Diffusion imaging markers of bipolar versus general psychopathology risk in youth at-risk.

Bipolar disorder (BD) is highly heritable. Thus, studies in first-degree relatives of individuals with BD could lead to the discovery of objective risk markers of BD. Abnormalities in white matter structure reported in at-risk individuals could play an important role in the pathophysiology of BD. Due to the lack of studies with other at-risk offspring, however, it remains unclear whether such abnormalities reflect BD-specific or generic risk markers for future psychopathology. Using a tract-profile approach, we examined 18 major white matter tracts in 38 offspring of BD parents, 36 offspring of comparison parents with non-BD psychopathology (depression, attention-deficit/hyperactivity disorder), and 41 offspring of healthy parents. Both at-risk groups showed significantly lower fractional anisotropy (FA) in left-sided tracts (cingulum, inferior longitudinal fasciculus, forceps minor), and significantly greater FA in right-sided tracts (uncinate fasciculus and inferior longitudinal fasciculus), relative to offspring of healthy parents (P < 0.05). These abnormalities were present in both healthy and affected youth in at-risk groups. Only offspring (particularly healthy offspring) of BD parents showed lower FA in the right superior longitudinal fasciculus relative to healthy offspring of healthy parents (P < 0.05). We show, for the first time, important similarities, and some differences, in white matter structure between offspring of BD and offspring of non-BD parents. Findings suggest that lower left-sided and higher right-sided FA in tracts important for emotional regulation may represent markers of risk for general, rather than BD-specific, psychopathology. Lower FA in the right superior longitudinal fasciculus may protect against development of BD in offspring of BD parents.

Reward-related neural activity and structure predict future substance use in dysregulated youth.

BACKGROUND: Identifying youth who may engage in future substance use could facilitate early identification of substance use disorder vulnerability. We aimed to identify biomarkers that predicted future substance use in psychiatrically un-well youth. METHOD: LASSO regression for variable selection was used to predict substance use 24.3 months after neuroimaging assessment in 73 behaviorally and emotionally dysregulated youth aged 13.9 (s.d. = 2.0) years, 30 female, from three clinical sites in the Longitudinal Assessment of Manic Symptoms (LAMS) study. Predictor variables included neural activity during a reward task, cortical thickness, and clinical and demographic variables. RESULTS: Future substance use was associated with higher left middle prefrontal cortex activity, lower left ventral anterior insula activity, thicker caudal anterior cingulate cortex, higher depression and lower mania scores, not using antipsychotic medication, more parental stress, older age. This combination of variables explained 60.4% of the variance in future substance use, and accurately classified 83.6%. CONCLUSIONS: These variables explained a large proportion of the variance, were useful classifiers of future substance use, and showed the value of combining multiple domains to provide a comprehensive understanding of substance use development. This may be a step toward identifying neural measures that can identify future substance use disorder risk, and act as targets for therapeutic interventions.

Predicting clinical outcome from reward circuitry function and white matter structure in behaviorally and emotionally dysregulated youth.

Behavioral and emotional dysregulation in childhood may be understood as prodromal to adult psychopathology. Additionally, there is a critical need to identify biomarkers reflecting underlying neuropathological processes that predict clinical/behavioral outcomes in youth. We aimed to identify such biomarkers in youth with behavioral and emotional dysregulation in the Longitudinal Assessment of Manic Symptoms (LAMS) study. We examined neuroimaging measures of function and white matter in the whole brain using 80 youth aged 14.0 (s.d.=2.0) from three clinical sites. Linear regression using the LASSO (Least Absolute Shrinkage and Selection Operator) method for variable selection was used to predict severity of future behavioral and emotional dysregulation measured by the Parent General Behavior Inventory-10 Item Mania Scale (PGBI-10M)) at a mean of 14.2 months follow-up after neuroimaging assessment. Neuroimaging measures, together with near-scan PGBI-10M, a score of manic behaviors, depressive behaviors and sex, explained 28% of the variance in follow-up PGBI-10M. Neuroimaging measures alone, after accounting for other identified predictors, explained ~1/3 of the explained variance, in follow-up PGBI-10M. Specifically, greater bilateral cingulum length predicted lower PGBI-10M at follow-up. Greater functional connectivity in parietal-subcortical reward circuitry predicted greater PGBI-10M at follow-up. For the first time, data suggest that multimodal neuroimaging measures of underlying neuropathologic processes account for over a third of the explained variance in clinical outcome in a large sample of behaviorally and emotionally dysregulated youth. This may be an important first step toward identifying neurobiological measures with the potential to act as novel targets for early detection and future therapeutic interventions.

