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Section II:
Theories of Panic Disorder Neurobiological Theories Biological
theorists conceptualize PD as a distinct psychiatric condition
that stems from an underlying biological dysfunction. The recognition of
PD as a distinct syndrome is credited to Donald Klein, who demonstrated
that the tricyclic antidepressant imipramine successfully blocked spontaneous
panic attacks but failed to reduce generalized anxiety, while benzodiazepines
reduced generalized anxiety but did not block panic attacks.[3] Although
subsequent research has demonstrated that both benzodiazepines and tricyclic
antidepressants can alleviate spontaneous panic attacks and generalized
anxiety, there still exists a large body of evidence that supports the
view that panic is distinct from generalized anxiety and has a neurobiological
etiology. Support for a biological etiology of PD comes from several lines
of evidence, including: (a) genetic studies; (b) laboratory provocation
of panic models; (c) studies assessing the effects of drugs on particular
neurotransmitter systems; and (d) respiratory and hyperventilation theories.
Genetic studies. Evidence for the genetic transmission of PD can be found
in the fact that panic tends to run in families.[4] For example, approximately
one half of all PD patients have at least 1 relative with PD, and first-degree
relatives of PD patients are approximately 5 times more likely to develop
PD than first-degree relatives of normal controls. Although the magnitude
of difference is not as high, rates of PD are still considerably higher
for first-degree relatives of patients with PD than for first-degree relatives
of patients with agoraphobia alone. Stronger confirmation of a genetic
link for PD is provided by results from a twin study that indicate that
PD and agoraphobia with panic attacks are more than 5 times as frequent
in monozygotic twins than in dizygotic cotwins of patients with PD. However,
these results may be explained by the fact that monozygotic twins may share
more similar environmental experiences and may also be treated more alike
than dizygotic twins. Therefore, studies that examine rates of the disorder
in children of PD patients who were adopted at birth and raised by a healthy
parent are still needed to provide further evidence for a genetic etiology
of PD. Further, although data from family and twin studies suggest a strong
genetic component to PD, it is still unclear if what is inherited is a
specific vulnerability for panic or merely a general trait such as "negative
affectivity" that then translates into a specific anxiety or depressive
disorder depending upon environmental influences. Laboratory provocation
of panic. Since panic attacks are difficult to capture under natural conditions,
scientists have developed laboratory models of panic attacks. For the most
part, laboratory models involve provoking a panic attack by administering
a panicogenic substance to the patient. To date, much of what is known
about the biochemical, physiological, and psychological changes that occur
during a panic attack come from laboratory-provocation studies.[5] Although
many substances have been used over the years, the most commonly researched
substances include sodium lactate, carbon dioxide (CO2), yohimbine, and
caffeine. Overall, findings from these studies suggest that (a) patients
with PD experience a greater number of panic attacks during administration
of these substances, compared with normal controls and patients with other
psychiatric disorders; (b) laboratory-provoked attacks resemble naturally
occurring panic attacks; and (c) drugs used to treat PD also block laboratory-provoked
panic attacks from occurring. By studying the effects of substances that
provoke panic attacks and those that block the attacks from occurring,
researchers aim to elucidate biological factors involved in the etiology
of PD. They hypothesize that the various substances that provoke attacks
in PD patients but not in normal controls or other psychiatric patients
do so by activating an inherited biological dysfunction. Alternatively,
those agents that block the attacks from occurring are believed to treat
the underlying biological dysfunction. However, critics contend that provocation
studies such as these have so far been unable to provide conclusive evidence
for a biological etiology of PD. Several lines of evidence indicate that
psychological factors may mediate the provocation of panic within the laboratory.
