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Anxiety Disorders
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CHAPTER 1 6
Anxiety Disorders
CARL F. WEEMS AND WENDY K. SILVERMAN
HISTORICAL CONTEXT
ALTHOUGH THE OXFORD ENGLISH Dictionary reports evidence for the noun ‘‘anx-
iety’’ as early as the 1500s, interest in childhood anxiety problems can
be traced as far back as the writings of Hippocrates in ancient Greece
(Silverman & Field, 2011). Descriptions of child anxiety and phobias also can be
found in writings from early America (e.g., Benjamin Rush), and in many famous
case reports (e.g., Freud’s Little Hans; Watson’s Little Albert; see Silverman & Field,
2011, for review). In the second edition of the Diagnostic and Statistical Manual of
Mental Disorders (DSM-II ; American Psychiatric Association [APA], 1968) there was
only one specific childhood anxiety category: overanxious reaction. The DSM-III
(APA, 1980) then introduced—and the DSM-III-R (APA, 1987) retained—a new
broad category termed anxiety disorders of childhood and adolescence. Within this
broad category three specific anxiety disorders were introduced: (1) separation anx-
iety disorder, (2) overanxious disorder, and (3) avoidant disorder. Children could
also receive diagnoses of other anxiety/phobic disorders classified among adults,
with identical criteria to the adult depictions.
Claims were soon made that the majority of new DSM-III categories and subcate-
gories, including those relating to anxiety, were overrefined, untested, and excessive
in number (see Silverman, 1992). It was also contended that the use of similar diag-
nostic criteria in children and adults was inconsistent with developmental changes
in the expression of psychopathology across the life span. These were serious issues,
and the research community was faced with the challenge of providing empirical evi-
dence to either support or refute the validity of each new diagnostic category. Hence,
a great deal of time and energy was devoted toward establishing basic requirements
of a useful taxonomic scheme, including reliability, coverage, descriptive validity,
and predictive validity (Blashfield, 1989). This work spurred concentrated efforts
toward developing and evaluating structured interviewing procedures as a way to
yield improved reliability of diagnoses (e.g., Silverman & Rabian, 1994; Silverman,
Saavedra, & Pina, 2001; see Silverman & Ollendick, 2005).
513

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514 Internalizing Behavior Disorders
The fourth version of the DSM (APA, 1994) witnessed major changes. The broad
category of anxiety disorders of childhood and adolescence (and its subcategories:
overanxious disorder, avoidant disorder) from the DSM-III and DSM-III-R were
abandoned. Only separation anxiety disorder was retained as a distinct child anxi-
ety disorder under ‘‘other disorders of infancy, childhood or adolescence.’’ Thus, in
theDSM-IV the same basic definitions of anxiety disorders apply to children, adoles-
cents, and adults, with the exception of separation anxiety disorder which requires
onset before age 18 although this requirement has been questioned (Manicavasagar,
Silove, Curtis, & Wagner, 2000). For specific phobia, social phobia, obsessive com-
pulsive disorder, posttraumatic stress disorder, and generalized anxiety disorder
there are notes in the diagnostic criteria delineating child specific considerations
(e.g., for specific phobia, Criterion C indicates that children may not recognize that
the fear is unreasonable).
TERMINOLOGICAL AND CONCEPTUAL ISSUES
Anxiety is viewed as a higher-order feeling state produced by specific brain mech-
anisms responsible for basic emotion (Damasio, 2003). We define anxiety in this
chapter as the product of a multicomplex response system, involving affective,
behavioral, physiological, and cognitive components (e.g., Barlow, 2002; Lang,
1977). Worry, for example, is one component of anxiety that can be viewed as
a cognitive process preparing the individual to anticipate future danger. Fear, in
contrast, is part of the response system that fosters preparation for either freezing
to avoid impending punishment or escaping as part of the fight/flight response
(Barlow, 2002; Gray & McNaughton, 2000; Mathews, 1990).
A core defining feature of anxiety is emotion dysregulation of the anxiety response
system (Weems, 2008). Such dysregulation may involve intense and disabling worry
that does not help anticipate true future danger, or intense fear reactions in the
absence of true threat. Distress/impairment may also result from dysregulation in
corresponding negative emotional states (e.g., being upset or overconcerned). For
convenience we refer to these primary features of anxiety problems as anxious emo-
tion. These core features of anxiety may be expressed behaviorally (e.g., avoidance),
cognitively (e.g., concentration difficulties), physiologically (e.g., dizziness, racing
heart), or interpersonally (e.g., difficulty making friends). These features cut across
all of the anxiety disorders in the DSM-IV . In contrast, secondary features of anxiety
are aspects that differentiate specific categories of anxiety disorder (Weems, 2008).
For example, worry about separation from parents is specific to separation anxiety
disorder, being embarrassed in public is specific to social anxiety disorder, and
uncued panic attacks are specific to panic disorder (APA, 1994).
DIAGNOSTIC ISSUES AND DSM-IV CRITERIA
The conceptualization and classification of the anxiety disorders in the DSM-IV
(1994, 2000) currently dominate the field. The fifth edition of the DSM is anticipated
for release in May 2013. Several changes to the classification scheme for anxiety

