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2 Pearson Education Limited Edinburgh Gate Harlow Essex CM20 2JE England and Associated Companies throughout the world Visit us on the World Wide Web at: Pearson Education Limited 2014 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without either the prior written permission of the publisher or a licence permitting restricted copying in the United Kingdom issued by the Copyright Licensing Agency Ltd, Saffron House, 6 10 Kirby Street, London EC1N 8TS. All trademarks used herein are the property of their respective owners. The use of any trademark in this text does not vest in the author or publisher any trademark ownership rights in such trademarks, nor does the use of such trademarks imply any affiliation with or endorsement of this book by such owners. ISBN 10: ISBN 13: British Library Cataloguing-in-Publication Data A catalogue record for this book is available from the British Library Printed in the United States of America

3 sergei Impairment in Functioning Sergei is a 17-year-old former high school student. Only a year or so ago Sergei seemed to be a normal adolescent with many talents and interests. Then, almost overnight he was transformed into a lonely outsider, excluded from social life by his psychological disabilities. Specifically, he was unable to stop washing. Haunted by the notion that he was dirty in spite of the contrary evidence of his senses he began to spend more and more of his time cleansing himself of imaginary dirt. At first his ritual ablutions were confined to weekends and evenings and he was able to stay in school while keeping them up, but soon they began to consume all his time, forcing him to drop out of school, a victim of his inability to feel clean enough. Rapoport, 1989, p. 83. concerning adults, in which obsessions and compulsions are reported at fairly equivalent rates. There appear to be two broad themes to the excessive concerns and rituals: The first theme is a preoccupation with cleanliness, grooming, and averting danger, and the second theme is a pervasive doubting not knowing when one is right. Childhood obsessive-compulsive disorder is often recognized only when symptoms are very severe. If a youth reaches out for help, it is frequently only after years of suffering. Young people often admit having kept their problems a secret. Among those who do seek help, many indicate that their parents were unaware of their problem. Table 7 For example, diagnostic interviews conducted with a community-based sample of youths ages 9 through 17 and their mothers found that of the 35 cases of OCD identified, 4 youths were diagnosed as having OCD on the basis of the parent s report, and 32 as the result of the youth s report, but in only 1 case did the youth and parent concur (Rapoport et al., 2000). epidemiology Epidemiological studies of nonreferred adolescents suggest a prevalence rate of about 1% and a lifetime prevalence rate for OCD of about 1.9% in the general adolescent population (Flament et al., 1988; Rapoport et al., 2000). Most estimates also suggest that at younger ages, boys outnumber girls, but that by adolescence, the genders are equally represented (March et al., 2004; Rapoport et al., 2000). Among a sample of 70 consecutive child and adolescent cases seen at NIMH, 7 had an onset prior to the age of 7 years, and the mean age of onset was 10 years of age. The onset of obsessive-compulsive symptoms in boys tended to be prepubertal (mean age 9), whereas in girls, the average onset was around puberty (mean age 11) (Swedo et al., 1989c). Similar age differences in onset of OCD symptoms have also been reported among community samples (Rapoport et al., 2000). Most children and adolescents diagnosed with obsessive-compulsive disorder meet the criteria for at least one other disorder (Geller et al., 2003a; Rapoport & InhoffGermain, 2000). Multiple anxiety disorders, attentiondeficit hyperactivity disorder, conduct and oppositional disorders, substance abuse, and depression are commonly reported (Leonard et al., 2005; Rapoport & InhoffGermain, 2000). Obsessive-compulsive disorder also often occurs with Tourette syndrome (a chronic disorder with a genetic and neuroanatomical basis characterized by motor Some Common Obsessions and Compulsions Obsessions Contamination concerns (e.g. dirt, germs, environmental toxins) Harm to self or others (e.g. death, illness, kidnapping) Symmetry, order, exactness Doing the right thing (scrupulosity, religious obsessions) Compulsions Washing, grooming Repeating (e.g. going in and out of a door) Checking (e.g. doors, homework) Ordering or arranging 162