For example, several studies have demonstrated that psychological treatments
block laboratory-provoked panic attacks. In addition, other studies have
demonstrated that psychological factors, such as variations in instructional
set, the presence of a doctor, and illusion of control over administration
of the panicogenic agent, have influenced the incidence and severity of
panic attacks in the laboratory. Critics have also debated if the laboratory-provoked
panic attack is, in fact, the result of underlying neurochemical changes
or if PD patients merely demonstrate elevations on physiological measures
at baseline. For example, although individuals with and without a history
of panic attacks report differences in levels of fear when given sodium
lactate, they do not differ on a variety of physiological measures. This
suggests that both groups may experience many similar physical sensations
but that only patients with PD respond with fear to these sensations, presumably
because they have a history of panic attacks. Neurotransmitter theories.
Researchers[6] attempt to provide an indirect link between PD and specific
neurotransmitter systems by assessing the effects of drugs on particular
neurotransmitter systems. Specifically, they attempt to demonstrate that
drugs used to treat panic increase availability of a specific neurotransmitter
or its metabolite while drugs that induce panic decrease availability of
the same neurotransmitter. Conversely, an association may be established
by demonstrating that antipanic drugs decrease availability of a specific
neurotransmitter while panic-provoking drugs increase availability of the
same neurotransmitter. Neurotransmitters commonly implicated in the etiology
of PD include norepinephrine, serotonin, and gamma-aminobutyric acid (GABA).
Respiratory and hyperventilation theories. Respiratory physiology theories[3]
propose that panic attacks may be caused by a dysfunctional respiratory
system. Substances such as sodium lactate and CO2, which are not believed
to trigger any one neurotransmitter system, are believed to provoke panic
attacks by stimulating the respiratory system. Since the symptoms of a
panic attack closely resemble those experienced during hyperventilation,
several theories[3] have suggested that hyperventilation may be causally
related to panic attacks. During hyperventilation, there is an imbalance
between oxygen inhaled and CO2 exhaled, so that more CO2 is exhaled than
produced, thus lowering CO2 levels in the body. In an effort to compensate
for the reduction in respiratory rate caused by hyperventilation, patients
experience a host of symptoms, including shortness of breath, dizziness,
trembling, and palpitations. The greater the loss of CO2 as a result of
hyperventilation, the stronger these secondary symptoms. Hyperventilation
theories of panic differ according to whether they consider hyperventilation
to be primary or secondary to other factors, such as fear. Proponents of
the former position suggest that PD patients misattribute the sudden, unexpected,
and inexplicable somatic symptoms which arise immediately following hyperventilation
(especially shortness of breath and heart palpitations) and, in doing so,
experience the initial fear typically reported in PD. This initial sense
of fear is then believed to activate the autonomous nervous system in preparation
for fight or flight, which leads to a subsequent increase in heart and
respiration rates. If the individual does not flee or fight, these increases
will eventually lead to a further drop in CO2, thus increasing the symptoms
of hyperventilation. Hyperventilation theorists propose that PD patients
are chronic hyperventilators who acutely increase breathing during stress,
leading to episodes of panic. However, since forced hyperventilation induces
panic attacks in only a subgroup of patients and evidence for the existence
of chronic hyperventilation is mixed, the primary hyperventilation hypothesis
may be insufficient to account for the etiology of PD. An alternate theory
of hyperventilation proposes that hyperventilation is secondary to the
experience of fear. This model suggests that the fear of having a panic
attack gives rise to somatic symptoms, which in turn, lead to increased
fear, hyperventilation, and so on, until the individual experiences a full-blown
panic attack. This theory has been criticized on several grounds, including
its inability to elucidate the specific events that give rise to the experience
of fear or explain why panic attacks are not caused in all individuals
who experience fear. Opponents of this theory also assert that psychological
factors, while capable of mediating laboratory-provoked attacks, have not
been shown to provoke attacks in and of themselves. A more recent formulation
by Donald Klein and colleagues proposes that the essential disturbance
in PD may be a dysfunctional suffocation monitor (a "false suffocation
alarm"). Throughout the course of evolution, a highly sensitive "alarm
system" has developed to detect when an organism is in danger of suffocation.