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Anxiety Disorders 515
disorders have been proposed. At the time of the writing of this chapter, no final
decisions had been made. However, it does appear that anxiety disorders included
inDSM-IV will continue to be included in DSM-5 . These include (1) specific phobias,
(2) social anxiety disorder, (3) generalized anxiety disorder, (4) separation anxiety
disorder, (5) obsessive compulsive disorder, (6) panic disorder, and (7) posttraumatic
stress disorder (PTSD). These disorders can appear at any age, with the exception of
separation anxiety disorder, which is diagnosed only if it emerges before age 18.
According to the DSM-IV (APA, 1994, 2000), specific phobias are characterized
by extreme and unreasonable fears of a specific object or situation such as dogs,
loud noises, or the dark; social anxiety disorder is characterized by an extreme
and unreasonable fear of being embarrassed or humiliated in front of other youths
or adults. Next, generalized anxiety disorder is characterized by persistent and
excessive worry about a number of events or activities, whereas separation anxiety
disorder is characterized by excessive worry concerning separation from home or
loved ones. Obsessive compulsive disorder (OCD) is characterized by recurrent
thoughts or behavior patterns that are severe enough to be time consuming, dis-
tressful, and highly interfering, including repeated thoughts about contamination,
repeated doubts, having things in a particular order, and aggressive or horrible
impulses. Panic disorder is characterized by sudden and severe attacks of anxiety.
In addition, a child or adolescent who experiences a catastrophic or otherwise
traumatic event may develop posttraumatic stress disorder (PTSD; APA, 1994,
2000). The traumatic event must involve a situation in which someone’s life has been
threatened or severe injury has occurred. Following exposure to the trauma, the
youth may exhibit agitated or confused behavior as well as intense fear, helplessness,
anger, sadness, horror, and/or denial. Youth with PTSD usually avoid situations
or places that remind them of the trauma. They also may become depressed,
withdrawn, emotionally unresponsive, and detached from their feelings.
The DSM anxiety disorders exhibit high rates of comorbidity with one another
(Costello, Egger, & Angold, 2004; Curry, March, & Hervey, 2004). In fact, only
secondary features outlined above, such as social concerns in social anxiety disor-
der and worries about separation in separation anxiety disorder, distinguish the
anxiety disorders from one another. Moreover, genetic risk for anxiety disorders is
nonspecific (Gregory & Eley, 2011). With the exceptions of OCD and possibly PTSD,
there is little evidence that anxiety disorders are related differentially to treatment
outcomes, although it is recognized that such null findings may be attributed in part
to insufficient sample sizes (see Berman, Weems, Silverman, & Kurtines, 2000; see
also Dadds, James, Barrett & Verhulst, 2004; Saavedra & Silverman, 2001). Finally,
longitudinal research on the stability of child and adolescent anxiety disorders has
produced inconsistent results (e.g., Last, Perrin, Hersen, & Kazdin, 1996; Newman
et al., 1996).
PREVALENCE
Anxiety disorders are one of the most common emotional problems in childhood
and adolescence. In a recent meta-analysis, Costello, Egger, Copeland, and Angold

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516 Internalizing Behavior Disorders
(2011) reported that the mean estimate for any anxiety disorder is 12.3% for
children between ages 6 and 12, with the following disorders being most prevalent:
specific phobia (6.7%), separation anxiety disorder (3.9%), social phobia (2.2%), and
generalized anxiety disorder (1.7%). For adolescents, the prevalence estimate for any
anxiety disorder was 11.0%. The following specific disorders were most prevalent:
specific phobia (6.6%), social phobia (5.0%), separation anxiety disorder (2.3%),
generalized anxiety disorder (1.9%), and panic disorder (1.1%).
RISK FACTORS AND ETIOLOGICAL FORMULATIONS
To understand the development of anxiety problems, a number of biological,
cognitive, behavioral, and social risk factors are salient. Some of these may be part of
‘‘normal’’ developmental processes (e.g., biological maturation) or may be atypical
experiences (e.g., traumatic event). Symptoms of anxiety and phobic disorders can
be understood as stemming from transactions among biological vulnerabilities (e.g.,
genetic, neural) and environmental risk factors (e.g., parenting, exposure to trauma)
that produce emotion dysregulation, distress, and impairment. These factors give
rise to undifferentiated anxious emotion. Specific anxiety disorders are then shaped
by biological, cognitive, behavioral, and social processes (Vasey & Dadds, 2001;
Weems & Stickle, 2005). For example, genetic predispositions and early experiences
may render a child vulnerable to elevated levels of anxiety and distress, sometimes
termed trait anxiety (or behavioral inhibition). More specific experiences such as
being excluded or teased by peers upon school entry may foster the development of
social anxiety; a frightening experience with a dog may result in an animal phobia;
and biological vulnerability such as the experience of uncued physiological arousal
may lead to panic disorder.
In understanding the etiology of childhood anxiety we use a developmental
perspective that emphasizes complex transactions among various vulnerabilities and
factors (Weems, 2008; Weems & Silverman, 2006). From this perspective, behavior
patterns among individuals have varying trajectories over time (Baltes, Reese, &
Lipsitt, 1980; Baltes, Reese, & Nesselroade, 1988), resulting in both equifinality and
multifinality (see Chapter 1).
Specific etiological influences on the development of problematic anxiety span
genetics, temperament, and physiology (biology); operant, observational, and
respondent learning (associative learning); information processing and stimulus/
event interpretation (cognition); attachment relations and sociability (socialization),
and interactions among these processes in diverse contexts (e.g., parent–child
relationships, family, home, school, community).
Biological Processes
Genetic influences . Twin studies suggest that about a third of the variance in childhood
anxiety symptoms is accounted for by heritable influences (see Eley, 2001; Gregory &
Eley, 2011). Heritability may help to account for children’s early anxious styles,
including physiological reactivity and avoidance behaviors. It is important to note,