Altered functioning of reward circuitry in youth offspring of parents with bipolar disorder.

BACKGROUND: Offspring of parents with bipolar disorder (BD) (BO) are at higher risk of BD than offspring of parents with non-BD psychopathology (NBO), although both groups are at higher risk than offspring of psychiatrically healthy parents (HC) for other affective and psychiatric disorders. Abnormal functioning in reward circuitry has been demonstrated previously in individuals with BD. We aimed to determine whether activation and functional connectivity in this circuitry during risky decision-making differentiated BO, NBO and HC. METHOD: BO (n = 29; mean age = 13.8 years; 14 female), NBO (n = 28; mean age = 13.9 years; 12 female) and HC (n = 23; mean age = 13.7 years; 11 female) were scanned while performing a number-guessing reward task. Of the participants, 11 BO and 12 NBO had current non-BD psychopathology; five BO and four NBO were taking psychotropic medications. RESULTS: A 3 (group) × 2 (conditions: win-control/loss-control) analysis of variance revealed a main effect of group on right frontal pole activation: BO showed significantly greater activation than HC. There was a significant main effect of group on functional connectivity between the bilateral ventral striatum and the right ventrolateral prefrontal cortex (Z > 3.09, cluster-p < 0.05): BO showed significantly greater negative functional connectivity than other participants. These between-group differences remained after removing youth with psychiatric disorders and psychotropic medications from analyses. CONCLUSIONS: This is the first study to demonstrate that reward circuitry activation and functional connectivity distinguish BO from NBO and HC. The fact that the pattern of findings remained when comparing healthy BO v. healthy NBO v. HC suggests that these neuroimaging measures may represent trait-level neurobiological markers conferring either risk for, or protection against, BD in youth.

The influence of comorbid disorders on the episodicity of bipolar disorder in youth.

OBJECTIVE: Bipolar disorder (BP) frequently co-occurs with other psychiatric disorders. We examine whether course of anxiety disorders (ANX), attention deficit hyperactivity disorder (ADHD), disruptive behavior disorders (DBD), and substance use disorders (SUD) influence likelihood of recovery and recurrence of depression and mania in BP youth. METHOD: Weekly ratings of psychiatric disorder intensity were obtained from 413 participants of the Course and Outcome of BP Youth project, followed for an average of 7.75 years. Multiple-event Cox proportional hazards regression analyses examined worsening of comorbid disorders as predictors of mood episode recovery and recurrence. RESULTS: Increased severity in ANX and SUD predicted longer time to recovery and less time to next depressive episode, and less time to next manic episode. Multivariate models with ANX and SUD found that significant effects of ANX remained, but SUD only predicted longer time to depression recovery. Increased severity of ADHD and DBD predicted shorter time to recurrence for depressive and manic episodes. CONCLUSION: There are significant time-varying relationships between the course of comorbid disorders and episodicity of depression and mania in BP youth. Worsening of comorbid conditions may present as a precursor to mood episode recurrence or warn of mood episode protraction.

Borderline personality disorder in transition age youth with bipolar disorder.

OBJECTIVE: To determine the longitudinal impact of borderline personality disorder (BPD) on the course and outcome of bipolar disorder (BP) in a pediatric BP sample. METHOD: Participants (N = 271) and parents from the Course and Outcome of Bipolar Youth (COBY) study were administered structured clinical interviews and self-reports on average every 8.7 months over a mean of 93 months starting at age 13.0 ± 3.1 years. The structured interview for DSM-IV personality disorders (SIDP-IV) was administered at the first follow-up after age 18 to assess for symptoms of BPD. BPD operationalized at the disorder, factor, and symptom level, was examined as a predictor of poor clinical course of BP using all years of follow-up data. RESULTS: The number of BPD symptoms was significantly associated with poor clinical course of BP, above and beyond BP characteristics. Affective dysregulation was most strongly associated with poor course at the factor level; the individual symptoms most strongly associated with poor course were dissociation/stress-related paranoid ideation, impulsivity, and affective instability. CONCLUSION: BPD severity adds significantly to the burden of BP illness and is significantly associated with a more chronic and severe course and outcome beyond what can be attributable to BP characteristics.