High CO2 levels usually serve as an indicator that the organism is in danger
of imminent suffocation, since high levels of CO2 correspond with low levels
of oxygen. Klein suggests that for PD patients, this suffocation threshold
is pathologically lowered (ie, their suffocation monitor becomes hypersensitive
to CO2), with low levels of CO2 becoming a signal for low oxygen supply.
As a result, the brain's suffocation monitor incorrectly signals a lack
of oxygen, and thus triggers a false suffocation alarm. He hypothesizes
that since PD patients believe they are suffocating, (a) they experience
shortness of breath and (b) they begin hyperventilating in order to keep
CO2 levels well below the suffocation threshold. Therefore, according to
Klein, rather than cause panic attacks, hyperventilation is a consequence
and actually a defense against panic onset. Klein distinguishes between
panic and fear, suggesting that while panic is a false suffocation alarm,
fear is not. Integrating laboratory provocation studies of panic, Klein
suggests that "respiratory" panicogens such as sodium lactate, CO2, and
isoproterenol elicit a false suffocation alarm (ie, a panic attack). Conversely,
"neurochemical" panicogens such as yohimbine, caffeine, and mCPP produce
general autonomic surges or changes similar to those created by fear, stress,
or pain, and may be evident in both anxiety disorders and normal emergency
reactions. There appears to some empirical support for CO2 hypersensitivity
in PD. For example, studies suggest that following CO2 inhalation, patients
with PD exhibit a more rapid increase in respiration than normal controls
and other psychiatric patients. However, the false suffocation alarm hypothesis,
although it is a compelling integration of seemingly disparate physiological
and pharmacological data, has yet to be empirically tested. Psychological
Theories Several psychological theories of PD have been advanced that are
well supported by empirical data, indicating the importance of psychological
factors in the etiology and maintenance of PD. In fact, many of the biological
findings can be explained within these psychological theories. Data showing
that (a) psychological interventions alleviate panic attacks; (b) psychological
treatments block laboratory-provoked attacks; and (c) psychological factors
mediate laboratory-provoked attacks suggest that any valid theory of PD
must include both biological and psychological factors. Although much of
the empirical data have attempted to test hypotheses conceptualized by
cognitive and behavioral models, a psychodynamic model of PD is also presented
below. Psychodynamic models. According to Freud's early formulation, pathologic
anxiety occurs when unacceptable libidinal thoughts, impulses, memories,
and desire break through into consciousness. The psychic energy attached
to these previously repressed components then appears in a disguised form
(eg, a panic attack). In a subsequent formulation, Freud suggested that
anxiety leads to repression instead of the other way around. This later
formulation proposed that anxiety is a signal to the ego that it is in
danger. As a result, the ego attempts many psychic "maneuvers," including
repression, to try and reduce anxiety and avoid the dangerous situation.
A panic attack, then, is a neurotic symptom that results when memories
of past events are inadequately repressed. Freud also suggested that the
phobic behavior exhibited by these patients might be a result of their
fear of having panic attacks. Modern psychoanalytic theorists propose that
both anxiety and panic attacks are invoked by triggers that are symbolically
related to infantile wishes and/or fears. Unconscious or conscious cues
become associated with earlier innate psychological and biological threats
to the organism, such as castration, separation, or parental disapproval,
and serve as a trigger for panic onset in adults. Specifically, when defense
mechanisms are unable to control the unconscious fantasies linked to these
infantile fears, panic attacks develop. A newer psychodynamic formulation
integrates findings from temperament studies and psychological assessments
of PD patients, and proposes that PD is an interaction between temperament
and environmental factors. According to this model, PD patients enter the
world with an inborn physiological reactivity that predisposes them toward
early fearfulness. When this inborn trait interacts with an inadequate
parental style (eg., parents who are incapable of managing a constitutionally
fearful baby), a psychological vulnerability for PD develops. Such individuals
struggle with dependency conflicts, develop weak representations of themselves
coupled with a powerful representation of others, and use poor strategies,
such as avoidance, to cope with life stresses. These psychological vulnerabilities,
in turn, exacerbate the underlying physiologic sensitivity and, in the
face of stress, lead to further psychological and physiological changes.