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Anxiety Disorders 517
however, that genes do not act directly on behavior. Genes code for proteins, which
in turn affect brain structures and regulative processes, such as neurotransmitter
receptors. The heritability of anxiety also depends on many other factors including
the type of anxiety assessed, the age and sex of the population, the specific assessment
method, and whether anxiety is viewed as a personality trait or a clinical disorder
(Gregory & Eley, 2011). It is also important to note that the heritability of anxiety
increases considerably in adolescence and young adulthood, a phenomenon seen
for many psychiatric disorders (Bergen, Gardner, & Kendler, 2007). This pattern
suggests that genetic vulnerabilities unfold across development as environmental
risks mount (see Chapter 3).
Molecular genetics studies of anxiety have also grown rapidly. Such investigations
have focused on genes encoding components of the 5-HT and GABA systems. Results
have been mixed, but the strongest findings have linked genes to anxiety-related
traits such as behavioral inhibition and not to specific disorders. Such findings point
to the importance of differentiating between primary and secondary features of
anxiety (see earlier). For example, the gene encoding the GABA-synthetic enzyme
GAD65 has been associated with behavioral inhibition, a risk factor for anxiety
disorders such as panic disorder, yet no genes encoding GABA receptors have
been linked directly to panic disorder (see Gordon & Hen, 2004). One of the most
promising lines of research suggests that polymorphisms in the promoter region of
the gene for the 5-HT transporter (5-HTT) may also be associated with behavioral
inhibition, particularly among individuals exposed to environmental risk (Fox et al.,
2005). However, the particular polymorphisms in genes identified (e.g., the 5-HTT)
may not simply lead to increased risk under negative environments but rather
may be associated with malleability to both positive and negative environmental
influences (Belsky & Beaver, 2011; Belsky, & Pluess, 2009).
Temperament theorists have drawn from genetic models, suggesting that anxiety
problems stem from biological predispositions to react negatively to novelty (Bieder-
man et al., 1990, 1993; Kagan et al., 1988; Kagan, Reznick, & Gibbons, 1989; Kagan,
Reznick, & Snidman, 1987; see Lonigan, Phillips, Wilson, & Allan, 2011, for review).
Temperamentally inhibited children display many of the same behavioral, affec-
tive, and physiological characteristics as children with anxiety disorders, including
avoidance and withdrawal from novelty, clinging or dependence on parents, fear-
fulness, and autonomic hyperarousal (Kagan et al., 1987). Such children are more
likely than their peers to respond to potentially fearful situations (e.g., interactions
with a stranger, separations from mother) with heightened physiological reactivity,
which may result from a lower threshold of amygdalar and hypothalamic activity.
Central nervous system . The concept of a behavioral inhibition system (BIS) is a
good starting point for understanding central nervous system structures involved in
the anxiety response (Gray, 1982). The BIS comprises the septohippocampal system,
including the amygdala, noradrenergic projections of the locus coeruleus, and
serotonergic projections of the median raphe (Gray 1982; Gray & McNaughton, 2000).
Important for this discussion, the BIS is activated under conditions of perceived
threat, helping us avoid exposure to punishment and danger. Overactivation of the
BIS is associated with excessive fear, hyperarousal, and negative emotionality.

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518 Internalizing Behavior Disorders
Among septo-hippocampal structures, the amygdala has received particular atten-
tion in theories of the pathogenesis of anxiety (e.g., Davis, 1998; LeDoux, 2000). The
amygdala is a collection of nuclei found in the anterior portion of the temporal lobes.
It functions to evaluate the emotional significance of incoming stimuli after receiving
input from the cortex, hippocampus, and thalamus. The amygdala projects to other
brain structures in the frontal cortex (choice), the hippocampus (memory consoli-
dation), the striatum (approach/avoidance), and the hypothalamus and brain stem
(autonomic responses, startle, corticosteroid response) (see Gordon & Hen, 2004;
LeDoux, 2000). Importantly, no single structure, neurotransmitter, or gene controls
the experience of anxiety or any other complex behavioral trait (see Pine, 2011;
Chapter 3).
As noted, negative affect is an important component of anxiety. Functional brain
studies suggest normal threat assessment and emotional learning may involve
differential hemispheric activation. Electroencephalography (EEG) research has
demonstrated increased right prefrontal and anterior temporal region activation
during the experience of negative emotion and increased left prefrontal activation
during the experience of positive emotion (Davidson, 1998). Furthermore, increased
left prefrontal activation is associated with the ability to suppress startle responses
to negative stimuli (Davidson, 1998; Davidson, Marshall, Tomarken, & Henriques,
2000). Davidson et al. (2000) have also demonstrated greater relative right versus
left prefrontal activation among adults with social anxiety and depression. These
findings have been replicated in infants (Davidson & Fox, 1989) and school-age
children (8 to 11 years) with diagnosable anxiety disorders (Baving, Laucht, &
Schmidt, 2002). Similar findings have emerged in anxious youth using functional
magnetic resonance imaging (fMRI) techniques, with research implicating frontal
regions in anxiety disorders in youth (Carri ´on, Garrett, Menon, Weems, & Reiss,
2008). The greater spatial resolution of fMRI has recently shown sensitized amygdala
and hippocampal activation to facial expressions in youth with PTSD symptoms.
For example, youth with PTSD symptoms (ages 11 to 17) showed faster right
amygdala activation in response to angry faces than age and gender matched
controls (Garrett et al.,2012). In addition, a number of specific neurotransmitters
and neurotransmitter systems have been implicated in anxiety and anxiety-related
behavior. Both gamma-aminobutyric acid (GABA) and serotonin (5-HT) have been
the foci of research. This interest follows from findings that anti-anxiety (anxiolytic)
medications such as benzodiazepines and selective serotonin reuptake inhibitors
(SSRIs) modulate GABA and 5-HT neurotransmission. The noradrenergic sys-
tem also has been implicated in the expression of anxiety disorders (Gordon &
Hen, 2004).
Another theoretically important system is the hypothalamic-pituitary-adrenal
(HPA) axis. Activation of the HPA axis often follows from fight/flight reactions
in response to stress and fear, although its time course is considerably longer,
spanning minutes to hours. Fear reactions are associated with elevations in the
secretion of cortisol, a corticosteroid hormone produced by the adrenal cortex
(see Gunnar, 2001). The release of cortisol is controlled by the hypothalamus,
where corticotropin-releasing hormone (CRH) is secreted. CRH then stimulates the

