Vasey 2014
Vasey 2014
Vasey 2014
Psychopathology of Anxiety 27
Michael W. Vasey, Guy Bosmans,
and Thomas H. Ollendick
Anxiety and fear are common in childhood and improved understanding of such disorders and
adolescence, with their focus typically reflecting the factors contributing to their development,
important developmental themes and challenges persistence, and amelioration so as to foster their
(Muris & Field, 2011) that are largely consistent early detection, treatment, and prevention.
across cultures (Ollendick, Yang, King, Dong, & In this chapter we provide a roadmap to
Akande, 1996). As such, anxiety is an adaptive research on the central issues in understanding
emotion that prepares the individual to detect and the developmental psychopathology of youth
deal with threats, thereby fostering survival anxiety. First, we consider issues in the defini-
(Marks & Nesse, 1994). However, high levels of tion of anxiety disorders and their epidemiology,
anxiety have strong potential to interfere with with particular emphasis in each case on the
development, raising risk for a wide range of implications of development. Second, we con-
maladaptive outcomes, including impaired inter- sider factors contributing to the etiology of such
personal and academic functioning (Rapee, problems, again with emphasis on the impact of
Schniering, & Hudson, 2009). Consequently, development. Unfortunately, space does not per-
such problems have strong potential to initiate mit discussion of developmental issues in the
negative developmental cascades. assessment, treatment, and prevention of child-
Anxiety disorders are the most prevalent hood anxiety disorders. Interested readers are
form of psychopathology in youth (Lepine, directed to recent reviews of these issues (e.g.,
2002). Furthermore, these disorders often per- Lyneham & Rapee, 2011; Rapee et al., 2009;
sist and carry risk for other disorders in adoles- Silverman & Ollendick, 2008).
cence and adulthood, particularly depression
(Rapee et al., 2009). Thus, there is a need for
Definitional Issues
normal anxieties are best thought of as different generalized anxiety disorder (GAD), obsessive–
forms (i.e., categories) or as different only in compulsive disorder (OCD), and a specific phobia
degree (i.e., dimensions). Bernstein and Zvolensky (SP, i.e., fear of injury). The best-fitting model
(2011) suggest that future work will likely con- was a single, higher order anxiety factor associ-
verge on hybrid models including both categorical ated with these six subdimensions. Thus, these
and dimensional aspects, and it was expected that results converge fairly well with DSM-5.
the fifth edition of the Diagnostic and Statistical However, consistent with the high rates of comor-
Manual (DSM-5; American Psychiatric bidity among these disorders, they also show that
Association [APA], 2013) would take the first these anxiety disorders share much in common
steps toward such a hybrid model. For example, (i.e., a higher order factor). This overlap may stem
dimensional assessments could be used to supple- from inadequacies in our current nosology but
ment categorical diagnosis. This would allow clini- also likely reflects a high degree of commonality
cians and researchers to capture not only the level in the risk factors and causal processes involved in
of severity of a given disorder’s symptoms but also these disorders’ etiology and maintenance.
the full range of symptoms an individual experi-
ences regardless of diagnosis (e.g., levels of other
forms of anxiety or of depressive or attention defi- Diagnostic Categories
cit hyperactivity disorder symptoms). Such defini-
tional changes were ultimately deemed premature DSM-IV described seven major anxiety disor-
by the DSM-5 Task Force but remain an important ders commonly diagnosed in youth: (1) SAD, (2)
emphasis for future research (APA, 2013). Finally, SP, (3) SoP, (4) PD with and without agoraphobia
it is unclear how anxiety disorders should be dif- AG, (5) GAD, (6) OCD, and (7) post-traumatic
ferentiated. Should they be organized based on stress disorder (PTSD). DSM-5 largely retained
their descriptive psychopathology (as in the DSM), these diagnoses although AG was promoted to a
etiology, or the function served by symptoms (see, standalone diagnosis and OCD and PTSD were
e.g., Kearney & Silverman, 1990)? moved to separate sections. Below, we discuss
There is also ambiguity as to what is the best the major features and epidemiology of each of
approach to answering these questions (Bernstein these except OCD and PTSD, which are not con-
& Zvolensky, 2011). Should we proceed empiri- sidered because they are addressed in separate
cally, with a minimum of assumptions (i.e., a chapters in this volume.
