International Journal of Behavioral Development 2006, 30 (1), 511 http://www.sagepublications.

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2006 The International Society for the Study of Behavioural Development DOI: 10.1177/0165025406059967

The pathogenesis of childhood anxiety disorders: Considerations from a developmental psychopathology perspective
Peter Muris
Erasmus University, Rotterdam, The Netherlands
Anxiety disorders are among the most prevalent psychiatric problems in children and adolescents. The present article summarizes the main evidence that has accumulated on the pathogenesis of childhood anxiety disorders during the past two decades. Various risk and vulnerability factors (e.g., genetics, behavioral inhibition, disgust sensitivity, negative life events, family inuences), protective factors (e.g., effortful control, perceived control), and maintaining factors (e.g., avoidance, cognitive biases) will be discussed. The information will be described in terms of a developmental psychopathology perspective, which assumes that (a) most forms of psychopathology are the result of multiple causal inuences; (b) both successful and unsuccessful adaptation are important for understanding the origins of psychopathology; and (c) psychopathology occurs in a developing organism.

Introduction
Anxiety phenomena such as fear, worry and scary dreams are common in childhood (Muris, Merckelbach, Gadet, & Moulaert, 2000). In most cases, these phenomena are shortlived and dissipate within a brief period of time (see Craske, 1997). Initially, this has led many child psychologists to the faulty conclusion that childhood anxiety should not be taken too seriously, and as a result the phenomenon received little research attention. During the past decade, this opinion has changed as researchers have increasingly demonstrated that a substantial minority of children do suffer from such high anxiety levels that a diagnosis of an anxiety disorder is clearly warranted (Muris, Meesters, Merckelbach, Sermon, & Zwakhalen, 1998; Muris, Merckelbach, Mayer, & Prins, 2000; Muris, Merckelbach, Ollendick, King, & Bogie, 2001). In fact, epidemiological studies have shown that anxiety disorders are among the most prevalent forms of psychopathology in youths (Costello, Mustillo, Erkanli, Keeler, & Angold, 2003; Ford, Goodman, & Meltzer, 2003). Moreover, there is evidence indicating that a signicant proportion of childhood anxiety disorders have a chronic course and, although they may change form, even last into adulthood (Keller, Lavori, Wunder, Beardslee, & Schwartz, 1992; Last, Perrin, Hersen, & Kazdin, 1996). The understanding that childhood anxiety should be viewed as a clinically relevant phenomenon has yielded a host of studies on the pathogenesis of excessive anxiety in children and adolescents. While the majority of this research has focused on single factors, it has become clear that an understanding of the pathways by which childhood anxiety disorders develop, persist and remit is likely to require consideration of a wide range of inuences and, most impor-

tantly, their potential for complex, dynamic, transformational interactions (i.e., transactions) across development (Vasey & Dadds, 2001, p. 3). Clearly, this notion ts nicely with the major tenets of the developmental psychopathology perspective (Cicchetti & Cohen, 1995), which imply that (a) most forms of psychopathology are the result of multiple causal inuences; (b) both successful and unsuccessful adaptation are important for understanding the origins of psychopathology; and (c) psychopathology occurs in a developing organism, which is of course particularly relevant in childhood and adolescence, when developmental changes are most pronounced. The present article summarizes the main evidence that has accumulated on the etiology of childhood anxiety disorders during the past two decades. First, a number of vulnerability and risk factors that are thought to play a role in the development and maintenance of childhood anxiety disorders will be described. Then it will be argued that protective factors also play an important role in the development of pathological anxiety in vulnerable children. More precisely, children who have the disposal over protective mechanisms are able to cope successfully with anxietyprovoking situations, whereas those without such protective mechanisms are prone to developing high and persistent levels of fear and anxiety. Next, factors will be discussed which are thought to play a role in the maintenance of childhood anxiety disorders. Following this, developmental issues that are relevant for understanding the pathogenesis of childhood anxiety will be considered. The article will end with a discussion in which the information is integrated and linked to the earlier mentioned developmental psychopathology perspective. Finally, some directions for future research in this area will be pointed out.

