The evidence does not permit a confident reply to the question of whether anxiety disorders in preschool children are precursors of similar disorders in adolescents. Retrospective data, which are always fallible, indicate that adolescents with anxiety disorders recalled their first onset of anx iety being at around 7 years of age (Costello, Erkanli, Federman, & Angold, 1999; Orvaschel et al., 1995). The Great Smoky Mountains Study revealed that specific phobias, GAD, separation anxiety, and social phobia all appeared around the time the child began school, while agoraphobia, OAD, and OCD appeared several years later, usually at 9 to 11 years of age (Costello et al., 2003).

Although early anxiety disorder appears to be a precursor of later depression (Alloy, Kelly, Mineka, & Clements, 1990; Breslau, Schultz, & Peterson, 1995; Kendler, Neale, Kessler, Heath, & Eaves, 1992; Lewinsohn, Zinbarg, Seeley, Lewinsohn, & Sack, 1997; Silberg, Rutter, & Eaves, 2001a, 2001b; Silberg, Rutter, Neale, & Eaves, 2001), we do not know the influence of anxiety on the timing or occurrence of other psychiatric disorders, with the sole exception that early separation anxiety and GAD have different predictive consequences for the later abuse of alcohol (Kaplow, Curran, Angold, & Costello, 2001).

Separation anxiety and phobic disorders are seen in early childhood but become rare by adolescence. However, panic disorder and agoraphobia have the opposite developmental profile; they are rare in childhood and increase in adolescence. We do not yet know whether some adolescent disorders are later manifestations of an underlying syndrome that was displayed earlier or whether they represent new forms of psychiatric illness. An answer to this question requires longitudinal research.

Early behavioral models for the treatment of anxiety have been based on two primary suppositions. First, fears and phobias are acquired through classical conditioning, i.e., through the formation of association between a neutral stimulus and an aversive stimulus such that the for

mer acquires the aversive properties of the latter. The neutral stimulus is then designated as a conditioned stimulus (CS) and the original aversive stimulus is called an unconditioned stimulus (US). Second, the acquired fears can be unlearned through extinction, i.e., through presentation of the CS in the absence of the US. This conceptualization gave rise to exposure therapy, in which patients are taught to systematically confront their feared situations, objects, responses (e.g., tachycardia), or memories, under safe circumstances with the goal of extinguishing their phobic fear. While there have been debates about the mechanisms through which exposure therapy reduces anxiety symptoms, the benefit of this therapy has been demonstrated by a large body of research (cf., Barlow, 2001; Ollendick & March, 2004).

Discontent with nonmediational (automatic) accounts for acquisition and extinction of pathological anxiety led to the development of theories that posited a pivotal role for cognitive factors in anxiety (e.g., Beck, Emory, & Greenberg, 1985). The assumption here is that it is not the events themselves but rather their threat “meaning” that is responsible for the evocation of anxiety. Meaning in these theories is often assumed to be represented in language. Accordingly, in cognitive therapy for anxiety disorders, verbal discourse is used to challenge the patient's threat interpretations of events and to help replace them with more realistic ones, especially so with adolescents. With young children, however, cognitive therapy frequently takes the simpler form of thought replacement such that fearful thoughts are replaced with brave ones (e.g., “I am a brave boy. I can handle this.”). The child is provided new thoughts to replace the old ones (see Ollendick & Cerny, 1981).

The focus on the meaning of events as accounting for pathological anxiety paralleled the reconceptualization of conditioning in learning theories. For example, Rescorla noted that “conditioning depends not on the contiguity between the CS and US but rather in the information that the CS provides about the US” (Rescorla, 1988, p. 153) and that the “organism is better seen as an information seeker using logical and perceptual relations among events along with its own pre-conception to form a sophisti cated representation of its world” (Rescorla, 1988, p. 154). In the same vein, when discussing the phenomenon of extinction, Bouton (1994, 2000) stated that “in the Pavlovian conditioning situation, the signal winds up with two available `meanings'” (Bouton, 2000, p. 58). Obviously, for rats the meaning of events cannot be represented in verbal language; rather, it is represented as associations among stimuli, responses, and outcomes.

Advances in information processing theories of conditioning and of pathological anxiety (e.g., Lang, 1977) influenced conceptualizations of treatment for the anxiety disorders. One such conceptualization, emotional processing theory, was proposed by Foa and Kozak (1986). In this theory, fear is viewed as a cognitive structure in memory that serves as a blueprint for escaping or avoiding danger that contains information about the feared stimuli, fear responses, and the meaning of these stimuli and responses. When a person is faced with a realistically threatening situation (e.g., a car accelerating at you, a fierce-looking dog approaching you) the fear structure supports adaptive behavior (e.g., swerving away, running away). A fear structure becomes pathological when the associations among stimulus, response, and meaning representations do not accurately reflect reality; in this instance, harmless stimuli or responses assume threat meaning. In emotional processing theory, meaning is thought to be embedded in associations among stimuli, responses, and consequences (as in Rescorla, 1988), as well as in language, especially in the form of thoughts, beliefs, and evaluations (as in Beck, 1976).