bottom-up approach) or should we begin by
defining anxiety disorders based on consensus or
theory (i.e., a top-down approach). Although Separation Anxiety Disorder
bottom-up approaches have a long history in the
study of child psychopathology (Achenbach, The hallmark of SAD is developmentally inap-
1982), top-down approaches have predominated propriate, recurrent, and excessive anxiety con-
since the introduction of DSM-III (APA, 1980). cerning separation from home or attachment
The anxiety disorder categories defined in figures. Affected children experience excessive
DSM-5 (APA, 2013) reflect a largely top-down worry about losing or harm befalling major
approach to distinguishing among types of anxi- attachment figures or that events will separate
ety problems. Very little bottom-up research has them from caregivers. Associated features
been done. However, there is factor analytic evi- include reluctance or refusal to attend school,
dence that generally supports many of the DSM-5 fear of being alone, nightmares concerning sepa-
anxiety disorders. Spence (1997) used confirma- ration, and physical symptoms (e.g., stomach
tory factor analysis of children’s self-reports aches) in anticipation of or following separation.
regarding the major symptoms of each of six The disorder must persist for at least 4 weeks and
DSM-IV anxiety disorder subcategories: panic cause clinically significant distress and/or inter-
disorder (PD) with agoraphobia (AG), separation ference with functioning in academic, social, or
anxiety disorder (SAD), social phobia (SoP), other important domains.
27 The Developmental Psychopathology of Anxiety 545
SAD changed only slightly from DSM-IV to or retreating from the feared stimulus. Typically
DSM-5. The main change was to allow onset this distress leads to efforts to avoid, although
after age 18 years. Such a change is consistent some individuals endure feared situations
with research showing that SAD may have onset despite intense distress. The avoidance and/or
in adulthood (Cyranowski et al., 2002). However, distress must interfere with normal functioning
in such cases (i.e., ages ≥ 18 years) duration is or there must be marked distress about having
required to be at least 6 months). Adults with the phobia. Also, in children there must be evi-
SAD are described as tending to be overcon- dence of the capacity for age-appropriate social
cerned about loved ones (e.g., a spouse) and relationships with familiar people, and the anxi-
intensely anxious when separated from them ety must occur with peers and not just in inter-
(APA, 2013). actions with adults.
DSM-5 made few changes to SoP. One change
which had been proposed was to make selective
Specific Phobia mutism a behavioral specifier to SoP rather than
a disorder in its own right. Although this change
SPs involve marked, persistent fear of specific ultimately was not made, such a change would be
objects or situations lasting at least 6 months. In consistent with evidence of high comorbidity
children, this fear may take the form of tantrums, between selective mutism (SM) and SoP, which
crying, freezing, or clinging (APA, 2013). To dis- suggests that SM is best regarded as an avoidance
tinguish phobias from normal fears, particularly pattern that is particularly relevant to the expres-
in children, severity must be sufficient to inter- sion of social anxiety in young children (Bögels
fere significantly with normal functioning. Like et al., 2010).
DSM-IV, DSM-5 distinguishes among five foci:
animals, situations (e.g., elevators, flying), blood-
injection-injury, natural environment (e.g., Panic Disorder with or Without
storms, heights), and other. These fear foci are Agoraphobia
avoided or endured with intense distress. Whereas
adults may recognize their fears are excessive or Recurrent, unexpected panic attacks are the
unreasonable, children typically do not. hallmark of PD. Such attacks involve intense
Changes to the specific phobia category under fear accompanied by somatic symptoms of sym-
DSM-5 are minor (APA, 2013), largely involving pathetic nervous system arousal and by cata-
wording changes intended to reduce ambiguity strophic cognitions (e.g., fear of having a heart
(e.g., the term “marked” was operationalized as attack). PD is often associated with AG, which
“intense”). involves pronounced anxiety about being in
places or situations where escape may be diffi-
cult or embarrassing in the event that a panic
Social Phobia attack were to occur. These situations are
avoided or endured with significant distress.
SoP is characterized by pronounced, persistent Few changes were made to PD under DSM-5
(at least 6 months) fear of one or more social but AG became codeable as a separate disorder
performance situations in which embarrassment (APA, 2013). This change is in keeping with evi-
and negative social evaluation may occur or in dence showing that panic and AG are not closely
which the individual encounters unfamiliar peo- linked in youth. For example, Wittchen et al.
ple. This phobia can be limited to specific con- (2008) found that adolescents with panic disorder
texts (e.g., public speaking) or generalized or panic attacks were only moderately more
across social situations. In the feared situation likely to develop agoraphobia than those without.
intense anxiety is experienced, often taking the Furthermore, the majority meeting criteria for
form of a panic attack. In children, this anxiety agoraphobia had never experienced a panic
may take the form of crying, tantrums, freezing, attack.
