Anxiety disorders are among the most common
mental disorders, with the adult lifetime preva-
lence rate at 33.7% (Kessler, Petukhova, Samp-
son, Zaslavsky, & Wittchen, 2012). Symptoms of
anxiety are regularly experienced by healthy indi-
viduals and despite not reaching clinical levels,
are found to be correlated with negative health
consequences, work absenteeism, and lowered
productivity (Borkovec & Sharpless, 2004). Clark
and Beck (2010) remark: “Today, as never before,
calamitous events brought about by natural disas-
ters or callous acts of crime, violence, or terrorism
have created a social climate of fear and anxiety in
many countries around the world” (p. 3). Our aim
in this chapter is to describe how biofeedback can
help ameliorate this problem.
Anxiety is both a physiologically based response,
influenced by genetic predisposition, and one that
is a result of learning processes. The physiologi-
cal aspect is of central importance in treatment,
because anxiety is at its core a physiological phe-
nomenon. Indeed, the term “anxiety” typically
refers to a collection of physiological symptoms,
including shortness of breath, trembling, and nau-
sea, for instance (Bourne, 2005).
When a threatening situation arises, the sym-
pathetic component of the nervous system is trig-
gered in order to enable either defense against or
escape from the threat, commonly known as the
fight-or-flight response (Cannon, 1929). Internal
changes such as increased alertness, rapid heart-
beat, tensing of muscles, amplified sweating, hur-
ried breathing rate, and increased oxygen in the
body enable more effective preparation of the body
to fight or flee the “enemy” and preserve safety
(Sadock & Sadock, 2003). Therefore, those expe-
riencing an anxiety disorder may be considered to
have a an overreactive fight-or flight response, in
that even the perception of a physical threat, and
in some cases, a psychological threat, can act as
triggers. Sympathetic nervous system response,
such as elevated cardiovascular function, has
indeed been correlated with worry (Pieper, Bross-
chot, Van Der Leeden, & Thayer, 2010).
An overproportional focus on danger and
extreme sensitivity to potential threat, combined
with inefficient functioning of physiological sys-
tems, can result in the establishment of a sustained
state of fear, either of the sensation of anxiety itself
or the perceived risks this experience poses. The
intensity of the physiological experience presum-
ably makes it difficult for the person to consider
and/or accept that their perception of external
threat is not real, whereas the internal symptoms
are. In concordance with this general understand-
ing of anxiety, the preferred treatment for anxi-
ety is cognitive-behavioral therapy (CBT) with
or without medication (e.g., Smits, Berry, Tart
& Powers, 2008; Stewart & Chambless, 2009).
The proposition herein is that biofeedback can
enhance CBT as it addresses certain shortcom-
ings of cognitive aspects of therapy. This proposal
C h a p t e r 2 6
Arnon Rolnick, Dana Bassett, Udi Gal, and Anat Barnea
Schwartz_Biofeedback4E.indb 439 11/12/2015 5:24:26 PM
440 VI. CLINICAL APPLICATIONS: TRADITIONAL GENERAL BIOFEEDBACK PRACTICE
is made increasingly plausible with further discus-
sion of the physiological aspects of clinical anxiety.
Classical cognitive therapy is based on the
ABC model, which purports a linear activa-
tion from (A), the activating event, via (B), the
beliefs of the patient, to (C), the inevitable con-
sequences (Ellis, 1994). However, developments
in the understanding of neural processes deem
the ABC assumption’s validity to be questionable.
LeDoux (2002) asserts that there exist two neu-
ral information-processing pathways that contest
the ABC assumption. One pathway, shorter and
quicker acting, relays information about external
stimuli to the amygdala directly from the thala-
mus, while the second pathway, longer and slower
acting, relays the information a short while later,
from the thalamus through the cortex to the
amygdala. These pathways differ in not only the
speed of response but also their accuracy (LeDoux,
2002). The shorter, quicker path is highly valu-
able in situations that demand a quick response
for survival. However, this pathway is subject to
inaccuracy, because it does not involve the cortex,
which is responsible for the augmented analysis of
information. Therefore, its activation may lead to
a conditioned anxiety response before any cogni-
tive processing has occurred. This conditioning
process has a valuable aspect in that it enables one
to learn the connection between situations/places
where danger is truly present. However, this pro-
cess is subject to fault in that it may also repeatedly
err in its production of a response when the envi-
ronment is devoid of any real danger. This auto-
maticity, an inherent aspect of the conditioning
process, produces anxiety and defensive responses
as the quicker path acts on partial information.
The work of CBT appears to be somewhat discor-
dant with this pathway and may be a contribut-
ing factor in the variable success rate of therapy,
which is sometimes as low as 50% (e.g., Fisher &
Wells, 2005; DiMauro, Domingues, Fernandez, &
Tolin, 2013). It is in fact this pathway, according to
LeDoux's (2002) model, that is responsible for the
emotional response that occurs and is subjectively
misunderstood, which sheds light on the maladap-
tive pattern of functioning that is a main feature
in pathology. On the other hand, LeDoux's model
also notes the importance of cognitive interven-
tion in that it explains the need for the cortical
path to regulate the amygdala's response. The
slower pathway has the potential either to amplify
or to regulate the anxiety response. “However,
because the direct [shorter] pathway bypasses the
cortex, it is unable to benefit from cortical pro-
cessing. As a result it can only provide the amyg-
dala with a crude representation of the stimulus.
The cortex's job is to prevent the inappropriate
response rather than to produce the appropriate
one” (pp.106–107, LeDoux, 2002). This is where
CBT is focused.
The term “anxiety” is used to refer to a cluster
of psychophysiological manifestations across the
psychotherapeutic, learning-based, and neurobio-
logical literature. In clinical psychopathology lit-
erature the term also refers to a fear response that
is both incongruous and exaggerated given the
context in which it occurs (Pine, 2009).
In this chapter we refer to anxiety in its vari-
ous manifestations, such as that occurring within
generalized anxiety disorder, social anxiety disor-
der, phobias, panic disorder, obsessive–compulsive
disorder, and trauma disorders. There is some dis-
agreement about whether all of these syndromes
are best considered anxiety disorders and in fact
the Diagnostic and Statistical Manual of Mental
Disorders modifed the classification of anxiety dis-
orders between its fourth and fifth editions (DSM-
IV and DSM-V, respectively) such that several of
these syndromes are no longer regarded as anxiety
disorders despite the fact that anxiety is a feature.
The justification for this system of classifica-
tion has been repeatedly subjected to criticism.
Whereas some researchers emphasize the differ-
ences between various kinds of anxiety, positing
several distinct disorders, each with its own etiol-
ogy, phenomenology, and treatment. Others focus
on the similarities among the manifestations of
anxiety and postulate the unity of all anxiety dis-
orders (Barlow, 2002). Moreover, there has been
a recent tendency in the psychotherapy literature
for interventions to utilize a unified protocol for
transdiagnostic treatment, designed to be appli-
cable across the entire range of anxiety-related
disorders (Barlow et al., 2011).
of Anxiety Disorders
Clark and Beck (2010) in their review of the
symptoms of anxiety, list the following as possible
physiological manifestations of anxiety: increased
heart rate, palpitations, shortness of breath, rapid
breathing, chest pain or pressure choking sensa-
Schwartz_Biofeedback4E.indb 440 11/12/2015 5:24:26 PM
26. Anxiety Disorders 441
tion, dizzy, lightheaded, sweaty, hot flashes, chills,
nausea, upset stomach, diarrhea, trembling, shak-
ing, tingling or numbness in arms, legs, weakness,
unsteady, faintness, tense muscles, rigidity, and dry
Many symptoms of anxiety are manifestations of
autonomic nervous system (ANS) activity (Brad-
ley, 2000). Activation of the sympathetic nervous
system (SNS) is the most prominent physiologi-
cal response in anxiety, inducing symptoms of
hyperarousal such as constriction of the peripheral
blood vessels, increased strength of the skeletal
muscles, increased heart rate and force of contrac-
tion, dilation of the lungs to increase oxygen sup-
ply, dilation of the pupils for possible improvement
of vision, cessation of digestive activity, increased
basal metabolism, and increased secretion of epi-
nephrine and norepinephrine from the adrenal
medulla (Bradley, 2000).
These SNS manifestations can be addressed via
biofeedback. The goal is for patients to learn to
influence each physiological incident of the entire
cluster of symptoms to achieve symptom manage-
ment and/or reduction. It was initially purported
that the goal of biofeedback is to decrease sym-
pathetic activity. However, recent research reveals
that the picture is somewhat more complicated.