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Anxiety Disorders 519
pituitary gland, resulting in the release of adrenocorticotrophic hormone (ACTH),
which in turn causes the adrenal cortex to release cortisol. Cortisol helps to regulate
behavioral and emotional responding through a feedback loop to the pituitary and
hypothalamus.
Cortisol secretion may underlie protective mechanisms on exposure to danger;
however, prolonged exposure to glucocorticoids such as cortisol may also be
neurotoxic and related to anxiety problems. For example, animal studies demonstrate
hippocampal atrophy in rats and primates exposed to either psychological stress
or elevated levels of glucocorticoids (see Sapolsky, 2000). Maltreated children with
PTSD symptoms and those diagnosed with PTSD demonstrate dysregulation in
diurnal cortisol rhythms (Carri ´on et al., 2002; De Bellis et al., 1999a), and symptoms
of social anxiety disorder are associated with heightened cortisol reactivity among
clinic referred youth (Granger, Weisz, & Kauneckis, 1994; see Gunnar, 2001, for
a review). Moreover, youth who have experienced severe stress are more likely
to display reductions in cerebral volume and frontal lobe asymmetry, possibly
due to effects of prolonged cortisol secretion (Carri ´on et al., 2001; De Bellis et al.,
1999b). Carri ´on, Weems, and Reiss (2007) found that cortisol levels were associated
with changes in the volume of the hippocampus in a sample of youth ages 8 to
14 who were exposed to traumatic stressors. Higher cortisol levels were related
to decreases in hippocampal volume over a 1-year period. Finally, research on
behavioral inhibition, a risk factor for later childhood anxiety disorders (see Kagan,
this volume), has linked the construct with increased cortisol levels in very young
children (e.g., Kagan et al., 1987, 1988). Carri ´on, Weems, Richert, Hoffman, and
Reiss (2010) have also found decreased prefrontal cortical volume associated with
increased bedtime cortisol in traumatized youth.
Peripheral nervous system . A growing body of research suggests that youth with
anxiety disorders are marked by excessive sympathetic nervous system (SNS)
activity, expressed by increased heart rate, blood pressure, and electrodermal
responding (e.g., Beidel, 1991; Carri ´on et al., 2002). Behavioral inhibition is also
associated longitudinally with elevated heart rates in community samples of youth
(Kagan et al., 1987, 1988). Data available from youth with elevated anxiety scores
also suggest different physiological responses to anxiety provoking stimuli. For
example, in a community sample of children with and without test-taking anxiety,
Beidel (1991) found significant group differences in pulse rate and systolic blood
pressure during social evaluative tasks. Scheeringa, Zeanah, Myers, and Putnam
(2004) found that young children with symptoms of PTSD exhibited higher heart
rates during recall of their trauma memories than matched controls.
In a community-recruited sample, Weems, Zakem, Costa, Cannon, and Watts
(2005) examined skin conductance and heart rate responses among youth exposed
to a fear-eliciting stimulus (video of a large dog), and their relation to youth- and
parent-rated anxiety symptoms and cognitive bias. Heart rate and skin conductance
were associated with youth ratings of anxiety disorder symptoms. These responses
were associated uniquely with youth-rated symptoms of anxiety but not depression.
There are also individual differences in absolute levels of arousal that individuals
comfortably tolerate. Indeed, research on anxiety sensitivity shows that absolute

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520 Internalizing Behavior Disorders
levels of arousal are not crucial for anxiety problems to develop (Schmidt, Lerew, &
Jackson, 1997). Anxiety sensitivity involves the belief that anxiety sensations (e.g.,
heart beat awareness, increased heart rate, trembling, shortness of breath) have
negative social, psychological, and/or physical consequences (Reiss, 1991). One’s
interpretation of arousal symptoms appears to be especially important in influencing
his or her experience of anxiety (Reiss, 1991; Weems, Hammond-Laurence, Silver-
man, & Ginsburg, 1998). In other words, some individuals experience considerable
negative affect and distress with relatively little physiological arousal.
Associative Learning Processes
Behavioral conceptualizations of anxiety disorders propose respondent (classical
or Pavlovian conditioning), vicarious (social modeling), and operant (Skinnerian
conditioning) mechanisms of the acquisition of fear. Limitations of early classical
conditioning accounts involving the direct pairing of stimuli with aversive events
(e.g., a large dog bites a child, resulting in fear of dogs) have prompted theorists
to posit multiple learning pathways to anxiety and phobic disorders (Bouton,
Mineka, & Barlow, 2001). Although the following focuses on specific conditioning
events it is important to realize that many individuals with phobias and anxiety
disorders do not develop these problems following a single exposure to a feared
stimulus (Bouton et al., 2001), bespeaking the role of preexisting vulnerabilities and
additional risk factors in the generation of clinical-level problems. Although recent
conceptualizations highlight the complexities involved in learning processes with
respect to fear and anxiety development and maintenance, we focus here on three
pathways posited by Rachman (1977).
One pathway is through classical aversive conditioning (Wolpe & Rachman,
1960). A large body of research suggests that exposure to traumatic events is
associated with increased risk for anxiety disorders, particularly PTSD (indeed,
the diagnostic criteria for PTSD mandate exposure to life-threatening trauma).
Events that have been researched extensively as traumatic during childhood include
experiences of child abuse, maltreatment, and exposure to community violence.
Between 25% and 55% of youth with past histories of physical and sexual abuse meet
criteria for PTSD (Ackerman, Newton, McPherson, Jones, & Dykman, 1998; Kiser,
Heston, Millsap, & Pruitt, 1991). Exposure to natural disasters, such as earthquake
and hurricanes, is also associated with PTSD symptoms in youth (e.g., La Greca,
Silverman, Vernberg, & Prinstein, 1996). Furthermore, the level of PTSD symptoms
a child or adolescent experiences is related to the number of disaster exposure events
(La Greca, Silverman, & Wasserstein, 1998). Importantly, preexisting vulnerabilities
such as trait anxiety confer susceptibility to postdisaster PTSD and predict symptoms
beyond exposure to the stressful event (La Greca et al., 1998).
The second of Rachman’s pathways is vicarious acquisition through observational
learning or modeling. Via this pathway, children may acquire fears by observing the
actions of salient others such as parents, caregivers, siblings, or friends (Bandura,
1982). For example, a child who sees his or her mother react fearfully to a dog may
begin to model this reaction.