Correspondence should be sent to Professor Peter Muris, Institute of Psychology, Erasmus University Rotterdam, Burgemeester Oudlaan

50, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands; e-mail: muris@fsw.eur.nl

MURIS / THE PATHOGENESIS OF CHILDHOOD ANXIETY

Vulnerability and risk factors Genetics

Behavioral-genetic research has yielded clear support for the genetic transmission of childhood anxiety disorders. For example, Stevenson, Batten, and Cherner (1992) obtained fear scores in monozygotic and dizygotic twins aged between 8 and 16 years. Results showed that a twins level of fearfulness could be predicted from a co-twins score. Also, the frequency of fears was more similar in monozygotic than in dizygotic twin pairs, yielding a signicant heritability estimate of .29. Several other studies have examined the genetic contribution to anxiety phenomena in children and adolescents (Eley et al., 2003; Legrand, McGue, & Iacono, 1999; Topolski et al., 1997). These studies have provided further support for the heritability of childhood anxiety. Genetic inuences were particularly prominent in the case of trait anxiety, with heritability estimates as high as .50. It is important to note that the genetic vulnerability to anxiety disorders is represented in general and specic factors (e.g., Taylor, 1998). The general genetic factor acts as a vulnerability factor to a wide range of anxiety disorders, while specic factors only predispose to certain types of anxiety disorders. The general genetic factor may constitute the biological substrate of what is typically referred to as neuroticism, which may manifest itself in children at a behavioral level as behavioral inhibition (Craske, 1997).

levels of cortisol may sensitize subcortical arousal circuits (e.g., amygdala, hypothalamus) and this would make children more prone to develop serious anxiety symptoms. Interestingly, work on psychophysiological parameters that tap subcortical fear responsivity (e.g., the eye blink startle reex; Vrana, Spence, & Lang, 1988) supports such an interpretation. For example, Grillon, Dierker, and Merikangas (1997) measured startle reexes in children with a parental history of an anxiety disorder (who often meet the criteria of behavioral inhibition) and control children. It was found that the startle magnitude was relatively elevated in children of parents with an anxiety disorder. This is in agreement with the notion that anxietyprone (i.e., behaviorally inhibited) children have hyperexcitable subcortical circuits that may promote fear and anxiety.

Disgust sensitivity
Disgust sensitivity is a genetically based personality trait that should be viewed as a specic vulnerability factor as it is only relevant for certain types of anxiety disorders (Muris, Merckelbach, Schmidt, & Tierney, 1999). More precisely, disgust sensitivity seems to be involved in the pathogenesis of childhood phobias, and in particular animal phobias. Evidence for this notion comes from a study by De Jong et al. (1997) who assessed fear of spiders, disgust sensitivity, and spiders disgust-evoking status in spider-phobic girls, non-phobic controls, and the parents of both groups of children. Phobic girls were tested twice, before and after behavioral treatment. The idea that disgust is an important aspect of spider phobia was supported by the following ndings. First of all, compared with non-phobic girls, spider-phobic girls exhibited higher levels of disgust sensitivity and considered spiders per se as more disgusting. Second, after treatment, the reduction in spider fear was closely paralleled by a decline in spiders disgust-evoking status. Third, mothers of spider-phobic girls also more frequently attributed a high disgust-evoking status to spiders, a nding that either points in the direction of modeling experiences or the genetic transmission of disgust sensitivity. In a follow-up study by De Jong and Muris (2002), spiderphobic and non-phobic girls were confronted with vignettes describing potential encounters with spiders. Both groups of girls then rated the subjective probability of spiders entering their private living space, their tendency to approach and make physical contact, and the probability of spiders doing physical harm. In addition, all girls indicated their eagerness to eat a favorite food item after a spider had contacted it. Results showed that phobic girls reported relatively high ratings concerning spiders tendency to enter their private living space and to approach and make physical contact, and low ratings of eagerness to eat a spider-contaminated food item. This nding seems to indicate that spider phobia results from the convergence of disgust and the probability of physical contact. All these results indicate that disgust plays a role in this type of phobia.