Behavioral and emotional dysregulation trajectories marked by prefrontal-amygdala function in symptomatic youth.

BACKGROUND: Neuroimaging measures of behavioral and emotional dysregulation can yield biomarkers denoting developmental trajectories of psychiatric pathology in youth. We aimed to identify functional abnormalities in emotion regulation (ER) neural circuitry associated with different behavioral and emotional dysregulation trajectories using latent class growth analysis (LCGA) and neuroimaging. METHOD: A total of 61 youth (9-17 years) from the Longitudinal Assessment of Manic Symptoms study, and 24 healthy control youth, completed an emotional face n-back ER task during scanning. LCGA was performed on 12 biannual reports completed over 5 years of the Parent General Behavior Inventory 10-Item Mania Scale (PGBI-10M), a parental report of the child's difficulty regulating positive mood and energy. RESULTS: There were two latent classes of PGBI-10M trajectories: high and decreasing (HighD; n=22) and low and decreasing (LowD; n=39) course of behavioral and emotional dysregulation over the 12 time points. Task performance was >89% in all youth, but more accurate in healthy controls and LowD versus HighD (p<0.001). During ER, LowD had greater activity than HighD and healthy controls in the dorsolateral prefrontal cortex, a key ER region, and greater functional connectivity than HighD between the amygdala and ventrolateral prefrontal cortex (p's<0.001, corrected). CONCLUSIONS: Patterns of function in lateral prefrontal cortical-amygdala circuitry in youth denote the severity of the developmental trajectory of behavioral and emotional dysregulation over time, and may be biological targets to guide differential treatment and novel treatment development for different levels of behavioral and emotional dysregulation in youth.

El Trastorno Bipolar Pediátrico: ¿Sabemos detectarlo? / Pediatric Bipolar Disorder: Do we know how to detect it?

Objetivo: Revisar la literatura sobre el Trastorno Bipolar Pediátrico (TBP), centrándonos en su epidemiología, clínica característica, comorbilidad, curso y pronóstico y claves para su diagnóstico. Método: Búsqueda sistematizada por Pub Med de los artículos publicados desde 1980. Resultados: En los últimos años se ha extendido el diagnóstico del TBP, señalándose una incidencia entre el 1% y el5% según los estudios. Si bien se había señalado un presentación clínica atípica con un predominio de la irritabilidad y un curso crónico, estudios recientes observan síntomas patognonómicos de manía ya en edades precoces, demostrando la utilidad de los actuales criterios diagnósticos DSMIV para el TBP, con un predominio del fenotipo BPNOS. Los casos donde la irritabilidad es el único síntoma, parece que evolucionarían hacia otros trastornos afectivos más que a Bipolares. En el TBP la comorbilidad sería muy elevada, especialmente con TDAH y los trastornos de conducta. En su evolución se observan elevadas tasas de recaídas y síntomas subsindrómicos persistentes. El diagnóstico debe basarse en la clínica, con información colateral de la familia. Se han desarrollado pruebas psicométricas con buena fiabilidad para el diagnóstico del TBP. Conclusiones: En la actualidad es posible un diagnóstico fiable del TBP, pero persisten dudas sobre su categorización, y evolución en el tiempo. Son necesarios futuros estudios longitudinales que puedan aclarar su presentación (AU)

Objective: To review the literature covering the epidemiology, clinical characteristics, longitudinal course, prognosis and clues for the assessment of the Pediatrics Bipolar Disorder (PBD). Method: A computerized search in Pub Med, looking for published articles since 1980. Results: During the last years, the PBD diagnosis has proliferated largely, with some studies reporting incidences between 1% and 5%. In the past, some researchers reported that atypical symptoms could be more common than the classical symptoms in the PBD. However, current studies confirm the presence of typical mania symptoms in the youngest. Also, they confirm the utility of the diagnostic criteria DSM-IV in this population, with the PBD-NOS as the most prevalent phenotype. Those cases with irritability and without any other maniac symptom are still not clear, but the evidence shows a possible evolution towards others non-bipolar affective disorders. The PBD has high comorbidity, especially with ADHD and Disruptive Behavior Disorders. In the longitudinal evaluation, the PBD cases show high rates of relapse and persistent subsyndromical symptoms. The diagnosis is based in the clinical presentation, with collateral information provided by the family. Screening scales and standardized interview has been developed. Conclusions: Now days is possible the diagnosis of PBD, although there is not enough information about the categorization and the longitudinal course of the PBD. Future studies are needed in order to clarify these shadows (AU)

Pediatric Bipolar Disorder: Do we know how to detect it?