546 M.W. Vasey et al.
to non-shared environmental factors (Muris, (Gregory & Eley, 2011). Endophenotypes are
2007). However, the magnitude of genetic and characteristics that are presumed to be closer to
shared environmental effects varies with age the genotype than a disorder phenotype and
(Gregory & Eley, 2011). Specifically, heritability therefore they permit easier identification of
of anxiety appears to increase and the influence genetic effects. Several recent studies reveal the
of shared environment to decrease with age promise of research focused on such characteris-
(Gregory & Eley, 2011). This is consistent with tics (e.g., Battaglia, Pesenti-Gritti, Medland,
the increasing potential for individuals to select Ogliari, & Spatola, 2009; Eley et al., 2007).
their own environment as they get older, thereby For example, Battaglia et al. (2009) studied an
increasing the potential for anxiety-promoting endophenotype presumed to be linked to PD—
gene–environment correlations. hypersensitivity to a CO2 inhalation challenge—
Most studies of genetic effects to date assume and found that the variance it shared with diagnoses
that genes and environments have additive of PD and SAD was largely (89 %) a function of
effects. However, it is clear that interactive (e.g., shared genes, with the remaining 11 % linked to
gene × environment [G × E]) effects should be childhood parental loss. Epigenetic effects reflect
expected and research has begun to isolate them factors that regulate gene expression and thus are
(Lau, Gregory, Goldwin, Pine, & Eley, 2007). For the processes by which genes are turned on or off
example, Silberg, Rutter, Neale, and Eaves over time. For example, a growing body of animal
(2001) found that genetic effects on GAD symp- research shows there is significant potential for
toms were strongest among girls exposed to high early experiences to impact risk for anxiety disor-
levels of negative life events. ders (Nolte, Guiney, Fonagy, Mayes, & Luyten,
Although a number of gene-linkage and asso- 2011). Weaver et al. (2004) found that rat pups
ciation studies of youth anxiety have begun to licked and groomed to a greater extent by their
appear, few consistent findings have yet emerged. mothers were more stress resistant as adults and
However, there are several likely candidate genes that difference was mediated by methylation
or gene regions, among the most promising of changes in the promoter region of a gene linked to
which are the serotonin transporter polymor- a glucocorticoid receptor in the hippocampus.
phism (5-HTTLPR) and the gene for catechol-O-
methyltransferase (COMT), an enzyme involved
in the metabolism of dopamine and other cate- Neurobiology
cholamines (Arnold & Taillefer, 2011; Gregory
& Eley, 2011). The s-allele of the 5-HTTLPR has A rapidly growing body of animal and human
been linked to heightened fear conditionability research provides an increasingly clear picture of
(Lonsdorf et al., 2009) and vulnerability to anxi- the brain circuits underlying anxiety and fear
ety (and depression), although results in youth responses and their regulation, with particular
studies thus far have been mixed (Gregory & emphasis on bidirectional connections between
Eley, 2011). Homozygosity for the met-allele of the amygdala and the prefrontal cortex (PFC;
the COMT gene has been linked to poor fear LeDoux, 2000). Although undoubtedly an over-
extinction learning (especially in individuals simplification, pathological anxiety appears to
with the 5-HTTLPR s-allele (Lonsdorf et al., involve hypersensitivity of the amygdala interact-
2009) and to increased odds for phobic anxiety ing with deficient regulatory processes mediated
disorder in youth (McGrath et al., 2004). Future by the PFC (Nolte et al., 2011). The former is
research will likely specify other genes linked to shown by hypervigilance characterized by rapid
these and other neurotransmitters, including the orienting to threat stimuli presented for very brief
gamma-aminobutyric (GABA), corticotropin- intervals whereas the latter is shown by delayed
releasing hormone (CRH), and estrogen systems disengagement of attention from threat stimuli
(Gregory & Eley, 2011). presented for longer intervals (Pine, 2011 ).