4 and vocal tics and related urges) or other tic disorders (Scharf et al., 2012; Swain et al., 2007). Tics are sudden, rapid, recurrent, stereotyped motor movements or vocalizations. The various ways in which OCD may present have led to the idea of a group of related disorders and the suggestion to use the term Obsessive Compulsive Spectrum to describe this situation. It remains unclear whether children and adolescents with tics represent a distinct subtype of OCD with regard to symptomatology and response to treatment (Storch et al., 2008; Swain et al., 2007). Developmental course and Prognosis Behavior with obsessive-compulsive qualities occurs in various stages of normal development (Evans & Leckman, 2006). For example, very young children may have bedtime and eating rituals or may require things to be just so. Disruption of these routines often leads to distress. Also, young children are often observed to engage in repetitive play and to show a distinct preference for sameness. In his widely read book for parents, Benjamin Spock noted that mild compulsions such as stepping over cracks in the sidewalk or touching every third picket in a fence are quite common in 8-, 9-, and 10-year-olds (Spock & Rothenberg, 1992). Many readers of this text likely recall engaging in such behaviors. Behaviors that are common to the youth s peer group are probably best viewed as games. Only when they dominate the young person s life and interfere with normal functioning is there cause for concern. In addition, the specific content of OCD rituals generally does not resemble common developmental rituals and OCD rituals have a later stage of onset. It is not clear whether developmental rituals represent early manifestations of obsessive-compulsive disorder in some children (Evans & Leckman, 2006). There is heterogeneity regarding the course of OCD. The disorder follows a course in which symptoms emerge and fade over time. Multiple obsessions and compulsions are usually present at any one time, and usually the symptoms change in content and intensity over time (Leonard et al., 2005; Rettew et al., 1992). Research also suggests that the disorder is likely to be chronic. Although about threequarters of youths receiving treatment may show substantial improvement, problems persist. However, persistence may be lower than once thought (Leonard et al., 2005). mechanisms continues to evolve and be informed by ongoing research. biological Influences There is evidence for a genetic contribution to anxiety disorders (Smoller, Gardner-Schuster, & Misiaszek, 2008). Aggregation of anxiety disorders in families is consistent with a genetic contribution. For example, family studies indicate that children whose parents have an anxiety disorder are at risk for developing an anxiety disorder (Beidel & Turner, 1997; Merikangas, 2005), and parents whose children have anxiety disorders are themselves likely to have anxiety disorders (Last et al., 1991). In addition, more specific examinations of the influence of inheritance (e.g., twin studies, genome-wide association studies) indicate a genetic component that, along with environmental influences, contributes to the development of anxiety disorders (Franić et al., 2010). Estimates of the degree of heritability for anxiety disorders vary but moderate heritability is suggested. In the Virginia Twin Study of Adolescent Behavioral Development (Eaves et al., 1997), heritability estimates for anxiety tended to be lower than for other disorders; however, other findings suggest higher heritability estimates (Bolton et al., 2006). Heritability may depend on the nature of the anxiety presentation and is perhaps greatest for generalized anxiety and OCD (Eley et al.,2003). Also, some research suggests that heritability may be greatest for younger children. As children grow up, the relative contribution of genetic influences may decrease and the influence of shared family environment may increase (Boomsma, van Beijsterveldt, & Hudziak, 2005). In sum, findings suggest that genetic factors may play a role in the development of anxiety disorders. There etiology OF ANxIety DIsORDeRs The development of anxiety disorders is influenced by multiple risk factors that interact with one another in complex ways (Barlow, 2002; Bosquet & Egeland, 2006; Pliska, 2011). Our understanding of risk factors and causal Keeping things in certain specific locations and order is common. It is only when these kinds of behaviors interfere with a young person s normal functioning that they should cause concern for clinicians and other adults. 163

5 may be different patterns of inheritance for different anxiety disorders. Alternatively, what may be inherited, rather than a specific anxiety disorder, is a general tendency, such as emotional and behavioral reactivity to stimuli. Furthermore, this general tendency may be a risk factor for depression as well as anxiety. These findings also indicate a substantial contribution of environment to anxiety disorders. Thus, there may be a general genetic risk and unique experiences may contribute to specific expressions of this vulnerability (Boomsma, van Beijsterveldt, & Hudziak, 2005; Gregory & Eley, 2007; Lichenstein & Annas, 2000; Muris, 2006; Smoller et al., 2008; Williamson et al., 2005). Genetic influences may be expressed through differences in specific brain circuits and neurotransmitter systems (Pliska, 2011). For example, neurotransmitters such as serotonin are thought to play a role in the development of anxiety and panic. The neurotransmitter gamma aminobutyric acid (GABA) also has received attention. GABA is known to inhibit anxiety. Anxious individuals have low levels of GABA in particular areas of the brain. Attention also has focused on corticotrophin-releasing