OBJECTIVE: To review the literature covering the epidemiology, clinical characteristics, longitudinal course, prognosis and clues for the assessment of the Pediatrics Bipolar Disorder (PBD). METHOD: A computerized search in PubMed, looking for published articles since 1980. RESULTS: During the last years, the PBD diagnosis has proliferated largely, with some studies reporting incidences between 1% and 5%. In the past, some researchers reported that atypical symptoms could be more common than the classical symptoms in the PBD. However, current studies confirm the presence of typical mania symptoms in the youngest. Also, they confirm the utility of the diagnostic criteria DSM-IV in this population, with the PBD-NOS as the most prevalent phenotype. Those cases with irritability and without any other maniac symptom are still not clear, but the evidence shows a possible evolution towards others non-bipolar affective disorders. The PBD has high comorbidity, especially with ADHD and Disruptive Behavior Disorders. In the longitudinal evaluation, the PBD cases show high rates of relapse and persistent subsyndromical symptoms. The diagnosis is based in the clinical presentation, with collateral information provided by the family. Screening scales and standardized interview has been developed. CONCLUSIONS: Now days is possible the diagnosis of PBD, although there is not enough information about the categorization and the longitudinal course of the PBD. Future studies are needed in order to clarify these shadows.

Amygdala response to fearful faces in anxious and depressed children.

BACKGROUND: Alterations in amygdala function have been implicated in the pathophysiological characteristics of adult anxiety and depressive disorders. Studies with healthy adults and children, as well as with adults who have amygdala lesions, have found facial expressions of emotion to be useful probes of amygdala activity. Our study examined the amygdala response to fearful and neutral facial expressions in healthy, anxious, and depressed children. We hypothesized that children with anxiety and depression may show atypical amygdala responses to emotional stimuli. METHODS: Twelve children (8-16 years of age) with generalized anxiety or panic disorder and 12 healthy comparison children underwent noninvasive functional magnetic resonance imaging while viewing photographs of fearful and neutral facial expressions. In a second comparison, 5 girls with major depressive disorder were compared with 5 anxious and 5 healthy girls from the previous sample. RESULTS: Children with anxiety disorders showed an exaggerated amygdala response to fearful faces compared with healthy children, whereas depressed children showed a blunted amygdala response to these faces. In addition, the magnitude of the amygdala's signal change between fearful and neutral faces was positively correlated with the severity of everyday anxiety symptoms. CONCLUSIONS: Our results suggest that amygdala function is affected in both anxiety and depression during childhood and adolescence. Moreover, this disruption appears to be specific to the child's own rating of everyday anxiety.

Relation between anxiety and depressive disorders in childhood and adolescence.

Current research indicates that there is a strong relationship between pediatric anxiety disorders and depression. Assessment measures show high rates of correlation between depression and anxiety and much of the overlap may be related to a common domain of negative affectivity. Anxious youth and depressed youth share a cognitive style marked by a negative bias in information processing. Anxiety disorders and depression are frequently comorbid in children and adolescents. About 25-50% of depressed youth have comorbid anxiety disorders and about 10-15% of anxious youth have depression. Twin and family studies have demonstrated that pediatric anxiety disorders and depression likely share some common genetic factors or influences. Selective serotonin reuptake inhibitors and cognitive-behavioral therapy have been shown in randomized controlled trials to be efficacious for both pediatric depression and anxiety disorders. Integrating the treatment literature with studies of phenomenology, biology and genetics indicates that pediatric anxiety disorders and depression may share a genetically determined neurobiological component that could involve neural circuits that include or are modulated by serotonergic neurons. This component could contribute to the negative affective temperament that appears to be common in both pediatric depression and anxiety disorders.

Fluoxetine in adolescents with major depression and an alcohol use disorder: an open-label trial.