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Anxiety Disorders 521
The third pathway is through verbal transmission of information. Through this
mechanism, children may acquire fears by talking about fearful things with parents,
caregivers, siblings, or friends. For example, the type of information (positive versus
negative) youth receive about a potential fear stimulus (e.g., an animal) changes
the valence of fear beliefs (Field, 2006; Field, Argyris, & Knowles, 2001; Field &
Lawson, 2003).
Ollendick, Vasey, and King (2001) have suggested a fourth pathway to anxi-
ety problems through negative reinforcement, also called escape conditioning .T h i s
account suggests that if a child learns to cope with normative anxiety and fear
responses through avoidance of the anxiety or fear-provoking stimulus, then nor-
mal anxiety responses may be maintained at high levels and may eventually turn into
problematic anxiety. Withdrawal from the stimulus may be negatively reinforced
by reduction in anxiety after withdrawing; in addition, avoidance may be positively
reinforced by caregivers through approval of avoidance behaviors. Exposure to
feared stimuli fails to occur, maintaining anxious and avoidant responses. Con-
siderable evidence exists to support these learning pathways in anxiety disorders
generally (Craske et al., 2009) and in childhood anxiety in particular (see Ollendick,
Vasey, & King, 2001, for a review).
Cognitive Processes
Proponents of cognitive and information processing models propose that various
cognitive processes, such as encoding, interpretation, and recall, may contribute to
the etiology and maintenance of anxiety disorders (see Field, Hadwin, & Lester,
2011; Vasey, Dalgleish, & Silverman, 2003). According to these models, anxious
children have biased interpretations, judgments, and memories, as well as attentional
selectivity (Vasey & MacLeod, 2001). These biases are hypothesized to work together
to foster and maintain heightened anxiety. Weems and Watts (2005) developed
a model of the cognitive influences on childhood anxiety, which suggests that
attentional biases may foster selective encoding of threat information into memory,
and such selective attention could increase negatively biased threat memories.
Memory biases, in turn, may become internalized in cognitive working models or
cognitive schemas, fostering interpretive and judgment biases. For example, existing
threat memories may bias attention toward only the threatening part of the situation
and away from mitigating aspects of the situation (such as safety signals), thereby
fostering anxiety provoking interpretations. Existing threat memories may then bias
the new interpretation of the event and help to consolidate existing interpretation
and judgment biases.
In conjunction with biological and learning accounts, cognitive factors may foster
or hamper learning acquisition, exacerbate biological predispositions, and maintain
anxiety disorder symptoms. Selective attention, memory biases, interpretation biases
(e.g., negative cognitive errors) and judgment biases are four broad forms of cognitive
processes that have begun to garner attention in relation to youth anxiety symptoms.
Selective attention involves focusing attention toward a category of stimuli (e.g.,
threatening stimuli) when such stimuli are placed in a context with other categories

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522 Internalizing Behavior Disorders
of stimuli (e.g., neutral or other nonthreatening stimuli). A predisposition for
attending to and processing potentially threatening stimuli is thought to charac-
terize anxious individuals and may maintain anxiety by overallocating intellectual
resources toward threat (Mathews, 1990). Studies demonstrate a link between child-
hood anxiety problems and selective attention (e.g., Dalgleish et al., 2003; Vasey,
Daleiden, Williams, & Brown, 1995). Using a dot-probe detection task, Vasey et al.
(1995) demonstrated that youth with anxiety disorders show shorter detection laten-
cies for threat words than do controls. Similar results have been found among
test-anxious youth (Vasey, El-Hag, & Daleiden, 1996) and among youth with gener-
alized anxiety disorder (Dalgleish et al., 2003). It is important to note that such studies
do not inform us about causal or directional associations between such cognitive
biases and anxiety. However, an exciting line of research using the modification of
attentional biases has suggested causal linkages. When attentional biases toward
threat are trained in nonanxious individuals, anxiety symptoms increase (e.g., Math-
ews & Mackintosh, 2000; Mathews & MacLeod, 2002; Salemink, van den Hout, &
Kindt, 2010). Moreover, training anxious individuals toward neutral or away from
threat improves anxiety disorder symptoms (e.g., Amir, Beard, Burns, & Bomyea,
2009) with evidence for a similar effect in youth samples (Bar-Haim, Morag, &
Glickman, 2011).
Memory biases refer to a predisposition to recall threatening information (see
Vasey & MacLeod, 2001). Similar to research on selective attention, evidence supports
a link between memory biases and anxiety problems in children (Daleiden, 1998;
Moradi, Taghavi, Neshat-Doost, Yule, & Dalgleish, 2000). More research is needed to
examine associations between both selective attention and memory biases and youth
anxiety symptoms to determine whether these differences exist only in extremely
impaired individuals. Most past research on youth anxiety compared groups that
represent the extremes of anxious psychopathology (e.g., those with diagnosed
disorders compared to groups with no history of psychiatric diagnosis).
Interpretive bias involves predisposition toward negative or erroneous interpre-
tations of neutral, ambiguous, or potentially threatening stimuli. Negatively biased
cognitions have long been implicated in both anxiety and depression (e.g., Beck,
1976). Clinically anxious youth presented with ambiguous vignettes and asked to
explain what is happening are more likely to provide interpretations indicating threat
than nonanxious controls (Barrett, Rapee, Dadds, & Ryan, 1996). A well-validated
measure for assessing negative interpretive biases is the Children’s Negative Cog-
nitive Error Questionnaire (CNCEQ; Leitenberg, Yost, & Carroll-Wilson, 1986).
Research using the CNCEQ suggests that cognitive biases are associated with symp-
toms of anxiety and can be assessed validly in both children and adolescents (Epkins,
1996; Leitenberg et al., 1986; Leung & Wong, 1998; Weems, Berman, Silverman, &
Saavedra, 2001). Research has also implicated anxiety sensitivity as a risk factor for
panic attacks, panic disorder, and other anxiety problems (e.g., Maller & Reiss, 1992;
Schmidt et al., 1997, 1999; Weems et al., 1998, 2001; Weems, Hammond-Laurence,
Silverman, & Ferguson, 1997). Anxiety sensitivity involves the belief that anxiety
sensations have negative social, psychological, and/or physical consequences (Reiss,
1991) and so involves a negative interpretation of anxiety related sensations. Anxiety