The research on electrodermal activity (EDA)
specifically sheds light on this issue. The electro-
dermal system, primarily controlled by the SNS,
has been studied extensively, yet the results are
inconclusive. Certain models have linked anxiety
with excessive autonomic lability and reactivity
(e.g., Cruz & Larsen, 1995; Brenner, Beauchaine,
& Sylvers, 2005). In support of these models, some
research indicates that elevated electrodermal
baseline levels and heightened responses are corre-
lated with both PTSD and panic (Pole, 2007; Wil-
helm, Gevirtz, & Roth, 2001). Electrodermal reac-
tivity in anxious subjects has been demonstrated
in a well-controlled study using virtual reality
(Wilhelm et al., 2005). However, in his review,
Crider (2008) argues that a substantial number of
studies have failed to find any consistent relation-
ship between electrodermal lability and self-report
anxiety measures. Additionally, a diminished
range of EDA responding has been found in panic,
as well as GAD (Hoehn-Saric & McLeod, 1988;
Hoehn-Saric, McLeod, Funderburk, & Kowalski,
2004). A broader view of anxiety disorders also
considers the role of the PNS, which is involved in
symptoms such as tonic immobility, drop in blood
pressure, and fainting. The effects of PNS stimu-
lation include decreased heart rate and force of
contraction, constricted pupils, relaxed abdominal
muscles, and constriction of the lungs (Bradley,
HRV is a good indicator of both SNS and PNS
activation, because the information provided by
frequency analysis can differentiate between the
two systems (Gevirtz, 2009; Gevirtz, Lehrer, &
Schwartz, Chapter 13, this volume). It has been
suggested that diminished HRV in patients with
PTSD is a marker of autonomic dysregulation
(Gevirtz, 2009). Other research has found both
diminished HRV and reduced vagal tone to be
associated with panic and GAD (Thayer, Fried-
man, & Borkovec, 1996; Pittig, Arch, Lam, &
Craske, 2012) as well as PTSD and SAD (Chalm-
ers, Quintana, Abbott, & Kemp, 2014).
The research on respiratory sinus arrythmia
(RSA), a variation in heart rate that occurs dur-
ing a breathing cycle, and on heart rate variability
(HRV) indicates that there needs to be movement
from a simplistic homeostatic view to a homeody-
namic view of biological functioning (Friedman,
Vascular constriction, as measured by skin tem-
perature, is a known marker of stress, and skin
temperature biofeedback provides training in
stress reduction that has been widely accepted as
efficacious (Shusterman & Barnea, 1995; Peper &
Gibney, 2003). However, there appears to be a pau-
city of research describing a correlation between
skin temperature and anxiety disorders.
Two instruments that measure patterns in respi-
ration, the “pneuomograph,” a flexible rubber ves-
sel that records the velocity and force of chest and
abdominal movements during respiration and the
“capnograpgh,” a device that monitors the concen-
tration or partial pressure of carbon dioxide (Co2)
in the respiratory gases, may be good indicators of
anxiety because abnormalities in respiration have
been postulated as a central component in anxiety
disorders (e.g., Meuret, Wilhelm, & Roth, 2001)
and exercises that regulate breathing have been
shown to moderate ANS activity (e.g., Jerath,
Crawford, Barnes, & Harden, 2015). One hypoth-
esis of the etiology of panic attacks specifies hyper-
ventilation as a key mechanism, proposing that
panic attacks considered to be spontaneous are
actually episodes of chronic or episodic hyperven-
tilation of which the patient is unaware (Meuret et
al., 2001; Meuret, Wilhelm, & Roth, 2008). The
capnometric assessment is therefore considered
a good tool for the assessment of panic disorder
(Moss, 2003; Khazan, 2013). Additionally, it is
imperative that the interconnectedness of emo-
Schwartz_Biofeedback4E.indb 441 11/12/2015 5:24:26 PM
442 VI. CLINICAL APPLICATIONS: TRADITIONAL GENERAL BIOFEEDBACK PRACTICE
tions and respiration be further deciphered if the
treatment of stress, anxiety, and mood disorders is
to be improved (Jerath et al., 2015).
Electromyograph (EMG) has long been estab-
lished as a measure of relaxation (Lehrer, 2007).
In anxiety disorders elevated excessive muscle
tension has been found in GAD, and inter-
preted as reflecting generalized psychophysiologi-
cal response rigidity to environmental stimuli
(Hoehn-Saric & McLeod, 1988;,Yucha & Mont-
The brain wave pattern (electroencephalo-
graphic [EEG]) that is characteristic of most anxi-
ety disorders shows abnormalities in basal levels of
waking cortical arousal. This is indicative of some
cerebral system instability, and sensory gating
problems that suggest pathophysiology in brain-
stem structures that are critical to the passage of
exteroceptive information to cortical structures,
and subsequent difficulties in the capacity for
controlled information processing, indicating dys-
function in working memory systems mediated by
cortical network operations (Clark et al., 2009).
It is generally agreed that anxiety is associated
with increased activity in the beta range in con-
junction with a decrease of activity in lower fre-
quencies (Moss, 2003; Thompson & Thompson,
2007). Some discrepancy exists among reports
regarding the specific range of beta activation,
which is set to be elevated in anxiety, as well as the
specific range of lower frequency activation, which
is said to be reduced at the same time. Thompson
and Thompson suggest that anxiety usually cor-
responds to an increase in 19- to 22-Hz activity in
conjunction with a decrease in 15- to 18-Hz activ-
ity. Moss (2003) presents a different view, propos-
ing that excessive fast wave activity (24–32 Hz) in
combination with deficient amounts of slow wave
activation is a cortical pattern of anxiety. This
higher beta activation is often seen in conjunc-
tion with a decrease in SMR, beta wave activity
in the frequency of 12–15 Hz. Bursts of increased
high beta activity in the low 20s seem to be a state
marker, as the person reports feeling tense.
Our own clinical experience suggests that anxi-
ety of any kind is most often associated with an
increase in frontal beta activation and occasion-
ally with an increase in beta activation through-
out the entire cortex. These observations suggest
a general EEG biofeedback protocol for treating
anxiety of any kind, essentially, reducing activa-
tion in the beta range that seems excessive in an
individual relative to the norm.
Overall, it appears that important psychophysi-
ological indices, such as elevated basal arousal
level, slower habituation, and reduced autonomic
flexibility, are associated with anxiety disorders.
However, generalization of findings across the
anxiety subtypes is not possible, because different
physiological response patterns may distinguish
phobia, panic disorder, and GAD. The homeody-
namic model stresses the importance of physiolog-
ical variability in maintaining organismic stability
(Friedman, 2007). Despite the various manifes-
tations that exist across the subtypes of anxiety
and psychophysiological measures, there exist
two commonalities. One relates to the subjective
experience of the person so affected, an innate
understanding that something is wrong. The sec-
ond relates to the inherent inflexibility within the
ANS. This accords with the proposal made by
Borkovec and Sharpless (2004) that autonomic
rigidity is a correlate of anxiety (GAD) that pre-
vents healthy coping. Clark and Beck (2010) sug-
gest that diminished autonomic flexibility might
contribute to the misinterpretation of threat that
is the core cognitive feature of anxiety. Similarly
Craske (2003) has suggested that the likelihood
of experiencing intense and acute autonomic sen-
sations may heighten the salience of, and threat
attributed to, bodily sensations.
The clinician may train the patient to develop
flexibility of responses so that physiological activ-
ity can be reduced and/or increased in accordance
with the situation, and simultaneously change the
patient's interpretation of his or her physiologi-
cal condition, such that perception of control is
regained. The current discourse aims to outline
the ways in which biofeedback can be used as a
tool to assist in the regulation of physiological
response, conditioned response, and cognitive pat-
terns across the various subtypes of anxiety.
The Use of Biofeedback in Anxiety
Several theories of anxiety disorders propose that
reports of fear and anxiety reflect an underlying
state of physiological hyperarousal (Lang & McTe-
ague, 2009). Yucha and Gilbert (2004) reported
that reductions in both state and trait anxiety
have been demonstrated with biofeedback (Hur-
ley & Meminger, 1992; Wenck, Leu, & D'Amato,
Yucha and Montgomery (2008) reviewed
numerous controlled studies supporting the effi-
cacious status of biofeedback (Bont, Castilla, &
Maranon, 2004; Coy, Cardenas, Cabrera, Zirot, &
Claros, 2005; Dong & Bao, 2005). Several other
independent studies provide additional support for
Schwartz_Biofeedback4E.indb 442 11/12/2015 5:24:27 PM
26. Anxiety Disorders 443
this finding (Hitanshu, Maman, & Jaspal, 2007;
Reiner, 2008; Zucker, Samuelson, Greenberg, &
Gevirtz, 2007; Gevirtz & Dalenberg, 2008; Agni-
hotri, Paul, & Sandhu, 2007).