Recently, a first placebo-controlled study of an selective serotonin reuptake inhibitor (SSRI) medication was conducted among a sample of adolescents with major depression by Emslie et al. [Arch. Gen. Psychiatry 54 (1997) 1031.]. That study demonstrated efficacy for fluoxetine vs. placebo for treating adolescents with major depression. However, to date, no studies have been conducted to assess the efficacy of fluoxetine or any other SSRI medication in adolescents with major depression in combination with an alcohol use disorder (AUD). In this study, the authors investigated whether fluoxetine decreases the depressive symptoms and the drinking of adolescents with comorbid major depression and an AUD. The authors conducted a 12-week open-label study of fluoxetine (20 mg) in 13 adolescents with current comorbid major depression and an AUD. A significant within-group decrease (improvement) was found for both depressive symptoms and drinking during the course of the study. The fluoxetine was well tolerated during the study. These data suggest promise for fluoxetine for decreasing both the depressive symptoms and the drinking of adolescents with comorbid major depression and an AUD.

Efficacy of paroxetine in the treatment of adolescent major depression: a randomized, controlled trial.

OBJECTIVE: To compare paroxetine with placebo and imipramine with placebo for the treatment of adolescent depression. METHOD: After a 7- to 14-day screening period, 275 adolescents with major depression began 8 weeks of double-blind paroxetine (20-40 mg), imipramine (gradual upward titration to 200-300 mg), or placebo. The two primary outcome measures were endpoint response (Hamilton Rating Scale for Depression [HAM-D] score < or = 8 or > or = 50% reduction in baseline HAM-D) and change from baseline HAM-D score. Other depression-related variables were (1) HAM-D depressed mood item; (2) depression item of the Schedule for Affective Disorders and Schizophrenia for Adolescents-Lifetime version (K-SADS-L); (3) Clinical Global Impression (CGI) improvement scores of 1 or 2; (4) nine-item depression subscale of K-SADS-L; and (5) mean CGI improvement scores. RESULTS: Paroxetine demonstrated significantly greater improvement compared with placebo in HAM-D total score < or = 8, HAM-D depressed mood item, K-SADS-L depressed mood item, and CGI score of 1 or 2. The response to imipramine was not significantly different from placebo for any measure. Neither paroxetine nor imipramine differed significantly from placebo on parent- or self-rating measures. Withdrawal rates for adverse effects were 9.7% and 6.9% for paroxetine and placebo, respectively. Of 31.5% of subjects stopping imipramine therapy because of adverse effects, nearly one third did so because of adverse cardiovascular effects. CONCLUSIONS: Paroxetine is generally well tolerated and effective for major depression in adolescents.

Biological studies in depressed children and adolescents.

The objective was to review the literature on the biological correlates of major depressive disorder (MDD) in children and adolescents. A computerized search for articles published during the last 20 years was done and selected studies presented. To date, examination of growth hormone (GH), prolactin, and cortisol levels after pharmacological stimulation have shown abnormalities in the secretion of these hormones (e.g. blunted GH secretion after the administration of growth hormone releasing hormone). Identical results have been found in never-depressed children at high risk to develop MDD due to high family loading for MDD suggesting that alteration in certain hormonal systems may be trait markers for MDD. Other biological studies (e.g. the hypothalamic--pituitary axis, sleep electroencephalogram) have yielded more inconsistent results with subjects with melancholic symptoms, severe depressions, and older age showing some abnormalities similar to the ones reported in adults with MDD. Factors such age, sex, maturation, psychiatric family history and exposure to stress need to be considered since they also affect the same biological systems associated with the aetiology of MDD. Considerable biological research has been done in youth with MDD. Further research is needed to investigate whether these markers predict the development of new episodes of MDD, recurrences, and treatment response. Also, these and other studies using more sophisticated methods (e.g. functional MRI) aimed at elucidating the interrelationship between biological and other risk factors are needed.

Subsyndromal depression in adolescents after a brief psychotherapy trial: course and outcome.

INTRODUCTION: Subsyndromal depression has been associated with an increased risk of the development of major depressive disorder (MDD). Since treatment trials of adolescent MDD often result in subsyndromal depression as the outcome, the long-term course of these youth would be useful to understand. METHODS: 107 adolescents with MDD participated in a clinical psychotherapy trial, of whom 99 were followed up for two years after acute treatment. Those with subsyndromal depression (2-3 symptoms) at the end of acute treatment were compared to those who were well (< or =1 symptom) and those who were still depressed (> or =4 symptoms) on presentation at intake, the end of treatment, and over the two-year follow-up. RESULTS: Of the 99 youth, at the end of acute treatment 26 were well, 18 were subsyndromal, and 55 were still depressed. A substantial proportion of the subsyndromally depressed youth were functionally impaired (38%), and showed a protracted time to recovery. The risk of recurrence was similar to those who were without depression at the end of acute treatment (46% vs. 44%). Recurrence was predicted by depressive symptom severity and family difficulties at the end of acute treatment. LIMITATIONS: A large proportion of the subsyndromal groups received open treatment that may have altered their course. Also, this was a referred sample, rather than an epidemiological one. CONCLUSIONS: In clinical samples treated with psychotherapy, subsyndromal depression poses a significant risk for functional impairment and protracted recovery. Depressive recurrence may be prevented by targeting reduction of symptom severity and of family difficulties.

