Early biofeedback treatment modalities leveraged the emerging understanding that subjects were able to gain volitional control over their own body systems if provided feedback. Initially, feedback referred to the use of devices to feed-back biometric data such as a subject’s muscle tension, hand temperature or heart rate to assist the client in learning how to self regulate their physical state. As research expanded to human subjects, we gained the understanding that in self regulating our own physiology, we are regulating our levels of physiological arousal, and thus indirectly regulating intertwined states of attention and emotion (Schwartz, 1995; Demos, 2005).
New neuroimaging tools such as functional MRI (fMRI), Positron Emission Tomography (PET), Magnetoencephalography, and quantitative Electroencephalograph (qEEG) now allow feedback of brain biometric data such as brain activity images, brain wave amplitude, and brain wave frequencies. The use of brain biometric data in therapy is alternately called neurofeedback, neurotherapy, neurobehavioral therapy, biofeedback, and as I will refer to it in this paper, EEG Biofeedback (EBF).
The field of EBF includes two distinct approaches: self regulation and stimulation. Self regulation is accomplished by feeding back brain biometric data; these devices are frequently called neuro-trainers. Stimulation is accomplished either through direct stimulation such as: Cranial Electrical Stimulation (CES), Transcranial Magnetic Stimulation (TMS), Vagal Nerve Stimulation (VNS); or brain wave rhythmic entrainment, through devices called Audio Visual Entrainment devices (AVE).
For purposes of this paper, I will review research related only to neuro-trainers and AVE stimulation. These are used commonly in conjunction in practice. Although there is one CES device now that does entrainment through stimulation of a specific hertz (Siever, 2007), traditionally the FDA has approved CES devices only of very low levels such as .35-1.0 hertz. There is no body of research available to review for this new CES technique.
It is important to mention that reviewing research
in EBF warrants a tailored approach for a number of reasons. With the exception
of ADHD and qEEG (which has applications in the pharmaceutical marketplace), it
is not typically feasible to conduct a double blind, well controlled randomized
clinical trial in EBF. The course of EBF treatments common in clinical practice
ranges from 20 to 40 treatments. A well controlled trial for that duration is
expensive and a rarely found without motivated funding sources. Secondly, it is not shown to be possible in
studies to “blind” the EBF participant (Othmer, Othmer, & Kaiser, 2007).
Although clinicians can be blinded, clients being treated with EBF can feel
when blood flow and brain states change and are not fooled by placebo
treatments. Thirdly, there is some evidence that RCT do not extrapolate well to
clinical community (
To evaluate the empirical support in the literature, I will be drawing on literature and guidelines sometimes outside traditional psychological journals. With the exception of ADHD and qEEG, I was not finding most EBF articles published in mainstream psychological journals. Within psychology related journals (Masterpasqua & Healey, 2003), there is found sufficient research evidence accumulated to support the effectiveness of EBF with ADHD only. I will focus not on the controversies, but in gathering details that support a holistic picture.
The
Robust EBF therapy begins by taking a baseline reading of the client’s current brain wave state. This is done through neuroimaging tools such as 19 or 24 channel (number of electrode locations) qEEG or Single Photon Emission Computer Tomography (SPECT) to determine how the client’s brain differs from brain wave norm databases that are available. Many studies do not include 19 channel qEEG in the study design, possibly because the equipment is expensive and requires additional training to operate. It is good to keep in mind that rather than evaluating studies which were designed to normalize a specific individual’s anxious brain state by applying harmonizing brain wave rhythms; most studies apply a standard anxiety protocol for all study participants regardless of what and where the individual’s specific brain wave deficit or surplus might be.
There is a significant body of work using PET, SPECT, fMRI and qEEG which links specific pathologies to specific non-typical brain wave patterns and asymmetries. Many psychological disorders can be seen to have distinct sub-types with qEEG. It has even been recommended for use in neuropsychological assessment (Shenal, Rhodes, Moore, Higgins, & Harrison, 2001). QEEG patterns are also being used to predict medication success in treatment resistant patients. Changes in a qEEG metric called cordance, when measured at the prefrontal site, have been found to be a good predictor of a client’s response to affective medications (Bares, Brunovsky, Kopecek, Stokova, Novak, Kozeny, & Hoschl, 2007).