Behavioral inhibition
Behavioral inhibition is a temperamental trait characterized by the tendency to be unusually shy and to react with fear and withdrawal in situations that are novel and/or unfamiliar (Kagan, 1994). Research has shown that behaviorally inhibited children and adolescents are at increased risk for developing anxiety disorders. Noteworthy in this regard is a 3-year longitudinal study by Biederman et al. (1993) who found that children initially identied as behaviorally inhibited were subsequently more likely to develop anxiety disorders compared to control children (i.e., children who at study onset were not classied as behaviorally inhibited). Further support for a link between behavioral inhibition and anxiety in older youths comes from a series of studies conducted by Muris and colleagues (Muris, Meesters, & Spinder, 2003; Muris, Merckelbach, Schmidt, Gadet, & Bogie, 2001; Muris, Merckelbach, Wessel, & Van de Ven, 1999; Van Brakel, Muris, & Bgels, 2004). In these studies, children, adolescents, and their parents completed a questionnaire measuring childrens behaviorally inhibited temperament. Results showed that children who were identied as high on behavioral inhibition displayed higher levels of anxiety symptoms compared to children who were classied as low on behavioral inhibition. All the abovementioned studies suggest that behavioral inhibition is associated with the development of a broad range of anxiety symptoms and anxiety disorders (for reviews of studies on behavioral inhibition and anxiety see Biederman, Rosenbaum, Chaloff, & Kagan, 1995; Turner, Beidel, & Wolff, 1996). As to the biological correlates of behavioral inhibition, relevant parameters have been identied by Schmidt, Fox, Rubin, and Sternberg (1997). These researchers noted that behaviorally inhibited children exhibit relatively high morning levels of the stress hormone cortisol. They speculated that high

Negative learning experiences

Besides general (e.g., neuroticism, behavioral inhibition) and specic (e.g., disgust sensitivity) genetically based vulnerability factors, it is clear that negative learning experiences also play an important role in the pathogenesis of childhood anxiety

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disorders. A useful framework for discussing these learning experiences is Rachmans (1991) three-pathways theory. Briey, this theory posits that anxiety phenomena are acquired in three ways: (a) classical conditioning, (b) observational learning or modeling, and (c) negative information transmission. In their famous experiment, but questionable from an ethical point of view, Watson and Rayner (1920) demonstrated that classical conditioning is indeed involved in the development of certain childhood anxiety disorders. They introduced a white rat to an 11-month-old boy, Little Albert, who initially showed no fear of the animal and appeared to want to play with it. However, whenever Albert approached the rat, the experimenters produced a loud noise (the UCS) by striking a steel bar behind his head, causing him great fright (the UCR). After ve such experiences, Albert became very upset (the CR) by the sight of the white rat, even without the presentation of the loud noise. Obviously, the fear originally associated with the loud noise had come to be elicited by the previously neutral stimulus, the white rat (now the CS). Although some phobias seem to be acquired by classical conditioning, it should be borne in mind that current views of this learning mechanism are more complicated and stress the importance of cognitive processes (such as stimulus evaluation; Dadds, Davey, & Field, 2001). Evidence for the role of observational learning in the origins of childhood fear and anxiety was provided in an experimental study by Gerull and Rapee (2002). These authors investigated the inuence of modeling on the acquisition of fear and avoidance toward novel, fear-relevant stimuli in a sample of 15- to 20-month-old toddlers. The toddlers were shown a rubber snake and spider, which were alternately paired with either negative or positive facial expressions by their mothers. Both stimuli were presented after a brief delay, and fear and avoidance reactions were assessed. Results clearly indicated that children showed more fear and avoidance following negative reactions from their mothers. Conversely, children displayed less fear and more approach behavior when their mothers responded positively to the stimuli. Field, Argyrus, and Knowles (2001) carried out a prospective study on the role of negative information in the exacerbation of childhood fear. Seven- to 9-year-old children received either negative or positive information about an unknown monster doll. Results showed that negative information signicantly increased childrens fear ratings, whereas after positive information fear ratings slightly decreased. These results were replicated by Muris, Bodden, Merckelbach, Ollendick, and King (2003), who provided children with either negative or positive information about an unknown, dog-like animal, called the beast. This study demonstrated that informationinduced fear effects endured over a 1-week follow-up period and generalized to other stimuli, that is, children who became more fearful of the beast after receiving negative information also became more apprehensive of other dogs and predators.

reported stressful life events. Results indicated that anxietydisordered children differed signicantly from healthy controls in the number of negative life events reported by their parents over their lifetime and the year preceding referral. Furthermore, anxiety-disordered children differed signicantly from their non-referred siblings in the number of negative life events. Although Boer et al. also found some evidence indicating that parents tended to appraise the impact of life events as more negative for their anxious child than for their non-anxious child, the conclusion that negative life events contribute to the development of high levels of anxiety symptoms in youths was still justied (see also Goodyer, Wright, & Altham, 1990).