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Anxiety Disorders 523
sensitivity differentiates youth with panic disorder from youth with other anxiety
disorders (Kearney, Albano, Eisen, Allan, & Barlow, 1997) and predicts the onset
of panic attacks in adolescents (Hayward, Killen, Kraemer, & Taylor, 2000; Weems,
Hayward, Killen, & Taylor, 2002).
Judgment bias involves negative and/or lowered estimates of the individual’s
coping ability or style. Several investigators have emphasized a key role for the
construct of control in anxiety and anxiety disorders in youth (e.g., Capps, Sigman,
Sena, Henker, & Whalen, 1996; Cortez & Bugental, 1995; Granger et al., 1994;
Muris, Schouten, Meesters & Gijsbers, 2003; see Chorpita & Barlow, 1998; Weems &
Silverman, 2006, for reviews). For example, Chorpita and Barlow (1998) described
how early childhood experiences with diminished control may result in a cognitive
style that increases the probability of interpreting events as out of one’s control.
Based on these findings, Chorpita and Barlow proposed a model in which perceived
control (or lack thereof) may represent a psychological vulnerability for anxiety
problems. Barlow’s (2002) model of anxiety suggests that a perceived lack of control
over ‘‘external’’ threats (events, objects, situations that are fear producing) and/or
negative ‘‘internal’’ emotional and bodily reactions are central to the experience
of anxiety problems. Nonpathological anxiety is differentiated from pathological
anxiety both by subjective anxiety responses to the experience and by the belief that
the event is uncontrollable. Empirical support exists for the importance of control
cognitions in youth (Ginsburg, Lambert, & Drake, 2004; Muris et al., 2003; Weems,
Silverman, Rapee, & Pina, 2003).
Watts and Weems (2006) examined links among selective attention, memory bias,
cognitive errors, and anxiety problems in a community sample of youth ages 9 to
17. Selective attention, memory bias, and cognitive errors were each independently
associated with childhood anxiety symptoms. Cannon and Weems (2010) found
that both interpretive biases (CNCEQ) and judgment biases (ACQ-C) each provided
incremental discrimination of youth meeting DSM-IV criteria for anxiety disorders
from matched comparison youth. Furthermore, Weems, Costa, Watts, Taylor, and
Cannon (2007) found that each was independently associated with anxiety symptoms
in a community sample.
Models integrating the affective, cognitive, and physiological components of
anxiety suggest that cognitive biases may exert their effect by exacerbating negative
feelings that heightened physiological responding elicit. Thus, negative cognitive
biases may not be correlated with physiological reactivity but should interact
with physiological responses to produce negative affective states that characterize
anxiety disorders (see Alfano, Beidel, & Turner, 2002; Vasey & Dadds, 2001.) As
noted above, Weems et al. (2005) examined the physiological responses of youth
exposed to a mildly phobic stimulus. Heart rate response to threat interacted
with cognitive biases (CNCEQ scores) in predicting anxiety disorder symptoms
indicating that those with high cognitive errors and a high heart rate reaction had
the greatest anxiety disorder symptoms. Studies integrating the affective, cognitive,
and physiological components of anxiety while simultaneously placing them in a
broader developmental context are needed (Muris, Vermeer, & Horselenberg, 2008;
Weems & Pina, 2010).

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524 Internalizing Behavior Disorders
Social and Interpersonal Processes
Interpersonal theories focus on children’s relationships with others. Research sug-
gests important peer (Bell-Dolan, Foster, & Christopher, 1995) and parenting (Berg,
1976; B ¨ogels & Phares, 2008; Creveling, Varela, Weems, & Corey, 2010; Dadds,
Barrett, Rapee, & Ryan, 1996) influences on childhood anxiety. Moreover, social con-
textual approaches suggest that factors such as poverty, parental psychopathology,
exposure to trauma, and exposure to violence can exacerbate vulnerability to anx-
iety disorders. According to attachment theory, for example, a child’s interactions
with the environment are influenced by the underlying quality of the parent–child
relationship, and a number of factors influence the quality of that relationship
(e.g., poverty, parental psychopathology). Attachment theory suggests that human
infants form enduring emotional bonds with their caretakers (Bowlby, 1977; Cassidy,
1999). When the child’s caretakers are responsive, the resultant emotional bonds can
provide a lasting sense of security that continues even when the caretaker is not
present. However, an inconsistently responsive caretaker, a neglectful caretaker, or
some other disruption in the parent–child bond may be associated with insecure
attachment. Children with insecure attachments have particular difficulty during
separations from their parents (Ainsworth, Blehar, Waters, & Wall, 1978).
The reactions of children with anxiety disorders such as separation anxiety
disorder (SAD) can be similar to those reported of insecurely attached children
in the Strange Situation (Ainsworth et al., 1978). For example, children with SAD
protest desperately when separation is imminent, cry and become agitated during
separation, and may act angrily or aggressively toward the parent on return.
Warren, Huston, Egeland, and Sroufe (1997) found that children classified as
anxious/resistant in their attachment (assessed at 12 months of age) were more
likely than children with other types of attachment to have anxiety disorders at age
17, even when controlling for measures of temperament and maternal anxiety.
Overcontrolling parenting may also influence childhood anxiety, although it is not
clear if such patterns are maintaining factors or truly causal. For example, anxiety
in either member of the mother-child dyad tends to elicit maternal overcontrol
during interactions (Whaley, Pinto, & Sigman, 1999; Woodruff-Borden, Morrow,
Bourland, & Cambron, 2002), and higher levels of maternal control are observed
in anxious mother-child dyads than in control dyads (e.g., Siqueland, Kendall, &
Steinberg, 1996). Costa and Weems (2005) tested a model of the association between
maternal and child anxiety that included mother and child attachment beliefs and
children’s perceptions of maternal control as mediators. Maternal anxiety was asso-
ciated with child anxiety and maternal anxious attachment beliefs, whereas child
anxiety was associated with maternal anxious attachment beliefs, child insecure
attachment beliefs, and children’s perceptions of maternal control. Maternal anx-
ious attachment beliefs also mediated the association between maternal and child
anxiety. Taken together, research suggests that parents who exhibit overcontrolling,
overinvolved, dependent, or intrusive behavior may (a) prevent youth from facing
fear-provoking events, a developmentally important task that allows children to
face fear; and/or (b) send the message that particular stimuli are threatening, which

