Internalizing Conditions

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CHAPTER 18 Internalizing Conditions

18A. Mood Disorders

There is a growing emphasis on psychosocial problems in pediatric care, and pediatricians are in a unique position to monitor children over time to prevent, identify, and address psychosocial concerns.1 Primary care visits account for an increasing portion of mental health visits, and pediatricians play an important role in the management of childhood mood disorders.2,3 Mood disorders in childhood and adolescence have received increased clinical and research attention. Mood disorders include those characterized by depressed or irritable moods (major depressive disorder (MDD), dysthymic disorder, and depressive disorder not otherwise specified) and those characterized by fluctuations between depressed and manic or hypomanic moods (bipolar I disorder, bipolar II disorder, cyclothymic disorder, and bipolar disorder not otherwise specified). This chapter summarizes how depression and bipolar disorder in childhood and adolescence are currently understood, focusing on research concerning the significance, causes, diagnosis, and treatment of these disorders. Current practice standards, as well as issues necessitating further research, are discussed.

SIGNIFICANCE

Prevalence

The incidence of depression in adolescents is similar to that found in adults, ranging from 0.4% to 8.3%. Rates are lower in preadolescents, ranging from 0.4% to 2.5%.4 Epidemiology studies rarely include preschool-aged children; however the available data suggest that depression occurs in approximately 1% of preschool children.5,6 Gender ratios in rates of depression also change with age. Among preadolescents, similar rates of depression are found in boys and girls. In adolescence, the rate of depression in girls increases dramatically, resulting in a gender ratio of 2 : 1, similar to that found among adults.4

Estimation of the prevalence of bipolar disorder in childhood and adolescence is complicated by the general lack of agreement concerning the core characteristics of the disorder, which are discussed further in the diagnosis section of this chapter.7 No epidemiological studies currently exist for children. In a study of 14- to 18-year-olds, Lewinsohn and colleagues8 found lifetime prevalence rates for a diagnosis of bipolar disorder to be approximately 1%; an additional 5.7% reported subthreshold symptoms. Adolescents with subsyndromal symptoms of bipolar disorder experienced functional impairments similar to those in adolescents with bipolar disorder, which continued into young adulthood. This study was based solely on interviews with adolescents, however, and more recent research has emphasized the importance of including parent report in diagnosing bipolar disorder.9

These incidence rates indicate that a significant proportion of children and adolescents suffer from mood disorders. In addition, the overall rates of depression in children and adolescents appear to be increasing.5

Effect on Child and Family

Mood disorders can affect several aspects of a child’s development, including social and academic development. Children accomplish many developmental tasks through normal interactions with their environment, such as interpersonal relationships and academic tasks. Mood disorders interrupt these normal interactions. For example, social interaction may be disrupted when a child experiences social withdrawal or is rejected by peers because of unusual behaviors. Similarly, a child may miss considerable instructional time in the classroom because of impaired concentration or behavioral problems related to irritability or disruptive manic behaviors. Once a child has fallen behind in social or academic development, catching up can be extremely difficult. When children experience long mood episodes and frequent relapses, the effect on development is dramatic. As one example, U.S. Department of Education statistics indicate that only 29% of children with an “emotional disturbance” graduated with a standard high school diploma in 2001, whereas 65% dropped out, in comparison to an 86% high school completion rate for all students in the same year.12,13 Teachers rate children with depression as having more withdrawn and disruptive social behaviors than do nondepressed peers.14 Adolescents with MDD also experience impairments in social, family, and academic functioning.15 In comparison with children with attention-deficit/hyperactivity disorder (ADHD), children with bipolar disorder have been found to have impaired relationships with parents and peers, higher rates of placements in special education classes, and higher rates of hospitalization.16,17

A child’s mood disorder can affect the entire family. Symptoms of irritability and mood lability can increase conflict in the child’s family interactions. Parenting stress also increases because parents are faced with a child’s mood and behavior problems that do not respond to typical parenting strategies.18 Besides the stress associated with managing the child’s symptoms, families can also suffer from the financial burden associated with the cost of medication and other treatments and lost time from work for doctor appointments. With more severe cases of mood disorders, multiple hospitalizations and legal difficulties related to the child’s behavior further disrupt family life.

Effect on Society

Beyond the direct effect of these conditions on the child and family, there is also a significant effect on society in terms of both human and financial costs. These costs are difficult to estimate, because they include the amount of money invested in treatment and educational services, reduced productivity, lost employment, mortality, and juvenile justice services.19 Ringel and Sturm3 estimated a national annual expenditure of $11.68 billion on child mental health services (inpatient treatment, outpatient treatment, and psychotropic medications) in the United States, with average costs of $293 per adolescent, $163 per child, and $35 per preschooler. In addition, in 2001, more than 475,000 students aged 6 to 21 received educational services for emotional disturbance under the Individuals with Disabilities Education Act (IDEA); this population constituted 8.1% of all students served under IDEA.13 The risk of death or physical injury related to mood disorders is also substantial. Approximately 2000 adolescents in the United States die from suicide every year, many of whom suffer from mood disorders, and an additional 700,000 require medical attention after a suicide attempt.20 According to World Health Organization estimates, MDD is the first and bipolar disorder is the fifth leading cause of years of living with a disability among 15- to 44-year-olds worldwide.19

CAUSES

Genetics

There is considerable evidence for the heritability of mood disorders in adult populations, with bipolar disorder more strongly influenced by genetics than is unipolar depression. Meta-analyses of adult studies have attributed approximately 60% of the variance in bipolar disorder and 37% of the variance in MDD to genetic factors.21,22 More recent research, using family and twin studies, has focused on the genetic influences on child and adolescent mood disorders. There is some evidence that earlier onset of a mood disorder is associated with increased prevalence of mood disorders in family members in comparison with later onset, which suggests that earlier onset may signify a more substantial genetic basis.21

Studies of the offspring of depressed parents have clearly demonstrated a familial association in childhood and adolescent depression, which could be the result of genetic influences, parent-child interactions, or other environmental influences. Having a parent with depression is one of the strongest predictors of depression in childhood and adolescence.5 Several twin studies have been conducted to explore heritability; results have varied widely, depending on measurement strategy, informant, age, and gender. Heritability estimates of parent-rated depressive symptoms range from 30% to 80%.23 Twin studies have been based on questionnaire reports of depressive or more general internalizing symptoms, and further research is needed with clinical interviews to establish diagnosis.23

Studies of parents with bipolar disorder have indicated that their offspring are at increased risk for mood disorders in general and bipolar disorder specifically. Among children of parents with bipolar disorder in a meta-analysis, 52% developed some type of mental disorder (2.7 times the risk in comparison with parents without bipolar disorder), 26.5% developed a mood disorder (4 times the risk in comparison with parents without bipolar disorder), and 5.4% developed bipolar disorder (in comparison with none of the control group).24 Studies have consistently demonstrated that for children with bipolar disorder, the rates of bipolar disorder in family members are higher, and younger age at onset is related to stronger family statistical loading of bipolar disorder.7,21 Children with psychotic depression also tend to have a family history of bipolar disorder and have a higher chance of going on to develop bipolar disorder.7 Twin studies of childhood-onset bipolar disorder have yet to be conducted, but the evidence available from family studies suggests that early-onset bipolar disorder may have a particularly strong genetic basis, and young patients may be good candidates for molecular genetic studies.21,25 Investigators are beginning to explore the molecular genetics of childhood-onset bipolar disorder, but consistent findings have yet to emerge.7,21

Biological Factors

Research in adults has identified several neurobiological correlates of mood disorders, including abnormalities in basal cortisol, cortisol regulation, corticotropin-releasing hormone, thyroid hormones, growth hormone regulation, and electroencephalographic sleep measures. Research in children and adolescents has been relatively sparse and has inconsistently replicated adult patterns.26,27

A review by Kaufman and colleagues26 indicates that consistency among child, adolescent, and adult studies has been found only in response to the dexamethasone suppression test and to selective serotonin reuptake inhibitors (SSRIs). Across the lifespan, patients with depression demonstrate nonsuppression of cortisol after the dexamethasone suppression test, which is suggestive of dysregulation of the body’s stress response system. There is also evidence that children and adolescents with depression respond to some SSRI medications in similar ways as do adults, which is discussed in more detail later in this chapter. However, responses to serotonergic probes in children have generally opposed findings in the adult literature, which indicates that there may be developmental differences in the dysregulation of the serotonergic system.26

Other neurobiological studies have yielded inconsistent findings. Studies in children with depression indicate that they show blunted response to agents that trigger growth hormone release, which is similar to adults’ responses; however, results have not been as consistent in adolescents.26 Blunted responsiveness to growth hormone has also been found in nondepressed children who are at increased risk for depression because of family history; this finding indicates that this response may reflect a predisposition to depression.5 Sleep studies have shown that adolescents with depression may demonstrate some electroencephalographic sleep responses similar to those of adults with depression, including reduced rapid-eye-movement latency and increased rapid-eye-movement density; however, these patterns have typically not been found in children.26 In contrast to the adult literature, abnormalities in basal levels of thyroid hormones, basal cortisol levels, and corticotropin-releasing hormone have not been consistently observed in children and adolescents.26

Investigators have only begun to examine the brain anatomy and functioning of children and adolescents with mood disorders; therefore, many results are preliminary. Neuroimaging studies with adults can be confounded by long duration of illness and the effects of treatment. Studies with children hold particular promise for identifying brain regions associated with the pathogenesis of mood disorders.28

The prefrontal cortex is influential in mood regulation and has been the focus of much of the neuroimaging research in adult depressive disorders.5,29 A growing series of child and adolescent studies have also focused on this area. One study revealed patients with MDD who had no family history of mood disorder had larger prefrontal cortical volume than did control patients and patients with MDD who did have a positive family history of mood disorder.28 In another study, glutamatergic concentrations in the anterior cingulate cortex were shown to be decreased by approximately 19% in patients with MDD in comparison with matched controls.30,31 In addition, significant increases in choline compounds have been found in the left dorsolateral prefrontal cortex of child and adolescent patients with MDD.32,33 Together, these studies reveal anatomical and biochemical anomalies in the prefrontal cortex in childhood and adolescent MDD. Furthermore, within a group of patients with MDD, Ehilich and colleagues34 found that white matter hyperintensities were associated with history of suicide attempts. Replication and extension of these findings are necessary to establish a clearer understanding of the role of the prefrontal cortex in childhood mood disorders.

In at least 11 studies, children and adolescents with bipolar disorder have been studied with magnetic resonance imaging.35 As reviewed by Frazier and associates,35 these studies collectively show that early-onset bipolar disorder is associated with a variety of functional, anatomical, and biochemical abnormalities in brain regions associated with emotional regulation and processing, including the limbic-thalamic-prefrontal circuit and the limbic-striatal-pallidal-thalamic circuit.

Environmental Factors

The strong familial association in early-onset mood disorders, discussed earlier, probably reflects a combination of genetic influences and family environment influences. Parental mood disorders can affect parent-child interaction, as well as events in the home. In comparison with control families, parent-child interaction in families with depressed children is characterized by higher levels of criticism, less warmth, more conflict, and poorer communication.15,3639 Research on expressed emotion has suggested that a low level of parental criticism is predictive of recovery from depressive symptoms, whereas a high level of criticism is associated with the persistence of the mood disorder.40 The depressed child’s behavior also plays a role in evoking more negative interactions from parents.41 Disruptions in the family environment, such as marital discord, abuse, and poor support, can also affect parent-child interaction and the child’s risk for depressive symptoms.4,42 Furthermore, life stressors in general have been found to precede and exacerbate depressive symptoms.5

The mechanisms by which environmental factors are associated with depressive symptoms have been the focus of more recent research. Diathesis-stress models suggest that depression results from an interaction between an internal predisposition and environmental stressors. This predisposition can take the form of a genetic or biological tendency or may be related to cognitive factors, such as poor coping skills or depressive cognitive style. According to the review by Hammen and Rudolph,5 several investigators have tested the diathesis-stress model as it pertains to cognitive vulnerabilities and have found significant interactions between cognitive style and stressful events.

The association between family or psychosocial factors and depressive disorders has been clearly demonstrated across the lifespan.4,5 In a few studies, Researchers have also begun to examine those factors in childhood bipolar disorder. In Geller and colleagues’ long-term follow-up of children with bipolar disorder, children experiencing poor maternal warmth were about four times more likely to suffer relapse after recovery than were children with high maternal warmth.11,43 Children and adolescents with bipolar disorder have also been found to experience more life stressors than children with ADHD and children with no psychiatric diagnosis.44 These stressors included those clearly caused by the child’s symptoms or behavior (e.g., hospitalization), those possibly related to the child’s symptoms or behavior (e.g., removal from the home), and those unrelated to the child’s symptoms or behavior (e.g., death of a parent).

DIAGNOSIS

Accurate diagnosis of mood disorders in children is important, because underdiagnosis and misdiagnosis can lead to delays in the delivery of appropriate treatment or to the selection of treatments that may be harmful.45 For example, some research findings suggest that the use of SSRIs or stimulants can induce mania in children and adolescents with bipolar disorder; although not all researchers have replicated these findings.7,46

Barriers to Identification

The rate of recognition and treatment for children with psychological disorders in general is quite low. Data suggest that approximately 20% to 50% of children with a psychological problem are identified and only a portion of those cases are referred for evaluation and treatment.1,47,48 Internalizing problems, such as mood disorders, are identified much less frequently than are externalizing problems and are more likely to be identified when they are accompanied by a comorbid externalizing condition.49 In view of the negative effects of mood disorders on the child’s school, social, and family functioning, as well as the suicidal behaviors that can accompany mood disorders, the low rate of identification and treatment is a significant concern. Because of low rates of identification and treatment, outcomes in community settings have not kept pace with advances in the development of effective treatments for mood disorders in children and adolescents.50

Primary care pediatricians are in an ideal position to identify mental health conditions in general and mood disorders in particular. Most children have at least one primary care visit per year, and children with psychological problems are likely to have more frequent visits.49 Many children, particularly those from families of low socioeconomic status, receive care from only a primary care pediatrician.1 Several factors can prevent accurate identification in a primary care setting, including pediatricians’ limited training in mental health issues, parents’ failure to report mental health concerns without direct questioning, limited time available for screening of nonsomatic concerns, limited referral resources, and limited availability and use of screening instruments.1 Pediatricians can play a very important role in improving identification of mood disorders but may require education and resources to support them in this role.1,49 The development of screening instruments and the availability of onsite support and treatment options are promising strategies for removing these barriers to identification and treatment.1,2,50

Symptom Manifestation

The same criteria used for adults are used to diagnose childhood mood disorders. There is consensus that childhood depressive disorders have the same clinical features as the adult form of the disorders, with a couple of differences as outlined in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision (DSM-IV-TR)51 (i.e., irritability can take the place of depressed mood; considering failure to make expected weight gains; 1-rather than 2-year duration for dysthymia). The child’s cognitive and emotional development can affect symptom manifestation and profile over time, but the clinical features of depressive disorders remain fairly consistent over time.52

There is controversy, however, over the definition of bipolar disorder in children. The core symptoms necessary for diagnosis, the necessity of discrete episodes, and the definitions of cycling in children all continue to be points of debate in the literature, and definitions of bipolar disorder have varied across studies.7 DSM-IV-TR diagnostic criteria for a manic episode include “a distinct period of persistently elevated, expansive, or irritable mood.”51 However, because irritability is so pervasive across childhood disorders, some investigators have required hallmark criteria of expansive/elated mood or grandiosity to help distinguish mania in children. In addition, many children meet symptom criteria for mania, with the exception of the duration criterion. These children may have intense rapid mood swings and often receive a diagnosis of Bipolar Disorder Not Otherwise Specified.

To help clarify the various conceptualizations of childhood mania, Leibenluft and colleagues53 proposed definitions for narrow, intermediate, and broad phenotypes of mania. In the most narrow phenotype, children meet strict DSM-IV-TR criteria for mania or hypomania, with the hallmark symptoms of elevated mood and/or grandiosity, and meet full duration criteria. Two intermediate phenotypes were identified: mania not otherwise specified (hallmark symptoms present, but symptoms do not meet duration criteria) and irritable mania (irritability without hallmark symptoms; full duration criteria met). The broad phenotype includes symptoms of severe mood and behavioral dysregulation without the hallmark symptoms or episodic cycling. Further research is needed to determine how these various phenotypes are related and whether there are differences in terms of etiology, treatment, and prognosis among the types.