Schoenberg and Anthony (2014) recently con-
ducted a meta-analytic review of the use of bio-
feedback in psychiatric disorders, in which they
reported that anxiety disorders were the most
commonly treated (68.3%). Overall, 80.9% of
research reviewed reported some level of clinical
amelioration resulting from biofeedback exposure,
65% of these to a statistically significant level
of symptom reduction, as assessed via standard-
ized clinical parameters. The authors admit that
results must be interpreted with caution due to the
heterogeneity of studies included; however, they
also note the strong indication that biofeedback
has the potential to unlock the channels of com-
munication between mind and body with some
proficiency, and that both therapeutic interaction
and individual realizations can thus be augmented
(Shoenberg & Anthony, 2014).
Many of the research studies assessing biofeed-
back have investigated it as a stand-alone inter-
vention (Clough & Casey, 2011). For example, an
early study of GAD demonstrated that both EEG
and EMG biofeedback can reduce GAD (Rice,
Blanchard, & Purcell, 1993). A later study sup-
ported these findings, with results indicating that
state and trait anxiety diminished significantly
via EEG and EMG interventions (Agnihotri et
al., 2007). Possibly, biofeedback might actually
have the potential for even more promising results
when integrated with interventions such as CBT
(Reiner, 2008; See Hamiel and Rolnick, Chapter
11, this volume) and supportive intersubjective
psychotherapy (Rolnick & Rickles, 2010). Indeed,
some authors have investigated the combination
of biofeedback with specific interventions (Kleen
& Reitsma, 2011; Khazan, 2013). In this chapter
we first attend to biofeedback as a stand-alone
intervention and then explore the application of
biofeedback in combination with other types of
Biofeedback as a Stand‑Alone Intervention
in Anxiety Disorders
Arousal Reduction and Biofeedback as Tools
for Alleviating Anxiety
Biofeedback may be used effectively in the treat-
ment of anxiety disorders as an arousal reduc-
tion tool. The reason for this becomes clear when
considering the need to regulate the ANS as an
integral aspect of treating anxiety disorders. As
discussed, some anxiety disorders involve over-
activation of the SNS, while others involve an
active avoidance of thoughts and behaviors that
are likely to trigger this overactivity.
Utilizing biofeedback to regulate the initial
overarousal can be achieved in various ways: the
reduction of muscle tension using EMG, regula-
tion of the sympathetic response using EDA, bal-
ance of the sympathetic–parasympathetic interac-
tion using HRV or temperature, and control and
prevention of hyperventilation with a breathing
belt or capnometry (e.g., Lehrer, 2007).
A meta-analysis of the treatment of anxiety dis-
orders has shown that relaxation is highly effective
whether the technique used is progressive muscle
relaxation (PMR), autogenic training, breathing,
applied relaxation, or meditation (Manzoni, Pag-
nini, Castelnuovo, & Molinari, 2008). Biofeed-
back may both enhance these relaxation methods
or be used by people who are unable to use these
other techniques (Rice et al., 1993). Indeed, Yucha
and Montgomery’s (2008) review outlines studies
that indicate the efficacy of biofeedback training
that has not included relaxation techniques.
Although research does not consistently show
that biofeedback as a sole intervention provides
superior results to relaxation, combining bio-
feedback training in therapy may provide several
advantages. For instance, motivation and belief
in personal ability to gain control are established
and strengthened as a function of the feedback, as
objective immediate proof of technique efficacy is
provided. Indeed, a study by Reiner (2008) indi-
cated that participants found portable biofeedback
devices to be more helpful than other relaxation
techniques, such as yoga, meditation, and other
unassisted breathing techniques.
Relaxation-induced anxiety (RIA) is an occa-
sionally reported difficulty that patients experi-
ence with common relaxation techniques (Heide
& Borkovec, 1983). Patients with RIA frequently
report that relaxing may be harmful. Biofeed-
back can address this challenge. For instance, if a
heightened sense of lack of control is experienced
when asked to keep their eyes closed, they may
respond more positively to biofeedback, because
they can keep their eyes open. Alternatively, even
if patients close their eyes, auditory input can indi-
cate to them that all is continuing as expected.
Apart from the hypothesized motivational
advantages, relaxation skills can be built via trial
and error due to the feedback provided. Results
achieved by Corrado, Gottlieb, and Abdelha-
mid (2003) indicated that subjects receiving bio-
Schwartz_Biofeedback4E.indb 443 11/12/2015 5:24:27 PM
444 VI. CLINICAL APPLICATIONS: TRADITIONAL GENERAL BIOFEEDBACK PRACTICE
feedback and relaxation training had reductions
on measures of both anxiety and somatization.
When one begins to reduce arousal, the effects
can be immediately observed. If the patient is not
responding to a particular technique, therapist
and patient can try other techniques, and both
are immediately made aware of any reduction in
arousal. In fact, the uniqueness of biofeedback lies
within the inherent phenomenon that no tech-
nique per se is actually needed to achieve arousal
reduction. The act of receiving feedback, and the
reinforcement provided each time there occurs a
desired change, propels arousal reduction. This is
of specific significance in cases in which patients
have suffered continued tension and do not know
what it feels like to be in a state of nonarousal.
The moment they begin to reduce arousal, as the
feedback shows, this awareness can be cultivated.
Once this has been achieved, patients can begin
to use arousal reduction skills in their everyday
lives as they attend to their growing awareness of
aroused versus nonaroused states.
A review of early research that compared vari-
ous biofeedback measures to one another or bio-
feedback to relaxation techniques, such as PMR,
autogenic training, and systematic desensitiza-
tion, concluded that EMG biofeedback is superior
to PMR in the specific achievement of muscle
relaxation (Lehrer, Carr, Sargunaraj, & Woolfolk,
To cultivate low arousal, various biofeedback
sensors can be used. For PMR (Jacobson, 1938),
the use of EMG, either from the frontalis or wrist
flexor or wrist-to-wrist placement can be of bene-
fit. Although Jacobson objected to the use of phys-
iological measurements during PMR (Lehrer et al.,
1994), using EMG provides patients with infor-
mation about the tonus of their muscles, and it is
the receipt of this information that helps to build
self-awareness, ultimately leading to relaxation. In
a similar vein, the other biofeedback sensors pro-
vide information that also assist in developing self-
awareness. To achieve relaxation through breath-
ing techniques, a breathing belt, capnometry, or
HRV can be used. Autogenic training and mind-
fulness methods, as well as guided imagery relax-
ation, also stand to be enhanced using feedback
based on skin temperature and EDA.
The clearest illustration of biofeedback as a stand-
alone intervention is provided by neurofeedback.
Best understood within a learning paradigm of
trial and error, neurofeedback relies more heavily
on a patient's response to reinforcement and is less
dependent on interpersonal or cognitive factors.
Several studies suggest this technique is efficacious
(e.g., Hammond, 2005; Walker, 2009).
Anxiety disorders have brain biomarkers (EEG
patterns) that can help with diagnosis and treat-
ment prognosis (Clark et al., 2009). These EEG
patterns may form the basis of the rationale for
treating anxiety disorders not only psychothera-
peutically but also with neurofeedback, which
appears to offer specific benefits due to high sensi-
tivity and high specificity.
Neurofeedback has been researched and suc-
cessfully applied in disorders of attention (Ams,
Ridder, Strehl, Breteler, & Coenan, 2009; Barnea,
Rassis, & Zaidel, 2005). Attention and anxiety
have an interconnected nature, in that anxi-
ety increases attention to threat-related stimuli
(Eysenck, Derakshan, Santos, & Calvo, 2007) and
in turn reduces the capacity for self-regulation.
Anxiety is often considered in terms of attention
deviation (e.g., Eysenck et al., 2007) and since it
has central biomarkers in addition to peripheral
ones, it is plausible to suggest that neurofeedback
can be used as a primary, or complementary, treat-
ment tool. Indeed, anxiety is a systemic phenom-
enon that affects the individual on cognitive,
emotional, and physical levels.
