofeedback relies on self-control and attention in the rewiring of EEG

frequency bands to get people back to their healthy, normalized EEG levels in accordance to

their age group (Hammond, 2011). Further research is needed on utilizing neurofeedback as a

treatment and diagnostic tool for PTSD though the current amasses of research published reveal

a strong scientific basis for the efficacy of multiple sub-types of neurofeedback involving PTSD

symptoms. With the base-level of research completed, more should be conducted over the

separate subgroups of neurofeedback as well as pairing neurofeedback training with different

trauma-informed psychotherapies as a method of discovering the most effective form of

treatment for PTSD so that everyone affected by trauma has the best chance at total recovery.
NEUROFEEDBACK & PTSD 27

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