hormone (CRH). CRH, when released in reaction to stress or a perceived threat, has effects on other hormones and areas of the brain implicated in anxiety. The limbic system and the amygdala, in particular is the portion of the brain that is most often thought to be associated with anxiety. Neuroscience research has examined processes such as attention, fear conditioning, and other emotional learning and has made use of neuroimaging techniques such as the fmri. Findings suggest that the amygdala and portions of the prefrontal cortex play a role in anxiety. For example, anxious and non-anxious youth shown threatening stimuli have been found to exhibit different reactions in these regions of the brain (Pine, Guyer, & Leibenluft, 2008). Many professionals have come to believe in a biological basis for obsessivecompulsive disorder (Evans & Leckman, 2006; Leonard et al., 2005; McMaster, O Neill, & Rosenberg, 2008). Twin and family studies also suggest considerable heritability for OCD (Eley et al., 2003; Matthews & Grados, 2011). For example, the disorder has been found to be more prevalent among youngsters with a first-degree relative with obsessive-compulsive behavior than among the general population, and many parents of youngsters with the disorder meet diagnostic criteria for OCD or exhibit obsessive-compulsive symptoms. In addition, a number of studies have reported that both OCD and Tourette syndrome (or less severe tic disorders) occur in the same individuals at higher-than-expected rates, and these studies have found a familial association between the two biological INFLueNces FOR OcD 164 disorders (Spessot & Peterson, 2006; Swain et al., 2007). It seems likely that OCD and Tourette s syndrome have some shared genetic basis (Matthews & Grados, 2011). Research is ongoing to identify the network of genes involved in the development of OCD (Grados, 2010). Neuroimaging studies have suggested that obsessive-compulsive disorder is linked to neurobiological abnormalities of the basal ganglia, a group of brain structures lying under the cerebral cortex and several areas of the prefrontal cortex (Evans & Leckman, 2006; Leonard et al., 2005; Rauch & Britton, 2010). A subset of cases of obsessive-compulsive disorder, known as PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections), has been noted. This subset of OCD involves a sudden onset or exacerbation of OCD symptoms following infection and the youth also exhibitstics. Although a clear picture regarding this potential subgroup of OCD remains to be established, they are believed to result from an autoimmune reaction produced when antibodies formed by the body against the streptococcal cells react with and cause inflammation in cells of the basal ganglia (Leckman et al., 2011). The general vulnerability to anxiety discussed earlier may be associated with aspects of the child s temperament biologically based, possibly inherited, individual differences in emotionality, attention, behavioral style, and the like (Bosquet & Egeland, 2006; Fox, 2010; Pérez-Edgar & Fox, 2005; Rapee & Coplan, 2010). An important contribution to an understanding of the relationship of temperament and anxiety disorders has been described by Jerome Kagan and his colleagues (Kagan, 1997). Their findings are based on longitudinal research regarding the temperament quality known as behavioral inhibition (BI). Behaviorally inhibited children are identified as hypervigilant of their environment, particularly in novel or unfamiliar situations, and extremely likely to withdraw from unfamiliar people or events. It is suggested that about 15 20% of children would display heightened behavioral inhibition and that about half of these children will continue to display these characteristics across childhood (Degnan & Fox, 2007; Fox et al., 2005). Particular autonomic and brain activity patterns, including greater autonomic system reactivity, elevated morning cortisol levels, and heightened activation in the amygdala to novel or threatening stimuli have been reported (Degnan, Almas, & Fox, 2010; Fox & Pine, 2012; Perez-Edgar et al., 2007). Of particular interest is the development of internalizing problems in these inhibited children. At 5.5 years of age, children who were originally classified as inhibited had developed more fears than had uninhibited children. temperament

6 Furthermore, whereas fears in uninhibited children could usually be related to a prior trauma, this was not true for the inhibited children (Kagan, Reznick, & Snidman, 1990). Other research also suggests that inhibited children are at risk for developing anxiety disorders such as social anxiety, separation anxiety, and agoraphobia. Inhibited children, compared with noninhibited children, also seem more likely to meet the criteria for multiple anxiety disorders. While there are conceptual and methodological issues with regard to the temperament anxiety relationship, this and other evidence suggests that BI and similar temperamental differences may, in the context of certain environmental influences such as parenting styles or peer relationships, be a vulnerability pathway towards the development of anxiety disorders during later childhood, adolescence, and