Clark et al.’s (2009) seminal paper provides a
systematic, evidence-based medicine (EBM) revi-
sion of the field of electrophysiology with relation
to anxiety disorders. Despite the fact that quan-
titative EEG (QEEG) is not yet a diagnostic tool
that can stand alone, research nevertheless sug-
gests that QEEG is a tool that can efficiently guide
neurofeedback training (Kropotov, 2009).
Research indicates that the various anxiety syn-
dromes disorders are characteristically different in
their electrophysiological profile patterns, indicat-
ing differences in underlying structural/functional
pathology (Clark et al., 2009). Notwithstanding,
there are some commonalities in the classes of
measures characterizing dysfunction, all of which
highlight difficulties with information processing.
Thus, most of these disorders present with abnor-
malities in basal levels of waking cortical arousal.
This in turn suggests some cerebral system instabil-
ity, accompanied by sensory gating problems that
indicate pathophysiology in brainstem structures
that are critical to the passage of exteroceptive
information to cortical structures. Subsequently,
there is a decrease in the capacity for controlled
information processing (Ludewig et al., 2005).
Schwartz_Biofeedback4E.indb 444 11/12/2015 5:24:27 PM
26. Anxiety Disorders 445
Based on EEG recordings, taken from the whole
scalp, that have been quantitatively analyzed and
compared to norms, the therapist can decide
which protocol is most appropriate (e.g., which
frequency should be enhanced, which should be
decreased, and the site where electrodes should
be placed). These two aspects of neurofeedback,
frequency and electrode placement, are central
to the successful use of neurofeedback (Walker &
Anxiety disorders tend to be characterized by a
surplus of high-frequency waves (beta) and a defi-
ciency in low-frequency waves (alpha) (Clark et
al., 2009). In a limited number of cases, the reverse
is true, in that anxiety is marked by excessive low-
frequency waves and a paucity of high-frequency
waves. Neurofeedback aims to reduce the power
of high-frequency waves and increase that of low-
frequency waves. Accordingly, the classic way to
conduct neurofeedback is guided by the “bull-
dozer” principle, which states that when one tries
to normalize the pathological brain, the amplitude
of the overactive brainwave frequency needs to
be reduced, while the frequency that is less active
requires enhancement (Moss, 2009). Given that
the typical pattern of EEG in anxiety disorders
is a surplus of beta waves, it is presumed that an
increase of alpha waves is necessary. This increase
is typically observed when one enters a meditative
state (Travis, 2001).
Thompson and Thompson (2007) suggest that
raising high alpha (11–12 Hz) and semsorimo-
tor rhythm (SMR; a beta wave in the frequency
of 12–15 Hz), at the midline between Cz and Fz,
and teaching diaphragmatic breathing at a rate
of about six breaths per minute, produces relax-
ation and improved motor control, and may cause
a peaceful feeling.
Davidson (1998) has proposed the existence
of two motivation systems operating in separate
hemispheres and subserving different forms of
behavior and affect. The right hemisphere has
been said to be especially active during process-
ing of negative events, while the left hemisphere
is more active in response to positive events. Thus,
an additional direction that may be adopted in the
use of neurofeedback is based on Davidson’s model,
in that most anxiety disorders involve hemispheric
asymmetry. It is possible that bipolar placement of
the electrodes, one in each hemisphere, in F3 and
F4 positions, forms part of the treatment in that
it provides feedback about the different activity
between the hemispheres, the purpose of which is
to enhance or reduce the hemisphere's asymmetry,
or to increase left-hemisphere activity by enhanc-
ing beta frequencies.
Walker (2009) reported successful results with
23 patients with PTSD whose QEEGs showed
both high beta and a high anxiety rate (measured
by self-report questionnaire). After several QEEG-
guided neurofeedback sessions of reducing beta
and enhancing alpha bands, a significant reduc-
tion in anxiety was reported and remained stable
throughout follow-up 1 month later. However,
these results must be replicated before conclusions
may be reached. Although studies assessing the
use of neurofeedback for PTSD have been ongoing
(Peniston & Kulkosky, 1991; Othmer, 2011), vali-
dation studies remain sparse. This area is likely to
benefit significantly from studies being conducted
on the efficacy of neurofeedback for PTSD suffer-
ers in more than 15 military and Veteran Admin-
istration facilities, as reported by leading trauma
researcher van der Kolk (2014).
That neurofeedback may have the potential to
be sensitive and specific is strongly suggested by
results overall, but further research is required.
Integrating Biofeedback with Psychotherapy
The efficacy of biofeedback has been examined in
several published studies; however, very few have
used it as a technique to enhance current psycho-
therapy practices (Clough & Casey 2011).
As noted earlier, research has effectively estab-
lished that biofeedback combines well with certain
behavioral components of CBT such as breathing
training and PMR (often referred to as “relax-
ation exercises”), and leads to positive gains (e.g.,
Hawkins, Doell, Lindseth, Jeffers, & Skaggs, 1980;
Reed & Saslow, 1980; Reiner, 2008).
One case study, in which biofeedback, relax-
ation, and CBT techniques of cognitive challeng-
ing and exposure were combined, reported that
panic attacks and agoraphobic avoidance ceased
completely at the end of treatment (Goodwin &
Montgomery, 2006). Reiner (2008) paired a por-
table biofeedback device with CBT for a range
of anxiety disorders and reported significant
decreases in trait anxiety across subjects.
Investigation of the potential efficacy of HRV
biofeedback plus psychotherapy as a treatment for
PTSD indicated that veterans receiving face-to-
face treatment of HRV biofeedback with psycho-
therapy showed significant reductions in PTSD
symptoms, while those receiving only psycho-
therapy did not (Tan, Dao, Farmer, Sutherland,
& Gevirtz, 2011). Kleen and Reitsma (2011) suc-
Schwartz_Biofeedback4E.indb 445 11/12/2015 5:24:27 PM
446 VI. CLINICAL APPLICATIONS: TRADITIONAL GENERAL BIOFEEDBACK PRACTICE
cessfully integrated third-wave behavior therapies
with HRV biofeedback and found that this was an
effective method of training clients’ to increase
both their HRV and mindfulness skills. Although
these results are promising, demonstrating that
the addition of biofeedback can enhance the ther-
apeutic intervention, the general lack of empiri-
cal research and, specifically, replication data, is
a problem that must be rectified. A review of the
rationale for its use in the treatment of anxiety dis-
orders, primarily as a vehicle to enhance psycho-
therapeutic processes, follows.
Integrating Biofeedback with Desensitization
Most current CBT methods are based largely on
exposure or desensitization as the major inter-
vention. Biofeedback can be very easily paired
with desensitization and prolonged exposure. In
line with Wolpe's classical research (1958, 1973)
desensitization of conditioned responses may be
achieved by first training patients to utilize PMR
during imaginal confrontation with the feared
object. Biofeedback helps in the training of vari-
ous relaxation techniques whose aim is to reduce
arousal by providing detailed feedback in real-time
about changes in level of arousal. The therapist
is guided to provide better instructions during
the desensitization process, because the feedback
allows creation of a parallel in reaction to the
patient’s responses. The arrangement of stimuli in
a hierarchy is the second component of systematic
desensitization. Biofeedback assists with the cre-
ation of the hierarchy by providing an objective
measure of response to imagined stimuli (Wood et
al., 2008); that is, biofeedback reveals to therapist
and patient the point at which a particular trigger
activates the anxiety response.
Prolonged or repeated exposure is based on
the phenomenon of habituation of the CNS, an
automatic process that brings about a reduction
in the intensity of a response when exposed to an
arousal-inducing stimulus for long periods (Foa
et al., 2005). Biofeedback displays provide evi-
dence of inherent ability to control a physiologi-
cal response and as such can be used to manage
anxiety, further reinforcing a belief in ability to
cope with exposure overall. Wiederhold and Wie-
derhold (2003) found that, compared to exposure
alone, exposure with feedback was associated
with better results. Whereas prolonged exposure
requests that patients “grin and bear it” until such
time that control is gained, biofeedback provides
immediate reinforcement, in that it shows, objec-
tively, the changes the patient has brought about,
thus strengthening the patient's motivation and
ability to persist. This result may be a function of
the increase in one’s sense of control. When using
biofeedback, there is a sense that balance in the
arousal level of the PNS and SNS can be achieved
while maintaining control, as opposed to relax-
ation techniques that rely on closed eyes, which
decreases the sense of control.