Family factors
Family factors are also thought to be involved in the pathogenesis of childhood anxiety disorders (e.g., Dadds & Roth, 2001). A factor that seems to be relevant in this context is attachment. Research has, indeed, shown that early attachment relationships are predictors of fear and anxiety in later childhood. For example, in their prospective study, Warren, Huston, Egeland, and Sroufe (1997) examined whether insecurely attached infants run greater risk for developing anxiety disorders than infants who are securely attached. At 12 months of age, infants were classied as either securely or insecurely attached using the strange situation observation procedure. When children reached 17.5 years of age, current and past anxiety disorders were assessed by means of an interview schedule. Results indicated that insecurely attached children more frequently displayed anxiety disorders than children who were securely attached (see also Muris, Meesters, Van Melick, & Zwambag, 2001). Other studies have examined the role of specic parental rearing behaviors in the development of childhood anxiety. For example, a number of studies focused on childrens perception of their parents rearing behavior, and have reported signicant and positive relationships between anxious rearing, parental control, and rejection, on the one hand, and anxiety symptoms in youths, on the other hand (Grner, Muris, & Merckelbach, 1999; Muris, Meesters, & Van Brakel, 2003; Muris & Merckelbach, 1998).

Protective factors
Genetically based variables such as behavioral inhibition and disgust sensitivity and other vulnerability and risk factors such as negative learning experiences, stressful life events, and adverse family factors will make children prone to develop anxiety disorders. Fortunately, there are also protective inuences, which may serve to shield children and adolescents against the development of an anxiety disorder. Although several authors have carefully described the characteristics of such resilience in children (Masten & Coatsworth, 1998), relatively few attempts have been made to study protective factors in relation to the development of anxiety problems in youths.

Life events
Research has also found that there is a link between negative life events such as parental divorce and death of signicant family members and childhood anxiety. For example, in a recent study by Boer et al. (2002), anxiety-disordered children were compared with non-clinical controls, and with their nearest in age non-referred sibling on the number of parent-

Effortful control
While behavioral inhibition is a temperament factor predisposing to anxiety disorders, it is of interest to note that there are also temperament variables that may buffer against the emergence of such problems. These protective temperament

MURIS / THE PATHOGENESIS OF CHILDHOOD ANXIETY

variables have been subsumed under the construct of effortful control. Effortful control refers to regulative, executive functioning-based processes, which include the focusing and shifting of attention (i.e., attentional control) and the ability to inhibit behavior when appropriate (i.e., inhibitory control; Rothbart, Ellis, & Posner, 2004). While most research has focused on the role of effortful control in the pathogenesis of disruptive behavior disorders (e.g., Eisenberg et al., 2000), several authors have recently noted that low levels of these regulative temperament factors may also promote childrens proneness to develop anxiety disorders (e.g., Lonigan & Phillips, 2001; Muris, 2004). A number of recent studies have examined the relation between effortful control and anxiety symptoms in youths (Meesters, Muris, & Van Rooijen, submitted; Muris, De Jong, & Engelen, 2004; Muris, Meesters, & Rompelberg, submitted). Although these studies were cross-sectional in nature and relied on non-clinical samples of children and adolescents, results have indeed demonstrated that low levels of effortful control are associated with high levels of anxiety symptoms in youths of various ages. Further, some evidence emerged showing that children are particularly prone to anxiety when low levels of effortful control are combined with the presence of certain vulnerability factors. For instance, the study by Meesters et al. (submitted) demonstrated that low effortful control was most strongly linked to anxiety in children with a neurotic temperament.

anxious child would not have the opportunity to learn that the stimulus or situation is in fact harmless or safe. While the role of avoidance behavior in the maintenance of anxiety disorders seems self-evident (Ollendick, Vasey, & King, 2001), there are also a number of cognitive distortions that promote continuation of these psychopathological problems. Cognitive distortions refer to cognitive processes that are biased and erroneous, and therefore yield dysfunctional and maladaptive thoughts and behaviors. Typically, in anxiety disorders, such distortions reect the chronic overactivity of schemas organized around themes of danger and threat (Kendall, 1985).