Diagnosis of mood disorders in children and adolescents can evolve and change over time. Seventy percent of children with dysthymic disorder eventually experience a major depressive episode, and 20% to 40% of children who initially present with MDD eventually experience a manic episode.4 It is important to monitor the progression of symptoms over time to ensure that appropriate treatment strategies are used. Children who have early-onset depression, depression with psychotic features or psychomotor retardation, a family history of bipolar disorder, or a very strong family history of any mood disorders are at increased risk for developing mania.4

The clinical symptoms of mood disorders in children are often different from those typically seen in adults. Depressed affect, low self-esteem, and somatic complaints are more common in children than in adults, whereas anhedonia, diurnal variation, hopelessness, psychomotor retardation, and delusions increase with age.54 Children with bipolar disorder are more likely than adults to display continuous cycling (<365 cycles per year), mixed episodes, irritable mood swings with an insidious and chronic course beginning in early childhood, and high rates of comorbidity.16,45,55

It is important to consider developmentally relevant symptom manifestations in diagnosis in children. Cognitive maturation influences the ways children experience and express emotion.56 Children may be less able to express symptoms such as hopelessness, which require abstract thought until around puberty, when children begin to develop more abstract cognitive abilities.56 As another example, during their early school years, children become cognitively capable of comparing and evaluating themselves with regard to others; thus, the symptom of low self-esteem is more relevant than in younger years.56 In diagnosing childhood mania, it is particularly important to consider how DSM-IV-TR symptoms such as grandiosity, “increase in goal-directed activity,” and “excessive involvement in pleasurable activities” may manifest at different ages and how they differ from typical childhood behaviors. Children have certain constraints on their behavior by virtue of being monitored by adults, being required to attend school and other activities regularly, and not having resources such as credit cards or independent transportation to engage in the types of behaviors that adults may display.

DEPRESSION: CASE ILLUSTRATION

Eight-year-old Sara often states that nobody loves her, and she wishes she could run away and be adopted by a new family. Several days per week, she is irritable and uncooperative for most of the day. Her parents describe a “look in her eye” that indicates she is having a bad day. She was brought for assessment after an episode when she tried to run away from school and ran into traffic. She no longer initiates play dates with friends but does play when asked. Sara has episodes of tearfulness three to four times per week and sometimes reports that she is crying because she misses her dog, which ran away 3 years ago. When asked what she is good at, Sara has difficulty thinking of a response. Her parents report that she takes 1 to 2 hours to fall asleep at night. She has visited her pediatrician five times over the past year because of persistent stomachaches, which have caused her to miss school. Her parents have also recently asked Sara’s pediatrician about ways to help her sleep.

Sara experiences a mixture of irritability and depressed mood, which is common among children with depressive disorders. Parents of children with mood disorders commonly describe a different look in their child when the child’s mood is at an extreme level, such as a “look in her eye,” even if the child is not able to report feeling different. Although Sara does not report suicidal ideation, she clearly conveys a desire to escape her current life and distress by running away, which is an age-typical response. Sara’s grief over the loss of her dog is prolonged and perseverative and appears to be part of her depressive disorder rather than a typical grief reaction. Sara’s case also illustrates the increased use of health care services because of somatic complaints. Often children with mood disorders do not present for mental health treatment until symptoms become severe or cause significant distress to others. Sara’s pediatrician would be in a good position to screen for and identify mood problems at an earlier stage when she presented with somatic complaints and sleep problems.

BIPOLAR DISORDER: CASE ILLUSTRATION

David is 10 years old. His predominant mood state is irritability; however, he also experiences daily periods of elevated mood, lasting 30 to 60 minutes, when he becomes unusually silly and goofy and cannot settle down. According to his mother, David thinks that he “knows everything” about a variety of topics and picks fights with peers and adults if his knowledge is challenged. David has also become fearless on his bicycle and tries stunts that his peers do not attempt. David has recently decided to expand his lemonade stand to a restaurant in his mother’s kitchen so that he can earn more money, and he has started advertising his new restaurant to his neighbors. In the past week, David has been sleeping approximately 5 hours per night. When he cannot sleep, he stays up making menus for his restaurant and making lists of various things he wants to do the next day. When he gets bored, David builds webs with string. He recently filled his entire bedroom with an intricate web of string in a short time. His mother additionally reports that David has been making inappropriate sexual comments and recently got into trouble for taking pictures of his genitals in his bedroom, pictures that were later found on the family camera.

Pretend play is normal in childhood, but the child who describes elaborate scenarios and cannot readily identify the play as pretend may be experiencing grandiosity, particularly if the play becomes inappropriate for the situation and impairs functioning.57 In David’s case, grandiose thoughts that are causing interference can be seen in his elaborate plans to run a restaurant to make money. He also provides several examples of increased goal-directed activity. His intense focus on making plans for his restaurant and creation of string webs that fill his bedroom reflect his increased energy and goal-directed activity. Children are not able to display typical adult pleasurable activities, such as spending sprees, but may instead display excessive “daredevil” behaviors without considering the dangerous consequences, or they may become hypersexual; David exhibits both behaviors.

Response to Bereavement

When a child or adolescent has experienced a loss, such as the death of a loved one or pet, a family move, or a broken relationship, symptoms of depression are common. Children’s reactions to the death of a loved one can vary and may include dysphoria, crying spells, clinging to familiar routines and caregivers, impairments in school functioning, behavior problems, bedwetting, loss of interest in activities, sleep problems, and psychosomatic symptoms.59 These symptoms are usually transient and can be differentiated from a mood disorder on the basis of the duration and associated impairment.60 According to DSM-IV-TR criteria, symptoms of bereavement should not be diagnosed as a mood disorder unless they last longer than 2 months or are associated with significant functional impairment, worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.

In children who have experienced parental death, grief or sadness lasting a year or more is common.61 In the largest prospective study to date of children after parental death, Cerel and colleagues62 found that bereaved children demonstrated more impairment over a 2-year period than did a control group but less impairment than did a comparison group of nonbereaved children with a diagnosis of a depressive disorder. Overall impairment and depressive symptoms improved significantly in the bereaved group over 2 years, and this improvement was more rapid than that seen in the depressed group. Level of impairment and coping skills should be carefully monitored after parental death, because up to 20% of children display symptoms serious enough to warrant specialized treatment.61 A child is more likely to display clinical levels of disturbance after parental death when he or she had a psychiatric disorder before the death, when the surviving parent displays high levels of depression before or after the death, or when the family has fewer socioeconomic resources.61,62 The presence of multiple stressors in the child’s life is associated with slower improvement in depressive symptoms and overall impairment.62 Parental death by suicide is also related to higher levels of overall psychopathology.63 When children witness elements of a traumatic death, such as parental murder or suicide, they are at risk for posttraumatic stress disorder.61

After the death of a parent, many children experience suicidal ideation; however they are less likely to attempt suicide than are children with depressive disorder.64 The suidical ideation expressed by bereaved children more often reflects a desire to be with the deceased parent rather than a wish to end their lives.61,64 As with all reports of suicidal ideation, bereaved children who report such thoughts should be carefully assessed for risk factors, development of a suicide plan, and access to means of harming themselves.

ASSESSMENT

As with all childhood mental health concerns, a thorough assessment is necessary to establish an accurate diagnosis. Mood problems can reflect underlying medical conditions or drug reactions; therefore, medical causes for symptoms should be explored and ruled out as part of the assessment process.45 Gathering data from multiple informants is important, because agreement between parent and child report is often low.65 Children are generally better reporters of internal mood states, whereas parents tend to be more accurate in reporting behavioral symptoms and symptom history, although exceptions to this generalization are readily found in clinical settings.66 Teachers also have a unique perspective, inasmuch as they see children in a structured setting where behavior can differ from home and have experience with a same-age comparison group. If possible, data from teachers, such as questionnaires, notes, and report cards, should also be integrated into the clinical assessment process.

A clinical interview with the child and at least one parent is a critical component of the assessment process. The clinical interview should cover several main topics, including an evaluation of a broad spectrum of childhood conditions to establish a differential diagnosis and identify comorbid conditions, the gathering of detailed information about mood symptom severity, reconstruction of the history of mood symptom evolution and treatment, and family history data. Questionnaires may also be used to complement the interview process.

Differential Diagnosis

Cross-sectionally, the symptoms of mood disorders can appear similar to other childhood disorders and may be misdiagnosed as ADHD, anxiety disorders, developmental disorders, or behavior disorders. Furthermore, differential diagnosis among the mood disorders can present a challenge when only current symptoms are considered. Examination of the evolution of symptoms over time can help establish the presence of episodic mood changes and whether other symptoms fluctuate with mood. For example, symptoms of social withdrawal and self-doubt may reflect depression or social anxiety, which can be difficult to distinguish with a cross-sectional assessment. A history of social anxiety preceding the development of other symptoms of depression would signify the presence of an anxiety disorder. If the symptoms developed at the same time or became significantly worse along with other mood symptoms, then they could be considered symptoms of depression.

Irritability is frequently a symptom of childhood mood disorders, but it can also be prominent in ADHD, behavior disorders, anxiety disorders, and pervasive developmental disorders, as well as in children without psychopathology who are hot, hungry, tired, or stressed.45 Manic irritability often can be distinguished by its episodic, intense, and prolonged nature.

Children with ADHD also tend to experience difficulties with emotional regulation related to general impairments in behavioral inhibition, which can lead to quick expressions of emotional reactions that change easily.67 Children with mood disorders also have difficulty with emotional regulation; however, they can be differentiated by their intensity, duration, associated symptoms, and environmental triggers. Children with ADHD typically experience emotional overarousal in response to environmental disorganization and overstimulation. Children with depressive disorders, on the other hand, experience depression or irritability as their predominant mood state, and their mood does not change as much in response to environmental triggers. Bipolar disorder can be distinguished from the emotional overarousal of ADHD by the episodic, intense, and prolonged nature of emotional reactions, which are accompanied by associated symptoms not typically seen in ADHD.

Because of the symptom overlap between mania and ADHD, differential diagnosis can be particularly difficult. Distractibility, rapid speech, and increased energy are symptoms of mania that overlap with those of ADHD. Geller and colleagues55 identified five symptoms of mania that provide the best discrimination between mania and ADHD: elated mood, grandiosity, racing thoughts, decreased need for sleep, and hypersexuality. In assessment for bipolar disorder, the clinician should pay careful attention to these distinguishing symptoms, as well as symptom fluctuation with mood changes over time. In children with comorbid ADHD, distractibility, rapid speech, and increased energy should be considered symptoms of mania only when they increase beyond the child’s unique baseline level as his or her mood changes.

Hypersexual symptoms, such as those demonstrated by the example of David previously, are common in childhood-onset bipolar disorder. In Geller and colleagues’ sample,55 43% of children displayed hypersexuality. Children who display hypersexual behaviors should be carefully assessed for evidence of sexual abuse or exposure to sexual content inappropriate for the child’s age.68 Sexual behavior with a pleasure-seeking quality that fluctuates with other mood symptoms may be a symptom of mania.69

Psychosis is common in both MDD and bipolar disorder in childhood and may be incorrectly diagnosed as a schizophrenia spectrum disorder.5,70 Psychotic symptoms that are congruent with mood and fluctuate with mood symptom severity are more likely to be an associated symptom of the mood disorder.70

Mood Symptoms

Specific information should be gathered during the clinical interview about severity of mood symptoms. Mood symptoms should be evaluated in the context of an understanding of normal variations in children’s mood. Frequency, intensity, number, and duration (FIND) guidelines can be used to assist in establishing the presence or absence of mood symptoms45: Individual symptoms should fluctuate with mood and occur most days of the week (frequency), at a level that causes impairment (intensity), several times per day (number), and should last a significant portion of the day (duration).45

Prospective mood charting can be helpful in making a diagnosis, as well as monitoring progress. Daily mood logs completed by parents or adolescents can provide valuable information about situational variables that trigger mood symptoms and response to treatment. Examples of mood logs can be found at www.bpkids.org/site/PageServer?pagename=lrn_mood or can be individually tailored to meet the needs of a particular child and family.

Clinician-rated mood scales can also be helpful in summarizing mood symptom severity and in tracking progress. The Children’s Depression Rating Scale-Revised has been shown to be a reliable, valid, and sensitive measure of depressive symptoms in both inpatient and outpatient samples.71 The Young Mania Rating Scale, which was developed for adult populations, has been shown to have acceptable reliability and validity in child samples.72,73 Although widely used, this scale has several limitations, including a lack of published developmentally appropriate anchor criteria for interview-based ratings.69 The Kiddie Schedule for Affective Disorders and Schizophrenia (KSADS) Mania Rating Scale and Depression Rating Scale are promising new instruments developed for child and adolescent populations and are based on DSM-IV-TR criteria.74 Preliminary studies have found that these instruments have good psychometric properties, and further validation with larger samples is under way.69,74

Family History

Information about family history can further help establish the probability of mood disorder.69 Although a family history of mood disorders is not diagnostic of mood disorders per se, it does add additional information about the child’s risk for the disorder.69 Furthermore, because data suggest that children with MDD who have a family history of bipolar disorder are at increased risk for developing a manic episode in the future, this information may guide treatment decisions and follow-up strategies.4

Structured Interviews

It is important to assess for behavior, anxiety, mood, and other symptoms as part of the clinical interview. Structured or semistructured interviews can be used to systematically gather information about various childhood problems. Several options have demonstrated sensitivity and specificity in identifying relevant conditions and require varying levels of training and time to administer. Examples include the Diagnostic Interview Schedule for Children,75 Children’s Interview for Psychiatric Symptoms (ChIPS),76,77 Diagnostic Interview for Children and Adolescents,78 and the Washington University at St. Louis KSADS (WASH-U-KSADS),79 which includes an expanded section on the diagnosis of manic symptoms. Variations of the KSADS, such as the WASH-U-KSADS, are most commonly used in research settings, but require extensive time and specialized training for administration, which makes this instrument impractical for clinical use.69 Symptoms of mania are often not thoroughly evaluated in developmentally appropriate terms in the briefer structured interviews; however the ChIPS shows the most promise for identifying manic symptoms in youth.69

Questionnaires

Diagnosis of mood disorders can never be made on the basis of questionnaires alone. However, questionnaires can be useful as screening instruments to guide a clinical interview or as another source of information to integrate with interview data. The Child Behavior Checklist (CBCL) is a norm-referenced and widely used instrument in clinical practice and research to assess a variety of behavior problems in children and adolescents.80 The CBCL behavior scales are not specific enough to differentiate depressive from anxiety disorders; however, high scores on the internalizing scale signal that additional information should be gathered about specific mood and anxiety disorders. The Children’s Depression Inventory81 is a self-report measure specifically designed to assess the severity of depressive symptoms. This inventory has been shown to differentiate between psychiatric patients and control subjects, but it does not differentiate well among psychiatric diagnoses.82

Low scores on the externalizing scales of the CBCL are useful in ruling out bipolar disorder, but high scores are not specific enough to draw conclusions about the presence of bipolar disorder.9 The General Behavior Inventory83 is a questionnaire that is used specifically to assess manic symptoms. Parent and youth versions of this inventory have demonstrated excellent psychometric properties; however, the complexity of many items may make it difficult for individuals with limited education or reading abilities.69 Data suggest that youth and teacher questionnaires do not add anything beyond parent questionnaire data in the prediction of bipolar disorder diagnosis.9

The Pediatric Symptom Checklist84 has been developed specifically to screen for a variety of mental health problems in primary care settings. It is brief, has empirically derived cutoff scores, and has been validated with racially diverse populations and populations of low socioeconomic status.1 In settings in which resources are available to score and interpret the CBCL, it may be administered before the clinician meets with the family and used to help guide the interview. When a mood disorder is suspected, the Children’s Depression Inventory or General Behavior Inventory may be useful in the decision of whether to refer for a more thorough evaluation.