Hughes and John (1999), reviewed over 200 studies and arrived at the conclusion that EEG patterns are so apparent that qEEG can be used as a diagnostic tool for assessment of psychological disorders such as ADHD, LD, mood disorders, substance abuse and schizophrenia. Masterpasqua and Healey (2003) reviewed existing literature and concluded qEEG has significant well documented evidence that it can discriminate specific pathologies by their characteristic qEEG signatures.
Amen (1998) has documented (via SPECT imaging shown below) higher than normal cerebral blood flow to the basal ganglia in clients with anxiety disorders. He describes the increase as setting the “idle speed” of the brain too high and resulting in increased dopamine, tension, and beta brain wave activity.
Although anxiety may present with right frontal
beta, it can just as easily occur with excess beta in other location such as
midline, center, or parietal areas. There are several potential profiles that
reflect redundant systems in the brain (
With Obsessive Compulsive disorder (OCD) anxiety; a number of PET and SPECT studies have found increased blood flow and activity in the mediofrontal, anterior cingulate, right frontal or orbitofrontal areas (Hammond, 2005). Others have found two distinct subtypes of OCD: one with an excess of alpha and frontal beta, and the other with an excess of posterior and temporal theta. Each distinct sub-type has the potential of predicting an individual’s response to treatment. Over 80% of the high theta group is non responders to SSRIs. Responders were characterized with excess alpha, which is consistent with the decrease in alpha production which results for SSRI use (Hurley, Saxena, Rauch, Hoehn-Saric, & Taber, 2002; Prichep, Mas, Hollander, Leibowitz, John, Aimas, Decaria, & Levine, 1993).
Because of this, practitioners emphasize that the treatment site is crucial. Numerous studies do not mirror a concern for treatment site, and may use a single site for all study participants. This is not to say that they don’t inform us, only that many of the seemingly contradictory results form a clearer coherent picture when viewed in terms of profiles and subtypes.
Discussing early studies may be the most expedient way to describe the contradictory conclusions that were possible. Plotkin and Rice (1981) conducted an experiment to determine if alpha enhancement and/or alpha suppression training could reduce anxiety. While their data showed rightly that there is no simple direct relationship between alpha increases and anxiety reduction, they concluded that the anxiety reduction their experiment showed, was thus unrelated to EBF.
By using only the occipital site, a small number of participants (ten), a lack of eyes closed protocol, and concurrent relaxation training, they were able to document anomalies such that one participant who increased alpha did not reduce anxiety, and others who did reduce anxiety did not increase alpha. The protocol they used: alpha suppression/then alpha enhancement is similar to protocols used in practice to encourage brain wave flexibility; which could easily result in reduced anxiety as well (Plotkin & Rice, 1981).
Studies encompassed a variety of protocols such as
alpha suppression, theta enhancement, alpha enhancement, alternating alpha
enhancement and suppression and, for the PTSD study, alpha-theta oscillation.
Even in light of his methodological concerns, he concludes that alpha
enhancement, theta enhancement and alpha-theta oscillation are effective
treatments for anxiety disorders. He
concluded that alpha suppression was possibly effective for anxiety reduction.
His conclusion was chosen based on the fact that twelve of the fourteen studies
showed significant reductions in anxiety. Only two showed no marked changes (
Moore (2000)
references that the Hardt and Kamiya’s
Generalized Anxiety Disorder study which used an alpha wave enhancing protocol,
worked in reducing anxiety for high trait anxiety subjects, but not low trait
anxiety subjects. It also demonstrated that alpha suppression increased anxiety
at the occipital sites, but it did not increase anxiety at the central sites.
He further references that in the Rice, Blanchard and Purcell’s GAD study,
while muscle tension reduction and alpha increase reduced anxiety
significantly, only a real increase in alpha waves resulted in an improvement
in heart rate reactivity to stress. He
summarizes by recommending future studies separate anxiety by severity, improve
rigor for electrode placement protocols, and better discriminate between alpha
training and alpha increase attainment (
PTSD appears to be another anxiety related disorder that is elucidated by further sub-typing and sub-type treatment selection through qEEG (Trudeau, Anderson, Hansen, Shagalov, Schmoller, Nugent, & Barton, 1998). The above exploratory study of a small number of veterans describes distinct qEEG signatures accompanying distinct recovery difficulties for a subtype of veterans who experienced blast concussions. Although the veterans did not show MTBI in CT brain scans, their qEEG profiles and symptomology indicated possible permanent micro brain damage may have occurred. Again this demonstrates the importance of sub-typing by qEEG signature and electrode location within research studies.