Finally, changes such as a decrease in feelings of safety or physiological
changes associated with feelings of loss of control, along with an increase
in negative emotions (such as anxiety, anger, guilt, and shame), culminate
in an initial panic attack. Although psychodynamic formulations are interesting,
one drawback to these models is the lack of research data to validate the
proposed concepts. Since many of these theories propose unconscious etiologies
for PD, the proposed hypotheses may be difficult to test directly and even
more difficult to refute since, given a panic attack, an unconscious etiology
may be presumed. Therefore, researchers need to develop measures to test
these concepts without presuming their existence solely on the presence
or absence of panic symptoms. The cognitive model. The cognitive model
of PD[7,8] proposes that panic attacks occur when individuals perceive
certain somatic sensations as considerably more dangerous than they truly
are, and then interpret them to mean that they are about to experience
sudden, imminent disaster. For example, individuals may develop a panic
attack if they misinterpret heart palpitations as signaling an impending
heart attack or if they misinterpret jittery, shaky feelings as indicating
that they will lose control or go crazy. Clark[7] believes that these "catastrophic
misinterpretations" may arise not only from fear but also from a variety
of other emotions (eg, anger) or from other stimuli (eg, caffeine, exercise).
The vicious cycle culminating in a panic attack develops when a stimulus
perceived as threatening creates a feeling of apprehension. If the somatic
sensations that accompany this state of apprehension are catastrophically
misinterpreted, the individual experiences a further increase in apprehension,
followed by elevated somatic sensations and so on, until a full-blown panic
attack occurs. The fact that PD patients themselves report having thoughts
of imminent danger during their panic attacks (eg, heart attacks, insanity)
and report that these thoughts typically occur after they notice specific
bodily sensation, provides convincing support for the cognitive model of
panic. Other evidence in support of Clark's hypothesis is the finding that
laboratory-provoked attacks may lead to similar physiological sensations
in PD patients and normal controls, but only PD patients who catastrophically
misinterpret these sensations will go on to develop panic attacks. Furthermore,
only patients who develop panic attacks in the laboratory following the
administration of a panicogenic substance report fears of going crazy or
losing self-control. Additional support for Clark's cognitive model comes
from studies demonstrating that panic attacks can be alleviated with cognitive
techniques, such as cognitive restructuring, which attempt to challenge
and substitute catastrophic misinterpretations with rational thoughts.
Critics contend that the cognitive model does not explain why PD patients
continue to misinterpret these somatic sensations despite evidence to the
contrary (ie, when the catastrophic predictions do not come true). However,
since PD patients take a variety of precautions to prevent the occurrence
of an attack (eg, avoid or escape situations in which they are likely to
occur), it is likely that they never truly learn that their panic attacks
will not lead to catastrophes no matter what safeguards they may use. An
integrated model. Barlow conceptualizes the initial panic attack as a "false
alarm," in which fear or panic occurs in the absence of any life-threatening
stimulus, learned or unlearned.[9] He contrasts these with "true alarms,"
in which fear or panic occurs in the presence of an event that is truly
dangerous or life-threatening to the organism (eg, being attacked by a
gunman). According to Barlow,[9,10] individuals with PD have a genetically
based biological vulnerability (ie, they are "hard-wired" to respond to
the stress of negative life events with exaggerated neurobiological activity).
This neurobiological overreaction or false alarm occurs because such individuals
perceive life stressors as if they were truly dangerous or life-threatening.