ASSOCIATED CONDITIONS

Comorbidity

Comorbidity is common among childhood diagnoses. Approximately 40% to 70% of children and adolescents with depression have at least one other psychiatric condition.4 A meta-analysis by Angold and colleagues85 found that depression is most closely associated with anxiety disorders (odds ratio, 8.2), followed closely by conduct disorders (odds ratio, 6.6) and ADHD (odds ratio, 5.5). Substance abuse disorders are also commonly comorbid with depression and tend to begin an average of 4.5 years after the onset of the depressive disorder.4

High rates of comorbidity have also been found with early-onset bipolar disorder, particularly with ADHD, behavior disorders, and anxiety disorders. Rates of comorbidity range from 66% to 75% for ADHD, 46% to 75% for oppositional defiant disorder, 5.6% to 37% for conduct disorder, 12.5% to 56% for anxiety disorders, and 11% for pervasive developmental disorders.7,69 The rates of comorbid substance abuse disorders increase with age, with rates up to 40% in adolescents.7

Treatment of Comorbidity

In treating conditions comorbid with bipolar disorder, it is important to first stabilize the mood symptoms and then evaluate the need for psychosocial or pharmacological treatment of any comorbid conditions.45 There are no clear guidelines for the treatment of comorbid conditions with depression. If the mood disorder appears to be secondary to another condition, such as social anxiety or posttraumatic stress disorder, it may be useful to treat the primary condition first or concurrently with the treatment for depression.

Suidical Ideation

Children with mood disorders are at increased risk for suicidal ideation, attempt, and completion. Suicidal ideation has been reported in more than 60% of depressed children and adolescents, and MDD is the most common diagnosis among suicide victims.5,86 Children with bipolar disorder are also at high risk for suicide, particularly when depressed, during a mixed episode, or when psychotic.8,55,87 Geller and colleagues55 reported suicidal ideation in 25% of their 7- to 16-year old participants with bipolar disorder. Comorbidity between mood disorders and substance abuse or disruptive behavior disorders further increases the risk of suicide.86 These data highlight the importance of assessing suicidality in youths with mood disorders. Data from a randomized controlled trial indicate that assessing for suicidal ideation does not increase distress or suicidal ideation in adolescents.88

In assessing for suicide risk, several factors should be taken into account; these are outlined in the American Academy of Child and Adolescent Psychiatry’s 2001 Practice Parameters regarding the assessment and treatment of adolescent suicidal behavior.20 In addition to the presence of a mood and/or substance abuse disorder, individuals with previous suicide attempts, suicidal thoughts, plans for suicide, agitation, and psychosis are at greatest risk for suicide.20 Other risk factors include family history of suicide; history of physical or sexual abuse; school problems; poor communication with parents; recent suicide of a peer; and gay, lesbian, or bisexual orientation.86 Several questionnaires that have been developed to assess risk of suicide have high sensitivity but poor specificity because of the low base rates of suicide.86 These questionnaires can best be used as screening tools in community samples. In children and adolescents at high risk for suicide, such as those with mood disorders, assessment should include direct interview with the child and parent.20

Psychosis

Psychosis is more common in child and adolescent mood disorders than in adult mood disorders. Approximately 33% to 50% of preadolescents with MDD and up to 31% of adolescents with MDD experience hallucinations, most commonly auditory hallucinations.5 Estimates of the rates of psychosis in early-onset bipolar disorder range from 16% to 88%, depending on assessment strategy.70 The most common type of psychotic symptom reported in early-onset bipolar disorder is mood-congruent grandiose delusions.70

TREATMENT

As evidenced by the prevalence, chronicity, and impairment associated with mood disorders described previously, effective intervention strategies are needed to manage these conditions. Treatment outcome studies for both biological and psychosocial therapies have helped informed treatment decisions for children with mood disorders. Considerable research on treatments for MDD has accumulated.89,90 Much of the treatment research on childhood bipolar disorder, in contrast, is preliminary and is currently evolving.45

Depression

BIOLOGICAL INTERVENTIONS

Tricyclic antidepressants have not been found to be effective in the treatment of children and adolescents.26 Only one SSRI, fluoxetine, has received approval from the U.S. Food and Drug Administration (FDA) to be marketed for children and adolescents.

Cheung and associates91 reviewed the efficacy and safety of published and unpublished randomized controlled trials of antidepressants in children and adolescents. Throughout the studies reviewed, various outcome measures were used; however, a Clinical Global Impression Improvement (CGI-I) rating of 1 or 2 (very much improved or much improved) was the most frequent definition of response to treatment that produced significant results and these response rates are reported as follows: (1) Three large double-blind placebo-controlled trials of fluoxetine indicated significant differences in clinician-rated response and symptom level between fluoxetine and placebo across all three studies; response rates for fluoxetine ranged from 53% to 60%, in comparison with 33% to 37% rates for placebo.90,92,93 (2) Of three double-blind, placebo-controlled studies of paroxetine, the one published study demonstrated superiority of paroxetine over placebo (66% response to paroxetine, 48% to placebo), whereas the other two adequately powered but unpublished studies failed to demonstrate significant results.94 (3) Two studies of sertraline, combined a priori for analysis, were identified. Response rates were 69% for the sertraline recipients and 59% for the placebo recipients. The difference was statistically significant because of the large number of subjects; however, neither study produced significant results when analyzed separately.95 (4) Two studies of citalopram were reviewed, one published and one unpublished, with an unusual pattern of results. Neither study revealed differences in CGI-I response rates; however, one did reveal group differences in depression symptom severity, as rated by the Children’s Depression Rating Scale-Revised.96 The meaning of this finding without CGI-I response differences is unclear. (5) Two studies of nefazodone were identified; one revealed a significant effect of the drug (65% response rate in comparison with 46% response rate with placebo), whereas the other study revealed no significant effect.97 (6) In two studies of venlafaxine and two studies of mirtazapine, no differences were found between the drugs and placebo on any measure.98 Additional details about the methods and results of all these studies were described by Cheung and associates.91

In October 2004, the FDA issued a black box warning requiring that antidepressant medications be accompanied by information indicating that antidepressant use is associated with increased risk of suicidality in children and adolescents. This warning was based on a review of 26 studies that demonstrated that the average risk of suicide-related events was 4% with antidepressants, in comparison with 2% with placebo.99 No deaths by suicide were reported in any of the studies reviewed.99 Examining the risk of suicidal behavior associated with naturalistic antidepressant use in the United Kingdom, Jick and colleagues100 found that risk was increased in the first month after initiation of antidepressant therapy and was highest in the first 1 to 9 days. Concerns have also been raised concerning children’s and adolescents’ risk of becoming agitated or switching to mania with antidepressant medications, which was found to occur in very small numbers of patients participating in randomized controlled trials.91 The Society for Adolescent Medicine emphasizes the high risk of suicide associated with untreated depression, however, and supports the continued use of antidepressant medication in adolescents along with careful monitoring, particularly at the beginning of treatment and after dose changes.99

Herbal remedies are gaining popularity, and St. John’s wort has been shown to have antidepressant effects superior to those of placebo in mild to moderate adult depression.101 Open-label pilot studies in children and adolescents have indicated that St. John’s wort is well tolerated and may be beneficial in treating MDD in youth.101,102 Randomized clinical trials are needed to further evaluate the safety and efficacy of St. John’s wort in children and adolescents.

Among adults who experience seasonal variation in mood symptoms, exposure to bright light or to dawn simulation has been found beneficial. Research extending these findings to pediatric samples has shown that light therapy is effective and superior to placebo in children and adolescents.103

Electroconvulsive therapy has been shown to be a very effective treatment for severe depression in adults, with remission rates of 70% to 90% in clinical trials.104 Since 1990, several studies of the use of electroconvulsive therapy in adolescents with a variety of diagnoses have been published.105 Response rates range from 50% to 100%, with higher response rates reported for mood disorders. In addition, high rates of satisfaction with the treatment have been reported among adolescents who received electroconvulsive therapy.105 There are not enough data on the use of electroconvulsive therapy in preadolescents with which to draw conclusions about its efficacy. The American Academy of Child and Adolescent Psychiatry practice parameters advised that electroconvulsive therapy be considered for adolescents after previous interventions have been ineffective and if a second psychiatrist agrees to the appropriateness of the treatment.105 Overall, electroconvulsive therapy is rarely used in adolescents despite the efficacy data and American Academy of Child and Adolescent Psychiatry guidelines.106 Lack of both knowledge and experience with electroconvulsive therapy among child and adolescent psychiatrists and public controversy surrounding the treatment may contribute to the low rates of utilization.105

PSYCHOSOCIAL TREATMENT

The most extensively researched psychosocial treatment for depression in children and adolescents is cognitive-behavioral therapy (CBT). Compton and colleagues89 reviewed 12 randomized controlled trials of CBT for depression in children and adolescents. Overall these studies showed that CBT is superior to no treatment. One study found that CBT was superior to an attentional control group;107 however others have failed to find differences in comparison with nonfocused therapy, treatment as usual, or pill placebo.90,108,109 In comparison with other specific treatment modalities, CBT has been found to be superior to relaxation training110 and systemic behavior family therapy,107 but no differences were found with interpersonal therapy.111

The cognitive-behavioral model is based on the idea that depression is maintained by cognitions and behavioral patterns that decrease effective interaction with the world.89 Cognitive distortions are thought to bias the way an individual obtains and interprets information from the environment, leading to negative thoughts about one’s self, the world, and the future and to attribution of negative events to stable, internal, and global factors. Deficits in social skills and problem solving also prevent successful interactions with the environment. Further, decreased participation in potentially enjoyable activities decreases opportunities for pleasure. Specific components of CBT include psychoeducation, goal setting, problem solving, and tailored interventions based on the individual’s cognitive and behavioral patterns. As family conflict and disruption is quite common in child and adolescent depression, a parent or family component is often included in treatment. Two studies have specifically investigated the effect of adding a family component to individual therapy, and have failed to find group differences, however this may be due to insufficient power to detect incremental differences in treatment efficacy.112,113

Another psychosocial treatment that shows promise in the treatment of adolescents with depression is interpersonal psychotherapy (IPT). In randomized clinical trials, IPT has been shown to be more effective than control groups and has shown similar efficacy to CBT.111,114,115 IPT focuses treatment on patterns of interpersonal interaction and communication. Specific targets of treatment include the problem areas of grief, interpersonal disputes, role transitions, interpersonal deficits, and single-parent families.116

COMBINATION BIOLOGICAL AND PSYCHOSOCIAL TREATMENT

The Treatment of Adolescents with Depression (TADS) study90 is the first to systematically explore the relative efficacy of fluoxetine, CBT, and their combination in adolescent depression. Results suggest that the combination is most effective, followed by fluoxetine, which was superior to both CBT alone and placebo. The TADS study90 showed that combination pharmacotherapy and CBT are more effective in decreasing both depressive symptoms and suicidal behavior than either intervention alone in adolescents with depression, highlighting the importance of a combination of interventions in the treatment of childhood-onset mood disorders.

Bipolar Disorders

BIOLOGICAL INTERVENTIONS

Pharmacological interventions are an essential component of comprehensive treatment for bipolar disorder.116a The only medication approved by the FDA for adolescent bipolar disorder is lithium. Only five randomized placebo-controlled studies to date have evaluated medications for use in child and adolescent bipolar disorder.7 Lithium was shown to improve global functioning in adolescents with bipolar disorder and comorbid substance use disorders.117 The only other study of lithium monotherapy, however, did not find continuing effects of lithium in a randomized discontinuation study.118 Following mood stabilization with combination lithium and divalproex sodium, a comparison of the two medications indicated that they were equally effective in maintenance treatment.119 DelBello and colleagues120 found that the combination of quetiapine with divalproex sodium was more effective in treating adolescent mania than dovalproex sodium alone. In a study of children and adolescents with comorbid ADHD, the addition of Adderall following mood stabilization with divalproex sodium was found to be effective in treating the ADHD symptoms.121 Much of the data used in determining treatment options for bipolar disorder in children and adolescents come from open trials, adult studies, and clinical experience.45

Kowatch and colleagues45 developed treatment guidelines for children and adolescents with bipolar disorder based on the evidence currently available. For bipolar mania, with or without psychosis, various combinations of treatment with mood stabilizers and/or atypical antipsychotics were recommended. Following nonresponse to multiple medication trials, clozapine or electroconvulsive therapy was recommended. See Kowatch et al45 for detailed treatment algorithms. No algorithm was developed for the treatment of bipolar depression, as the currently available data are too limited to draw conclusions about the treatment of depressive symptoms.

Despite the limited efficacy data for child and adolescent bipolar disorder treatments, mood stabilizers and antipsychotics are commonly used for the treatment of early onset bipolar disorder in clinical settings. American Academy of Child and Adolescent Psychiatry practice parameters recommend considering the evidence from child and adult studies, symptom presentation, phase of illness, medication safety profile, child’s history of medication response, and family preference in choosing medication(s).116a The practice parameter also suggests that most youth with bipolar disorder will require ongoing medication treatment to prevent relapse.116a

PSYCHOSOCIAL TREATMENT

Medication is a critical component of treatment for bipolar disorder; however psychosocial interventions play an important role in promoting medication compliance and teaching skills to help decrease relapse.7,116a Outcome studies of medication treatment in children and adolescents are limited, as described above, however adult studies describe residual symptoms, poor outcomes for bipolar depression, and high medication nonadherence rates.122 Additionally, while the cause of bipolar disorder in children appears to be strongly influenced by biological factors, the course can be shaped by psychosocial factors.123 Adjunctive interventions are clearly needed to enhance treatment outcome and adult studies indicate family-based psychosocial interventions decrease relapse by 33%.124,125

The addition of psychotherapy to pharmacotherapy has been recommended as soon as the child’s mood is stable enough to learn new skills.45 Research to identify efficacious treatments for bipolar disorder is in the early stages of development and three research teams have developed and reported preliminary data on therapies for bipolar disorder. These therapies are all adjunctive, include family involvement, and are psychoeducationally focused.

Fristad and colleagues have conducted the only randomized controlled trials of a psychoeducational treatment for families of children with mood disorders to date. These studies included children age 8-11 with both depression and bipolar disorder. In a pilot study of 35 children, 46% of whom had bipolar disorder, Multi-Family Psychoeducation Groups (MFPG) were found to increase parental knowledge about mood disorders, increase positive family interactions, increase the parental support perceived by children, and increase utilization of appropriate services by families.126 MFPG involves parents and children meeting separately in a group format to receive education, support, and learn skills to cope with symptoms and improve the child’s functioning. Forming groups of children with both bipolar disorder and depressive disorder diagnoses had the benefits of making it easier and faster to recruit an adequate number of families to start a group. Due to the significant portion of children initially diagnosed with MDD who later develop bipolar disorder, it was also considered important to provide information on the symptoms and management of bipolar disorder to families of children with both diagnoses. No difficulties were found in conducting these combined groups, but it was considered beneficial to include at least two children with each type of diagnosis in a group. In the pilot study, families of children with bipolar disorder had worse mood symptoms, a history of more treatment experiences, and greater knowledge about mood disorders at the beginning of treatment than the families of children with depressive disorders; however families of children with bipolar disorder and depressive disorders both benefited from treatment.127 A larger randomized controlled trial of 165 children is currently underway to evaluate MFPG.