Also holding considerable promise is research As discussed below (see Cognitive Factors), such
focused on endophenotypes and epigenetic factors effects have been documented in relation to a
550 M.W. Vasey et al.
range of anxiety-related individual differences EC are associated with heightened risk for anxi-
including BI temperament, trait anxiety, and ety and depression (Muris, 2007). Furthermore,
anxiety disorders. Lonigan and Phillips (2001) postulated an interac-
The functioning of this fear circuitry changes tive relation between NA and EC such that height-
with development. For example, Lau et al. (2011 ) ened NA is most likely to lead to anxiety problems
report evidence of developmental change in when coupled with deficits in EC. A growing
threat learning between early adolescence and body of evidence supports this model (Lonigan
adulthood. Young adolescents were less able than et al., 2011). For example, Lonigan and Vasey
adults to discriminate threat and safety cues in (2009) showed that high NA was associated
their verbal ratings of fear and these results were with an attentional bias toward threat only when
mirrored by fMRI results. Specifically, whereas EC was low, and Lonigan et al. (2011) report
both groups showed a similar pattern of amyg- finding the NA × EC interaction to be significant
dala response to threat versus safety cues, only in relation to concurrent symptoms of SAD,
adults showed evidence of activation in the GAD, and PD/AG.
dorsolateral (dl)PFC in response to safety cues. There are at least four ways in which tempera-
Lau et al. (2011 ) interpret their findings as being ment can influence anxiety problems, often in
consistent with maturation of the dlPFC, which transaction with environmental influences
likely supports the capacity for reappraisal of (Lonigan et al., 2011). First, temperament may
potentially threatening stimuli. Failures to predispose to the development of anxiety disor-
develop this capacity may contribute to persistent ders in interaction with environmental stressors
anxiety disorders (Britton et al., 2011 ). (i.e., the diathesis-stress model). Second, the
pathoplasticity model postulates that tempera-
ment may influence the symptoms or course of an
Temperament anxiety disorder without having a direct causal
role in its onset. For example, even before the
The genetic risk for anxiety disorders is mediated onset of a phobia, children with BI temperament
by temperamental factors, particularly early are likely to have taught their parents to protect
emerging individual differences in negative them from anxiety-provoking experiences,
affectivity (NA, Clark, Watson, & Mineka, 1994) thereby fostering the persistence of a phobia
and associated constructs such as behavioral following its onset. Third, under the complica-
inhibition (BI) to the unfamiliar (Degnan & Fox, tion or scar model, enduring changes to tempera-
2007). BI temperament, both as a dimension and ment that foster anxiety emerge as a complication
as a categorical construct, has received the most of developing an anxiety disorder. For example,
attention, with research consistently supporting an anxious child’s avoidance and protective
its link to heightened risk for anxiety problems in responses to the child’s anxiety by parents and
childhood, especially SoP (e.g., Hirschfeld- others may increase a child’s level of NA. Fourth,
Becker et al., 2007). This is particularly true for under the continuity model, anxiety disorders and
that subset of children who show stable BI from temperament are seen as reflecting the same
infancy through middle childhood. Lonigan, underlying processes. Of course, these models
Phillips, Wilson, and Allan (2011) suggest that are not mutually exclusive.
such stable BI likely reflects not only high levels
of NA but also deficient competence at regulating
emotional reactions. Indeed, a second aspect of Parental Influences
temperament thought to contribute to anxiety
pathology is effortful control (EC), which is the Many of the experiences through which chil-
capacity for self-regulation (i.e., the capacity to dren’s fears are acquired and shaped involve their
override one’s automatic, reactive tendencies and parents (Dadds & Roth, 2001). Murray, Creswell,
substitute more adaptive responses). Deficits in and Cooper (2009) described three paths by
27 The Developmental Psychopathology of Anxiety 551
which parents may contribute to their child’s anx- process of fear habituation or mastery (Vasey &
iety problems. First, parents may adopt Dadds, 2001). Similarly, they may foster vulner-
approaches to socialization that lead their child to ability by failing to grant and support the child’s
perceive the world as full of uncontrollable dan- autonomy, instead limiting contact with chal-
gers, with which he or she is incompetent to cope. lenging situations or exerting intrusive control as
Second, if anxious themselves, parents may pro- the child copes with such challenges. A growing
mote anxiety through modeling and verbal infor- body of evidence supports an association between
mation transmission, as discussed below in the parental control and child anxiety (Creswell,
context of respondent conditioning influences. Shildrick, & Field, 2011). For example, in their
Third, whether they are anxious or not, parents meta-analysis, McLeod et al. (2007) found an
may respond to their child’s anxious responses in average correlation of r = −0.42 between parental
ways that contribute to their maintenance and autonomy granting and child anxiety.