In some of these individuals, the initial false alarm becomes associated
(via classical conditioning) with the somatic sensations that accompany
feelings of anxiety (eg, dizziness, palpitations). This association or
conditioning leads to the development of "learned alarms," wherein these
individuals learn to become fearful of these somatic sensations because
they believe they will lead to another attack. They become increasingly
anxious and apprehensive over having additional alarms or panic attacks
in the future and, as a result, go on to develop PD. Their inborn predisposition
to be somatically preoccupied becomes intensified as they focus even more
attention on themselves, with the result being that they become even more
sensitive to false alarms than they were when they had their first attack.
Occasional false alarms are more common among the general population than
previously realized.[10] However, most individuals who experience false
alarms do not become apprehensive about having future panic attacks. Barlow
proposes that several variables, including constitutional factors, a combination
of personality and cognitive dispositions (eg, overly dependent personality),
and a lack of social support may determine which individuals become susceptible
to stress and go on to develop PD. Further, Barlow believes that the avoidance
behaviors that develop subsequently as a means of coping with unexpected
panic and are also determined at least partly by cultural, social, and
environmental factors. Barlow's theory of panic has received support from
several sources. A number of studies indicate that many PD patients describe
one or more negative life events as preceding their first panic attack,
thus providing circumstantial evidence for the notion that the initial
false alarm may result from an overreaction to a life stress. However,
these results must be interpreted with caution since the studies have been
shown to have many methodological deficiencies. Further, other studies
indicate that stress may also play a role in precipitating other psychiatric
and physical disorders, suggesting that the relationship between stress
and panic onset may not be unique.[10] There is clear evidence, however,
those internal or somatic cues can become conditioned to anxiety, supporting
Barlow's claim that false alarms can become associated with somatic sensations.
In addition, findings that PD patients exhibit a greater fear over somatic
sensations than do other psychiatric patients and normal controls support
his contention that PD patients learn to become apprehensive about somatic
cues.[11]
Section III:
Empirically Supported Treatment Components The following
psychological interventions have been shown to be efficacious
-- either alone or in a "package" of treatment strategies -- for PD in
controlled research studies. (For a review of empirically supported psychological
treatments, see Woody & Sanderson.[12])
Psychoeducation
By the time PD patients consult with a mental health professional, they
typically have been to many different doctors without receiving a clear
diagnosis and explanation of PD. In the absence of such information, these
patients often imagine that they are going to die, go crazy, or lose control.
In almost
all cases, they suspect that the doctor has overlooked some life-threatening
physical condition that would account for their symptomatology. Therefore,
the psychoeducation phase consists of a didactic presentation about PD,
within the framework of the cognitive behavioral model of panic.[13]
During the
initial session(s), anxiety, panic, and agoraphobia are defined. Each symptom
is identified as a feature of PD and shown to be harmless. Common myths
about the danger of panic attacks (eg, panic attacks are a sign of an undetected
brain tumor, palpitations cause heart attacks, hyperventilation leads to
fainting, etc.) are debunked.
The development
of the disorder is understood as a psychological response to stress, and
avoidance behavior and anticipatory anxiety are viewed as ways to ward
off a recurrence of the panic attacks.
Written materials,
such as pamphlets and books, are valuable educational tools since they
may be reread whenever the patient desires. We recommend several excellent
"self-help" books or Web sites which offer simple, supportive information
about PD.[13-16] In addition, we encourage patients to join the Anxiety
Disorders Association of America (6000 Executive Blvd., Rockville, MD 20852;
http://www.adaa.org). For a nominal fee, patients receive a bimonthly newsletter
providing self-help tips and educational information (eg, latest research
findings), and have access to many other valuable resources. In this way,
psychoeducation becomes an ongoing venture for the patient and not just
one component of the therapy. Cognitive Restructuring The cognitive restructuring
component of cognitive behavioral therapy (CBT) derives from Beck's seminal
work on how faulty information-processing may underlie anxiety and related
dysfunctional behaviors.[8] Therapeutic change is achieved as these faulty
cognitions (ie, thoughts, beliefs, and assumptions) are identified and
then subjected to rigorous reality testing. The first step is to help the
patient identify how certain cognitions accentuate or provoke panic. This
is done by retrospectively examining the thoughts, beliefs, and assumptions
elicited during a typical panic or anxiety episode.