The content of MFPG has also been adapted for delivery in individual family sessions, which has been tested in a pilot study of 20 children with bipolar disorder. Results suggest treatment led to decreased severity of mood symptoms, with improvements continuing for 12 months following treatment, improved treatment utilization, more positive family climate, and high levels of satisfaction with treatment.128 Further research with a larger sample size will be needed to more clearly evaluate the efficacy of individual family psychoeducation.128

Family-Focused Therapy (FFT) in adults with bipolar disorder has been shown to delay relapse, decrease hospitalization, decrease symptom severity, and improve medication adherence.129131 FFT involves patients and family members in education about bipolar disorder, communication training, and problem solving skills training. Miklowitz and colleagues132 have adapted FFT for an adolescent population (FFT-A), and in open trials the combination of FFT-A and pharmacotherapy was associated with improvements in symptoms of mania and depression and reductions in problem behaviors. Pavuluri and colleagues133 adapted the FFT model and combined it with cognitive behavioral principles to develop Child and Family-Focused Cognitive-Behavioral Therapy (CFF-CBT) for younger children. In open trials, CFF-CBT in addition to pharmacotherapy led to reductions in mood symptoms and improved global functioning.133

PREVENTION

Research has begun to address the prevention of depression in youth with subclinical symptoms. Group cognitive behavioral interventions for children and adolescents have shown promise in reducing symptoms and subsequent development of clinical depression; however data on the long term effects of these programs have been mixed.134136 Gilham and colleagues134 found that benefits were sustained and the prevention effects grew over the course of two years, while Spence and colleagues136 found that initial benefits were lost by one year follow up. Intervention programs in primary care have also targeted adolescents at risk for depression, and findings suggest that prevention programs can be successfully implemented in such settings with the consultation of mental health professionals or use of internet-based programs.50,137

Given the often chronic and relapsing course of mood disorders, the prevention of relapse in children who have had a prior mood episode is an important consideration. One study suggests that the continuation of fluoxetine treatment for depression may help reduce and delay relapse in children and adolescents over eight months.138 Follow-up studies of CBT for depression have indicated that treatment gains are generally maintained or continue one to nine months following treatment, but over longer term follow-up (nine months to two years), lack of recovery and relapse are common.89 Further research is needed to determine whether booster sessions of CBT may be helpful in maintaining treatment effects.89 Research on pharmacological and psychosocial strategies for reducing and delaying relapse for children and adolescents with bipolar disorder is in the early stages and has not yet yielded any conclusive findings.7

CLINICAL IMPLICATIONS

Mood disorders in pediatric populations are associated with impairment at home, at school, and with peers. The experience of a mood disorder also increases risk for suicide and future mood problems. Identification of these disorders in children and adolescents is a crucial first step in reducing the associated impairment and risks. Developmental-behavioral pediatricians, as well as other health and educational professionals, play an important role in identifying mood disorders in this population and recommending appropriate treatments. A significant portion of mental health services are currently provided in primary care settings, with primary care visits accounting for nearly 40% of all mental health services among a small sample of privately insured children.3 The availability of child and adolescent psychiatry services nationwide is far short of the need.139 These data highlight the importance of all child and adolescent health care providers being educated about the symptoms and effective treatments for mood disorders. Further, only about half of children referred for services with a mental health provider show up for their first appointment with that provider.1 Families may be more likely to follow through with treatment when services are available in the primary care setting or there is significant collaboration among professionals.1,2,50

Models of collaboration among professionals to treat mental health problems in a primary care setting have been developed and show promise for providing cost-effective, beneficial services for children and adolescents. A stepped-care approach has been shown effective in treating adult mood disorders and has been adapted for the treatment of child mental health problems.2,50,140 Campo and colleagues2 described a program in which primary care physicians, advanced practice nurses, social workers, and pediatric psychiatrists work together to provide appropriate levels of care for children and adolescents. In their model, primary care physicians identify children with possible mental health issues and provide treatment for less complex cases. Advanced practice nurses with training in psychiatry complete onsite mental health assessments, make diagnoses, and provide patient education and support as needed. Social workers provide case management and onsite psychotherapy for cases of moderate to severe complexity. The pediatric psychiatrist manages more complex cases and provides consultation for the team. The team also met regularly to discuss ongoing cases. With this level of support, two-thirds of mental health cases were successfully managed by the primary care pediatrician and advanced practice nurse. Asarnow and colleagues50 reported on a similar program testing the benefits of having a care manager with mental health training available in the primary care setting to coordinate and support the care of adolescents with depression. Adolescents who received the collaborative care reported fewer depressive symptoms, greater utilization of mental health services, and greater satisfaction with their treatment than those who received usual care. These models highlight the ways that mental health screening, in-house treatment options, and consultation among professionals can improve outcomes for children and adolescents.

RESEARCH IMPLICATIONS

Further research in childhood mood disorders is needed to improve prevention, identification, diagnosis, and treatment efforts. The existing research base is considerably stronger for depressive disorders than for bipolar disorders. There is a growing base of knowledge about the risk factors involved in mood disorders, including genetics, neurobiology, and environmental influences. Future molecular genetics research will improve our understanding and early identification of at-risk children. It will also be important for future research to examine the ways genetics, neurobiological factors, and environmental influences interact, which may lead to more targeted intervention strategies.139 Research is necessary to establish a clear definition of bipolar disorder in children and determine its continuity with adult forms of the disorder. To accomplish this, developmentally appropriate criteria with high interrater reliability and validity will need to be developed.139

We now have a growing base of randomized controlled trials of treatments for depression to guide treatment decisions. Future research should expand on this knowledge by examining treatment options for treatment-resistant depression, identifying the active components of psychotherapy through dismantling studies, increasing attention to prevention strategies, and examining effectiveness in community-based studies.139 There is currently very little research base for the treatment of bipolar disorder and the identification of effective pharmacological and psychosocial treatments will be very important in improving outcomes for the children and families who are coping with this chronic and relapsing condition.139

Changes are also needed in the way mental health services are provided to increase identification and appropriate treatment. Programs to increase knowledge about mood disorders among professionals who work directly with children, such as teachers and primary care physicians, should be developed and evaluated. Recent research has begun evaluating ways of incorporating mental health treatment into primary care.2,50 Continued research and public policy changes to allow for more effective treatment will help improve access to appropriate services.139

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61 Dowdney L. Annotation: childhood bereavement following parental death. J Child Psychol Psychiat. 2000;41:819-830.

62 Cerel J, Fristad MA, Verducci J, et al. Childhood bereavement: Psychopathology in the two years post-parental death. J Am Acad Child Adolesc Psychiatry. 2006;45:681-690.

63 Cerel J, Fristad MA, Weller EB, et al. Suicide-bereaved children and adolescents: A controlled longitudinal examination. J Am Acad Child Adolesc Psychiatry. 1999;38:672-679.

64 Weller RA, Weller EB, Fristad MA, et al. Depression in recently bereaved prepubertal children. Am J Psychiatry. 1991;148:1536-1540.

65 Tillman R, Geller B, Craney JL, et al. Relationship of parent and child informant to prevalence of mania symptoms in children with a prepubertal and early adolescent bipolar disorder phenotype. Am J Psychiatry. 2004;161:1278-1284.

66 Ryan ND. Diagnosing pediatric depression. Biol Psychiatry. 2001;49:1050-1054.

67 Barkley RA. Attention-Deficit Hyperactivity Disorder: A Handbook for Diagnosis and Treatment, 2nd ed. New York: Guilford, 1998.

68 Mackinaw-Koons B, Fristad MA. Research in practice: Early-onset bipolar disorder: What every child clinician should know. Soc Clin Child Adolesc Psychol Newsl. 2004;17(4):6-7.

69 Youngstrom EA, Findling RL, Youngstrom JK, et al. Toward an evidence-based assessment of pediatric bipolar disorder. J Clin Child Adolesc Psychol. 2005;34:433-448.

70 Pavuluri MN, Herbener ES, Sweeney JA. Psychotic symptoms in pediatric bipolar disorder. J Affect Disord. 2004;80:19-28.

71 Poznanski EO, Mokros HB. Children’s Depression Rating Scale, Revised Manual. Los Angeles: Western Psychological Services, 1996.

72 Fristad MA, Weller RA, Weller EB. The Mania Rating Scale (MRS): Further reliability and validity studies with children. Ann Clin Psychiatry. 1995;7:127-132.

73 Young RC, Biggs JT, Ziegler VE, et al. A rating scale for mania: Reliability, validity and sensitivity. Br J Psychiatry. 1978;133:429-435.

74 Axelson D, Birmaher BJ, Brent D, et al. A preliminary study of the Kiddie Schedule for Affective Disorders and Schizophrenia for School-Age Children mania rating scale for children and adolescents. J Child Adolesc Psychopharmacol. 2003;13:463-470.

75 Shaffer D, Fisher P, Lucas CP, et al. NIMH Diagnostic Interview Schedule for Children Version IV (NIMH DISC-IV): Description, differences from previous versions, and reliability of some common diagnoses. J Am Acad Child Adolesc Psychiatry. 2000;39:28-38.

76 Weller EB, Weller RA, Rooney MT, et al. Children’s Interview for Psychiatric Syndromes (ChIPS). Washington, DC: American Psychiatric Press, 1999.

77 Weller EB, Weller RA, Rooney MT, et al. Children’s Interview for Psychiatric Syndromes, Parent Version (P-ChIPS). Washington, DC: American Psychiatric Press, 1999.

78 Reich W. Diagnostic Interview for Children and Adolescents (DICA). J Am Acad Child Adolesc Psychiatry. 2000;39:59-66.

79 Geller B, Warner K, Williams M, et al. Prepubertal and young adolescent bipolarity versus ADHD: Assessment and validity using the WASH-U-KSADS, CBCL, and TRF. J Affect Disord. 1998;51:93-100.

80 Achenbach TM, Rescorla LA: Manual for the ASEBA School-Age Forms & Profiles. Burlington: University of Vermont, Department of Psychiatry, 2001.

81 Kovacs M. Children’s Depression Inventory. North Tonawanda, NY: Multi-Health Systems, 1999.

82 Fristad MA, Weller RA, Weller EB, et al. Comparison of the parent and child versions of the Children’s Depression Inventory. Ann Clin Psychiatry. 1991;3:341-346.

83 Depue RA, Slater JF, Wofstetter-Kaush H, et al. A behavioral paradigm for identifying persons at risk for bipolar depressive disorder: A conceptual framework and five validation studies. J Abnorm Child Psychol. 1981;90:381-437.

84 Jellinick M, Murphy JM. Screening for psychosocial disorder in pediatric practice. Am J Dis Child. 1988;109:371-378.

85 Angold A, Costello EJ, Erkanli A. Comorbidity. J Child Psychol Psychiatry. 1999;40:57-87.

86 Pfeffer CR. Diagnosis of childhood and adolescent suicidal behavior: Unmet needs for suicide prevention. Biol Psychiatry. 2001;49:1055-1061.

87 Dilsaver SC, Benazzi F, Rihmer Z, et al. Gender, suicidality and bipolar mixed states in adolescents. J Affect Disord. 2005;87:11-16.

88 Gould MS, Marrocco F, Kleinman M, et al. Evaluating iatrogenic risk of youth suicide screening programs: A randomized controlled trial. JAMA. 2005;293:1635-1643.

89 Compton SN, March JS, Brent D, et al. Cognitive-behavioral psychotherapy for anxiety and depressive disorders in children and adolescents: An evidence-based medicine review. J Am Acad Child Adolesc Psychiatry. 2004;43:930-959.

90 March J, Silva S, Petrycki S, et al. Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: Treatment for Adolescents With Depression Study (TADS) randomized controlled trial. JAMA. 2004;297:807-820.

91 Cheung AH, Emslie GJ, Mayes TL. Review of the efficacy and safety of antidepressants in youth depression. J Child Psychol Psychiatry. 2005;46:735-754.

92 Emslie GJ, Heiligenstein JH, Wagner KD, et al. Fluoxetine for acute treatment of depression in children and adolescents: A placebo-controlled, randomized clinical trial. J Am Acad Child Adolesc Psychiatry. 2002;41:1205-1215.

93 Emslie GJ, Rush AJ, Weinberg WA, et al. Double-blind placebo controlled study of fluoxetine in depressed children and adolescents. Arch Gen Psychiatry. 1997;54:1031-1037.

94 Keller MB, Ryan ND, Strober M, et al. Efficacy of paroxetine in the treatment of adolescent major depression: A randomized, controlled trial. J Am Acad Child Adolesc Psychiatry. 2001;40:762-772.

95 Wagner KD, Ambrosini PJ, Rynn M, et al. Efficacy of sertraline in the treatment of children and adolescents with major depressive disorder. JAMA. 2003;290:1033-1041.

96 Wagner KD, Robb AS, Findling RL, et al. A randomized placebo-controlled trial of citalopram for the treatment of major depression in children and adolescents. Am J Psychiatry. 2004;161:1079-1083.

97 Emslie GJ, Findling RL, Rynn MA, et al. Efficacy and safety of nefazodone in the treatment of adolescents with major depressive disorder. J Child Adolesc Psychopharmacol. 2002;12:299.

98 Emslie GJ, Findling RL, Yeung PP, et al: Efficcacy and safety of venlafaxine ER in children and adolescents with major depressive disorder. Presented at the annual meeting of the American Psychiatric Association, New York, May 2004.

99 Lock J, Walker LR, Rickert VI, et al. Suicidality in adolescents being treated with antidepressant medications and the black box label: Position paper of the Society for Adolescent Medicine. J Adolesc Health. 2005;36:92-93.

100 Jick H, Kaye JA, Jick SS. Antidepressants and the risk of suicidal behaviors. JAMA. 2004;292:338-343.

101 Simeon J, Nixon MK, Milin R, et al. Open-label pilot study of St. John’s wort in adolescent depression. J Child Adolesc Psychopharmacol. 2005;15:293-301.

102 Findling RL, McNamara NK, O’Riordan MA, et al. An open-label pilot study of St. John’s wort in juvenile depression. J Am Acad Child Adolesc Psychiatry. 2003;42:908-914.

103 Sweedo SE, Allen AJ, Glod CA, et al. A controlled trial of light therapy for the treatment of pediatric seasonal affective disorder. J Am Acad Child Adolesc Psychiatry. 1997;36:816-821.

104 Prudic J, Olfson M, Marcus SC, et al. Effectiveness of electroconvulsive therapy in community settings. Biol Psychiatry. 2004;55:3010-3312.

105 American Academy of Child and Adolescent Psychiatry. Practice parameter for use of electroconvulsive therapy with adolescents. J Am Acad Child Adolesc Psychiatry. 2004;43:1521-1539.

106 Walter G, Rey JM. An epidemiological study of the use of ECT in adolescents. J Am Acad Child Adolesc Psychiatry. 1997;36:809-815.

107 Brent DA, Holder D, Kolko D, et al. A clinical psychotherapy trial for adolescent depression comparing cognitive, family, and supportive therapy. Arch Gen Psychiatry. 1997;54:877-885.

108 Clarke GN, Hornbrook M, Lynch F, et al. Group cognitive-behavioral treatment for depressed adolescent offspring of depressed parents in a health maintenance organization. J Am Acad Child Adolesc Psychiatry. 2002;41:305-313.

109 Vostanis P, Feehan C, Gratten E, et al. A randomized controlled outpatient trial of cognitive-behavioral treatment for children and adolescents with depression: A nine-month follow-up. J Affect Disord. 1996;40:105-116.

110 Wood A, Harrington R, Moore A. Controlled trial of a brief cognitive-behavioral intervention in adolescent patients with depressive disorders. J Child Psychol Psychiatry. 1996;37:737-746.

111 Rossello J, Bernal G. The efficacy of cognitive-behavioral and interpersonal treatments for depression in Puerto Rican adolescents. J Consult Clin Psychol. 1999;67:734-745.

112 Clarke GN, Rohde P, Lewinsohn PM, et al. Cognitive-behavioral treatment of adolescent depression: Efficacy of acute group treatment and booster sessions. J Am Acad Child Adolesc Psychiatry. 1999;38:272-279.

113 Lewinsohn PM, Clarke GN, Hops H, et al. Cognitive-behavioral treatment for depressed adolescents. Behav Ther. 1990;18:85-102.

114 Mufson L, Weissman MM, Moreau D, et al. Efficacy of interpersonal psychotherapy for depressed adolescents. Arch Gen Psychiatry. 1999;56:573-579.

115 Mufson L, Dorta KP, Wickramaratne P, et al. A randomized effectiveness trial of interpersonal psychotherapy for depressed adolescents. Arch Gen Psychiatry. 2004;61:577-584.

116 Mufson L, Dorta KP. Interpersonal psychotherapy for depressed adolescents. In: Kazdin AE, Weisz JR, editors. Evidence-Based Psychotherapies for Children and Adolescents. New York: Guilford; 2003:148-164.

116a. American Academy of Child and Adolescent Psychiatry. Practice parameters for the assessment and treatment of children and adolescents with bipolar disorder. J Am Acad Child Adolesc Psychiatry. 2007;46:107-125.