Threat-perception biases
A good example of such cognitive distortion is interpretation bias, which refers to anxious childrens tendency to disproportionally impose negative interpretations upon ambiguous situations. For example, in a study by Barrett, Rapee, Dadds, and Ryan (1996), anxiety-disordered children and non-anxious controls were confronted with ambiguous stories and instructed to interpret them. Results indicated that anxietydisordered children were more likely to interpret ambiguous situations in a threatening way compared to control children. Furthermore, it has been observed that in anxious children even very minor threat cues may readily trigger subsequent processing and consequently anxious responding, a phenomenon that has been labeled as Reduced Evidence for Danger (RED) bias. Various studies have provided evidence for the existence of RED bias in anxious children and adolescents (e.g., Muris, Merckelbach, Schepers, & Meesters, 2003; Muris, Rapee et al., 2003). The general outline of these studies was as follows: Children were exposed to stories in which ambiguous situations were described. They were told that some of these stories were scary, i.e., these stories would have a bad end, whereas other stories were not scary, i.e., these stories would have a happy end. Children were instructed to nd out as quickly as possible whether the pertinent story was scary or not scary. Stories were read aloud sentence by sentence, and after each sentence children were asked whether they thought that the story would be scary or not scary. Results consistently indicated that highly anxious children needed to hear fewer sentences before deciding a story to be threatening compared to less anxious children.

Perceived control
According to Chorpita and Barlow (1998), there are clear individual differences in perceived control that are formed as a result of experiences during early childhood. More precisely, early experiences with diminished control may foster a cognitive style characterized by an increased probability of interpreting and processing subsequent events as being out of ones control, which may represent a psychological vulnerability for anxiety. The other way around, early experiences of adequate control may instill a cognitive style that is marked by certainty about the ability to control ones environment, which may serve as a buffer to anxiety. Support for these ideas comes from studies showing that there is a negative link between perceived control and symptoms of childhood anxiety. That is, children who report high levels of perceived control generally display lower levels of this negative emotion (e.g., Muris, Schouten, Meesters, & Gijsbers, 2003; Weems, Silverman, Rapee, & Pina, 2003). In passing, it should be mentioned that the literature lists several other protective factors that bear strong resemblance to perceived control, such as self-esteem (Harter, 1993) and self-efcacy (Bandura, 1997), which are also inversely related to childhood anxiety (e.g., Muris, 2002; Muris, Meesters, & Fijen, 2003).

Developmental issues
Research has shown that normal fear and anxiety follow a predictable course: In infancy, children become fearful and anxious of imaginary creatures (e.g., ghosts, monsters) and stimuli in their immediate environment, but as the child matures these emotions begin to incorporate anticipatory events and stimuli of an abstract nature (Gullone, 2000). It is assumed that this developmental pattern of fear and anxiety reects everyday experiences and to an important extent is mediated by childrens cognitive capacities (Marks, 1987). Empirical evidence for this notion is, however, extremely sparse. One exception is a study by Muris, Merckelbach, Meesters, and Van den Brand (2002), who examined the connection between cognitive development and worry. Children were interviewed about the presence and content of a personal worry. Furthermore, a worry elaboration score was obtained by encouraging children to think up potential

Maintaining factors
Once children and adolescents have developed an anxiety disorder, this condition is likely to be maintained, or even intensied, by a variety of inuences. The two-stage model of Mowrer (1960) suggests that avoidance behavior is responsible for the maintenance of anxiety problems. More precisely, avoidance would minimize direct and prolonged contact with the fear-provoking stimulus or situation, and, hence, the