Metzger, Carson, Paulus, Paige, Lasko and Pitman (2004) express concern regarding seemingly contradictory PTSD research about the presence or absence of asymmetrical qEEG signatures in clients. Their study of nurse veterans with PTSD was designed with tighter protocols to potentially highlight two separate neural systems underlying anxiety. One neural system is described as handling anxious physiological arousal such as panic or stress. This is associated with greater right sided posterior activity and asymmetry with a bias toward right sided activity. The other neural system for anxiety is described as handling anxious apprehension, such as rumination, or in OCD and GAD. This is associated with greater left sided anterior activity.
The team answered a few of their questions. They found that PTSD was associated with a relatively greater right-sided parietal asymmetry as corresponds to the anxious arousal subtype of qEEG signature. They also state that PTSD depression is biologically different from ordinary depression. Adding in depression as a variable more than doubled the study’s ability to explain variances in qEEG scores as anxiety and depression can counteract each other in a qEEG session. Increased depression and anxious arousal combined was highly correlated right parietal asymmetry. The study did not uphold literature hypotheses on qEEG signatures for depression and recommends new protocols for EBF research (Metzger, Carson, Paulus, Paige, Lasko, & Pitman, 2004).
In another study of anxious arousal, incredibly compelling neurobehavioral research has been published with respect to the high incidence of GAD and social anxiety in individuals with Autism spectrum disorders (ASD). It is estimated that as many as 35% of individuals with ASD also have GAD, and as many as 49% have social anxieties. One study concluded that the relationship between ASD and anxiety begins with a high resting degree of physiological arousal, this leads to a likelihood of being overwhelmed in social situations, and this leads to social withdrawal as a means of regulating arousal level, this in turn leads to impaired social skills and repeated social withdrawal. This cycle is exacerbated by the high resting level of physiological arousal which makes it more likely that the individual will be conditioned by negative social experiences (Bellini, 2006).
If correct, the implications to ASD-anxiety treatment of this more holistic research approach, are that the ability to self regulate physiological arousal is key to autism spectrum disorders. This makes tools like EBF invaluable in enabling individuals to be able to learn the social skills they need to reduce their distress. Further compelling and convincing research has been completed by the Pfeiffer treatment center which indicates that a compromised metal processing system in the body is one cause of the increased level of resting physiological arousal in children. They suggest this internal state of high physiological arousal can be readily mediated by nutrient and diet changes (Walsh, Usman, Tarpey, & Kelly, 2002).
Considerable discussion has occurred in the research pertaining to the meaning and interpretation of qEEG characteristic asymmetry and rhythmicity which have and have not been observed in various psychological and neurological conditions.
In a magnetoencephalography study of patients with affective disorders and other neurological conditions, a low frequency biased pattern of persistently occurring brain waves was documented. They found low frequency loops between the thalamus and cortex, which could be triggered by either the thalamus or the cortex. When the low frequency loop interacted with the cortex, it coincided with patient reports of positive symptoms of their condition (such as a tinnitus event) (Llinas, Ribary, Jeanmonod, Kronberg, & Mitra, 1999).
There is no disagreement in the research that these asymmetries exist; there is however, enormous variation in identifying, interpreting and applying these qEEG signatures. A meta-analysis of 34 studies on qEEG asymmetries concludes that both depressive and anxious clients show moderately strong correlation to right sided frontal qEEG asymmetry. In my opinion, tighter research protocols and clearer sub-typing of the underlying biological pathways will provide more clarity than a meta analysis of past research based on diagnostically heterogeneous study participants (Thibodeau, Jorgensen, & Kim, 2006).
Documenting an asymmetric qEEG pattern for a highly
targeted population such as anxiously aroused and depressed combat veterans
with PTSD and without blast concussions, could expand the potential for the
future success of EBF treatments such as Davidson, and other prominent
researchers in qEEG asymmetry are currently investigating (Llinas, Ribary, Jeanmonod, Kronberg, & Mitra,
1999). Clearer sub-typing could enable
treatments to be precisely targeted toward underlying redundant biological
pathways for affective disorders and remove other confounding variables as
well.