117 Geller B, Cooper TB, Sun K, et al. Double-blind and placebo-controlled study of lithium for adolescent bipolar disorders with secondary substance dependency. J Am Acad Child Adolesc Psychiatry. 1998;37:171-178.

118 Kafantaris V, Coletti DJ, Dicker R, et al. Lithium treatment of acute mania in adolescents: A placebo-controlled discontinuation study. J Am Acad Child Adolesc Psychiatry. 2004;43:984-993.

119 Findling RL, McNamara NK, Youngstrom EA, et al. Double-blind 18-month trial of lithium versus divalproex maintenance treatment in pediatric bipolar disorder. J Am Acad Child Adolesc Psychiatry. 2005;44:409-417.

120 DelBello MP, Schwiers ML, Rosenberg HL, et al. A double-blind, randomized, placebo-controlled study of quetiapine as adjunctive treatment for adolescent mania. J Am Acad Child Adolesc Psychiatry. 2002;41:1216-1223.

121 Scheffer RE, Kowatch RA, Carmody T, et al. Randomized, placebo-controlled trial of mixed amphetamine salts for symptoms of comorbid ADHD in pediatric bipolar disorder after mood stabilization with divalproex sodium. Am J Psychiatry. 2005;162:58-64.

122 Keck PE, McElroy SL. Pharmacological treatments for bipolar disorder. In: Nathan PE, Gorman JM, editors. A Guide to Treatments That Work. 2nd ed. London: Oxford University Press; 2002:277-299.

123 Lofthouse N, Fristad MA. Psychosocial interven tions for children with early-onset bipolar spectrum disorder. Clin Child Fam Psychol Rev. 2004;7:71-88.

124 Colom F, Vieta E, Martínez-Arán A, et al. A randomized trial on the efficacy of group psychoeducation in the prophylaxis of recurrences in bipolar patients whose disease is in remission. Arch Gen Psychiatry. 2003;60:402-407.

125 Miklowitz DJ, Richards JA, George EL, et al. Integrated family and individual therapy for bipolar disorder: Results of a treatment development study. J Clin Psychiatry. 2003;64:182-191.

126 Fristad MA, Goldberg-Arnold JS, Gavazzi SM. Multi-family psychoeducation groups (MFPG) in the treatment of children with mood disorders. J Marital Fam Ther. 2003;29:491-504.

127 Fristad MA, Goldberg-Arnold JS, Gavazzi SM. Multi-family psychoeducation groups (MFPG) for families of children with bipolar disorder. Bipolar Disord. 2002;4:254-262.

128 Fristad MA. Psychoeducational treatment for school-aged children with bipolar disorder. Dev Psychopathol. 2006;18:1289-1306.

129 Miklowitz DJ, Simoneau TL, George EL, et al. Family-focused treatment of bipolar disorder: One-year effects of a psychoeducational program in conjunction with pharmacotherapy. Biol Psychiatry. 2000;48:582-592.

130 Miklowitz DJ, George EL, Richards JA, et al. A randomized study of family-focused psychoeducation and pharmacotherapy in the outpatient management of bipolar disorder. Arch Gen Psychiatry. 2003;60:904-912.

131 Rea MM, Tompson M, Miklowitz DJ, et al. Family focused treatment vs. individual treatment for bipolar disorder: Results of a randomized clinical trial. J Consult Clin Psychol. 2003;71:482-492.

132 Miklowitz DJ, George EL, Axelson DA, et al. Family-focused treatment for adolescents with bipolar disorder. J Affect Disord. 2004;82(Suppl 1):S113-S128.

133 Pavuluri MN, Graczyk PA, Henry DB, et al. Child-and family-focused cognitive behavioral therapy for pediatric bipolar disorder: Development and preliminary results. J Am Acad Child Adolesc Psychiatry. 2004;43:528-537.

134 Gilham JE, Reivich KJ, Jaycox LH, et al. Prevention of depressive symptoms in schoolchildren: Two-year follow-up. Psychol Sci. 1995;6:343-351.

135 Clarke GN, Hawkins W, Murphy M, et al. Targeted prevention of uinpolar depressive disorder in an at-risk sample of high school adolescents: A randomized trial of group cognitive intervention. J Am Acad Child Adolesc Psychiatry. 1995;34:312-321.

136 Spence SH, Sheffield JK, Donovan CL. Long-term outcome of a school-based, universal approach to prevention of depression in adolescents. J Consult Clin Psychol. 2005;73:160-167.

137 Van Voorhees BW, Ellis J, Stuart S, et al. Pilot study of a primary care Internet-based depression prevention intervention for late adolescents. Can Child Adolesc Psychiatry Rev. 2005;14:40-43.

138 Emslie GJ, Heiligenstein JH, Hoog SL, et al. Fluoxetine treatment for prevention of relapse of depression in children and adolescents: A double-blind, placebo-controlled study. J Am Acad Child Adolesc Psychiatry. 2004;43:1397-1405.

139 Coyle JT, Pine DS, Charney DS, et al. Depression and bipolar alliance consensus statement on the unmet needs in diagnosis and treatment of mood disorders in children and adolescents. J Am Acad Child Adolesc Psychiatry. 2003;42:1494-1503.

140 Katon W, Von Korff M, Lin E, et al. Stepped collaborative care for primary care patients with persistent symptoms of depression: A randomized trial. Arch Gen Psychiatry. 1999;56:1109-1115.

18B. Anxiety Disorders

Anxiety is a multidimensional construct, involving three dimensions: subjective distress, physiological response, and avoidance or escape behaviors.1 Clinical levels of anxiety and anxiety disorders are common in both referred and nonreferred children and adolescents. Pediatric anxiety disorders co-occur with other childhood disorders; persist over time; interfere with functioning at school, at home, and with peers; and may be predictive of dysfunction in later childhood, adolescence, and adulthood.2,3 These conclusions are based on increased knowledge about the classification, etiology, assessment, and treatment of anxiety disorders in children and adolescents since the 1980s.4 The two most recent editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM)5,6 detail the diagnostic criteria for 12 anxiety disorders that are applicable to children, adolescents, and adults: Panic Disorder with and without Agoraphobia, Agoraphobia without History of Panic Disorder, Specific Phobia, Social Phobia, Obsessive-Compulsive Disorder (OCD), Posttraumatic Stress Disorder (PTSD), Acute Stress Disorder, Generalized Anxiety Disorder (GAD), Anxiety Disorder Due to a General Medical Condition, Substance-Induced Anxiety Disorder, and Anxiety Disorder Not Otherwise Specified.

This chapter provides an overview of key terms in describing anxiety and fear in children and adolescents, along with prevalence rates of anxiety disorders in youths and their effect on functioning. Diagnostic considerations are presented with a description of the varied assessment methods and measures for pediatric and adolescent anxiety disorders. The diagnostic criteria and prevalence, causes, and unique assessment measures are delineated for seven specific disorders: GAD, separation anxiety disorder (SAD), panic disorder, PTSD, social anxiety, OCD, and phobias. The chapter concludes with general intervention and referral guidelines for primary care pediatrician and developmental-behavioral pediatricians, as well as conclusions to foster future research and clinical practice. Other chapters in this book address psychological and pharmacological treatments for childhood anxiety disorders.

OVERVIEW

Definition of Key Terms

Anxiety, worry, and fear are related and yet distinct concepts, and the terms should not be used interchangeably.7,8 Simply stated, anxiety is a mood state characterized by worry or apprehension about future or anticipated situations.9 The definition given by Barlow10 is more elaborate: Anxiety is “a future-oriented emotion, characterized by perceptions of uncontrollability and unpredictability over potentially aversive events and a rapid shift in attention to the focus of potentially dangerous events or one’s own affective response to these events” (p 104). It is represented by a tripartite response system, including verbal or cognitive components, motor or behavioral components, and somatic or physiological components.11 The cognitive component pertains to thoughts, images, beliefs, and attributions about the situation and expected outcomes (e.g., “What if I have a heart attack because I cannot breathe?” “What if I fail this test and do not graduate?” “What if no one picks me up after school?”). The behavioral component consists of motor responses that involve escaping, avoiding, or taking action (e.g., trembling, running). The physiological component involves sensations of the flight-or-fight response or other somatic responses, such as muscle tension and increased heart rate.12

Worry involves thoughts and images that pertain to potentially threatening future events and is thus considered one of the cognitive components of anxiety.13 Borkovec and colleagues14 stated that “normal” worry manifests with minimal perceived or actual peripheral physiological activation and greater intrusions of negative thoughts in comparison with somatic aspects of anxiety. In addition, the content of worries differ from time to time and in response to changes in life circumstances. Silverman and Ollendick15 indicated that both worry and avoidance reflect maladaptive coping efforts in response to aversive states that are pervasive, intense, or uncontrollable. As worry persists and becomes excessive, it is deemed a dysfunctional process according to the fourth edition of the DSM (DSM-IV).5

Fear is an emotion that is related to the fight-or-flight system, which involves triggering the autonomic nervous system along with focusing attention on escaping the situation or fighting the potential threat.16 Thus, fear is viewed as a physiological response and is linked to the biological alarm system.8 Fear is essential in focusing attention to immediate danger, learning how to overcome dangerous situations, and learning how to differentiate threatening from harmless situations.12 Two key differences between anxiety and fear are whether the interpretation of threat is immediate or future oriented and whether the physiological arousal is an alarm reaction or excessive apprehension.9

Complicating the conceptual distinction between anxiety and fear is the high correlation with depression. The construct of negative affectivity refers to the nonspecific component of generalized distress that is common to anxiety and depression.15 Examples of symptoms that reflect negative affect include anxious or depressed mood, sleep difficulties, and irritability. An elaborate study implemented by Chorpita and colleagues17 confirmed the distinction among anxiety, fear, and depression as separate constructs. Their data indicate that anxiety reflected general distress; fear was equated with heightened physiological arousal; and depression corresponded to low positive affect. Additional research is needed to further distinguish these constructs from others, such as attention-deficit/hyperactivity disorder (ADHD), and to describe their course of development.12

Function of Worry

Borkovec and colleagues14,18 offered a detailed conceptualization of the formation and maintenance of worry, with implications for the development of anxiety disorders. According to these authors, worry represents the end result of an avoidance response to perceived threats. Behavioral inhibition is considered a temperamental category and appears related to the defensive reactions delineated by Barlow and colleagues.10,16 It is defined in terms of reactions of withdrawal, wariness, avoidance, and shyness in novel situations.

Defensive reactions are started when a threatening stimulus (object, person, situation) is perceived by a person; these reactions include automatic activation and inhibition, behavioral avoidance and or inhibition, catastrophic images and thoughts. Worry as a cognitive process is considered an example of long-term cognitive avoidance of future catastrophes or negative events. Barlow and collagues10,14 propose a suppression of physiological-affective processes as a direct outcome of such cognitive activity. They suggest that chronic worriers and nonanxious controls display activation of the frontal cortex during worrying, but chronic worriers display greater left than right frontal activation. Furthermore, worries about one topic tend to easily spread or generalize to related and unrelated topics. The results or consequences of such cognitive activity reportedly hinder new learning and maintain distressing emotional states.

Retrospective and prospective studies have linked certain early temperamental styles with anxiety and suggest that temperamental styles of high arousal, emotionality, and behavioral inhibition place youth at risk for developing later anxiety symptoms and disorders.19 In addition, adverse life events, especially uncontrollable ones, place individuals at greater risk of developing an anxiety disorder. Finally, the difference between a vulnerability and a disorder is probably a function of symptom severity and interference with daily activities.

Worry may serve two purposes or functions.20 One function is preparational, whereby worry at a moderate level may motivate a person to accomplish tasks. Within this function, worry supposedly suppresses somatic responses and decreases uncomfortable emotional reactions, thereby allowing the person to prepare for anticipated negative events.14 A second function of worry is avoidance, with regard to distracting the person from other emotional events and situations. Worry involves efforts to prevent the occurrence of negative events or to cope if and, when these events occur, through problem-solving strategies. Theorists also propose that although worry may offer some advantages, such as initial reduction of somatic distress, it interferes with emotional processing of negative events. As such, efforts at problem solving are not often effective, and the anxiety response is maintained.18,21

Normative Data on Worry

Many studies document the relatively common occurrence of fears in children. Almost 70% of children report worrying. Girls report more fears than do boys; at some point during their development, children experience between 9 and 13 fears on average 2 or 3 days per week.12,22 In studies on the frequency and content of children’s worries, investigators have identified developmental, gender, and potentially ethnic differences.8,23,24

The frequency of fears decreases, and their focus changes with age. From birth through age 18 years, fears change: Among preschool-aged children, they concern separation from caregivers and imaginary or supernatural creatures; in children aged 5 to 6 years old, they concern threats to physical well-being; among older children, they concern personal and social performance.24,25 In general, the worries of school-aged children (i.e., 7 to 14 years old) center on school performance, health, and personal harm. Young adolescents appear to worry more intensely about social issues, such as war, money, and disasters. Some studies (e.g., Vasey et al24) but not others (e.g., Silverman et al8) reveal age-related differences with regard to a greater number of worries in school-aged children than in younger children. Most experts in this area (e.g., Silverman et al8) suggest that the content of worries is associated with current social circumstances and media attention.

Girls are said to display more extreme symptoms and to report more worries than do boys in both clinical and community samples.8,26 Children of African-American ethnicity reported more worries than did white or Hispanic children.8

Several studies have focused on the frequency, intensity, and content of worries of clinically referred children in comparison with community samples. Overall, it appears that the intensity but not the number of worries differs between these two samples.27,28 The content of their worries—namely, school, health, disasters, and personal harm—are reflective of contemporary social challenges and concerns. The authors of these studies proposed that intensity more than specific content serves to differentiate children with anxiety syndromes or disorders from those without.

General Prevalence

The literature indicates that 18% of school-aged children are identified by their primary care clinicians as having a psychosocial problem.2931 Other studies (e.g., Wren et al32) have revealed that clinicians identify mood or anxiety syndromes on only 3.3% of visits. Differences in these rates appear related to how well the clinician knew the child, whether the visit was a well-child appointment rather than for acute care, and the presence of comorbid behavioral problems.30,32 Prevalence rates of specific anxiety disorders in children and adolescents typically range from 2% to 7%,3 whereas rates for clinical levels of anxiety among children range from 10% to 21%.33 Some guidelines help distinguish “normal” fears and worries from those that are dysfunctional and suggest a true anxiety disorder12: First, the intensity of the worry/fear is out of proportion to the actual threat of the situation. Second, the frequency of the worry/fear increases despite reassurance. Third, the content of the worry/fear concerns a harmless object or situation that poses minimal harm. Fourth, the worry/fear seems spontaneous. Finally, escape or avoidance is often in reaction to the worry/fear.

Effect of Anxiety Disorders

Children and adolescents with anxiety syndromes or disorders are at risk for a variety of problems across domains of functioning. Longitudinal studies have demonstrated an association between anxiety disorders and educational underachievement and between these disorders and alcohol and other drug use.3,34 The risk of other emotional problems is consistently documented in the literature3,34; the occurrence of anxiety disorders commonly precedes those of depressive disorders and substance abuse disorders.35,36 Alcohol and other drugs may be used to self-medicate or to manage symptoms of anxiety.37 Difficulties in social and peer relations that contribute to feelings of loneliness and low self-esteem also are related to anxiety disorders.38

The effect of anxiety disorders on health care utilization and health care costs is evident in the pediatric and adult literature. Studies on older adolescents and adults indicate high utilization of specialists and primary care physicians for symptoms of anxiety.39,40 Increased utilization results from frequent visits to physicians and emergency rooms, extensive laboratory tests, medications, and prolonged hospitalizations.40 Specialists most often seen include gastroenterologists for individuals with GAD, because of abdominal complaints; dermatologists and cardiologists for those with OCD, because of skin conditions and problems breathing; and neurologists and urologists for those with panic disorders, because of multiple physical symptoms. In one study, 54% of patients with irritable bowel syndrome had diagnoses of GAD, and 29% had diagnoses of panic disorder.41

Diagnostic Considerations

In a thorough review of the assessment literature on anxiety disorders, Silverman and Ollendick15 indicated that anxiety disorder diagnoses co-occur most frequently with other anxiety disorders, next most frequently with depression, and third most frequently with externalizing disorders, such as ADHD or oppositional defiant disorder. Symptoms of anxiety and resultant diagnoses tend to persist over time, and the condition is often refractory to intervention.42,43 Two constructs are critical in understanding the comorbidity patterns and course of anxiety disorders: (1) threshold for clinical significance and (2) sensitivity and specificity of assessment measures.