Fostering Awareness and Acceptance
A primary obstacle for anxious patients when
attempting to relax is their very high level of
arousal upon arrival, and their use of extreme
effort to reduce this arousal. Therapists who use
biofeedback can show patients that this goal may
be achieved without exertion and in fact will only
be completely achieved once the effort to control
is released (i.e., once a patient “lets go.” The prin-
ciple of effortless work and “letting go” is a primary
principle in acceptance and commitment therapy
(ACT; Hayes, Strosahl, & Wilson, 1999). ACT is
an example of a therapeutic approach that teaches
patients to observe reality without judgment
or criticism, and to cease efforts in the struggle
against anxiety. Biofeedback can certainly assist
with this aspect of change.
The importance of developing a sense of self-
awareness has been discussed by several psycholo-
gists (e.g., Borkovek & Sharpless, 2004) and has
been integrated as a principle aspect of various
therapies, including Kabat-Zinn’s mindfulness-
based stress reduction (MBSR; Kabat-Zinn, 1982),
mindfulness-based cognitive therapy (MBCT;
Teasdale, Segal, & Williams, 1995), and third-
wave therapies such as ACT (Hayes et al., 1999).
Originating from Eastern philosophy, the princi-
ple of self-awareness is an essential prerequisite of
change, because it reveals the function of behav-
ior to therapist and patient, enables the patient
to identify primary signals of change in internal
state, and guides the patient toward a focus on the
present (Borkovek & Sharpless, 2004).
Some patients may object to mindfulness and
meditation. People raised in a Western culture
have tended to seek a scientifically based, fast-
acting solution to their problems and, as such,
may respond to mindfulness-based techniques
with skepticism (Rolnick, 1999). On the other
hand, this general attitude to mindfulness and
meditation may have changed, as suggested by
recent data that has put the number of free and
Schwartz_Biofeedback4E.indb 446 11/12/2015 5:24:27 PM
26. Anxiety Disorders 447
paid meditation and mindfulness applications
available to Smartphone users in the thousands
(Plaza, Herrera-Mercadal, & Garcia-Campayo,
2013). Biofeedback meets the criteria of a scientific
approach, elegantly combines knowledge from
both Western and Eastern cultures, and is suitable
for use by both medical practitioners and laypeople
alike. Confidence about relaxation techniques can
only be strengthened once people see with their
own eyes how their body responds to the various
In a case study that combined HRV biofeed-
back with ACT principles, results indicated that
the patient was helped to accept anxiety rather
than attempt to suppress it (Gevirtz & Dalenberg,
2008). Kleen and Reitsma (2011) also studied the
effects and processes of an integrative approach in
which HRV biofeedback was combined with ACT.
Their findings suggest that HRV training may be
an effective way to train the client to be able to
increase both HRV and mindfulness skills.
Biofeedback, due to the feedback provided
and the reinforcement attained, can lead to both
arousal reduction and increased awareness, ulti-
mately benefiting the patient in ways that are
identical to the better known methods of relax-
ation, such as mindfulness and applied relaxation,
and guided imagery relaxation. Additionally, it
can be paired with these techniques to increase
their viability. The nature of the biofeedback para-
digm is observation, generating distance between
the patient and the physiological experience. Ulti-
mately this demonstrates to the patient that when
an attitude of acceptance is adopted and the effort
to exact control is relinquished, change may be
Biofeedback Enhances Cognitive Elements of Therapy
All patients arrive with a set of beliefs and ideas
regarding their anxiety (e.g., whether anxiety is
learned or innate; whether it can be managed or
eliminated; and whether it leads to loss of con-
trol). The role of psychoeducation when combined
with biofeedback is to address and alter beliefs
that prevent the adoption of a more realistic and
functional perspective. During biofeedback train-
ing, patients observe feedback from the computer,
leading to two types of learning: First, a specific
understanding of the physiological measure taking
place, and second, a more general understanding
of their abilities to exert control.
The use of biofeedback for treating disorders in
which inaccurate interpretation of bodily symp-
toms is a feature has been raised (Domschke, Ste-
vens, Pfleiderer, & Gerlach, 2010). The plausibil-
ity of biofeedback’s applicability is based on the
fact that misinterpretation of bodily symptoms co-
occurs with an excessive focus on the physiological
condition of the body; biofeedback can be used to
redirect attention, as well as introduce a new way
of understanding the body’s signals.
Sensors that monitor temperature and HRV
may be valuable additions to the cognitive stage
of therapy, because the patient can learn that con-
trol over the physiological state (e.g., temperature
or heartbeat) can be attained. Alternatively, the
visual contact with evidence of the body’s inter-
nal state may increase the patient’s willingness to
attend to something else and in this way, reach
the understanding that abandoning a focus on
the body does not result in any disastrous con-
sequences. The cognitive flexibility required to
think about bodily sensations in a more realistic
way is therefore facilitated.
Psychoeducation continues throughout therapy.
An example of how biofeedback can aid this pro-
cess is seen in the demonstration of the fight-or-
flight response. This idea is an aspect of many
therapeutic approaches, yet sometimes patients
may perceive the information as being uncon-
nected to their own cases. Alternatively, when
attached to biofeedback sensors, patients observe
the body's rate of response in reaction to a stimu-
lus and simultaneously connect the information
provided to their own experience. Furthermore,
patients learn that after the activation of the fight-
or-flight response, additional time is needed for the
body to regulate and regain a level of homeostasis.
Additional examples, psychophysiological demon-
stration of anticipatory anxiety, influences such as
acceptance and distraction, the restricting effects
of effort to control, and the thought–physiology–
emotion connection are provided by Hamiel and
Rolnick (Chapter 11, this volume).
The Unique Contribution of Biofeedback
in the Treatment of Anxiety Disorders
Biofeedback, as has been discussed, can be eas-
ily integrated with cognitive and behavioral
concepts. In addition, biofeedback offers its own
unique contributions in the treatment of anxiety
disorders that relate to two characteristics inher-
ent in biofeedback contingencies. The first of
these pertains to the dialogue that occurs between
clients and their physiology when exposed to their
own physiological reactions; the second concerns
Schwartz_Biofeedback4E.indb 447 11/12/2015 5:24:27 PM
448 VI. CLINICAL APPLICATIONS: TRADITIONAL GENERAL BIOFEEDBACK PRACTICE
clients’ exposure to situations wherein their stress
reaction is observed.
Exposure to One’s Own Physiological Reaction
The feedback of physiological information is usu-
ally considered to be the core process of learning
self-regulation; however, from a psychological per-
spective, the fact that a client is introduced to his
or her own physiology in an overt visual display
can initiate some important psychological pro-
Take, for instance, the case of health anxiety
and hypochondriasis. “Hypochondriasis” is char-
acterized by a focus on, and misinterpretation of,
bodily symptoms. The client reacts to the experi-
ence of all bodily sensations with fear due to the
belief that these sensations are indicative of ill-
ness. Biofeedback therapy involves direct exposure
to this very frightening stimulus. In several cases,
such exposure may produce sympathetic arousal
that will attenuate over time and teach the client
that his or her body is self-regulating. Moreover,
this exposure can instigate significant cognitive
change, such as the following: (1) The body’s reac-
tions are usually adaptive and self-regulating; (2)
there may be a significant discrepancy between
subjective experience and actual physiological
reaction; (3) one can learn to control his or her
reactions; and (4) the best way to gain control over
one’s physiology is by not trying too hard.
Exposure to the Arousal and Stress Reaction
Observed by the Therapist
Several anxiety disorders feature a fear that other
people will notice the existence of stress reactions.
This is clearly the case in social anxiety disorder,
in which the fear of embarrassment focuses on cer-
tain aspects of self-presentation, such as exhibit-
ing symptoms of anxiety. This sensitivity to the
criticism of other people is also central in panic
disorder, in which an aspect of the avoidance is
related to the fear that bystanders will notice the
panic attack. In fact, most of the avoidance behav-
ior seen in anxiety disorders is associated with the
fact that anxious people are afraid that their stress
reactions will be noticed, and their avoidance is
partly an attempt to prevent this exposure. Indeed,
there are a variety of situations in which people
feel shame at the idea that their stress reaction will
be observed (e.g., the fear of blushing in front of
others, that one’s trembling voice will be noticed,
that one’s hands are shaking or one’s palms are
wet), and there are several kinds of performance
anxiety, especially in sexual activity. Self-focused
attention is enhanced during anxious states, caus-
ing individuals to become acutely aware of their
own anxiety-related thoughts and behaviors. This
heightened attention to the symptoms of anxiety
serve to intensify one’s subjective apprehension.