Within emotional processing theory the anxiety disorders are thought to reflect the operation of specific pathological fear structures (cf. Foa & Kozak, 1985). For example, the fear structure of individuals with panic disorder is characterized by erroneous interpretations of physiological responses associated with their panic symptoms (e.g., tachycardia, difficulty breathing) as dangerous (e.g., leading to heart attack). As a result of this misinterpretation, individuals with panic disorder avoid locations where they anticipate experiencing panic attacks or similar bodily sensations, such as physical exertion. In contrast, the fear structure of individuals with OCD most

often involves the erroneous interpretation of safe stimuli (e.g., brown spots) as dangerous (e.g., AIDS-contaminated blood). Accordingly, the core pathology in panic disorder lies in the erroneous meaning of physiological responses, whereas the core pathology of OCD lies in the erroneous meaning of external events. The supposition that inaccurate negative cognitions underlie the anxiety disorders has also been at the heart of theories posed by cognitive therapists (e.g., Clark, 1986; Rapee & Heimberg, 1997; Salkovskis, 1985).

If fear and avoidance reflect the activation of an underlying cognitive fear structure, then changes in the fear structure should result in corresponding changes in emotions and behavior. Indeed, Foa and Kozak (1986) proposed that psychological interventions known to reduce fear, such as exposure therapy, achieve their effects through modifying the fear structure. According to emotional processing theory two conditions are necessary for therapeutic fear-reduction to occur: first, the fear structure must be activated; second, information that is incompatible with the pathological aspects of the fear structure must be available and incorporated into the existing structure. Thus, within this framework, exposure therapy is thought to correct the erroneous cognitions that underlie the specific disorder (e.g., tachycardia equals heart attack). This is also the explicit mechanism by which cognitive therapy is thought to reduce fear. In this way the mechanisms that are thought to operate during exposure greatly overlap with those of cognitive therapy. Moreover, some cognitive therapists explicitly posit that fear activation is necessary to refute the patient's false interpretations, and cognitive therapy programs routinely include an exposure component in the form of “behavioral experiments.” It must be noted that the evidence for change in cognitions as the central mechanism in fear reduction is somewhat incomplete at this time; accordingly, additional work on the mediators or mechanisms of change in both the cognitive and behavior therapies is drastically needed. Such research is especially needed with children and adolescents, in whom the exact role of cognitions has been less frequently examined (Prins & Ollendick, 2003).

The cognitive approach to anxiety disorders comprises two research traditions (McNally, 2001b). In one tradition, researchers assume that introspective self-reports of anxious individuals can reveal aberrant cognition underlying symptom expression. These scholars administer questionnaires and conduct interviews to ascertain, for example, the intensity, frequency, and content of the worries and fears of children and adolescents. One such study revealed that school-age children worry most about school, health, and personal harm, especially the latter (Silverman, La Greca, & Wassertein, 1995). Another indicated that children and adolescents suffering from anxiety disorders report the same kinds of worries as those of their healthy counterparts, but that the intensity (not the number) of worries distinguished youngsters with anxiety disorders from those without anxiety disorders (Weems, Silverman, & La Greca, 2000). Researchers in this tradition have also studied the fear of anxiety symptoms (i.e., anxiety sensitivity; Reiss & McNally, 1985). Silverman and colleagues have developed the Childhood Anxiety Sensitivity Index (CASI; Silverman, Fleisig, Rabian, & Peterson, 1991; Silverman & Weems, 1999) to investigate this phenomenon.

In the second tradition, researchers eschew self-report as insufficiently sensitive to measure abnormalities in cognitive mechanisms that often operate rapidly, and outside of awareness. These scientists apply the methods of experimental cognitive psychology to elucidate biases favoring processing of threat-related information in anxiety-disordered patients (McNally, 1996; Williams, Watts, MacLeod, & Mathews, 1997). In this section, we review experiments on information-processing biases in anxious children and adolescents (see also Vasey, Dalgleish, & Silverman, 2003; Vasey & MacLeod, 2001).

Although the exact timing of puberty is not easy to specify, scientists agree that the psychological and biological features of the era called adolescence are influenced by cultural setting. Some cultures, like our own, delay the assumption of adult roles; others require a clear transition, with or without a rite-of-passage ceremony (Schlegel & Barry, 1991). Nonetheless, there is an identifiable period between 12 and 18 years, ubiquitous across societies, characterized by changes in hormones, brain structure, and behavior. These properties may have been conserved over evolution to promote autonomy and to foster dispersal of some individuals from the natal territory to another in order to avoid inbreeding (Schlegel & Barry, 1991; Spear, 2000).

Adolescence is marked by a reactivation of the hypothalamic–pituitary–gonadal axis, development of secondary sexual characteristics, and the onset of reproductive capacity, even though the increased circulation of sex hormones does not account for much of the variance in the behavior of adolescents (Brooks-Gunn, Graber, & Paikoff, 1994). The timing of pubertal signs is influenced