The term threshold pertains to the frequency and intensity of symptoms necessary to detect the presence of a disorder, along with level of impairment. The phrase “clinical level” is used in a case when all diagnostic criteria are met and impairment is severe.29 The term subthreshold, refers to cases in which diagnostic criteria are met but impairment is mild to moderate. An optimal threshold for clinical significance is currently arbitrary, but low thresholds may help identify youth at risk for psychopathology, whereas higher thresholds help identify those requiring immediate treatment. Less stringent impairment thresholds may be preferred with regard to internalizing disorders, such as anxiety disorders, because the nature of the symptoms is less overt and disruptive than are symptoms.29,44

Silverman and Ollendick15 also proposed that discriminating between anxiety and other constructs is related to the diagnostic accuracy of anxiety assessment measures. The diagnostic value of these measures pertains to their sensitivity and specificity. Silverman and Ollendick15 defined sensitivity as the percentage of people who receive a diagnosis and who have been positively identified by rating scales, or true-positive cases. They defined specificity as the percentage of people who do not receive a diagnosis and who have not been identified by rating scales, or true-negative cases. Anxiety assessment measures are reviewed in the next section.

Research clearly indicates that anxiety disorders in youths share the same underlying constructs, display solid covariation with each other over time, seldom occur as singular conditions, and exhibit comparable familial constellations with adult anxiety and depressive disorders.4,10,45 Clinicians within primary care settings are expressing the need for practical and validated screening measures for mood syndromes and disorders in children and adolescents.32

ASSESSMENT METHODS

Since the 1980s, attention has been directed toward developing reliable and valid assessment measures for anxiety disorders in children and adolescents for accurate diagnosis and for formulating treatment plans and monitoring treatment outcome.4,46 Readers are referred to excellent reviews by Kearney and Wadiak,46 Silverman and Ollendick,15 and Velting and associates.4 The following discussion outlines recommended assessment protocols from these reviews; measures specific to individual disorders are listed in subsequent sections.

A multimethod and a multisource assessment approach is recommended for examining biological, cognitive, and behavioral aspects of anxiety from a variety of sources, such as the child, the parents, and the teachers, through the use of diverse methods, including structured interviews, rating scales, and observations. Kendall and colleagues47 also proposed a multistage sampling design in which a screening measure is administered first and followed by a more detailed diagnostic interview for persons identified from the initial screening. This process focuses on identifying the existence of an anxiety disorder and then determining the exact nature of the disorder. In general, self-report, parent, and teacher rating scales are frequently used for screening purposes. These rating scales also are administered to identify specific symptoms, to discriminate between anxiety and other constructs, and to examine treatment outcome. Semistructured and structured interviews are employed primarily to diagnose specific anxiety disorders, as well as to identify symptoms and to evaluate treatment effectiveness. Finally, rating scales, direct observations, and self-monitoring are used to identify specific aspects of anxiety that serve to maintain its occurrence and changes during treatment.

Various problems are evident with assessment methods and measures for anxiety disorders in youths. The predictive power of methods and measures requires further exploration. For example, a greater number of individuals may be identified as having anxiety symptoms or disorders at initial screening because of the higher false-positive values in comparison with true-positive values on self-report rating scales.34 Many assessment methods are limited in terms of developmental differences, including age and gender.46 Diagnostic interviews are difficult to administer, and self-report measures are less reliable with younger children.48 Furthermore, self-monitoring and behavioral observations may be more reactive with older children and adolescents. Many assessment measures lack appropriate cultural variations, such as idioms of distress and interpretation of worry.49

A medical condition or substance use should be confirmed or ruled out when anxiety symptoms are assessed.49 Therefore, a targeted medical examination should be completed before a final diagnosis is established, with the use of data from other methods. Individuals should be questioned about prescription medications; over-the-counter medications, especially those containing ephedrine and appetite suppressants; and caffeine intake, such as colas and chocolate. Othmer and Othmer50 provide a detailed list of medication side effects related to mental health symptoms. Fong and Silien49 describe a range of medical conditions associated with anxiety symptoms, such as specific neurological disorders (e.g., multiple sclerosis, temporal lobe epilepsy), endocrine disorders (e.g., hyperthyroidism, Cushing syndrome), immune and collagen disorders (e.g., lupus erythematosus), and cardiovascular disorders (e.g., anemia, mitral valve prolapse).

Semistructured and Structured Interviews

Semistructured and structured interviews offer the most reliable means of diagnosis because of the degree of information solicited from children and their parents.51 However, the 2 to 3 hours needed to complete these interviews may be prohibitive in some settings.4 The length appears related to the experience of the interviewer, the cooperation of the family, and the level of functional impairment of the youth. In addition, children report fewer symptoms than do their parents and may be less reliable in specifying symptom onset and duration.52 Examples of common interviews for school-aged children and adolescents include the Schedule for Affective Disorders and Schizophrenia in School-Aged Children53 and the Diagnostic Interview Schedule for Children.54 The Anxiety Disorders Interview Schedule for Children55 assesses for the presence and severity of anxiety, mood, and externalizing disorders, and it screens for learning and developmental disorders, substance abuse, eating disorders, psychotic symptoms, and somatoform disorders. This measure has strong psychometric properties and has been studied extensively in the literature on anxiety disorders.15

Self-Report Rating Scales

Self-report rating scales provide information from the youth’s perspective about the frequency and intensity of cognitive, behavioral, and physiological aspects of anxiety. The majority of self-report scales for anxiety disorders require a second to third grade reading level but take only about 10 to 15 minutes to complete and can be manually scored easily.4 Examples of self-report rating scales for general anxiety include the Revised Children’s Manifest Anxiety Scale (RCMAS),56 the State-Trait Anxiety Inventory for Children,57 the Screen for Anxiety and Related Emotional Disorders (SCARED),58 and the Children’s Anxiety Sensitivity Index.59 The Negative Affect Self-Statement Questionnaire60 may be considered because of the relevance of negative affect and comorbidity between anxiety and depression. Finally, the Youth Self-Report61 and the Behavior Assessment System for Children62 may be given as general self-report measures of both internalizing problems and externalizing problems. The SCARED appears to be useful in clinical practice, whereas the RCMAS and the State-Trait Anxiety Inventory for Children are used often in research.4,15 Appendix A provides a listing of resources for ordering specific self-report and parent and teacher rating scales. The specific websites should be consulted about restrictions of who may order and administer these measures. Measures not listed in Appendix A can be obtained by contacting the authors noted in the reference section.

Parent and Teacher Rating Scales

Data from multiple informants are crucial for accurate assessment because of the high parent-child discordance, especially with internalizing disorders such as anxiety and depression.15 The perspective of parents and teachers should be solicited with regard to the range of symptoms shown by the youth, in order to place the anxiety symptoms within a context of other problems.4 In addition, symptoms may be quantified and may be monitored over the course of treatment.15 These rating scales are time and cost efficient and are fairly easy to administer and to score, with the use of hand-scoring templates or computer programs, but the problem of self-disclosure is considerable.4,15 Examples of general, corresponding parent and teacher rating scales are the Child Behavior Checklist63 and the Teacher Report Form,64 the Conners’ Parent and Teacher Rating Scales,65 and a parent version of the SCARED. A measure of family environment, such as the Family Environment Scale,66 or of marital functioning, such as the Marital Adjustment Scale,67 also may be administered to obtain additional data about family factors that affect the presence of anxiety symptoms.

Behavior Observations

Behavioral observations include such procedures as behavioral approach tests, observational ratings, and role-play tests. Behavioral approach tests usually consist of five 5-minute phases that are held in analogue settings (e.g., giving speech), under stimulated conditions (e.g., tape recordings of thunder or visual displays of spiders), or in a naturalistic setting (e.g., at school): adaptation, baseline, walking baseline, approach, and post-baseline to assess social anxiety, specific phobias, or generalized anxiety.46 Observational ratings are provided by clinicians, parents, or teachers on diverse aspects of anxiety, including overt statements, trembling, and avoidance of the situation.68 Direct observational procedures are most useful in specialty clinics or experimental settings because of their obtrusive nature and complexity of implementation.15 An alternative approach may be to videotape at home and view the tape in the clinic setting.4 Examples of direct observational measures include the Observer Rating Scale of Anxiety,69 the Procedure Behavior Rating Scale,70 and the Behavioral Assertiveness Test for Children.71 An addition to these methods is to observe family interactions in order to examine the factors that may be maintaining anxiety symptoms, such as misinterpreting ambiguous situations and reinforcing avoidant behavioral styles.15 These observations are categorized as the Family Behavioral Test.17,72

Self-Monitoring

Self-monitoring involves monitoring and recording components of anxiety, including physical sensations, related thoughts, and behavior, along with the situation in which these symptoms occur.4 Self-monitoring is used to identify and quantify symptoms and controlling variables and to evaluate and monitor treatment outcomes.73 Self-monitoring is of limited value because in many trials, only between 31% and 39% of children record requested information for a full 2-week period.15 A brief description of symptoms, specific antecedents, and consequences of these symptoms can be recorded in a diary format. In addition, an anxiety rating (on a scale of 0 to 100) may be given to each description, as well as to an overall daily rating. Thought-listing and think-aloud procedures may be included within this method of assessment.46 Thought listing consists of recording thoughts associated with the anxious reaction,74 whereas think-aloud procedures involve audiotaping verbalizations of thoughts and placing these thoughts into categories.75

Physiological Assessment

Various physiological responses may be used as a measure of anxiety, although their reliability and validity have been mixed.4,15 In addition, there are few normative data by which to compare baseline responses or changes after interventions. Examples of physiological measures include heart rate and blood pressure, to examine cardiovascular reactivity; respiration and skin temperature, to assess blood flow to extremities and physiological arousal; and electromyography, to measure electrical activity in tense muscles.4,15

SPECIFIC ANXIETY DISORDERS

According to the DSM-IV,5 anxious apprehension is a critical process in all anxiety disorders; it is defined as the anticipation of future danger, accompanied by feelings of dysphoria or symptoms of tension. Multiple factors are judged to interact in the origin of anxiety disorders in children and adolescents, including biological predispositions, psychological vulnerabilities, environmental stressors, sociocultural demands, familial variables, and functional influences. Integrative models are currently emphasized, inasmuch as changes in cognitions and behaviors are assumed to effect neurobiological processes and genetic expression76 (see Albano et al12 for a review of integrative models of anxiety in children). Kearney and Wadiak46 suggested that contemporary models belong to one of three categories: behavioral, cognitive, and physiological. A behavioral model highlights the learning principles of classical and operant conditioning within Mowrer’s77 two-factor theory or Delprato and McGlynn’s78 approach-withdrawal theory. In general, anxiety or avoidance is learned through classical conditioning and maintained by reinforcement of nonaversive reactions and situations. Cognitive models of fear and anxiety disorders include Beck and Emery’s79 schema theory and Reiss’s80 expectancy-anxiety sensitivity theory. In these models, normal physiological responses are misinterpreted as negative. Individuals avoid situations that cue these response because they expect negative consequences. Physiological models address genetic factors revealed through family and twin studies, along with a range of biological variables such as changes in the basal ganglia (OCD); mitral valve prolapse (panic disorder); and dysfunctions in neurochemical substances, including γ-amino butyric acid (GAD), norepinephrine (panic disorder), and serotonin (OCD) (see Biederman et al,81 for a detailed review of these physiological processes).

Generalized Anxiety Disorder

DIAGNOSTIC CRITERIA

The diagnostic criteria for GAD are outlined in Table 18B-1. Worry that is difficult to control is the most prominent clinical feature of GAD. Some authors82 question the applicability of a GAD diagnosis in children because of differences in the occurrence of specific somatic complaints in children and adolescents. For example, headaches and stomachaches are the most common somatic complaints reported by children, but these complaints are not included in the symptoms of GAD in the fourth edition, text revision of the DSM (DSM-IV-TR).6 In addition, although muscle tension is one physiological response that discriminates adults with a diagnosis of GAD from nonanxious controls,83 muscle tension is least often reported by parents and children. On the other hand, reducing the number of symptoms required from criterion C in Table 18B-1 from three to one for children and adolescents may increase the diagnostic prediction of GAD.84

TABLE 18B-1 Diagnostic Criteria for Generalized Anxiety Disorder (GAD) and Obsessive-Compulsive Disorder (OCD)

Diagnostic Criteria for GAD

Diagnostic Criteria for OCD

Data from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text revision. Washington, DC: American Psychiatric Association, 2000.

Finally, for a diagnosis of GAD, symptoms of anxiety cannot be caused by a substance, a medical condition, or other mental health disorder. The level of impairment in functioning required by all DSM-IV-TR diagnostic categories may prompt parents and teachers to seek referrals to health care or mental health care professionals.

COMORBIDITY

Additional findings reveal comorbidity with mood disorders; generalized anxiety most often occurs before depression.36,85 Externalizing disorders, such as ADHD and oppositional defiant disorder, also appear to co-occur with GAD, but not more so than with any other anxiety disorder.85,86

PREVALENCE

The prevalence of GAD in children and adolescents is between 2% and 5%87; onset of the full syndrome generally occurs in later adolescence or early adulthood. The diagnosis is made twice as often in girls as in boys.88 GAD is associated with a lower spontaneous recovery rate than are other anxiety disorders.26

CAUSES

The combined roles of biological factors, psychological factors, and environmental factors are consistently delineated in the literature on the causes of GAD.19 Evidence is suggestive of a general predisposition toward anxiety rather than a specific heritability for GAD.89 It appears that affected individuals possess an anxious vulnerability that is manifested as heightened sensitivity, greater emotionality, and enhanced physiological arousal in response to threat. This greater emotionality and physiological arousal foster a tendency to interpret situations as threatening and to develop an avoidant coping style. Avoidance of novel situations is rewarding by reducing distress and obtaining attention from others in the environment. Also, an anxious temperament allows the individual to solicit behaviors from others in the environment that support avoidant and other maladaptive coping styles. For example, parents’ heightened attention to the youth’s efforts to prevent or cope with anxiety may actually increase the youth’s perception of the degree of threat, even though, if the threat were not real, minimal attention would be devoted to it. Modeling and verbal statements from the family, along with cultural and social influences, seem to transmit information about anxious behaviors to youths.