Furthermore, the presence of anxiety can impair
performance in certain “threatening” situations,
such as when a socially anxious person goes blank
in the middle of a speech or begins to perspire
profusely. Attending to these symptoms can eas-
ily interfere with the person’s ability to deliver
the speech. The anxious person is then left to
interpret the presence of anxiety itself as a highly
threatening event that must be managed immedi-
ately in order to minimize or avoid its “catastrophic
effects.” In this case, the person becomes anxious
about being anxious.
The case of blushing suggests that biofeedback
can enhance the therapy of anxiety disorders in
general, and social anxiety in particular, by acting
as a tool for simulating a situation in which the
client feels shame because another person can see
their stress. In this case, if a client is connected to
various peripheral physiological parameters (EDA
EMG, skin temperature, heart rate), the moment
he or she notices that the therapist has become
aware of any minute change in his or her physiol-
ogy, the client will experience an increase in stress.
There is a strong parallel between blushing, which
occurs primarily in social or interpersonal situa-
tions, and the biofeedback situation, wherein the
patient is aware that the therapist can observe his
or her internal reaction. This is a unique type of
exposure that CBT cannot create as easily, if at all.
As in all types of exposure, this situation allows
clients to face their fear that someone will notice
their anxiety. This experience tends to attenuate
the fear, and clients come to learn and accept that
they can survive the “shame.”
The Role of the Other
in the Self‑Regulation Process
The state of being observed by the therapist leads
to a wider issue about the role of the other in the
self-regulation process (Levit Binnun, Golland,
Davidovitch, & Rolnick, 2010). Originally based
on work by Winicott (1971), and later Bollas
(1987), anxiety disorders are perceived as a func-
tion of poor ability to self-regulate, a capacity that
typically develops throughout infancy via interac-
tion with parental figures.
Schwartz_Biofeedback4E.indb 448 11/12/2015 5:24:27 PM
26. Anxiety Disorders 449
It has been argued that in order to attain a sense
of safety, children typically react with fear in new
situations, resulting in fear-based dependence on
caregivers (Milrod, Busch, Cooper, & Shapiro,
1997). A parallel may be drawn within biofeed-
back-assisted psychotherapy. The fearful, anxious
patient is exposed as helpless and dependent before
the therapist, which may incite feelings of shame,
impotence, and hopelessness. In contrast to the
patient’s developmental experience, the biofeed-
physiological makeup with him or her provides an
opportunity for the therapist to validate this experi-
ence, label it, and explain emotional arousal. The
therapist also offers the patient an explanation of
the process that produces their arousal. Then the
therapist teaches self-regulation, fulfilling a role
that was absent in the original parenting unit.
This idea is also raised in the biosocial theory
proposed by Linehan (1993), who asserts that
individuals with emotional disorders are biologi-
cally vulnerable to experiencing emotions more
intensely than the average person, and also have
more difficulty modulating their intensity. In psy-
chophysiological terms, they are high reactors with
a very limited ability to calm down. The second
element in Linehan's theory states that emotional
disorders develop during childhood, wherein an
invalidating environment contributes to emotion
dysregulation. More specifically, the issues are that
parents fail to teach the child how to label and
regulate arousal, how to tolerate emotional dis-
tress, and when to trust his or her own emotional
responses as reflections of valid interpretations of
events. Therapy conducted with biofeedback calls
for validation, empathy, and the acquisition of self-
(Significant elements of the therapeutic alli-
ance within biofeedback-assisted therapy are fur-
ther discussed at www.marksschwartz.com.)
The value of biofeedback as a therapeutic tool in
the management of anxiety disorders is cogent.
The ease with which it can be integrated into
existing therapeutic models, regardless of their
theoretical and practical differences, is both
impressive and encouraging. Assuming that the
aim of clinicians, of all orientations, is to provide
patients with useful tools and experiences of mas-
tery, biofeedback has proved itself to be a suitable
complement that merges smoothly and effectively
into current modes of work. In the treatment of
anxiety disorders, biofeedback contributes directly
in three ways: (1) It provides a platform for direct
modulation of autonomic arousal; (2) it enhances
psychotherapuetic interventions; and (3) it cul-
tivates the therapeutic alliance and presents the
possibility for a unique reexperiencing of an early
interaction with a primary caregiver. The degree
to which the physiological aspect of anxiety is
addressed by the biofeedback paradigm strength-
ens the argument for its inclusion in treatment.
The use of biofeedback to augment other critical
aspects of treatment, such as the therapeutic alli-
ance, increased self-awareness, and an attitude of
acceptance, further warrants its utility. Further-
more, biofeedback meets requests of evidence-
based psychology standards, in that it provides an
ongoing objective measure of progress. Although
further research on biofeedback measures across
anxiety subtypes and its integrative qualities is
necessary to reinforce and consolidate the position
of biofeedback in the treatment of anxiety, its cur-
rent position as a valuable addition is sufficiently
discernible to merit its utilization.
Agnihotri, H., Paul, M., & Sandhu, J. S. (2007). Biofeed-
back approach in the treatment of generalized anxiety
disorder. Iran Journal of Psychiatry,2, 90–95.
Ams, M., Ridder, S., Strehl, U., Breteler, M., & Coenen, A.
(2009) Efficacy of neurofeedback treatment in ADHD:
The effect on inattention, impulsivity, hyperactivity:
A meta-analysis. Clinical EEG and Neuroscience, 40,
Barlow, D. H. (2002). Anxiety and its disorders: The nature
and treatment of anxiety and panic (2nd ed.). New York:
Barlow, D. H., Farchione, T. J., Fairholme, C. P., Ellard, K.
K., Boisseau, C. L., Allen, L. B., et al. (2011). The unified
protocol for transdiagnostic treatment of emotional disor-
ders: Therapist guide. New York: Oxford University Press.
Barnea, A., Rassis, A., & Zaidel, E. (2005). Effect of neu-
rofeedback on hemispheric word recognition. Brain and
Cognition, 59, 314–321.
Bollas, C. (1987). The shadow of the object: Psychoanalysis
of the unthought known. New York: Columbia University
Bont, J. I. C., Castilla, C. D. S., & Maranon, P. P. (2004).
Comparison of three fear of flying therapeutic programs.
Psicothemea, 16, 661–666.
Borkovec, T. D., & Sharpless, B. (2004). Generalized anxi-
ety disorder: Bringing cognitive behavioral therapy into
the valued present. In S. Hayes, V. Follette, & M. Line-
han, (Eds.), New directions in behavior therapy (pp. 209–
242). New York: Guilford Press.
Schwartz_Biofeedback4E.indb 449 11/12/2015 5:24:27 PM
450 VI. CLINICAL APPLICATIONS: TRADITIONAL GENERAL BIOFEEDBACK PRACTICE
Bourne, E. J. (2005). The anxiety and phobia workbook (4th
ed.). Oakland, CA: New Harbinger.
Bradley, S. J. (2000). Affect regulation and the development of
psychopathology. New York: Guilford Press.
Brenner, S. L., Beauchaine, T. P., & Sylvers, P. D. (2005). A
comparison of psychophysiological and self-report mea-
sures of BAS and BIS activation. Psychophysiology, 42,
Cannon, W. (1929). Bodily changes in pain, hunger, fear, and
rage. New York: Appleton.
Chalmers, J. A., Quintana, D. S., Abbott, M. J. A., &
Kemp, A. H. (2014). Anxiety disorders are associated
with reduced heart rate variability: A meta-analysis.
Frontiers in Psychiatry, 5, 1–11.
Clark, C. R., Galletly, C. A., Ash, D. J., Moores, K. A., Pen-
rose, R. A., & McFarlane, A. C. (2009). Evidence-based
medicine evaluation of electrophysiological studies of
the anxiety disorders. Clinical EEG and Neuroscience,
Clark, D. A., & Beck, A. T. (2010). Cognitive therapy of
anxiety disorders: Science and practice. New York: Guil-
Clough, B. A., & Casey, L. M. (2011). Technological
adjuncts to enhance current psychotherapy practices: A
review. Clinical Psychology Review, 31(3), 279–292.
Corrado, P., Gottlieb, H., & Abdelhamid, M. H. (2003).
The effect of biofeedback and relaxation training on
anxiety and somatic complaints in chronic patients.
American Journal of Pain Management, 13, 133–139.
