Clinical Psychology: Science and Practice

Kendall, Philip C.; Drabick, Deborah A. G.

doi: 10.1111/j.1468-2850.2010.01218.xpmid: 24058273

As an introduction to the Special Issue that includes a series of articles on comorbid mental health conditions among youth, some issues pertinent to the diagnostic system are considered. The discussion of illustrative issues that affect the diagnoses of mental health problems among youth includes reminders to consider the source, the time frame, what's normal, the situation, the data, and the effect of changing diagnostic criteria. We support the DSM and ICD efforts to continue to develop as instruments by relying on the data.

Drabick, Deborah A. G.; Kendall, Philip C.

doi: 10.1111/j.1468-2850.2010.01219.xpmid: 21243110

Recent years have evidenced a tremendous increase in research using a developmental psychopathology framework to examine clinical diagnoses among youth. Despite this increase, a relative dearth of literature systematically examines the development of co-occurring conditions among youth. In this introduction to the Special Issue on comorbidity among youth, we suggest that a developmental psychopathology perspective can provide an important foundation for the diagnosis of mental health problems among youth. As a potential framework for future investigations, we consider several developmental psychopathology principles that can inform assessment and diagnosis among youth psychological disorders. We use these principles as a foundation for considering co-occurring psychological disorders and provide potential explanations for comorbidity that can be addressed in future research that uses a developmental psychopathology perspective.

Wood, Jeffrey J.; Gadow, Kenneth D.

doi: 10.1111/j.1468-2850.2010.01220.xpmid: N/A

This article considers the nosology and pathogenesis of anxiety disorders in youth with autism. The comparability of anxiety in the autism spectrum disorder (ASD) population in relation to the typically developing population has been suggested by some recent findings, but conceptual and empirical ambiguities remain. It is suggested that anxiety may play at least three roles: (a) a downstream consequence of ASD symptoms (e.g., via stress generation through social rejection); (b) a moderator of ASD symptom severity, such that certain core autism symptoms like social skill deficits and repetitive behaviors may be exacerbated by anxiety; and (c) as a proxy of core ASD symptoms. Suggestions for clarifying the nature and function of anxiety in autism are made.

Garber, Judy; Weersing, V. Robin

doi: 10.1111/j.1468-2850.2010.01221.xpmid: 21499544

The high level of concurrent and sequential comorbidity between anxiety and depression in children and adolescents may result from (a) substantial overlap in both the symptoms and items used to assess these putatively different disorders, (b) common etiologic factors (e.g., familial risk, negative affectivity, information-processing biases, neural substrates) implicated in the development of each condition, and (c) negative sequelae of anxiety conferring increased risk for the development of depression. Basic research on their various common and unique etiologic mechanisms has guided the development of efficacious treatments for anxiety and depressive disorders in youth. Potential processes through which the successful treatment of childhood anxiety might prevent subsequent depression are described.

Drabick, Deborah A. G.; Ollendick, Thomas H.; Bubier, Jennifer L.

doi: 10.1111/j.1468-2850.2010.01222.xpmid: 21442035

Although oppositional defiant disorder (ODD) and anxiety disorders (ADs) often co-occur, the literature is mixed regarding the effects of such co-occurrence. For example, there is evidence that AD symptoms may mitigate ODD symptoms (buffer hypothesis) or exacerbate ODD symptoms (multiple problem hypothesis). A dual-pathway model incorporates previous research and addresses both hypotheses. We describe several possible etiological or risk processes that may underlie each of these ODD–AD pathways, including child temperament, aggression, limbic system processes, executive functioning abilities, and social information–processing biases, and suggest an integrated model. We conclude with implications for the model and directions for future research involving co-occurring ODD and ADs.

Burke, Jeffrey; Loeber, Rolf

doi: 10.1111/j.1468-2850.2010.01223.xpmid: N/A

Many studies have shown that conduct disorder (CD) and depression often co-occur in late childhood and adolescence and have historically been regarded as the primary point of comorbidity between internalizing and behavioral disorders. On the other hand, recent evidence suggests that oppositional defiant disorder (ODD), and not CD, may best explain the comorbidity between disruptive behavior disorders and depression. ODD typically onsets before CD and depression, changes in ODD symptoms predict changes in symptoms of CD and depression from one year to the next, and ODD in childhood and adolescence predicts depression in adulthood. Emerging evidence suggests that there are affective and behavioral dimensions of ODD symptoms, and those affective ODD symptoms (and not the behavioral symptoms) best predict later depression. These results are highly relevant not only for our understanding of the etiology of the disorders, but also for optimizing early interventions aimed at reducing irritability in some ODD children. The new findings also stimulate new questions to be addressed with future research.

Beauchaine, Theodore P.; Hinshaw, Stephen P.; Pang, Karen L.

doi: 10.1111/j.1468-2850.2010.01224.xpmid: N/A

Among boys, about one-third who exhibit severe attention-deficit/hyperactivity disorder (ADHD) in preschool follow a developmental trajectory to early-onset conduct disorder (CD) in later childhood and adolescence. Moreover, the vast majority of adolescent boys with early-onset CD also meet criteria for ADHD. Although trait impulsivity, a predisposing vulnerability to both ADHD and CD, is about 80% heritable, environmental risk factors play an important role in how impulsivity is expressed, including whether young children with ADHD eventually develop CD. In this article, we (a) describe how environmental risk potentiates early-onset conduct problems among trait-impulsive and therefore vulnerable individuals and (b) outline implications for conceptualizations of externalizing comorbidity. Although other pathways to CD exist, we focus on what is likely to be a common developmental trajectory to this costly psychiatric condition.

Conner, Bradley T.; Lochman, John E.

doi: 10.1111/j.1468-2850.2010.01225.xpmid: N/A

Conduct disorder (CD) and substance use disorders (SUDs) commonly co-occur. The high rates of comorbidity, in conjunction with similar developmental trajectories for CD and SUDs, suggest a common etiology. Both disorders are heritable, indicating a common genetic influence. Research suggests that a developmental pathways approach to the etiology, correlates, comorbidities, prevention, and treatment of CD and SUDs may improve our understanding of these disorders. Research that examines the genetic, neurophysiological, behavioral, and environmental connections among the CD and SUDs is reviewed. Study of the causes of these two disorders, either singly or in combination, is essential to prevent their occurrence and ameliorate the associated negative outcomes.

Youngstrom, Eric A.; Arnold, L. Eugene; Frazier, Thomas W.

doi: 10.1111/j.1468-2850.2010.01226.xpmid: 21278822

Published rates of comorbidity between pediatric bipolar disorder (PBD) and attention-deficit/hyperactivity disorder (ADHD) have been higher than would be expected if they were independent conditions, but also dramatically different across different studies. This review examines processes that could artificially create the appearance of comorbidity or substantially bias estimates of the PBD-ADHD comorbidity rate, including categorization of dimensional constructs, overlap among diagnostic criteria, over-splitting, developmental sequencing, and referral or surveillance biases. Evidence also suggests some mechanisms for “true” PBD-ADHD comorbidity, including shared risk factors, distinct subtypes, and weak causal relationships. Keys to differential diagnosis include focusing on episodic presentation and nonoverlapping symptoms unique to mania.