A multivariate twin analysis of more than 1000 pairs of twin girls90 suggests that the genetic influences for anxiety disorders are accounted for by two factors: one for phobia, panic, and bulimia and the other for GAD and major depression. Studies also support a familial basis of anxiety in that parents exhibit a cognitive bias toward threats and reinforce an avoidant response in their children.72

The literature dictates that worry as the principal component of GAD reflects a style of cognitive avoidance.19,23 Cognitive avoidance with regard to GAD is conceptualized as composed of cognitive activity or “verbal” content.91,92 The verbal content of worry allows the person to avoid fearful images and to decrease arousal. Subsequently, the avoidance of fearful images and physiological arousal maintains worry, but at the cost of not dealing with the emotional aspect of the worries. In relation to worry, key features of GAD are intolerance of uncertainty and poor problem orientation.93 This intolerance of uncertainty is defined as the way an individual perceives information in uncertain or ambiguous situations and responds to this information with a set of cognitive, emotional, and behavioral reactions.94

Obsessive-Compulsive Disorder

DIAGNOSTIC CRITERIA

The diagnostic criteria for OCD are listed in Table 18B-1. The obsessions appear to be irrational, are difficult to remove, and usually pertain to perceived risk or harm.96 The compulsions are performed in an effort to suppress, organize, or ignore the obsessive thoughts.97 Common content of obsessions include contamination by dirt or germs, aggression, inanimate-interpersonal objects (e.g., locks, bolts), sex, and religion.98 Compulsive behaviors often seen are hand washing, cleaning, checking, repetitive touching, counting, and ordering. These obsessions and compulsions generally take up more than an hour a day and cause distress or functional impairment in academics, with peers and family members, and with activities of daily living.5

Long-term follow-up studies of OCD in children and adolescents reveal a chronic, waxing-and-waning course, regardless of medication or behavior therapy treatment.99,100 Symptoms persist but change over time; for example, checking rituals may become ordering compulsions, and contamination fears may become counting rituals.100 In two follow-up studies of OCD in children,101,102 43% to 68% of children continued to meet diagnostic criteria for OCD, and 28% to 57% did not have the disorder at follow-up. The literature provides minimal information on prognostic indicators other than that developmentally appropriate rituals are not predictive of obsessions or compulsions.103,104

Subtypes of OCD in adults appear applicable to youths with OCD. The first classification pertains to the presence or absence of a tic disorder; the second classification pertains to familial versus nonfamilial OCD.105,106 Children without tics seem to have a higher incidence of contamination fears, washing, and repetitive requests for reassurance.107 Children with nonfamilial OCD may have other disorders suggestive of a central nervous system dysfunction.104 These subtypes may have implications for etiology and treatment response.105,107

There is some diagnostic confusion with regard to the phenomenological overlap between obsessions and worry and between pathological worry and covert compulsive behavior.108 Although both worry and obsessions involve cognitive activity, worry may be more abstract and verbal in nature, whereas obsession is more imaginative in form.109 Whether this distinction applies to children is not known, especially as it pertains to differential diagnosis between OCD and GAD.109 Compulsive behavior in children with OCD and in children with GAD may be distinguished in terms of frequency, rigidity, quality, and function, but empirical verification of these differences is not available in the literature.108

COMORBIDITY

Coexisting symptoms and disorders are common in children and adolescents with diagnosed OCD; 62% to 84% exhibit co-occurrence110 of SAD and GAD. Depressive symptoms and dysthymia106 also co-occur frequently. Neurological conditions, particularly tics and Tourette syndrome, frequently co-occur in this group, especially in boys. Youths with OCD and Tourette syndrome tend to display more violent and aggressive obsessions and harm-avoidance compulsions.111

PREVALENCE

The average age at onset of OCD is between 7.5 years and 12.5 years,112 and the prevalence is about 1% to 3%.113 Another 1% to 19% of children may show “subthreshold” or problem levels of OCD.114 It is diagnosed in twice as many boys as girls during childhood and adolescence, but this pattern reverses in adults with OCD.115 Earlier age at onset seems related to a familial pattern of OCD.116 Few differences appear in the frequency of specific obsessions or compulsions across age groups,100,117 although adolescent boys may report more religious/moral obsessions than do younger boys.107

CAUSES

Although the exact origin of OCD is not known, possible organic causes focus on focal brain lesions, specifically to the basal ganglia, and on immune-mediated sequelae of streptococcal infections.104,116 Through neuroimaging techniques, the frontal-striatal-thalamic pathway is implicated in the pathophysiology of OCD, along with the neurotransmitters serotonin and ocytocin.104,107

The role of heredity was elucidated through one twin study and several family studies, in which the prevalence of OCD was higher among first-degree relatives of patients than among those of controls (11% to 25% vs. 2.7%).118,119 Concordance for treated youths with OCD was 33% in monozygotic twins, in comparison with 7% in dizygotic twins.120 A familial component is also suggested by a higher incidence of OCD diagnosed in relatives of youths who received diagnoses of OCD before the age of 17 years.119 Even higher prevalence rates exist in parents considered to have subthreshold or problematic OCD (8.8% to 42%).

ASSESSMENT

A basic question that clinicians can ask youths is “Do you have thoughts that you cannot get out of your mind or have behaviors you do over and over?” The Leyton Obsessional Inventory-Child Version121 is a 20-item self-report measure of obsessions and compulsions used for diagnostic screening. Several factors include general obsessive thoughts and rituals, dirt-contamination fears, lucky numbers, and school-related habits. This measure does not provide a rating of severity. Separate child and parent interviews are necessary to determine the extent and the nature of the obsessions and compulsions because of the covert aspect of these symptoms.116 In addition, if parents have subthreshold or problematic obsessive and compulsive symptoms, they may either become involved in or accommodate the child’s ritual.116 The first choice for rating severity of OCD symptoms is the Children’s Yale-Brown Obsessive-Compulsive Scale.122 The basic 10-item scale is used to rate obsessions and compulsions in terms of degree of severity, interference, distress, resistance, and control. Normative data are available to assist with symptom identification and, subsequently, severity ratings.116

A neurological examination is recommended because of the high prevalence (33%) of soft signs and choreiform movements in youth with OCD,123 reports of streptococcal pharyngeal infections triggering obsessive-compulsive symptoms,124 and occurrence of obsessive-compulsive symptoms in various neurological disorders, including basal ganglia disorders, Huntington’s chorea, and Tourette syndrome.116 The presence of focal neurological signs may prompt a brain imaging study, such as computed tomography or magnetic resonance imaging study of the brain.116

Separation Anxiety Disorders

DIAGNOSTIC CRITERIA

Some difficulty separating from home or attachment figures is normal and expected for children aged 7 months to 6 years.26 When this distress lingers beyond normal development or is abnormally intense, a child may meet DSM-IV criteria for SAD.5 Furthermore, the DSM-IV specifies that the distress upon separation cannot be attributable primarily to pervasive developmental disorder or a psychotic disorder (e.g., schizophrenia) and, in adolescents, cannot be better accounted for by panic disorder with agoraphobia. Diagnostic criteria for SAD are provided in Table 18B-2.

TABLE 18B-2 Diagnostic Criteria for Separation Anxiety Disorder

Note: The DSM-IV-TR specifies that the distress on separation cannot be attributable primarily to pervasive developmental disorder or a psychotic disorder (e.g., schizophrenia) and, in adolescents, cannot be better accounted for by panic disorder with agoraphobia.

Data from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text revision. Washington, DC: American Psychiatric Association, 2000.

Children with SAD may first come to the awareness of a physician because of refusal to go to school or physiological symptoms, such as recurrent abdominal pain. In a physician’s office, these children may present as “clingy.” Parents may complain about bedtime routines, nightmares, or a child’s refusal to engage in normal peer relationships, such as spending time at a friend’s house. SAD may initially manifest in situations in which the child is expected to separate from a caregiver (e.g., school), when the child becomes extraordinarily distressed and avoidant of separation situations. Careful observation of these symptoms may reveal a cyclical pattern in which symptoms are exaggerated during times when a child is anticipating or has separated from home or parent.125 For example, if a child’s symptoms may increase just before a parent leaves for work. Refusal to go to school may also be seen in other disorders, such as specific phobia, social phobia, and/or depression.

Symptom manifestation is related to developmental stage: Younger children with SAD tend to have more symptoms and focus on unrealistic worry about harm to a caregiver, whereas older children exhibit excessive distress during times of separation. In adolescence, SAD is typified by somatic complaints and refusal to go to school.126

PREVALENCE

The prevalence rate of SAD is approximately 4% among children and adolescents in community samples; the incidence of SAD is higher among girls and younger children.87,127 The average age at first presentation is 7.5 years. In clinical samples, SAD accounts for approximately one third of anxiety referrals128 and is the most frequently occurring anxiety disorder in preadolescents.115 Although girls appear to show more symptoms of SAD than do boys in screening surveys, boys affirm separation anxiety more often in clinical samples, perhaps because these symptoms are less well accepted in boys. Therefore, SAD symptoms in boys may more likely result in a referral for treatment.129

CAUSES

Although the specific origin is largely unknown, SAD reportedly has an acute onset, with initial or subsequent occurrence often triggered by a major stressor, such as change of schools, death of a parent, or prolonged illness.128 Familial patterns are noted for SAD; the risk is increased for children whose parents have panic disorder with features of agoraphobia.130,131

The course of SAD is generally favorable for most children. In a study of over 150 children and adolescents with SAD, 80% of cases were improved at an average of 18-month follow-up.132 Individual and family factors related to a continued SAD diagnosis seem to include the presence of externalizing problems, such as oppositional defiant disorder or ADHD symptoms; parental psychopathology; and parental marital difficulties.125 In addition, children with persistent SAD may be more likely to receive diagnoses of depressive disorder or another anxiety disorder at a later date.

ASSESSMENT

Parents’ and children’s reports of SAD symptoms differ; children report more symptoms than do parents, which highlights the importance of multi-informant assessment in diagnosis.133 There is no parent or self-report questionnaire designed to assess solely diagnostic criteria for SAD. Several of the self-report measures of anxiety have separation anxiety subscales that can be used with children aged 8 years and older, including the SCARED,58 the Multidimensional Anxiety Scale for Children134 and the Spence Children’s Anxiety Scale.135 For the interested clinician, a full report regarding assessment of SAD can be found in Perwein and Bernstein.133 Specific questions suggested for use in initial assessment of SAD include the following: “Are you afraid of something that might happen to your mom or dad?”; “Do you sometimes get nervous when you are alone?”; and “Do you worry about getting lost or kidnapped?” Questions to ask parents include “Does your child have difficulty falling asleep or sleeping alone?”; “Does your child cry or have temper tantrums when anticipating being left with others?”; “Does your child follow you from room to room?”; “Does your child’s worries ever keep her or him from normal activities, including school or other fun activities away from home?”; and “Does your child complain of headaches, stomachaches, or body aches frequently on weekdays but not on weekends?”136

Posttraumatic Stress Disorder

DIAGNOSTIC CRITERIA

The types of trauma that children and adolescents may experience include motor vehicle collisions, house fires, natural disasters, child maltreatment, violence, and witnessing domestic abuse. These experiences make children vulnerable to PTSD. Table 18B-3 lists the DSM-IV-TR criteria for PTSD.6

TABLE 18B-3 Diagnostic Criteria for Posttraumatic Stress Disorder (PTSD)

Data from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text revision. Washington, DC: American Psychiatric Association, 2000.

If the child or adolescent’s response to the extreme stressor does not meet full criteria for PTSD, or if the pattern of PTSD symptoms occurs for a situation that is not extreme (e.g., parental divorce), a diagnosis of Adjustment Disorder should be considered. Presence of avoidance, numbing, and increased arousal before the stressor are suggestive of another underlining pathological process, such as a different anxiety disorder or mood disorder. If the symptoms have occurred for less than 1 month, a diagnosis of Acute Stress Disorder is warranted initially. The types of PTSD to be specified are acute (less than 3 months), chronic (longer than 3 months), or delayed onset (6 months after the most recent PTSD stressor).

Knowledge of developmental differences in the manifestation of PTSD is essential. Some scholars question the validity of the DSM-IV-TR criteria for very young children, because nearly half the criteria require verbal descriptions of thoughts and feelings that a young child is unlikely to articulate.137 Young children may have trauma-specific nightmares initially but more generalized nightmares as time passes. Young children with PTSD symptoms may also exhibit fear of the dark, awake frequently at night, and report generalized fears such as “monsters.”138,139 All children may have difficulties separating from parents in the days or weeks after the trauma. Older children and adolescents may report difficulties concentrating on schoolwork or may attempt to self-medicate with drugs and alcohol to alleviate painful reminders of the event.140 Adolescents may engage in risky behaviors to lesson emotional pain.141 In addition, older children and adolescents may report extreme levels of guilt for surviving a traumatic experience, when others did not survive.

COMORBIDITY

Children who meet criteria for a diagnosis for PTSD may also meet criteria for other psychiatric conditions, especially mood disorders, such as major depressive disorder and dysthymic disorder.142,143 The trauma experience, especially those involving maltreatment, may increase the susceptibility to a mood disorder144 or dissociative disorder.145 Comorbidity with externalizing disorders such as ADHD, oppositional defiant disorder, and conduct disorder suggests a need for a thorough psychological assessment.

PREVALENCE

The prevalence of PTSD in children and adolescents in the general population is largely unknown. In a clinical sample of children aged 6 to 18, just over 3% of youths in the juvenile justice system and 3% using mental health services met diagnosis for PTSD.146 Children who were the victims of parental abuse were nearly twice as likely to show signs of PTSD as were those who witnessed domestic violence,143 of whom 13% met criteria for PTSD.147 After a category 4 hurricane, 30% of 568 students in third through fifth grades demonstrated severe or very severe PTSD symptoms 3 months later,148 and 18% demonstrated severe or very severe symptoms 10 months after the hurricane.149 In a British study, of children who experienced an automobile collision, 35% met diagnostic criteria for PTSD.150 In general, girls tend to be more symptomatic than are boys.150,151

Children who are susceptible to anxiety conditions before a traumatic event are at greater risk for the development of PTSD after a stressor. For example, preexisting anxiety symptoms were predictive of a child’s PTSD symptoms 3 and 7 months after Hurricane Andrew.152 There is a strong association between PTSD and other anxiety conditions, such as GAD and SAD.153,154

ASSESSMENT

In order to make a diagnosis of PTSD, it is important to assess aspects of the child’s earlier functioning, severity of the trauma and child’s initial reaction, current symptoms, and their effect on the child’s life. PTSD-specific assessment measures can help determine whether a child should be referred to a mental health provider for further assessment and treatment. The Traumatic Events Screening Inventory for Children156 is a self-report checklist that assesses exposure and intensity of the child’s response to the trauma and can be used for children as young as 8 years of age. The Children’s Post-Traumatic Stress Reaction Index157 is a 20-item instrument that assesses the severity of PTSD symptoms; however, not all DSM-IV-TR criteria are represented. This index can be read aloud to children as a semistructured interview as well.158

Because it is difficult for children to assess their reactions at the time of the trauma, an observer report is helpful. However, parents may have difficulty accurately reporting the intensity of their child’s PTSD symptoms.159 Parents’ reports are necessary, but they should not be the sole informants. The Child Stress Disorders Checklist160 is a 36-item observer report measure of PTSD and acute stress disorder. This measure assesses PTSD symptoms in five domains: reexperiencing, arousal, avoidance, numbing and dissociation, and impairment in functioning. Parent and teacher information is important for gaining a better understanding of pretrauma functioning, inasmuch as young children may not be able to reflect accurately on their previous thoughts and behaviors, because of their relative cognitive immaturity.141

In addition to self-report and observer report instruments, empirical evidence supports asking children directly about the exposure in order to assess symptoms of PTSD.161 Initially, children should be given the opportunity to recall the event in their own words. Subsequently, prompts regarding specific aspects of the diagnosis are helpful: for example, “What did you think/feel/hear in your body when the trauma occurred?”158

Social Phobia

DIAGNOSTIC CRITERIA

The hallmark feature of social phobia, also known as social anxiety disorder, for children and adolescents is excessive fear of embarrassment in social or performance situations. These feelings of anxiety may advance into a panic attack,162 and refusal to go to school is a common presenting problem. The diagnostic criteria for social phobia as it relates to children and adolescence is outlined in Table 18B-4.

TABLE 18B-4 Diagnostic Criteria for Social Phobia, Specific Phobia, and Panic Disorder

Diagnostic Criteria for Social Phobia

Diagnostic Criteria for Specific Phobia

Diagnostic Criteria for Panic Disorder (without Agoraphobia)

Data from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed, text revision. Washington, DC: American Psychiatric Association, 2000.

Children and adolescents with social anxiety typically resist or avoid social activities or begin missing school because of the anxiety present in those social situations.163 This fear or avoidance of social situations must not be accounted for directly by the effects of medication or substance use or by another mental disorder such as SAD or panic disorder. If another medical or psychological problem is present, the marked fear must be unrelated to it.