Coy, P. C., Cardenas, S. J., Cabrera, D. M., Zirot, G. Z.,
& Claros, M. S. (2005). Psychophysiological and behav-
ioral treatment of anxiety disorder. Salud Mental, 28,
Craske, M. G. (2003). The origins of phobias and anxiety dis-
orders: Why more women than men. Oxford, UK: Elsevier
Crider, A. (2008). Personality and electrodermal response
lability: An interpretation. Applied Psychophysiology and
Biofeedback, 33, 141–148.
Cruz, M., & Larsen, R. J. (1995). Personality correlates of
individual differences in electrodermal lability. Journal
of Social Behavior and Personality, 23, 93–104.
Davidson, R. (1998). Affective style and affective disorders:
Perspectives from affective neuroscience. Cognition and
Emotion, 12, 307–330.
DiMauro, J., Domingues, J., Fernandez, G., & Tolin, D. F.
(2013). Long-term effectiveness of CBT for anxiety dis-
orders in an adult sample: A follow-up study. Behavior
Research and Therapy, 51(2), 82–86.
Domschke, K., Stevens, S., Pfleiderer, B., & Gerlach, A. L.
(2010). Interoceptive sensitivity in anxiety and anxiety
disorders: An overview and integration of neurobiologi-
cal findings. Clinical Psychology Review, 30(1), 1–11.
Dong, W., & Bao, F. (2005). Effects of biofeedback therapy
on the intervention of examination-caused anxiety.
Chinese Journal of Clinical Rehabilitation, 9(32), 17–19.
Ellis, A. (1994). Reason and emotion in psychotherapy—
revised and updated. New York: Birch Lane Press.
Eysenck, M. W., Derakshan, N., Santos, R., & Calvo, M.
G. (2007). Anxiety and cognitive performance: Atten-
tional control theory. Emotion, 7, 336–353.
Fisher, P. L., & Wells, A. (2005). How effective are cog-
nitive and behavioral treatments for OCD? Behaviour
Research and Therapy, 43, 1543–1558.
Foa, E. B., Hembree, E. A., Cahill, S. E., Rauch, S. A. M.,
Riggs, D. S., Feeny, N. C., et al. (2005). Randomized
trial of prolonged exposure for posttraumaticstress disor-
der with and without cognitive restructuring: Outcome
at academic and community clinics. Journal of Consult-
ing and Clinical Psychology, 73, 953–964.
Friedman, B. H. (2007). An autonomic flexibility–neuro-
visceral intregation model of anxiety and cardiac vagal
tone. Biological Psychology, 74, 185–199.
Gevirtz, R., (2009). Resonant frequency training to restore
autonomic homeostasis for treatment of psychophysi-
ological disorders. Biofeedback, 27, 7–9.
Gevirtz, R., & Dalenberg, C., (2008). Heart Rate Variabil-
ity Biofeedback in the treatment of trauma symptoms.
Biofeedback, 36, 22–23.
Goodwin, E. A, & Montgomery, D. D. (2006). A cognitive-
behavioral, biofeedback-assisted relaxation treatment
for panic disorder with agoraphobia. Clinical Case Stud-
ies, 5, 112–125.
Hammond, D. C. (2005). Neurofeedback with anxiety and
affective disorders. Child and Adolescent Psychiatric Clin-
ics of North America, 14, 105–123.
Hawkins, R. C., Doell, S. R., Lindseth, P., Jeffers, V., &
Skaggs, S. (1980). Anxiety reduction in hospital-
ized schizophrenics through thermal biofeedback and
relaxation training. Perceptual and Motor Skills, 51,
Hayes, S. C., Strosahl, K., & Wilson, K. G. (1999). Accep-
tance and commitment therapy: An experiential approach
to behavior change. New York: Guilford Press.
Heide, F. J., & Borkovec, T. D. (1983). Relaxation-induced
anxiety: Paradoxical anxiety enhancement due to relax-
ation training. Journal of Consulting and Clinical Psychol-
ogy, 51, 171–182.
Hitanshu, A., Maman, P., & Jaspal, S. S. (2007). Biofeed-
back approach in the treatment of generalized anxiety
disorder. Iranian Journal of Psychiatry, 2, 90–95.
Hoehn-Saric, R., & McLeod, D. R. (1988). The periph-
eral sympathetic nervous system: Its role in pathologi-
cal anxiety. Psychiatric Clinics of North America, 11,
Hoehn-Saric, R., McLeod, D. R., Funderburk, F., & Kow-
alski, P. (2004). Somatic symptoms and physiological
responses in generalized anxiety disorder and panic dis-
order: An ambulatory monitor study. Archives of General
Psychiatry, 46(12), 1113–1119.
Hurley, J. D., & Meminger, S. R. (1992). A relapse-preven-
tion program: Effects of electromyographic training on
high and low levels of state and trait anxiety. Perceptual
and Motor Skills, 74, 699–705.
Jacobson, E. (1938). Progressive relaxation (2nd ed.). Chi-
cago: University of Chicago Press.
Jerath, R., Crawford, M. W., Barnes, V. A., & Harden, K.
(2015). Self-regulation of breathing as a primary treat-
Schwartz_Biofeedback4E.indb 450 11/12/2015 5:24:27 PM
26. Anxiety Disorders 451
ment for anxiety. Applied Psychophysiology and Biofeed-
back, 40, 107–115.
Kabat-Zinn, J. (1982). An out-patient program in behav-
ioral medicine for chronic pain patients based on the
practice of mindfulness meditation: Theoretical consid-
erations and preliminary results. General Hospital Psy-
chiatry, 4, 33–47.
Kessler, R. C., Petukhova, M., Sampson, N. A., Zaslavsky,
A. M., & Wittchen, H. (2012). Twelve-month and life-
time prevalence and lifetime morbid risk of anxiety and
mood disorders in the United States. International Jour-
nal of Methods of Psychiatric Research, 21, 169–184.
Khazan, I. Z. (2013). The clinical handbook of biofeedback.
Chichester, UK: Wiley-Blackwell.
Kleen, M., & Reitsma, B. (2011). Appliance of heart rate
variability biofeedback in acceptance and commitment
therapy: A pilot study. Journal of Neurotherapy, 15(2),
Kropotov, J. D. (2009). Quantitative EEG, event-related
potentials and neurotherapy. New York: Academic Press.
Lang, P. J., & McTeague, L. M. (2009). The anxiety disorder
spectrum: Fear imagery, physiological reactivity, and dif-
ferential diagnosis. Anxiety Stress Coping, 22, 5–25.
LeDoux, J. (2002). The synpatic self. New York: Viking Press.
Lehrer, P. M. (2007). Biofeedback training to increase heart
rate variability. In P. M. Lehrer, R. L. Woolfolk, & W. E.
Sime (Eds.), Principles and practice of stress management
(3rd ed., pp. 227–248). New York: Guilford Press.
Lehrer, P. M., Carr, R., Sargunaraj, D., & Woolfolk, R. L.
(1994). Stress management techniques: Are they all
equivalent, or do they have specific effects? Biofeedback
and Self-Regulation, 19, 353–401.
Levit Binnun, N., Golland, Y., Davidovitch, A., & Rolnick,
A. (2010). The biofeedback odyssey: From Neal Miller
to current and future models of regulation. Biofeedback,
Linehan, M. M. (1993). Cognitive-behavioral treatment of
borderline personality disorder. New York: The Guilford
Ludewig, S., Geyer, M. A., Ramseier, M., Vollenweider, F.
X., Rechsteiner, E., & Cattapan-Ludewig, K. (2005).
Information-processing deficits and cognitive dysfunc-
tion in panic disorder. Journal of Psychiatry and Neurosci-
ence, 30, 37–43.
Manzoni, G. M., Pagnini, F., Castelnuovo, G., & Molinari,
E. (2008). Relaxation training for anxiety: A ten-years
systematic review with meta-analysis. BMC Psychiatry,
Meuret, A. E., Wilhelm, F. H., & Roth, W. T. (2001). Respi-
ratory biofeedback-assisted psychotherapy in panic dis-
order. Behavior Modification, 25, 584–605.
Meuret, A. E., Wilhelm, F. H., & Roth, W. T. (2008).
Feedback of end-tidal pCO2 as a therapeutic approach
for panic disorder. Journal of Psychiatric Research, 42,
Milrod, B., Busch, F., Cooper, A., & Shapiro, T. (1997).
Manual of panic-focused psychodynamic psychotherapy.
Arlington, VA: American Psychiatric Publishing.
Moss, D. (2003). Anxiety disorders. In D. Moss, A.
McGrady, T. C. Davies, & I. Wickramasekera (Eds.),
Handbook of mind–body medicine for primary care
(pp. 359–377). Thousand Oaks, CA: Sage.