Judging by research and case studies (Amen, 1998;
Demos, 2005; Joyce & Siever, 2000; Larsen, 2006; Robbins, 2000; Siever,
2002), the impact of EBF warrants major consideration as the effect size for
EBF is quite large. It is also reported as creating dramatic changes by the
treated individuals. In a study of mood
disorders

Any therapy which can, in just 19 sessions, improve the outlook for a chronically depressed individual, deserves to be seriously considered.
Siever (2000) reviews forty two small studies from 1929 forward on brain wave entrainment. He includes data on eight of his own studies; including one on situational anxiety during root canals which demonstrates that entrainment to 10Hz significantly reduces heart rate and other markers of anxiety during endodontic procedures. Although the studies he reviews might be classified as lacking controls, the sheer number of successful outcomes and potential implied therein is impressive. Case studies are numerous, document good results, and helpful from a qualitative perspective. There is not a question that brain waves can be entrained, the research questions relate to whether the particular device tested has the correct frequencies, power, visual range, and consistency to effect good entrainment.
AVE is a superb adjunct tool in that a client does not need insight, memory, cognitive speed, self esteem, motivation, lowered defenses, a belief in therapy, verbal skills, cultural knowledge, or psychological mindedness. Even severe attention deficiencies can be worked with through changing protocols. Clients with TBI, ADHD, developmental disabilities, dual diagnoses, treatment resistance, Alzheimer’s disease, and even substance abusers are all able to benefit. Anxious alcohol abusers who may be unable to produce alpha waves through neuro-training, can have therapeutic benefits from experiencing increased alpha waves through entrainment (Peniston, 2007).
After reviewing fifty five years of stalemated research into why psychotherapy works, Dr. Karla Moras (2006) makes a case for changing the questions we are asking. Rather than ask, why does psychotherapy work, she suggests that we begin to ask why and how very specific effective treatments work; and why and how those same effective treatments fail to work for some individuals. She feels with current neuroimaging techniques we can now know the mechanism, and glean the why from the how. Prichep, Mas, Hollander, Leibowitz, John, Aimas, Decaria, and Levine (1993) published research which is an excellent example of asking the question of why OCD treatment does not work for a specific group of people and arriving at why from the how.
In my opinion
based on a review of the literature, EBF research can help us precisely answer
the question of how and why certain treatments work. This implies that we may
learn why some current treatments sometimes fail to work as well.
For example, Dr. Moras discusses two operational pathways for memory in the brain; a hippocampally-dependent pathway and a non hippocampally-dependent pathway. High stress, hippocampally-dependent memories are accessed through situations and imagery, the day-to-day, non hippocampally-dependent memories are accessed through verbal processing. Divining and leveraging such knowledge of memory mechanisms adds clarity to the how of PTSD memory flashbacks and promises new progress on avenues to approach their resistant and enduring and nature (Moras, 2006).
It is also my opinion based on the literature review, that EBF research has the potential of enhancing the current DSM taxonomy by enumerating biologic subtypes.
In individuals with PTSD the medial prefrontal cortex activity is reduced and it is speculated that this prefrontal area fails to inhibit the amygdala that this event is a controllable/conquerable stressor (Nimh, 2007). The more we learn about the mechanism maintaining the situational memories, the closer Dr. Moras feels we will be to resolution of the distress (Moras, 2006).
Monitoring anxiety and panic real-time, neuroimaging can observe decreased medial prefrontal cortex activity (Amat, Baratta, Paul, Bland, Watkins, & Maier, 2005). With neuroimaging, we have observed clients responding to emotional stimuli real time who have a low sustained reactivity in the cingulate cortex and high activity in the amygdala; these show the greatest improvement with CBT. Decreased prefrontal activity is also seen in a number of conditions such as OCD, bipolar, aggression, schizophrenia, and substance abuse (Siegle, Carter, & Thase, 2006).
It is again my interpretation of the research, that EBF research has the potential of replacing an anxious client’s self reported experience under stress with objective brain metrics which may someday predict the likelihood of various treatments being effective for them personally. EBF gives us the opportunity to observe events like OCD checking in flight.