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Anxiety Disorders 525
may reinforce a child’s or adolescent’s anxiety (Rapee, 1997, 2009; Rapee, Wignall,
Hudson, & Schniering, 2000; Vasey & Ollendick, 2000).
Social-interpersonal models emphasize experiences in which behaviors of parents
are learned by children. These models are consistent with research showning
associations between children’s and mothers’ interpretation biases (Creswell &
O’Connor, 2006; Creswell, O’Connor, & Brewin, 2006). In discussing mediation in
this section, we have focused on possible behaviors of the parent or parent–child
relationship that foster children’s learning of anxious behaviors. However, some of
these processes may be influenced by genes. For example, in the Fox et al. (2005) study
noted earlier, neither genotype (i.e., the short allele for serotonin transporter) nor
low social support predicted behavioral inhibition alone. However, their interaction
was predictive. Thus, only among children with relatively low social support was
the short allele associated with behavioral inhibition. Such findings point to the
importance of considering Gene ×Environment interactions in developmental
psychopathology research on childhood anxiety (see Chapter 3). Moreover, the
literature implicates parenting behaviors as unique predictors, moderators of other
predictors (e.g., Costa, Weems, & Pina, 2009), mediators of other influences (Costa &
Weems, 2005), with possible bi-directional influences over time (Silverman, Kurtines,
Jaccard, & Pina, 2009). Integrative theories and research studies are needed to
elucidate not just for the specific parenting variables involved in childhood anxiety
but for their role in the context of other predictors.
DEVELOPMENTAL PROGRESSION
Childhood anxiety disorders are associated with adult anxiety and depressive
disorders (Pine, Cohen, Gurley, Brook, & Ma, 1998). As noted earlier, however,
results from prospective longitudinal studies of childhood anxiety disorders have
reported widely varying stabilities, ranging from 4% to 80% (e.g., Keller et al.,
1992; Last et al., 1996; March, Leonard, & Swedo, 1995; Newman et al., 1996). Such
wide-ranging stability estimates may exist for several reasons, including the type of
disorder, the informant, the sample, and the amount of time between evaluations.
Interestingly, studies show similarly wide estimates even for the same anxiety
disorder across similar time frames. For example, Last et al. (1996) found that 13.6%
of youth with social phobia retained the diagnosis after 3 to 4 years, whereas Newman
et al. (1996) found that 79.3% of youth with social phobia retained the diagnosis after
0 to 3 years. The main difference between these studies was the age of participants
(5 to 18 in Last et al., 1996; 11 to 21 in Newman et al., 1996). As already noted,
genetic influences on anxiety increase with age, which could account for some of the
discrepancy. Other possible sources of inconsistency include the types of assessment
instruments used, sample variations, different definitions of impairment, and limited
understanding and use of empirically derived developmental information in the
classification of anxiety disorders (see Curry et al., 2004; Scheeringa, Peebles, Cook, &
Zeanah, 2001).
Some authors have also posited specific age differences in the onset and expression
of phobic and anxiety disorders in youth (Warren & Sroufe, 2004; Weems, 2008;

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526 Internalizing Behavior Disorders
Westenberg, Siebelink, & Treffers, 2001). Drawing on stage theories (e.g., Loevinger,
1976), Westenberg et al. (2001) suggested that the predominant expression of fear
and anxiety symptoms may be tied in part to sequential developmental challenges.
For example, children ages 6 to 9 years have begun the process of individuation
and are expressing autonomy from their parents. The developmental challenge is
self-reliance, but this challenge is likely to give rise to concerns about separation
from or loss of parents. In contrast, youth ages 10 to 13 years are gaining insight into
mortality and broader world concerns. Finally, emerging social understanding and
comprehension in adolescence may lead to a predominance of social and evaluative
concerns in older youth (see Warren & Sroufe, 2004; Westenberg et al., 2001).
According to both Westenberg et al. (2001) and Warren and Sroufe (2004),
separation anxiety symptoms and animal fears are the predominant expression
of anxiety in children ages 6 to 9, compared with generalized anxiety symptoms
and fears concerning danger and death in children ages 10 to 13, and social
anxiety symptoms and social/performance related fears in adolescents around
ages 14 to 17. Epidemiological data from community samples are fairly consistent
with these assertions (see Costello et al., 2004), providing empirical evidence that
the predominant expression of phobic and anxiety symptoms is tied to normative
developmental milestones. Research in clinical samples also suggests that separation
anxiety disorder is more common in children whereas social phobia is more common
in adolescents (Weems et al., 1998; Weems, Silverman, Saavedra, Pina, & Lumpkin,
1999). Research examining specific fear and anxiety symptoms dimensionally across
age ranges also supports the notion of sequential developmental differences in
the expression of symptoms (Chorpita, Yim, Moffitt, Umemoto, & Francis, 2000;
Ollendick, Matson, & Helsel, 1985; Ollendick, King, & Frary, 1989).
In terms of a priori tests of the developmental hypothesis, Westenberg, Siebe-
link, Warmenhoven, and Treffers (1999) reported that separation anxiety disorder
precedes overanxious disorder (using DSM-III-R criteria). Moreover, Westenberg,
Drewes, Siebelink, and Treffers (2004) found that child self-rated fears of physi-
cal danger and punishment decrease with age and self-rated fears of social and
achievement evaluation increase with age, controlling for overall fears. Weems and
Costa (2005) tested this developmental theory and found that specific symptoms
dominated at certain ages, specificallyseparation anxiety in children 6 to 9 years,
death and danger fears in youth 10 to 13 years, and social anxiety and fears of
criticism in youth 14 to 17 years (see also Westenberg, Gullone, Bokhorst, Heyne, &
King, 2007). These findings suggest that models of the etiology of childhood anxiety
should consider differences across childhood and adolescence in developmental
expression. This concept has been termed heterotypic continuity (e.g., Moffitt, 1993).
COMORBIDITY
As noted earlier, comorbidity among anxiety disorders (i.e., homotypic comorbidity)
in youth is substantial, with estimates as high as 50% in population studies (see
Costello et al., 2004) and as high as 70% in clinical samples (Weems et al., 1998). Fur-
thermore, across studies, comorbidity of anxiety disorders with ADHD (heterotypic