Moss, D. (2009) Advances in the use of biofeedback and
neurofeedback with post traumatic stress disorder: Part
I. Biofeedback, 37(1), 1–2.
Othmer, S. (1991). Remediating PTSD with Neuro-
Peniston, E. G., & Kulkosky, P. J. (1991). Alpha-theta
brainwave neuro-feedback therapy for Vietnam veter-
ans with combat-related post-traumatic stress disorder.
Medical Psychotherapy, 4, 47–60.
Peper, E., & Gibney, K. H. (2003). A teaching strategy for
successful hand warming, Somatics, 14(1), 26–30.
Pieper, S., Brosschot, J. F., Van Der Leeden, R., & Thayer,
J. F. (2010). Prolonged cardiac effects of momentary
assessed stressful events and worry episodes. Psychoso-
matic Medicine, 72, 570–577.
Pine, D. S. (2009). Anxiety disorders: Introduction and
overview. In B. J. Sadock et al. (Eds.), Kaplan and
Sadock’s comprehensive textbook of psychiatry (9th ed.,
Vol. 1, pp. 1839–1926). Philadelphia: Lippincott Wil-
liams & Wilkins.
Pittig, A., Arch, J. J., Lam, C. W. I., & Craske, M. G. (2012).
Heart rate and heart rate variability in panic, social
anxiety, obsessive–compulsive, and generalized anxiety
disorders at baseline and in response to relaxation and
hyperventilation. International Journal of Psychophysiol-
ogy, 87, 19–27.
Plaza I. D., Herrera-Mercadal, P., & Garcia-Campayo, J.
(2013). Mindfulness-based mobile applications: Lit-
erature review and analysis of current features. JMIR
Mhealth Uhealth, 1(2), e24, 1–19.
Pole, N. (2007). The psychophysiology of posttraumatic
stress disorder: A meta analysis. Psychological Bulletin,
Reed, M., & Saslow, C. (1980). The effects of relaxation
instructions and EMG biofeedback on test anxiety, gen-
eral anxiety, and locus of control. Journal of Consulting
and Clinical Psychology, 36, 683–690.
Reiner, R. (2008). Integrating a portable biofeedback
device into clinical practice for patients with anxiety
disorders: Results of a pilot study. Applied Psychophysiol-
ogy and Biofeedback, 33, 55–61.
Rice, K. M., Blanchard, E. B., & Purcell, M. (1993). Bio-
feedback treatments of generalized anxiety disorder:
Preliminary results. Biofeedback and Self-Regulation, 18,
Rolnick, A. (1992). The application of biofeedback to psy-
chological problems in the military setting. Biofeedback
and Self-Regulation, 17(3), 235–236.
Rolnick, A. (1999). Biofeedback. Rosh Haayen, Israel. (in
Rolnick, A., & Rickles, W. (2010). Following Neal Miller's
footprints: Integrating biofeedback with the psychody-
namic, relational, and intersubjective approach. Biofeed-
back, 38(4), 131–135.
Sadock, B. J., & Sadock, V. A. (2003). Kaplan & Sadock’s
Schwartz_Biofeedback4E.indb 451 11/12/2015 5:24:27 PM
452 VI. CLINICAL APPLICATIONS: TRADITIONAL GENERAL BIOFEEDBACK PRACTICE
synopsis of psychiatry (9th ed.). Philadelphia: Lipincott/
Williams & Wilkins.
Schoenberg, P. L. A., & Anthony, S. D. (2014). Biofeedback
for psychiatric disorders: A systematic review. Applied
Psychophysiology and Biofeedback, 39(2), 109–135.
Shusterman, V., & Barnea, O. (1995). Spectral charac-
teristics of skin temperature indicate peripheral stress-
response. Applied Psychophysiology and Biofeedback, 20,
Smits, J. A., Berry, A. C., Tart, C. D., & Powers, M. B.
(2008). The efficacy of cognitive-behavioral interven-
tions for reducing anxiety sensitivity: A meta-analytic
review. Behaviour Research and Therapy, 46, 1047–1054.
Stewart, R. E., & Chambless, D. L. (2009). Cognitive-
behavioral therapy for adult anxiety disorders in clinical
practice: A meta-analysis of effectiveness studies. Jour-
nal of Consulting and Clinical Psychology, 77(4), 595–606.
Tan, G., Dao, T., Farmer, L., Sutherland, R., & Gevirtz, R.
(2011). Heart rate variability (HRV) and postraumatic
stress disorder (PTSD): A pilot study. Applied Psycho-
physiology and Biofeedback, 36(1), 27–35.
Teasdale, J. D., Segal, Z. V., & Williams, J. M. G. (1995).
How does cognitive therapy prevent depressive relapse
and why should attentional control (mindfulness) train-
ing help?: An information processing analysis. Behav-
iour Research and Therapy, 33, 25–39.
Thayer, J. F., Friedman, B. H., & Borkovec, T. D. (1996).
Autonomic characteristics of generalized anxiety disor-
der and worry. Biological Psychiatry, 39, 255–266.
Thompson, M., & Thompson, L. (2007). Neurofeedback for
stress management. In P. M. Lehrer, R. L. Woolfolk, &
W. E. Sime (Eds.), Principles and practice of stress manage-
ment (3rd ed., pp. 249–289). New York: Guilford Press.
Travis, F. (2001). Autonomic and EEG patterns distinguish
transcending from other experiences during Transcen-
dental Meditation practice. International Journal of Psy-
chophysiology, 42, 1–9.
van der Kolk, B. (2014). The body keeps the score: Brain,
mind, and body in the healing of trauma (Kindle Locations
8330-8331). Penguin Publishing Group.
Walker, J. E. (2009). Anxiety associated with post trau-
matic stress disorder—the role of quantitative electroen-
cephalograph in diagnosis and in guiding neurofeedback
training to remediate the anxiety. Biofeedback Volume,
Walker, J. E., & Kozlowski, G. P. (2005). Neurofeedback
treatment of epilepsy. Child and Adolescent Psychiatric
Clinics of North America, 14, 163–176.
Wenck, L. S., Leu, P. W., & D’Amato, R. C. (1996). Evaluat-
ing the efficacy of a biofeedback intervention to reduce
children’s anxiety. Journal of Clinical Psychology, 52,
Wiederhold, B. K., & Wiederhold, M. D. (2003). Three-
year follow-up for virtual reality exposure for fear of fly-
ing. CyberPsychology and Behavior, 6, 441–445.
Wilhelm, F. H., Gevirtz, R., & Roth, W. T. (2001). Respi-
ratory dysregulation in anxiety, functional cardiac, and
pain disorders. Assessment, phenomenology, and treat-
ment. Behavior Modification, 25, 513–545.
Wilhelm, F. H., Pfaltz, M. C., Gross, J. J., Mauss, I. B., Kim,
S. I., & Wiederhold, F. H. (2005). Mechanisms of vir-
tual reality exposure therapy: The role of the behavioral
activation and behavioral inhibition systems. Applied
Psychophysiology and Biofeedback, 30, 271–284.
Winnicott, D. W. (1971). Playing with reality. New York:
Wolpe, J. (1958). Psychotherapy by reciprocal inhibition as
the main basis of psychotherapeutic effects. Archives of
Neurology and Psychiatry, 72, 205.
Wolpe, J. (1973). The practice of behavior therapy (2nd ed.).
New York: Pergamon Press.
Wood, D. P., Murphy, J. A., Center, K. B., Russ, C., McLay,
R. N., Reeves, D., et al. (2008). Combat-related post-
traumatic stress disorder: A multiple case report using
virtual reality graded exposure therapy with physiologi-
cal monitoring. Studies in Health Technology and Infor-
matics, 132, 556–561.
Yucha, C., & Gilbert, C. (2004). Evidence-based practice
in biofeedback and neurofeedback. Wheat Ridge, CO:
Association for Applied Psychophysiology and Biofeed-
Yucha, C., & Montgomery, D. (2008). Evidence-based prac-
tice in biofeedback and neurofeedback. Wheat Ridge, CO:
Association of Applied Psychophysiology and Biofeed-
Zucker, T, Samuelson, K., Greenberg, M., & Gevirtz, R.
(2007). The effects of respiratory sinus arrhythmia bio-
feedback on heart rate variability and posttraumatic
stress disorder symptoms: A pilot study. Applied Psycho-
physiological Biofeedback, 34, 134–156.
Schwartz_Biofeedback4E.indb 452 11/12/2015 5:24:28 PM