Predictors of parent-rated credibility in a clinical psychotherapy trial for adolescent depression.

The authors have reported that adolescents with major depressive disorder had a higher remission rate with cognitive-behavioral therapy (CBT) than with systemic behavioral family therapy (SBFT) or nondirective supportive therapy (NST). Parent-rated treatment credibility deteriorated from baseline to end of treatment if patients were treated with SBFT or NST, compared with CBT. The present study evaluated the following variables as predictors of change in parent- rated credibility over time across the three treatment cells: severity of child's and parents' depression at baseline; parent-rated family climate at baseline; clinician age, gender, and years of clinical experience; and change in severity of child's depression and in family climate. The greater the baseline depression of children treated with CBT and NST, but not SBFT, the more favorable the change in parent-rated credibility at the end of treatment. Findings suggest that any improvement (for CBT) or a supportive therapeutic contact (for NST) may appeal to parents of severely depressed children.

Parent-child bonding and family functioning in depressed children and children at high risk and low risk for future depression.

OBJECTIVE: To evaluate parent-child bonding and familial functioning in depressed children, children at high risk for depression, and low-risk controls. METHOD: Diagnoses of children and their relatives were obtained via structured interviews with all available informants. Depressed children (n = 54) received a diagnosis of current major depressive disorder (MDD). The high-risk children (n = 21) had no lifetime diagnoses of mood disorders, but at least one first-degree relative with a lifetime history of depression. The low-risk controls (n = 23) had no lifetime psychiatric disorders and no first-degree relative with a lifetime history of mood disorders. Parent-child bonding was evaluated with the child's report on the Parental Bonding Instrument (PBI). Familial functioning was evaluated with each parent answering the Family Assessment Device (FAD). RESULTS: Significant differences were found between the MDD and low-risk children on most parameters of the PBI and FAD. The children with MDD reported significantly elevated maternal overprotection, and their fathers scored significantly lower on the FAD scales of Behavioral Control and General Functioning, compared with the high-risk children. Mothers of high-risk children had significantly lower scores on the Roles and Affective Involvement dimensions of the FAD compared with mothers of low-risk children. Current maternal depression had a deleterious effect on the child's perception of maternal protection and paternal care, mother's report on all FAD scales, and father's report on most FAD scales, whether interacting with the child's depression or existing even if the child was not depressed. CONCLUSION: Maternal depression and its interaction with the child's depression appear to have negative consequences for parent-child bonding and family functioning.

Screen for Child Anxiety-Related Emotional Disorders (SCARED): convergent and divergent validity.

The purpose of this study was to examine the Screen for Child Anxiety-Related Emotional Disorders' (SCARED) divergent and convergent validity and its ability to identify anxious children. The SCARED, the Child Behaviour Checklist (CBCL), and the State-Trait Anxiety Inventory for Children (STAIC) were administered to children, adolescents (n = 295), and their parents attending an outpatient mood and anxiety disorders clinic. DSM-IIIR/IV diagnoses were made using a semistructured interview (n = 130) or a symptom checklist (n = 165). The Multi-Trait Multi-Method Matrix was used to assess construct validity, and Receiver Operating Curve analysis was used to assess the sensitivity and specificity of the SCARED, CBCL, and STAIC. The SCARED correlated significantly better with the CBCL's internalizing factors than with the externalizing factors. In addition, parent and child forms of the SCARED correlated significantly with the trait and state subscales of the STAIC. Children with an anxiety disorder scored significantly higher on the SCARED than children with depression only or disruptive disorders only (P < 0.05), thus demonstrating the discriminant validity of the SCARED. The SCARED is a reliable and valid screening tool for clinically referred children and adolescents with anxiety disorders.