Cognitive-bio-behavioral treatments seek to address the underlying mechanism of low executive frontal activity which spans numerous DSM classifications. Increased amygdala activity is associated with inhibitory inputs to the prefrontal cortex, creating an emotional regulation cycle (Siegel, Ghinassi, & Thase, 2007).
Based on this
research, I have formed the opinion that if there are biologically different
types of anxiety and depression, EBF research provides us with a window into identifying
them and formulating more effective treatments for all of them individually. In addition to this, EBF appears to me as an
effective adjunct treatment which can work without requiring client skill or
understanding which changing client demographics begin to necessitate.
Cognitive Control Therapy (CCT) is an example of a new bio-behavioral or neurobiological therapy which utilizes what we know about brain mechanisms in finding resolutions that fit. Sustained attention and working memory work homework commonly assigned to individuals with Multiple Sclerosis which were noted not only to activate prefrontal cortex areas, but also coincidentally elevate mood. This curious side effect, interested researchers in new neurobehavioral techniques which aim to increase prefrontal activity, enhance executive functioning, and secondarily increase ability to self regulate emotions.
In a study of a merely two week course of treatment during the study, severely depressed and proven to be difficult to treat individuals were treated with CCT. They showed decreased rumination and decreased depressed symptomology (Siegel, Ghinassi, & Thase, 2007). These participants demonstrated normalized qEEG brain function and new symmetry of right and left brain activation.
The APA has in its mission statement to promote health. Although psychology practice is patterned after a medical model which identifies and treats disease, it is prudent to bear in mind that the medical model also provides a spectrum of services not centered on treating diseases at all, but designed to create positive health. Programs such as childhood immunizations, diabetic foot care education, well baby care, smoking cessation, memory exercises, relaxation training, and exercise-nutrition promotion all focus on positive health creation rather than illness.
It may well be our role to examine and present the positive side of pathologies such as anxiety. Performance anxiety, whether related to performance in sports, academics, music, theater, public speaking, or sexual functioning, has a natural positive twin: creating peak performance. (Reframing is after all, CBT’s business.)
Even if we do not consider positive psychology our role, research points toward anxiety and peak performance truly being twin halves of the same physiological phenomena. A link has been found between alpha-theta training (common to peak performance and creativity enhancement training) and reduced frontal high beta activity which reflects reduced anxiety and negative affect (Gruzelier & Egner, 2005). In any event, Kenny (2005) describes how what we have learned about performance anxiety can proactively help all who suffer from anxiety and stress to: maximize correct responses, minimize incorrect responses, and maximize the transfer of training to real life.
EBF is being used to improve sports and dance performance. In a study of dance performance, an EBF study group using and alpha/theta feedback protocol improved their musical performance by up to two grade points.(from third class to first class for example) Additionally, heart rate variability biofeedback(HRV) training was provided. It was discussed that dance “timing” was improved through EBF, and dance technique was improved through HRV training. The study was based on a small number of individuals. Those individuals had quite atypical qEEG signatures with higher theta than alpha at baseline, emphasizing again the importance of qEEG in setting baseline data for research (Raymonds, Sajid, Parkinson, & Gruzelier, 2005).
EBF research has also indicated that it will help us
teach individuals how to create peak immune system performance. In an eight
week extremely rigorous study of with a multidisciplinary team, employing 27
sites for electrode placement and well controlled protocols, anxiety was
reduced through left side anterior activation. This activation also resulted in
greater immune response to a flu shot. The increase in immune system response
was also directly proportionally to the left anterior activation increase
(Davidson, Kabat-Zinn, Schumacher, Rosenkranz, Muller, Santorelli, Urbanowski, Harrington, Bonus, &
It seems unreasonable to require randomized controlled trials in order to evaluate the effectiveness of EBF. With its complex physiological interrelationships, difficulty in blinding study participants, and prohibitive cost for a longer course of treatment, this research may never be available outside of ADHD and qEEG where there are tireless and a few dubiously motivated funding sources.
In cases where there is little harm to patients and significant potential gain, psychiatry will try a known drug for unproven diagnostic application. In my opinion, it would make sense for psychology to follow that same approach with EBF. EBF is in the unusual position of introducing almost zero risk to clients when standards are followed (Siever, 2000). EBF has the potential of moderating, to some degree, the entire spectrum of mental health concerns. Holding EBF to the gold standard of research in the current managed care environment will deprive many people of a least invasive and valuable therapeutic alternative.