intensification, as discussed below in the context Anxious parents, specifically mothers, have
of operant conditioning influences. However, next long been viewed as likely to behave in ways that
to these direct paths, research also suggests indi- promote anxiety in their offspring. Evidence
rect effects of interactions with parents through suggests they do indeed display more anxiety to
trust in parental support (Bosmans, Braet, Beyers, their children and that doing so increases the like-
Van Leeuwen, & Van Vlierberghe, 2011; lihood of later anxious responses by the child
Brumariu & Kerns, 2010). (Rapee et al., 2009). For example, Murray,
Cooper, Creswell, Schofield, and Sack (2007)
Direct Parental Influences observed mothers with SoP to exhibit more anxi-
Based on a recent meta-analysis, the effects of ety toward a stranger and to be less likely to
parental influences are small on average encourage their 10-month-old infants to engage
(McLeod, Wood, & Weisz, 2007). However, their with the stranger. Furthermore, such behavior
magnitude varies substantially, with the strongest was shown to increase the likelihood that infants
effects being seen in studies of younger children, would later show stranger avoidance.
clinical samples, and studies which use behav- Whereas early studies left it unclear if this
ioral observations rather than questionnaires association meant parental behaviors causally
(Creswell, Murray, Stacey, & Cooper, 2011). contribute to child anxiety or if anxious children
However, parenting influences do not operate in lead their parents to exert more control, recent
isolation, and evidence suggests that such effects evidence suggests both are true. Experimental
are likely to be substantially larger in interaction studies suggest that parental control does indeed
with other factors. For example, their impact is promote anxiety and related responses from
stronger among temperamentally vulnerable children (De Wilde & Rapee, 2008; Thirlwall &
children (e.g., Murray et al., 2008; Thirlwall & Creswell, 2010). However, Gar and Hudson
Creswell, 2010). Other research has begun to (2008) conducted an experimental study in which
reveal the processes that mediate the effect of mothers of children with and without anxiety dis-
parental influences on anxiety. For example, orders interacted with two unrelated children,
Perez-Olivas, Stevenson, and Hadwin (2008) one anxious and the other non-anxious. Mothers
found evidence that the impact of parental control were observed to be more involved and control-
on child anxiety is mediated by a tendency to ling with the anxious versus control child regard-
interpret ambiguous information as threatening. less of the anxiety status of their own children,
Parents may also foster anxiety in their child suggesting that anxious children engender con-
by being over-involved and exerting intrusive trolling responses from their parents.
control over the child’s experiences and behavior Parents may also exert control by fostering
(Cresswell et al., 2011). For example, parents their child’s selection of avoidant responses to
may limit their child’s exposure to fear-provok- anxiety-provoking situations. Barrett, Rapee,
ing stimuli, thereby interfering with the normal Dadds, and Ryan (1996) found that anxious chil-
552 M.W. Vasey et al.
dren chose avoidant solutions to challenging situ- should therefore face increased risk for the devel-
ations more often than normal controls, and this opment of anxiety disorders.
tendency was fostered by their parents in family Insecure attachment fundamentally alters
problem-solving discussions. Dadds, Barrett, children’s abilities to regulate distress, explaining
Rapee, and Ryan (1996) found that parents of links between attachment and anxiety (Nolte
anxious children were significantly more likely et al., 2011). When distressed, securely attached
than parents of normal controls to differentially children readily seek caregiver support and derive
reinforce their children’s mention of avoidance comfort from it. However, because insecurely
during problem-solving discussions. Further, attached children lack confidence in the care-
rates of such reinforcement were positively cor- giver, they must rely on less adaptive, secondary
related with the child’s selection of avoidant coping strategies (Brenning, Soenens, Braet, &
responses following the discussion. Bosmans, 2011; Mikulincer & Shaver, 2007).
The nature of these strategies depends on the
Indirect Parental Effects (Attachment) child’s insecure attachment style. Avoidantly
Research suggests that parenting effects on child attached children distance themselves from their
anxiety are at least partly mediated by the child’s caregivers and do not seek support, instead adopt-
lack of confidence in parental support. Moreover, ing a “deactivating” strategy involving emotional
in keeping with the finding that shared environ- suppression. In contrast, children with an anxious/
ment matters less with increasing age (Gregory & ambivalent attachment are highly dependent on
Eley, 2011), the direct effect of parenting declines caregiver support, but fear abandonment and
during adolescence. In contrast, confidence in rejection. Consequently, they adopt a “hyperacti-
parental support appears to remain important vating” strategy associated with pronounced anx-
(Bosmans et al., 2011). iety reactions in response to, and hypervigilance
These findings are unsurprising in light of for, threats (Nolte et al., 2011). Finally, children
attachment research. Multiple studies have shown exposed to highly unpredictable and negative
that lack of confidence in parental support, or caregiver interactions are at risk to develop a dis-
insecure attachment, is an important predictor of organized pattern of coping behavior character-
child anxiety problems (Brumariu & Kerns, 2010; ized by chaotic swings between hyperactivating
Groh, Roisman, van IJzendoorn, Bakermans- and deactivating responses (Groh et al., 2012).