As both the
first and most recent panic attacks are vividly remembered, a detailed
discussion of those 2 experiences is a useful place to begin this examination.
Through a series of questions, the therapist tries to determine the patient's
idiosyncratic panic sequence and to uncover unrealistic catastrophic thoughts.
Under such questioning, the validity of these cognitions is implicitly
and explicitly challenged.
A typical
panic sequence follows : I was sitting in a meeting at work; I noticed
my heart began to beat faster (physical symptom); I assumed these palpitations
were the early signs of a panic attack, and that I would lose control and
start to yell. Everyone would think I was crazy! (catastrophic thought);
I became even more anxious, worried about losing control, and started to
perspire profusely (escalation of physical symptom); I excused myself from
the meeting (escape and avoidance); I felt depressed and discouraged because
I couldn't even handle an innocuous work meeting (hopelessness).
This description
reveals the PD patient's interior monologue. In therapy, it is necessary
to make these private thoughts explicit since most patients are unaware
of their own thinking.
For the most
part, people process information automatically, and stimuli are interpreted
rapidly. There is also a tendency to deny catastrophic ways of thinking
because these beliefs seem so incredible once the panic attack has subsided.
The therapeutic
setting should promote the patient's sense of comfort and acceptance in
order to facilitate disclosure. But in addition, we recommend that patients
self-monitor their cognitions during episodes of panic. A written numbered
format may be used, as in the example above. After several sessions of
reviewing these panic-related cognitions, a clear panic sequence emerges,
and patients begin to appreciate the role that cognitions play. Once the
patient becomes aware of the importance of their cognitions in eliciting
and fueling their panic attacks, they are in a position to re-evaluate
the validity of these cognitions and ultimately to challenge them.
In particular,
catastrophic misinterpretations of panic-related somatic cues are targeted.[7]
But other common misinterpretations involve the overestimation of the consequences
of panic (eg, public humiliation, losing one's job, interpersonal rejection).
We use a "thought
record" to quickly identify the patient's thoughts, examine their validity,
and challenge the patient to respond with more rational thoughts.[17] The
patient is provided with a list of 10 cognitive distortions, misinterpretations,
or types of illogic as defined by Burns.[14] For example, one of the more
common distortions is "jumping to conclusions" (anticipating that things
will turn out badly, even though there are no definite facts to support
this conclusion).
By identifying
distortions, the patient is able to correct the illogical conclusion by
substituting a more rational response. It is important to note that cognitive
restructuring is not "positive thinking," but instead is a focus on teaching
people to think realistically (ie, weighing out evidence). The final phase
of cognitive restructuring is to decatastrophize the situation with the
patient, especially when dealing with agoraphobic avoidance. This is easily
accomplished through a series of questions: What if your worst fears came
true -- would it really be as bad as you imagine?
Consider patients
who believe they will have a panic attack on a plane, causing them to scream
wildly and try to escape. In fact, if their worst fears were realized and
they did have a panic attack, the most likely outcome would be a feeling
of great discomfort, and not screaming, attempts to escape, and embarrassment.
Decatastrophizing greatly reduces the patient's need to avoid panic-related
situations. Respiratory Control Respiratory control helps the patient regain
a sense of control over the somatic features of panic and anxiety.
Patients are
taught a method of breathing that increases relaxation and prevents hyperventilation.[18]
Hyperventilation initiates a cascade of somatic symptoms such as dizziness,
chest pain, breathlessness, and parasthesias that culminate in panic. These
symptoms instill a frightening sense that one's body is out of control.