My opinion after a review of the literature is that EBF for anxiety can be held to the standard of ‘‘Clinical Guidelines’’ where Clinical guidelines are based on limited empirical evidence. The recommended procedures (EBF) will be helpful at least 75% of the time and should always be considered an alterative by the therapist; and thus should be offered to clients.
If the client treatment were not reason enough to recommend EBF, EBF offers psychology a holistic vein of gold that can be mined to provide connections to decades of research spanning countless disciplines. This has already resulted in new minds and vibrant new treatment approaches (such as CCT) being offered for some of our most intractable psychological problems. The neurotherapy vein has resulted in biological methods that work which help to select treatments; to measure treatment effectiveness for an individual, and to demonstrate broader efficacy.
I was left unable to draw a conclusion on the
enduring nature, or lack of it with EBF treatment for anxiety. Practitioners,
researchers, and case studies seem convinced of the enduring nature of EBF with
at least ADHD treatment. (Amen, 1998; Demos, 2005; Joyce & Siever, 2000; Larsen,
2006; Robbins, 2000; Siever, 2002)
Health professionals such as Michael Joyce, Vince Monastra,
and
Progress in EBF is visible toward identifying diagnostic subtypes, which could well transform the current DSM. Progress is visible toward using EBF in assessment and diagnosis which could well transform intake and reliance on self reports of behaviors for diagnosis or evaluating treatment success and client improvement. Progress is visible in EBF research toward helping psychology reclaim the Health in Mental Health through research on positive techniques to create mental balance and peak performance.
Finding only two articles in mainstream psychological journals which describe what EBF offers to psychotherapy practice, seems inconsistent with its true value (Moras, 2006; Cappas, Andres-Hyman, & Davidson, 2005). It is completely possible that they are present and I am not skilled in finding them.
The holistic and synergistic approach that EBF employs can shed light and meaning on our empirical, unambiguous knowledge of brain mechanisms and those ambiguous conclusions we are left with regarding the minds of human beings. For this reason alone, I would like to see EBF research play a prominent role in forthcoming research studies in the field of Psychology.
When millions of neurons fire at the same time, they produce sweeping electrical patterns or brain waves. The waves can be seen by an EEG and fall into four main categories, each indicative of various levels of physiological arousal.
· Beta: quick waves of low amplitude, cycling from 14 to 40 cycles per second or Hertz( Three subtypes, Gamma, Beta 2 and Beta1 when occur can be linked to over arousal states such as anxiety and fear)
· Alpha: alpha waves cycle between 8 and 13 cycles per second of hertz, these occur during sensorial rest, relaxation and dissociation
· Theta:these cycle between 4 and 8 hz, referred to as twilight or hypnogogic state
· Delta: These are even slower and cycle at 1 to 4 hz. These occur in sleep, healing and brain damage. (Siever, 2002)


Anxious patient higher basal ganglia and amygdala activations
Guidelines for recommending evidence-based treatments
· ‘‘Minimal Standards’’ [MS] are recommendations that are based on substantial empirical evidence (such as well-controlled, double-blind trials) or overwhelming clinical consensus. Minimal standards are expected to apply more than 95% of the time. i.e., in almost all cases. When the practitioner does not follow this standard in a particular case, the medical record should indicate the reason.
· ‘‘Clinical Guidelines’’ [CG] are recommendations that are based on limited empirical evidence (such as open trials, case studies) and/or strong clinical consensus. Clinical guidelines apply approximately 75% of the time. These practices should always be considered by the clinician, but there are exceptions to their applications.
· ‘‘Options’’ [OP] are practices that are acceptable but not required. There may be insufficient empirical evidence to support recommending these practices as minimal standards or clinical guidelines. In some cases they may be appropriate, but in other causes they should be avoided. If possible, the practice parameter will explain the pros and cons of these options.
· ‘‘Not Endorsed’’ [NE] refers to practices that are known to be ineffective or contraindicated.
(Greenhill LL, Pliszka D, Dulcan MK, et al. Practice parameter for the use of stimulant medications in the treatment of children, adolescents, and adults. J Am Acad Child Adolesc Psychiatry 2002;41(2 Suppl):26S–49S.)

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