Kranenburg, & Fearon, 2012). According to Across age-groups, cross-sectional and pro-
attachment theory, perceived threats activate the spective research has confirmed that anxiety
attachment system, triggering a cascade of pro- problems are linked to insecure attachment,
cesses targeted at reducing the threat and also especially the anxious/ambivalent pattern
serving to regulate the stress response itself (Nolte (Colonnesi et al., 2011), although some evidence
et al., 2011). Key among these threat responses in also supports a link to the disorganized pattern
infancy and childhood is the seeking of proximity (e.g., Brumariu & Kerns, 2010; Groh et al., 2012).
to and support from one’s caregiver (Cassidy, Furthermore, evidence suggests that attachment
2008). Over time however, the child develops interacts with other factors in association with
expectations regarding the caregiver’s reliability anxiety problems, including BI temperament
as a source of support depending on whether or (Brumariu & Kerns, 2010) and stressful life
not the caregiver is sensitive and responsive to the events (Dallaire & Weinraub, 2007).
child’s needs. A securely attached child builds an
internal working model of a sensitive caregiver
that enables the child to feel safe while exploring Learning Influences
the world (Cassidy, 2008). In contrast, the inse-
curely attached child’s model of an insensitive Respondent conditioning processes undoubtedly
and unreliable caregiver leads to feeling unsafe in play an important role in precipitating the onset
navigating the world (Bowlby, 1973). Such children of phobic anxiety but can contribute to anxiety
27 The Developmental Psychopathology of Anxiety 553
disorders in other ways as well (Dadds, Davey, & factors, they may also play predisposing, protec-
Field, 2001). Modern respondent conditioning tive, maintaining, exacerbating, and ameliorating
theories (see Field & Purkis, 2011) emphasize roles. For example, the phenomenon of sensory
the acquisition of an expectation that a previously preconditioning may explain why some children
neutral stimulus (i.e., the conditioned stimulus develop phobias despite lacking any apparent
[CS]) predicts the occurrence of a second stimu- history of direct conditioning involving the feared
lus that is appraised as aversive (i.e., the uncondi- stimulus (see Dadds et al., 2001). Similarly, to
tioned stimulus [UCS]), thereby provoking a fear the extent that children have non-traumatic expe-
response. By virtue of that expectation, the CS riences with a stimulus, they may be less likely to
comes to elicit a conditioned fear response (CR). acquire a fear of that stimulus subsequent to a
It is important to emphasize that direct experi- conditioning episode [i.e., latent inhibition, see
ences pairing the CS and UCS are not necessary; Dadds et al. (2001)]. Finally, such processes may
the requisite expectancy can be learned indirectly. contribute to the maintenance, intensification, or
Indeed, direct conditioning experiences may amelioration of phobic responses through stimu-
account for only a minority of childhood phobias, lus revaluation (see Dadds et al., 2001).
with a basis in vicarious learning and verbal infor- Operant conditioning also may play a role in the
mation transmission being more common acquisition of anxiety disorders [e.g., inept social
(Ollendick & King, 1991). Similarly, the aversive behavior may bring negative social evaluation and
stimulus need not be truly dangerous; it need only thus lead to social anxiety (Ollendick, Vasey, &
be appraised as such. Indeed, it need not even be King, 2001)]. However, the impact of such factors
real: an imagined aversive event is sufficient is perhaps greatest with regard to the maintenance,
(Field & Purkis, 2011). exacerbation, and amelioration of such problems.
There are one direct and two indirect paths by Subsequent to the onset of anxiety symptoms, there
which such conditioning occurs: (1) direct trau- are numerous opportunities for such responses to
matic conditioning, (2) vicarious (i.e., observa- be shaped by their consequences (Ollendick et al.,
tional) learning, and (3) verbal information 2001). For example, by virtue of their extreme dis-
transmission (Field & Purkis, 2011). Experimental tress, anxious children are likely to be effective at
evidence from child samples shows that all three punishing those around them for not accommodat-
paths are sufficiently powerful as to produce con- ing their desire for avoidance. Simultaneously,
ditioned fear responses to novel, neutral stimuli relief from the child’s intense reactions is likely to
as expressed through cognitive, behavioral, and be a potent source of negative reinforcement when
physiological response channels (see Field & others permit or foster such avoidance. Thus, those
Purkis, 2011). Furthermore, such conditioned around the anxious child may come to be con-
responses persist over time (Field & Purkis, trolled by the short-term reduction of the child’s
2011). However, as should be expected given that anxiety, at the expense of the child’s ultimate mas-
even direct traumatic conditioning episodes often tery of anxiety and the demands of anxiety-
do not result in phobias (Dadds et al., 2001), provoking situations (Vasey & Dadds, 2001).