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Anxiety Disorders 527
comorbidity) range from 0% to 21%, with conduct disorder and oppositional defiant
disorder from 3% to 13%, and with depression from 1% to 20% (Costello et al.,
2004). In general, there is a high degree of association between depression and
anxiety. Similar findings in community samples suggest that comorbidity is not
just a function of referral biases. Rates of comorbidity exceed those predicted by
intersecting base rates (see Costello et al., 2011; Curry et al., 2004).
CULTURAL CONSIDERATIONS
A large body of literature indicates cultural and ethnic differences in the expression
of anxious symptoms. For example, Latino children often report higher levels of
internalizing symptoms than white non-Latino children, both in terms of anxious
and somatic complaints (Ginsburg & Silverman, 1996; Pina & Silverman, 2004;
Roberts, 1992; Varela et al., 2004a, 2004b). Little is known about the mechanisms •Q1
underlying this cultural variability. Researchers have focused on the effects that
culture-specific socialization practices and family variables may have on emotion
expression. Some have speculated that because Latino culture is characterized by
a collectivistic ideal, emotions and willingness to express emotions will tend to
be consistent with cultural norms (Triandis, Leung, Villareal, & Clack, 1985). In a
collectivistic society, interdependence and subordination to the group are cultivated
through strict social norms and expectations of conformity, self-restraint, and social
inhibition.
Thus, symptom elevations in anxiety reflect the societal emphasis on those
particular mood states and behaviors (Weisz, Suwanlert, Chaiyasit, & Walter, 1987).
From this perspective, individualistic cultures such as the United States, which
emphasize autonomous, outgoing, self-promoting behaviors, should have more
children with disruptive behavior problems because this type of expression is
supported (Weisz et al., 1987). An alternative explanation for an association between
collectivistic cultures and internalizing symptoms is that an emphasis on the control
of emotions may stifle children’s understanding and managing of their internal
states (Varela et al., 2004a, 2004b). From this perspective, the social constraints on
expressing emotions may lead to a failure to develop emotion regulation skills,
which predicts greater emotional difficulties.
SEX DIFFERENCES
Girls and women experience higher levels of anxiety and related symptoms than
boys and men (Silverman & Carter, 2006), at a roughly 2:1 girl:boy ratio (Costello
et al., 2004). These findings are consistent with research on youth self-reports of
fear, which show that girls report more fears than boys (Ginsburg & Silverman,
2000; Ollendick et al., 1985; Ollendick et al., 1989; Ollendick, Langley, Jones, &
Kephart, 2001). Although these findings are consistent, the mechanisms responsible
for the observed sex differences remain obscure. Twin studies suggest there may
be a genetic basis for the sex difference, as the genetic contribution to individual
differences in anxiety appears to be greater for females (Eley, 2001).

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528 Internalizing Behavior Disorders
Genetic influences do not rule out socialization processes in the expression of
symptoms or in girls’ increased willingness to report certain types of symptoms
(Ginsburg & Silverman, 2000; Rutter, Caspi, & Moffitt, 2003). Recent research also
has broadened the theoretical frame for understanding observed sex differences.
For example, Carter, Silverman, and Jaccard (2011) recently found in a sample of
clinic-referred anxious youth that early pubertal development and self-reported
gender role orientation were significant contributors to levels of youth anxiety.
THEORETICAL SYNTHESIS AND FUTURE DIRECTIONS
In this chapter, we have provided a developmental psychopathology approach to
describing continuity and change in childhood anxiety disorders. Such an approach
suggests that a comprehensive theory of anxiety disorders requires differentiation
between primary and secondary features. Primary features of problematic anxi-
ety are (a) dysregulation of the anxiety response system, and (b) negative affect
and distress/impairment that result from physiological arousal. Secondary features
are aspects that distinguish the DSM-IV (APA, 1994) anxiety disorders from one
another (e.g., interpersonal concerns in social anxiety disorder, uncued panic attacks
in panic disorder). Significant advances have been made in understanding the devel-
opmental psychopathology of childhood anxiety disorders: research has identified
biological, behavioral, cognitive, interpersonal, and contextual processes important
to understanding the origins of childhood anxiety.
The developmental psychopathology view can be summarized via a hypothetical
child’s emotional development from childhood through adulthood. This child may
be behaviorally inhibited early in his or her life. This behavioral inhibition is
likely to be the product of genetic risk factors (e.g., short 5HTT allele), which may
interact with environmental risks (e.g., low social support, parental reinforcement
of avoidance). A child exposed to this combination of genetic vulnerability and
environmental risk is likely to experience elevated anxiety (i.e., dysregulation of
anxious emotion and corresponding distress), which is in turn shaped by normative
developmental processes and individual experiences. For example, a child with a
propensity for elevated arousal and avoidance may live with parents who are not
skilled in reducing the child’s anxious responding or who model withdrawn or
anxious behaviors in social contexts. Such parents may themselves be anxious. The
child may also be exposed repeatedly to socially challenging events that he or she
is allowed to avoid. This avoidance may result in a failure to develop cognitive,
social, and behavioral skills for facing social situations. Vulnerability to developing
an anxiety disorder is high for this child, and the specific set of risk factors may
potentiate social anxiety. Early in the child’s life, the resultant emotion dysregulation
may manifest as separation anxiety disorder; later, especially in adolescence, social
anxiety disorder may be the predominant expression of this child anxious emotion.
We encourage research that tests the hypothesized factors of influence on shaping
continuity and change in both the primary and secondary features of anxiety. Our
view emphasizes trajectories (versus purely categorical approaches) throughout the
period of childhood and adolescence, to determine common and unique pathways

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Anxiety Disorders 529
in anxious emotion. We also encourage research aimed at clarifying the role of the
factors that are hypothesized to shape these pathways. We suggest that taking an
approach emphasizing the distinction between core and secondary features of anx-
ious emotion will facilitate understanding the basic developmental psychopathology
of anxiety and also individual variation in expression of anxious emotion.
In closing it is important to note that the research literature indicates that
interventions, such as cognitive behavioral therapy, are efficacious in reducing
anxiety disorders in youth (see Silverman, Pina, & Viswesvaran, 2008; Silverman &
Motoca, 2011). Results suggest that cognitive behavior therapy is efficacious across
various types of childhood anxiety disorders and age groups (Berman, Weems,
Silverman, & Kurtines, 2000; Kendall, 1994; Scheeringa, Weems, Cohen, Amaya-
Jackson, & Guthrie, 2011), can serve preventative functions (Dadds, Holland, Barrett,
Laurens, & Spence, 1999), and is associated with long-term positive outcomes
(Saavedra, Silverman, Morgan-Lopez, & Kurtines, 2010). We encourage the use of
intervention research to further the understanding the mechanisms involved in
anxiety disorder development as well as the use of the empirical literature on the
developmental psychopathy of anxiety to inform the next generation of intervention
research.
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Beauch c16.tex V1 – 08/30/2012 10:26 P.M.
Queries in Chapter 16
Q1. Au: Add Roberts, 1992 to Refs.
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