young adulthood (Biederman et al, 1993; Chronis-Tuscano et al., 2009; Degnan et al., 2010; Hirshfeld-Becker et al., 2007; Nigg, 2006b). Gray (1987) has described a functional brain system, part of which is a behavioral inhibition system (BIS), involving multiple areas of the brain. The BIS system is related to the emotions of fear and anxiety, and tends to inhibit action in novel or fearful situations or under conditions of punishment or nonreward. Gray s model of inhibition has also informed thinking about the contribution of temperament to the development of anxiety disorders (Chorpita, 2001; Lonigan et al., 2004). Another approach to the contribution of temperament to anxiety disorders derives from Clark and Watson s (1991) model of emotion and the concept of negative affectivity (NA). NA is a temperamental dimension characterized by a general and persistent negative (e.g., nervous, sad, angry) mood. Research supports the hypothesis that the development of both anxiety and depression may be characterized by high levels of NA and that this may, in part, be responsible for high rates of co-occurrence of these disorders. Depression, but not anxiety, is thought to be characterized by low levels of the separate temperamental dimension of positive affectivity pleasurable mood (Chorpita, 2002; Gaylord-Harden et al., 2011; Lonigan et al., 2004). Negative affectivity may also combine with low levels of the temperamental factor of effortful control (EC), the ability to employ self-regulative processes (Lonigan et al., 2004). Children and adolescents with anxiety may show a bias toward attending to threatening stimuli. Anxious youths with high NA thus may attend to more negative stimuli and react more strongly to them. They would, therefore, have a need for greater EC. Thus, the combination of the temperamental qualities of low EC and high NA may contribute to the development and maintenance of anxiety and anxiety disorders. Psychosocial Influences Psychosocial influences are clearly a part of the complex interplay of risk factors that can lead to the development of anxiety disorders. Children and adolescents with a general vulnerability to anxiety may be exposed to a variety of experiences that alter their risk for anxiety disorders. One way of conceptualizing psychosocial influences is Rachman s three pathway theory. Rachman (1977; 1991) suggested three main ways in which fears and phobias might be learned: through the classical conditioning of fear, through modeling observing another s fearful reaction to a situation, and through transmission of verbal threat information. There is research support for each of these pathways toward the development of fear (Askew & Field, 2008; Field, 2006; Mineka & Zinbarg, 2006; Muris & Field, 2010). The first pathway, through classical conditioning, is illustrated by Watson & Rayner s case of Little Albert and there is support for this model as one potential route to the development of fears. The child s development of fear or anxiety, thus, may begin with exposure to some traumatic or threatening event and subsequent avoidance is reinforced by reducing anxiety. The second pathway, in which the child vicariously learns to fear some object or situation by observing another s fearful reactions, suggests that children may learn to be anxious from their parents who prompt, model, and reinforce anxious behavior. Parents, who are themselves anxious, in particular, express and model fearful behavior (Degnan et al., 2010). That children can learn from observing their parents reactions is illustrated in a study of toddlers who were presented with a rubber snake or rubber spider (Gerull & Rapee, 2002). The toddlers approach to or avoidance of these toys was measured. Toddlers whose mothers expressions were negative toward a toy in an earlier trial were less likely to approach and more likely to show negative emotional reactions to the toy. Similarly, infants of anxious mothers exhibited fearful behaviors and avoidance of a female stranger who had previously interacted with their mothers. The infants avoidance was related to the anxiety they saw expressed by their mothers and the mothers low level of encouragement (Murray et al., 2008). Rachman s third pathway suggests that fear may be acquired through the transmission of information. Thus, in addition to modeling anxious behaviors, parents may transmit information that a situation is threatening. A study by Field and Schorah (2007) illustrates the transmission of information pathway. Children 6 to 9 years of age were given information (threatening, positive, or no information) regarding unknown animals. The children 165