evidence shows that respondent conditioning
processes interact with other factors such as
parental characteristics (e.g., negative interac- Stress
tions with parents, e.g., Field, Ball, Kawycz, &
Moore, 2007) and temperament (e.g., trait anxi- Stressful life events appear to increase risk for
ety, e.g., Field & Price-Evans, 2009) to produce anxiety disorders in youth (Muris, 2007). For
heightened fear conditioning and resistance to example, the onset of SAD often follows a major
extinction in vulnerable individuals (e.g., Waters, stressor such as a move to a new school (Gittelman-
Henry, & Neumann, 2009). Klein & Klein, 1980). Although most of the evi-
Although respondent conditioning processes dence for this association is cross sectional and
are most commonly discussed as precipitating relies on retrospective reports of stress, a few pro-
554 M.W. Vasey et al.
spective studies also support the link. For exam- important etiological and maintaining roles.
ple, Grover, Ginsburg and Ialongo (2005) found These include anxiety-promoting beliefs such as
that total negative life events at baseline predicted low self-efficacy, lack of control, and anxiety sen-
anxiety levels six years later in a high-risk sample sitivity (see Muris, 2007) as well as information
of African-American children. However, it is processing biases. Despite some inconsistencies,
important to note that evidence also shows that the extant evidence shows that such cognitive
anxiety disorders predict the occurrence of such factors characterize anxious youth just as they do
events (Kim, Conger, Elder, & Lorenz, 2003). anxious adults (see Field, Hadwin, & Lester,
The controllability of environmental events, 2011). For example, studies using a variety of
especially early in childhood, may be particularly paradigms show that anxious children exhibit an
important in the development of anxiety disorders attentional bias in favor of threat-relevant stimuli
(Chorpita & Barlow, 1998). Specifically, early relative to controls and that effect sizes are gener-
exposure to controllable environments appears to ally comparable to those seen among adults
protect against anxiety, whereas uncontrollable (see Bar-Haim et al., 2007). Similarly, compared
environments predispose to anxiety. For example, to controls, anxious children show a bias toward
infant rhesus monkeys exposed to chronically interpreting ambiguous information as threaten-
uncontrollable environments responded to novel ing (see Field et al., 2011).
stimuli with greater fear and less exploration than To the extent that such biases are shown by
monkeys having control over their environment children prior to the onset of problematic anxiety,
(Mineka, Gunnar, & Champoux, 1986). The pre- they may contribute significantly to risk for its
disposing effects of uncontrollable environments development. Unfortunately, prospective studies
may be mediated, in part, by changes in the endo- addressing this possibility remain largely lacking.
crine systems associated with stress responses However, whether such cognitive biases predis-
that may increase reactivity to stress (Nachmias, pose to, or result from anxiety, a growing body of
Gunnar, Mangelsdorf, Parritz, & Buss, 1996). experimental evidence suggests they are causally
However, such effects are also likely to be medi- involved in its maintenance. Studies in youth and
ated by control-related cognitions formed through adult samples show that the attentional and inter-
experiences with controllable and uncontrollable pretive biases can be modified through computer-
events (Weems & Silverman, 2006). based training procedures and that the resulting
Relationship problems, especially peer rejection reductions in bias lead to commensurate reduc-
and victimization, are potent stressors that can tions in anxiety symptoms (e.g., Rozenmann,
contribute to the development of anxiety disorders Weersing, & Amir, 2011; Vassilopoulos, Banerjee,
(La Greca & Landoll, 2011). In their most extreme & Prantzalou, 2009). Similarly, evidence suggests
forms (e.g., bullying), such social stressors can pro- that risk for anxiety disorders in adolescents can
voke onset of SoP, PTSD, or other anxiety disor- be substantially reduced through a program
ders (Hawker & Boulton, 2000). Furthermore, designed to reduce anxiety sensitivity (Schmidt
once anxiety symptoms develop, especially social et al., 2007).