Under stress and anxiety, respiration rate often increases, characterized
by the use of chest muscles and short, shallow breaths. To combat this
tendency, the patient is taught diaphragmatic breathing (ie, breathing
which involves in-and-out movement of the abdomen, not chest) at a regular
rate (ie, approximately 12 breaths per minute).
This exercise
is then practiced outside of the session in many different situations.
The patients quickly learn to control their breathing and come to recognize
that this is an effective strategy that they can rely on in panic-provoking
situations.
Relaxation
Training Relaxation training is a progressive muscle exercise also intended
to help patients gain a greater sense of control over their bodies. It
is practiced daily as a way to identify and decrease tension that might
otherwise escalate into a full-blown panic attack. The basic technique
involves tensing and relaxing muscles to achieve a more serene state. Specific
step-by-step details regarding this exercise may be found in an excellent
text by Barlow and Cerny.[9]
Visualization
In therapy, discussion of anxiety-provoking situations and experiences
is all too often devoid of the vivid images, associations, and emotion
necessary to foster real change. Visualization is meant to enhance this
dialogue. When the patient closes her eyes and imagines such situations,
she is often flooded with anxiety.
By confronting
such anxiety-provoking situations in her mind's eye, the patient learns
how to cope before she has to confront them for real. The therapist helps
the patient to visualize the situation in as much detail as possible. As
the patient describes the image, the therapist asks relevant questions
about the associated thoughts and feelings.
This is meant
to elaborate the image, but it is also a useful assessment; reporting on
cognitions and emotions in an imagined situation in the present is usually
more accurate than recalling cognitions and emotions in a real situation
from the past.
In time, the
patient is asked to visualize effective coping techniques and responses.
In this way, visualization serves as an inoculation -- if the patient can
handle small amounts of manufactured anxiety (the anxiety that arises during
the imagery exercise), she will be better prepared to handle anxiety in
a natural setting.
Exposure Exposure
is the final component of CBT, in which the patient confronts anxiety-
and panic-provoking stimuli. These phobic stimuli may be external situations
or internal sensations (ie, interoceptive desensitization). By repeatedly
facing their anxiety in a structured situation, patients learn to develop
appropriate coping mechanisms and become further inoculated.
Based on the
patient's individualized hierarchy of feared situations, he or she is exposed
to each of these situations in a progressive, systematic fashion, where
the therapist guides the patient to use coping skills when confronting
anxiety-provoking situations.
For example,
an external situational exposure exercise may involve creating a hierarchy
of increasing distances from which a patient will drive from their home
on a highway or other feared road. Similarly, interoceptive exposure is
based on the patient's individualized hierarchy of feared internal sensations
(eg, dizziness, palpitations).
A simulation
of these sensations may be achieved using idiosyncratic methods, such as
overbreathing, spinning, and physical exertion (eg, ride an exercise bicycle
for 2 minutes).
The use of
a hierarchy of least feared to most feared stimuli allows the therapy to
progress and build on past accomplishments. The patient first learns to
cope with mildly anxiety-provoking situations and later faces the more
difficult situations.
Facing anxiety
within a supportive therapeutic setting helps the patient to use his or
her newly developed coping skills. The patient learns to tolerate anxiety
without the need to escape. This lesson is passed on from one anxiety-provoking
situation to the next. As always, practice between sessions is expected
and essential for rapid progress. We encourage patients to confront phobic
stimuli at least 3 times during the week between sessions.
First, the
patient completes the exposure exercise with the assistance of the therapist,
such as inducing heart palpitations by walking up and down stairs for 3
minutes, and later practices this exercise at home. The patient's self-confidence
soars as she realizes that the therapist has confidence that she can handle
this formerly anxiety-provoking experience on her own.
For a more
thorough presentation of these treatment components, see Barlow and Cerny.[9]
Dr. Alex
Wasserman Rosinsky
Médico
Psiquiatra
Dirección
E-Mail : dralwaro@hotmail.com
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del Dr. Alex Wasserman R.
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