7 were asked to approach and put their hand into a box that contained the novel animal. The children s heart rates were significantly higher when they approached the box that supposedly contained the animal for which they had received threatening information. In addition to modeling anxious behavior or relating information of fearful and traumatic experiences, parents may influence the development of anxiety through other parenting styles or practices (Degnan et al., 2010). For example, Dadds and his colleagues (1996) demonstrated that anxious children and their parents are more likely to perceive threat and therefore choose avoidant solutions to ambiguous social problems. Videotaped discussions between children 7 to 14 years old and their families revealed that parents of anxious children listened less to their children, pointed out fewer positive consequences of adaptive behavior, and were more likely to respond to a child s solutions that were avoidant. In contrast, parents of nonclinic children were more likely to listen to their children and agree with their children s plans that were not avoidant. Following the family discussion, children from both groups were asked for their plan for the situation. Anxious children offered more avoidant solutions. Parenting practices may thus contribute to the development of certain cognitive styles, for example, to the perception of situations as threatening (Field & Lester, 2010). The impact of parenting to the development of anxiety disorders may begin early in the caregiving process (Main, 1996). The quality of early caregiving can contribute to the development of anxious behavior, particularly among children with a fearful temperament (Fox, Hane, & Pine, 2007). For example, Hane and Fox (2006) investigated the impact of maternal care behaviors, defined by constructs such as sensitivity and intrusiveness. They found that infants receiving low-quality maternal care behaviors exhibited EEG and behavioral differences, including more fearful behavior, compared with infants who received highquality maternal care behaviors. It has been suggested that the psychosocial influences on the development of anxiety is related to the child s perception of control and the child s development of an avoidant coping style (Chorpita, 2001; Chorpita & Barlow, 1998; Rapee et al 2009). From birth, caregiving that is sensitive to the infant s needs helps to reduce/control arousal before it becomes overwhelming. It is thought that through such caregiving processes children learn to regulate their emotions. As children develop, what constitutes sensitive parenting changes with changes in the children s needs and in a way that fosters their developing abilities to self-regulate. Parents of anxious children have often been described as overprotective or intrusive. Such overprotective/ intrusive parenting is defined by parent child interactions 166 that anticipate threats, overly regulate and limit children s activities, and instruct children in how to think and feel (Rapee et al., 2009; Wood et al., 2003). Such parenting behavior may affect children s sense of control/effectiveness, and their development of adaptive problem-solving and coping styles. Mothers of anxious children have been observed to be more intrusive and more critical with their children than mothers of non-anxious children (Hudson & Rapee, 2002; Hudson, Comer, & Rapee, 2008). However, influences are likely bidirectional (van der Bruggen, Stams, & Bögels, 2008). An anxious child may evoke an overprotective and intrusive parental response (Hudson, Doyle, & Gar, 2009). Insecure mother child attachments have also been shown to be a risk factor for the development of anxiety disorders (Bögels & Brechman-Toussaint, 2006; Brumariu & Kerns, 2010; Colonnesi et al., 2011). As described earlier, the attachment relationship is thought to contribute to the child s development in a number of important ways including emotion regulation and the nature of social relationships. It is not surprising, then, that an insecure attachment may be one of the factors that contributes to the development of anxiety disorders. We have been discussing how families may contribute to the development of anxiety problems in children. We should also remember that families can protect children from developing these problems. Family support, for example, has been found to protect children who are exposed to traumatic circumstances (Donovan & Spence, 2000). And families may foster children s abilities to cope with potentially anxiety-provoking circumstances. Peer relationships are another aspect of socialization that can affect the development of anxiety in children and adolescents (Degnan et al., 2010). There may be several ways in which peer relationships influence the development of anxiety. Withdrawn/inhibited youth may be rated as less popular by their peers and peer exclusion may occur because children s withdrawn and inhibited behavior is contrary to childhood peer interaction norms (Rubin, Bukowski, & Parker, 2006). Being withdrawn and rejected or excluded by one s peers has been found to be associated with internalizing difficulties including high levels of anxiety (Klima & Repetti, 2008). Similarly, withdrawn children may be viewed as easy targets for bullying and victimization by peers and this, also, has been found to be related to high levels of anxiety. In contrast to the risk associated with being socially withdrawn, being part of a peer group may be a protective factor with regard to the development of anxiety even if one s crowd is not an in group (La Greca & Harrison, 2005). Similarly, having a close friend may protect a youth from the negative effects of rejection by the larger peer group. But the close