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negative outcomes associated with a series of worry topics. Finally, a number of Piagets (1970) conservation tasks were administered in order to assess childrens level of cognitive maturation. Results revealed a mediational model in which increased age and, in its wake, cognitive development lead to enhanced worry elaboration, which in turn increases the possibility of a personal worry to emerge. The authors conclude that worry becomes increasingly manifest in middle childhood when children reach a certain level of cognitive maturation (see also Vasey, Crnic, & Carter, 1994). Another example involves a recent investigation by Westenberg, Drewes, Goedhart, Siebelink, and Treffers (2004). These researchers examined developmental patterns in fears concerning physical danger and fears concerning social evaluation in a large sample of children and adolescents. In addition, participants level of sociocognitive maturation was assessed. Results demonstrated that fears of physical danger decreased with age, whereas fears concerning social evaluation increased as children were older. Most importantly, however, it was found that the age effect in social-evaluative fears was entirely explained on the basis of developmental differences in sociocognitive maturity. This led the authors to the conclusion that the social fear and anxiety which frequently arise during adolescence are a corollary of sociocognitive development. Both studies seem to indicate that, in particular, cognitive development plays a prominent role in the occurrence of various normal anxiety phenomena, and may herald periods in which vulnerable children are prone to develop high levels of fear and anxiety or even anxiety disorders. Meanwhile, it is also conceivable that greater cognitive capacity directly promotes children and adolescents vulnerability to anxiety. For example, according to the cognitive model, maladaptive cognitions are the vehicle behind pathological anxiety (Beck & Emery, 1985). More precisely, cognitive errors such as catastrophizing (i.e., anticipating the worst possible outcome for an event) lead to automatic negative thoughts, which guide an individuals interpretation of internal and external events, and eventually lead to feelings of anxiety and avoidance behavior. It is generally assumed that such cognitive errors are a function of childrens cognitive development (Alfano, Beidel, & Turner, 2002), and there is indeed some recent evidence to support this notion. Muris, Vermeer, and Horselenberg (submitted) demonstrated that the catastrophic interpretation of bodily sensations in most children occurs after the age of 7, when they have reached Piagets concrete operational stage of cognitive development. Meanwhile, it should also be kept in mind that cognitive development not only has a negative inuence by enhancing vulnerability to childhood anxiety, but it may also strengthen protective mechanisms against this negative emotion. For example, several studies have demonstrated that, under favorable circumstances, the increase of cognitive capacities may also promote regulative processes such as perceived control, effortful control, self-efcacy, self-esteem, and coping (Band & Weisz, 1990; Daniels, 1993; Kochanska, Murray, & Harlan, 2000; Velder, 1985; Weisz, Southam-Gerow, & McCarty, 2001). Altogether, it is clear that developmental issues, such as cognitive development, play a prominent role in the origins, manifestation, and continuation of anxiety problems in children and adolescents.

Discussion
During the past years, our knowledge of the factors that are involved in the etiology of childhood anxiety disorders has increased considerably. Not only a large number of vulnerability factors have been identied, but we also have a good notion of the protective inuences that might play a role in the pathogenesis of anxiety problems in youths. In the present article, I summarized the evidence for the involvement of various vulnerability, protective, and maintaining factors in the development of anxiety disorders in children and adolescents. As mentioned in the introduction, it is important to note that these factors do not operate in isolation. Rather, we should consider multifactorial models in which vulnerability and protective factors interact with each other to produce an adaptive or a maladaptive outcome (Craske, 1997; Manassis & Bradley, 1994; Vasey & Dadds, 2001). Clearly, this ts nicely with two of the major tenets of the developmental psychopathology perspective. The rst one implies that mental disorders such as anxiety disorders are the result of multiple causal inuences. The second one pertains to the fact that research of both successful and unsuccessful adaptation is important for understanding the origins of anxiety problems. That is, the study of unsuccessful adaptation will primarily focus on vulnerability and risk factors, whereas the investigation of successful adaptation will also call attention to resilience and protective factors. The article also stresses the importance of a third tenet of developmental psychopathology, namely that developmental issues play an important role in the pathogenesis of childhood anxiety. The marked developmental changes during childhood and adolescence seem to be involved in the manifestation of anxiety phenomena and occasionally may promote vulnerability to develop anxiety disorders (although such changes may also strengthen protective mechanisms). As mentioned earlier, most research on the etiology and maintenance of childhood anxiety disorders has studied the inuence of isolated vulnerability and protective factors (see Vasey & Dadds, 2001). As a result, we have little information on the extent to which various factors overlap and play a unique role in the pathogenesis of anxiety disorders. Moreover, the precise dynamics between the various factors are far from clear. While a number of recent studies have begun to examine the additive and interactive effects of multiple factors in the origins of childhood anxiety problems (e.g., Van Brakel, Muris, Bgels, & Thomassen, submitted), it is obvious that this issue requires more research attention. In particular, longitudinal research including various vulnerability and protective factors is greatly needed. Of course, such prospective studies are not easy to conduct precisely because they are time consuming and difcult to get funded. However, only in this way we will denitely learn more about the aetiological antecedents of anxiety disorders in children and adolescents.

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