For the physician, children with social phobia may present for an office visit with a range of physiological problems, including stomachache and headache. Young children may have tantrums, freeze, or display selective mutism. Black and Uhde164 reviewed selective mutism in children as it may relate to social phobia. Reports of performance anxiety, stage fright, and shyness are relatively normal in children and adolescents and should not be diagnosed as social phobia unless they interfere with the child’s normal development or cause marked distress.5

PREVALENCE

Social phobia affects between 1% and 4% of children and adolescents.87 Although age at onset varies substantially, children are most likely to present with social anxiety during adolescence165,166 and, typically, approximately 3 years after the onset of symptoms.167 At all ages, more girls than boys are affected.168 Earlier onset is often related to greater impairment in functioning and a higher rate of coexisting disorders.162

CAUSES

Several studies represent compelling arguments to suggest a familial link to social anxiety. For example, of children whose parents meet criteria for an anxiety disorder, more than one third themselves met criteria for a diagnosis of social anxiety.169 One tenth of children meet diagnosis criteria for social phobia when one parent has anxiety, whereas no children do when neither parent meets criteria. In addition, other psychopathological processes in parents may increase rates of social phobia in their children. For example, parental depression, panic disorder, and substance abuse increase the difficulties that children have in social situations.170 Social isolation, rejection of the child, parental overprotectiveness, and frequent moves may contribute to the development of social anxiety in children and adolescents.170,171

Children with social phobia may perceive peers as being more negative, may misread cues, and may have trouble evaluating the nature of their peers’ intentions. An information-processing framework has been used to describe the negative cognitions in which children with anxiety disorders perceive a neutral environment.172

ASSESSMENT

In comparison with other types of anxiety, the assessment of social phobia in children and adolescents is rather extensive. Morris and colleagues173 conducted a full review of the measures and techniques used in the assessment of social anxiety. Among the most useful and psychometrically sound tools are self-report instrument for children aged 8 and older. The Social Anxiety Scale for Children174 and the counterpart for adolescents, the Social Anxiety Scale for Adolescents,175 are useful tools in assessing social anxiety in a self-report format. Both scales are 22-item measures on a 5-point Likert-type scale in which the individual’s fear of negative evaluation, generalized social avoidance and distress, and social avoidance in situations with new or unfamiliar peers are evaluated.

The Social Phobia and Anxiety Inventory for Children176,177 is a 26-item self-report measure designed to assess behavioral, cognitive, and physiological features of social phobia as it relates to the DSM-IV criteria.5 This instrument can be used for children and adolescents 8 to 14 years of age and has five scales: assertiveness, general conversation, public performance, physical/cognitive symptoms, and behavioral avoidance. This measure has been noted to be particularly helpful in differentiating whether the anxiety is experienced with peers or adults, an important distinction in the diagnosis of social phobia in children and adolescence.173

Specific Phobias

PREVALENCE

Specific phobias are present in approximately 5% of children and adolescents, although reports from community samples vary from 2.4% in a sample of 11-year-olds in New Zealand179 to 9.1% in a sample 7- to 11-year-olds in the United States.180 Girls have higher prevalence rates for specific phobias than do boys.178 Rates are similar among white, Hispanic,181 and African American children.182

COMORBIDITY

Comorbidity patterns within the different types of specific phobias can be present in children, but rates are relatively low (5%).178 Specific phobia and other types of anxiety disorders co-occur frequently, with separation anxiety disorder25, social phobia, and obsessive compulsive disorder178 among the most commonly cited. As with anxiety disorders in general, children and adolescents with specific phobias often have concurrent depression.

Fears and prevalence of phobia appear to be developmental in nature. Younger children report greater fears of animals and being alone in the dark, whereas older children and adolescents report fears associated with failure and criticism around social situations, illness, and bodily injury.168 In short, fears tend to decline as a child grows older; the fear of death remains the top fear for all age groups.183,184

CAUSES

Specific phobias may develop quite early; animal phobias often emerge earliest. In reviews of the literature, Silverman and associates8,15 noted the complexities among the factors that influence the development of phobias in children. That said, much literature supports the notion of Rachman’s185 proposal of three nonexclusive pathways through which a child or adolescent develops a phobia: experiencing a harmful event themselves through direct conditioning (e.g., snakebite); observing anxiety on behalf of caregivers through modeling; and hearing information from peers, family, or media. Among parents of 30 dog-phobic children, 27% attributed the fear to direct experience with an aversive event involving a dog, 53% believed the behavior was modeled, and 7% identified information as the source of their child’s phobia.186 Children’s reported fears about a fictional, unknown doglike animal changed according to the type of information provided before exposure and generalized to similar animals.187

A Darwinian nonassociative viewpoint suggests that some individuals are primed to have fears associated with things that may have been a threat at one time and thus develop a fear at first exposure to the object or event.188 With repeated and successful exposures, these fears decrease considerably for most children. In a study evaluating both associative and nonassociative development of fear of spiders, 46% of the children were noted to have always been afraid of spiders, and 41% of parents of these children attributed this phobia to a direct experience.189

Although parental modeling appears to play a role in the development of specific phobia, parental role in genetics should not be discounted. In a study of twins with specific phobias, monozygotic twins reported more similar types and intensities of fears than did dizygotic twin pairs.190

ASSESSMENT

Multi-informant (e.g., child, parent, teacher) and multimethod assessment is the “gold standard” in the assessment of specific phobias.191 The Fear Survey Schedule for Children-Revised22 is an 80-item scale and aids in the identification of specific fear-producing stimuli in children and adolescents aged 7 and older. There are five factors relating to specific fear types: failure and criticism, the unknown, injury and small animals, death and danger, and medical problems. Self-monitoring approaches are also helpful in gaining an understanding of the intensity of the fear. The Fear Thermometer192 depicts a thermometer-like drawing and a scale from 1 to 10 for children to rate fears as they encounter potential stimuli throughout their day. Physiological measures, including heart rate, galvanic skin response, muscle tension, and blood pressure, are helpful in gauging the intensity of fear of the object.191 For the trained clinician, presentation of feared objects while monitoring the child or adolescent physiological response may be helpful.

Panic Disorder

Since the 1990s, attention to panic disorder in children and adolescents has increased. Inherent within the definition of panic disorder is an intense concern regarding panic attacks. According to the DSM-IV,5 a panic attack is a somatic event that contains four of the following physiological features in a 10-minute time frame: heart palpitations/tachycardia, hyperhidrosis, trembling, sensations of suffocation or shortness of breath, sensations of choking, chest pain or discomfort, abdominal distress/nausea, syncope episodes, derealization or depersonalization, fear of loss of control, fear of dying, paresthesias, and/or chills or hot flashes. Furthermore, panic attacks can be defined as uncued and unexpected, cued and expected in certain situations, and situationally predisposed, whereby the panic attack is probably but not invariably going to happen. For a diagnosis of panic disorder, children and adolescents must experience panic attacks that are uncued.

DIAGNOSTIC CRITERIA

Further diagnostic criteria for Panic Disorder without Agoraphobia are listed in Table 18B-4. It is important to determine whether the panic attacks are drug-related or caused by a general medical condition such as hyperthyroidism. In addition, before a diagnosis of panic disorder is made, the clinician must explore potential triggers that may or may not be known to the child. For example, if panic attacks happen as a result of being away from home or from relatives, SAD should be considered. Similarly, if a child has panic attacks in response to school or other evaluative situations, a diagnosis of social phobia is warranted.5

PREVALENCE

Children and adolescents were not traditionally thought to be susceptible to panic disorder; thus, there are only few reports regarding its prevalence. Prevalence rates in the community vary considerably; from 0.5% to 5% of children and adolescents have been reported to meet full diagnostic criteria for panic disorder.193,194 Onset peaks in late adolescence. In adult retrospective studies, nearly 40% of affected individuals reported initial onset in adolescence or earlier.193,194

Although studies have documented an equal male-female distribution,195 more severe panic attacks are reported by girls.196 In one clinical study of 2000 high school students, the femal : male ratio for lifetime history of panic disorder was 3 : 1. Panic attacks are not uncommon in adolescence; rates among adolescents are 10.2%, although clinician ratings may be lower than self-report ratings.196 Of the adolescents who experience panic attacks, 75% report heart palpitations and racing heart as primary symptoms.165

CAUSES

Both environmental and genetic influences contribute to the development of panic disorder. Children and adolescents with more severe panic attacks report less social support and higher rates of family stressors.197 Risk factors for panic disorder include a diagnosis of Major Depressive Disorder and family histories of depression and/or panic disorders.196 High negative affectivity and fearful response to symptoms of anxiety contribute to having a panic attack in adolescence.196

ASSESSMENT

There exist few assessment measures that are specific to panic disorder. The Panic Attack Questionnaire198 represents the only self-report instrument designed to assess specifically panic attacks in individuals older than 13. This measure helps assess the frequency, duration, intensity, and triggers of panic attacks. In addition to the diagnostic function of this instrument, it may be useful for self-monitoring. A parent and/or a child may document any triggers underlying panic attacks.

COLLABORATIVE CARE PRACTICES

A review of interventions for anxiety disorders in children and adolescents indicates that cognitive-behavioral therapy alone and cognitive-behavior therapy plus family anxiety management are considered probably efficacious.2 The short-term (e.g., 3.5 years) and long-term (e.g., 6 years) treatment gains of cognitive-behavioral therapy have been supported by results of randomized clinical trials.199,200 After a 16-week cognitive-behavioral treatment program for primary anxiety disorders (e.g., GAD, social phobias), 60% to 70% of youth demonstrated a positive response to treatment in terms of reduced anxiety, as well as decreased substance use-related problems.201 Variables related to nonresponders, such as attrition and intensity of treatments, merit further exploration in the literature.201

Although promising interventions for pediatric anxiety disorders appear to exist, few youths are referred for, and fewer receive, such interventions. In general, only 16% to 20% of youths with identified psychosocial problems are referred for specialty treatment.30,44 With regard to identified anxiety disorders, reports suggest that about 50% of such youths are not referred for treatment.202 One report indicates that even among those who are referred, the majority (up to 72%) of children and adolescents with an anxiety disorder do not actually receive any treatment.29

These differential referral and treatment rates seem related to a variety of factors, with lower rates for children with mild problems and for those from ethnic minority backgrounds.30,203 Patients in managed care plans, in comparison with those in fee-for-service plans, receive fewer referrals for specialty care and psychotherapy.204 Such differing rates also may appear related to varying levels of treatment acceptability, stigma of mental health services, and early detection.203 If pediatricians are the “de facto mental health service” for many children with psychosocial problems, knowledge about effective treatment options and referral sources is essential to ensure timely intervention.44

Methods to enhance the ability of pediatricians to identify and treat psychosocial problems include interdisciplinary training, training in specialties such as developmental-behavioral pediatrics, and anticipatory guidelines and prevention strategies offered through the American Academy of Pediatrics.205 In addition, some strategies developed in tertiary care settings to identify and treat psychosocial problems could possibly be modified to make them feasible in primary care settings.206 For example, a group of investigators outline a three-tiered approach to enhance the role of primary care in children with psychosocial problems.207,208 The first level of care is more consistent identification and management by primary care and community professionals, such as home health care managers and case managers. The second tier is management by mental health specialists working in primary care settings. The third approach pertains to consultation-liaison, in which the mental health specialist supports management by the primary care physician but does not assume primary therapeutic responsibility. In an extension of this approach, pediatricians and psychologists work jointly within a practice team, to which developmental-behavioral pediatricians serve as consultants.209

A chronic disease management approach may be more applicable for youths with diagnoses of anxiety disorders, especially in view of the high frequency of somatic complaints observed in these children and adolescents. In one such approach, recommended by von Korff and colleagues,210 the “patient” works with the health care provider to manage his or her disease by monitoring symptoms, adhering to medical regimens, and adopting more adaptive health habits and coping skills. This approach can be modified by including patients and parents in collaboration with their primary care and mental health care professionals in managing pediatric anxiety disorders. As in the study by von Korff and colleagues210 on adult patients with GAD, children and adolescents with an anxiety disorder and their parents can be given written material on the characteristics and nature of GAD, pharmacological and psychological treatment options, and basic strategies for managing worry and anxiety. Allied health clinicians may then be available to provide more in-depth services and follow-up as needed. Parent involvement would be crucial in ensuring practice of skills outside of the clinic setting, supporting generalization of these skills, and offsetting modeling and reinforcement of anxious behaviors. Such involvement of the family is considered essential with regard to positive outcomes and maintenance of treatment gains.2,201

Within all these approaches, continuity of care is essential as continuity improves clinician recognition of psychosocial problems, receipt of preventive services, and patient satisfaction with care.30,31 In addition, continuing medical education programs are needed for primary care physicians and other medical specialists to ensure optimal identification, diagnosis, and effective treatment options for mental health disorders, including anxiety disorders in youths.39,210 Finally, strategies are needed to ensure effective collaboration between primary care pediatricians and mental health professionals, either working side by side or functioning as a consultants. The role of other consultants, such as developmental-behavioral pediatricians, also requires delineation in the management of youths with anxiety disorders.

Black and Nabors211 outlined optimal strategies for psychologists for collaborating with pediatricians in primary care settings. These strategies also apply to collaboration with other consultants and subspecialists, such as developmental-behavioral pediatricians. One recommendation centers on novel strategies for screening and interventions. Prompt identification may be fostered by consistent use of behavior screening measures during primary care appointments. Changes in behaviors across visits could be monitored and referrals made as soon as the information indicates that these behaviors are outside normative values. Another recommendation pertains to training of both medical and mental health professionals with regard to knowledge about development and behavior, as well as factors that affect busy practices. For example, consistent use of the DSM-PC212 may increase communication among professionals and agreement about when referrals need to be made to mental health professionals and other subspecialists. The type and range of stressful situations and problematic clusters could be used as an algorithm to determine referral patterns, especially challenges to primary support groups, emotions, and moods. Coordination of care also would be enhanced when referral procedures are efficient in terms of point of contact and appointment scheduling. Periodic meetings or telephone conference calls could be made between consultants to address referral difficulties and specific cases. A particularly relevant issue concerns performance and economic indicators necessary to demonstrate treatment effectiveness and “need” for services. The separation of health insurance plans into physical health and behavioral health segments has, unfortunately, reemphasized single-provider models of care that may be less effective although more fiscally viable.211 The role of pediatricians and psychologists as professional educators, clinicians, and researchers is evident from these approaches to care and in continued attention to strategies to support collaboration.209

FUTURE DIRECTIONS

Research and clinical efforts since the 1980s have produced extensive information about all aspects of pediatric anxiety disorders. Further research is needed to facilitate early recognition, early identification, and intervention, as well as to develop clinical practice guidelines.

Two “normative-developmental” principles are relevant to accurate diagnosis and assessment. Normative data on anxiety, worry, and fears are necessary in order to examine quantitative and qualitative changes that occur with development and to compare behaviors across reference groups. Normative data on gender, race, culture, and socioeconomic status should be obtained. Such data will be critical in interpreting behaviors as “normal” or “excessive” and in tracking behavior change over time, with or without intervention.15 Differences in cognitive, social, and emotional capacities of children and adolescents will assist in categorizing symptoms as either essential or associated features within each anxiety disorder. Comer and colleagues108 are credited for this recommendation in terms of distinguishing worry and obsessions in youth diagnosed with GAD or OCD, but consideration of developmental differences is applicable to all pediatric anxiety disorders.

Most researchers and clinicians emphasize the need for brief and valid screening instruments.29,32 Development of an “integrated triage protocol” is encouraged for primary care settings, community settings, and specialty clinic settings. In addition, potential thresholds could be established for these settings through cross-validated factor analysis.32 Along these lines, a structured, comprehensive, reliable measure of functional impairment to determine the level of impairment is needed because of its relevance to diagnosis.29

Longitudinal research is crucial for examining manifestations of pediatric anxiety disorders and treatment outcome and for answering a range of questions. For example, is the function of worry similar in children, adolescents, and adults?18 Are the core features of worry and behavioral inhibition predictive of, or do they co-occur with, anxiety syndromes and/or disorders?28 Family studies, investigations of neurotransmitters, and phenomenological observations would be helpful in more fully clarifying the role of genetics, neurobiology, and risk-protective factors in anxiety disorders.116 Prospective studies are essential for delineating the pattern and course of specific symptoms to document disorder subtypes, along with the relationship between childhood-onset and adult-onset disorders.116

As researchers and clinicians explore these recommendations, there should be another surge of information regarding etiology, diagnosis, assessment, and treatment of pediatric anxiety disorders. Stephenson213 raised the question of whether underfunded and overburdened health care and mental health care systems can serve the needs of an increasing number of identified youths with anxiety disorders. Specific factors that interfere with referral practices of physicians and follow-through by families include limited availability of specialists, cost and payor requirements, and scheduling delays.31 In addition, impediments to mental health services involve social stigma, family beliefs and attitudes about such care, as well as socioeconomic factors in the family.29 These barriers must be explored in more detail to ensure early identification, accurate assessment, and effective intervention for all children and adolescents with anxiety disorders.

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