anxiety symptoms, they can lead to further rela- How such cognitive biases develop remains
tionship difficulties. For example, Blöte, Kint, and poorly understood. With regard to the attentional
Westenberg (2007) found that higher levels of and interpretational biases, Field et al. (2011) con-
social anxiety in adolescents predicted more nega- sider three possibilities. First, such biases may be
tive treatment by their peers. innate or emerge very early, distinguishing anxi-
ety-prone children even in infancy. Second, all
young children may show biases favoring threat,
Cognitive Factors which normally diminish with increasing age but
fail to do so in anxious children. Third, such biases
Anxiety disorders in youth are associated with a may be acquired, emerging only as children get
wide range of cognitive factors that may play older. However, these possibilities are not mutu-
27 The Developmental Psychopathology of Anxiety 555
ally exclusive. Indeed, although the situation is In keeping with this view, once typically studied
less clear for the interpretation bias (Field et al., in isolation, etiological factors are now often con-
2011), in the case of the attentional bias, evidence sidered in the context of or in interaction with
supports all three. Not surprisingly given their one another. Indeed, numerous scholars have
likely adaptive advantage, attentional biases offered complex, integrative developmental mod-
toward threat are present even in infancy (e.g., els of youth anxiety (e.g., Degnan & Fox, 2007;
LoBue & DeLoache, 2010) and can be found in Lau & Pine, 2009; Muris, 2007; Nolte et al., 2011;
non-anxious children (Field et al., 2011). However, Vasey & Dadds, 2001), and prospective tests of
there is also evidence that this bias is larger in anx- predictions from such models are increasingly
ious versus non-anxious samples among children common in the literature (e.g., Barrocas & Hankin,
as young as 3 to 4 years (e.g., Martin & Jones, 2011; Bosquet & Egeland, 2006; Creswell,
1992). Similarly, Perez-Edgar et al. (2011) found a Shildrick, & Field, 2011; White, McDermott,
link between an attentional bias toward angry Degnan, Henderson, & Fox, 2011).
faces and social withdrawal in 5-year-olds. Finally, For example, drawing on research on biologi-
it appears that such biases can be acquired through cal, temperamental, and cognitive biases, growing
experience (e.g., Field, 2006). Thus, although it evidence suggests that hypersensitivity of the
remains unclear if the bias is larger in anxiety- amygdala to threat cues and deficient regulation of
prone children even in infancy, it appears that the the fear circuit by the PFC reflect genetic influ-
difference emerges early in childhood and thus has ences and manifest in an anxiety-prone tempera-
significant potential to contribute to the etiology of ment reflecting high levels of NA and low levels of
anxiety disorders. Nevertheless, evidence also EC (Bosquet & Egeland, 2006; Lau & Pine, 2008).
suggests that the bias becomes stronger with age in This combination elevates risk for stable difficul-
anxious children and weaker in non-anxious chil- ties regulating anxiety (e.g., stable BI tempera-
dren, presumably reflecting developing capacity ment) that are associated with heightened vigilance
for executive control of attention (Lonigan et al., for and orienting to threat cues coupled with defi-
2004) and the operation of other factors promoting cient ability to disengage attention from such cues
anxiety. For example, the attentional bias appears (Lonigan & Vasey, 2009; White et al., 2011). Such
to mediate the link between maternal over-involve- biases are further instilled and fostered by attach-
ment and symptoms of SAD (Perez-Olivas et al., ment insecurity (Nolte et al., 2011) as well as
2008). Furthermore, it appears that the attentional parental modeling, verbal information transmis-
bias promotes the interpretation bias (White, sion, and reinforcement of threatening interpreta-
Suway, Bar-Haim, Pine, & Fox, 2011). tions of ambiguous information (Creswell et al.,
2011; Perez-Olivas et al., 2008). Parents respond
by limiting the child’s autonomy, likely leaving the
An Integrative Perspective child deficient in skills needed to master the chal-
lenges posed by threatening situations and the
It is highly unlikely that any one of the etiological anxiety they produce (Creswell et al., 2011).
influences reviewed above is sufficient to pro- Children following such a path have a low sense of
duce clinical levels of anxiety by itself. Rather, control and view anxiety itself as dangerous and
anxiety disorders in youth emerge via develop- themselves as incompetent to cope with threaten-
mental pathways involving many and varied ing situations and the anxiety they trigger (Weems
combinations of these influences, each operating & Silverman, 2006). Furthermore, it is easy to see
in transaction with the others (Vasey & Dadds, the potential for reciprocal links among these influ-
2001). Depending upon the configuration and ences, with each promoting the other in a negative
timing with which they occur, any given factor developmental cascade (Vasey & Dadds, 2001).
may lead to several different anxiety disorders, Evidence for such a cascade can be found in recent
to other forms of psychopathology, or to no dis- prospective studies (e.g., Barrocas & Hankin,
order at all. 2011; Bosquet & Egeland, 2006).
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