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Since Robins and Guze set out criteria for the establishment of diagnostic validity in psychiatric disorders in 1970 – that psychiatric categories should be constructed as distinct and homogeneous entities associated with consistent clinical features, specific biomarkers, a uniform clinical course, a clear delineation from other disorders, and a consistent pattern of familial aggregation – a substantial amount of research has improved the classification of child psychiatric disorders and been incorporated in the two currently established classification systems of ICD-10 and DSM-IV-TR. However, recent advances in neurobiological research in areas such as neuroimaging, molecular genetics, neuropsychology, and neurophysiology have increasingly shown shared biological abnormalities across child psychiatric disorders and substantial heterogeneity within specific diagnostic categories, questioning the diagnostic validity of the current categorical classificatory systems (e.g., Banaschewski et al., 2005; Happé, Ronald, & Plomin, 2006). The first two papers in this issue examine the diagnostic validity of child mental health conditions that share the clinical symptom of mood irritability, paediatric bipolar disorder and oppositional defiant disorder, and will be the focus of my Editorial.

Considerable debate regarding appropriate diagnostic criteria has been caused by the concept of paediatric bipolar disorder (PBD), particularly concerning the nosological status of children with nonepisodic, impairing irritability and hyperarousal, or severe mood dysregulation. In this issue, Baroni et al. review the current research on the diagnostic boundaries of bipolar disorder (BD) in youths, in particular the issues of episodicity and irritability, and provide recommendations to guide clinical assessment. Studies comparing children with severe, non-episodic irritability to those with narrow-phenotype bipolar disorder (i.e., discrete episodes of mania with elevated mood) suggest important differences between these phenotypes in clinical correlates, longitudinal course, family history, and psychophysiological mechanisms. The authors advise that, in diagnosing mania in youth, clinicians should stick to DSM criteria and focus on the presence of episodes that consist of a distinct change in mood accompanied by concurrent changes in cognition and behaviour. Thus, the diagnosis of BD should only be made in the presence of identifiable manic or hypomanic episodes. The diagnosis of BD-NOS (not otherwise specified) should be reserved for children with episodes too short to meet DSM-IV-TR duration criteria for mania or hypomania because these children may resemble BD-I and BD-II patients rather than those with nonepisodic, impairing irritability. Lumping both groups together in the BD-NOS category may obscure prominent differences between these two syndromes and constitute a clinically heterogeneous diagnostic category and create a barrier to research clinical practice.

The developmental trajectories of oppositional defiant disorder (ODD), one of the most common psychiatric childhood disorders, are not well understood. Although conceptualised as a disruptive behaviour disorder, longitudinal studies indicate an association between childhood ODD and young adult major depressive disorder. Based on cross-sectional data from the epidemiological surveys including representative groups of 18,415 five–sixteen-year-old children, Stringaris and Goodman examine whether the distinction of three dimensions within youth oppositionality would clarify the pattern of associations between oppositionality and other psychopathology in early and adult life. These three dimensions have distinctive external correlates, with irritability being the only predictor of emotional disorders, the hurtful dimension being particularly strongly associated with callousness and aggressive symptoms of later conduct disorder, and the headstrong dimension being most strongly associated with attention deficit hyperactivity disorder and non-aggressive symptoms of conduct disorder. The differential pattern of external associations of the three symptom dimensions raises the possibility that oppositional defiant disorder should rather be understood as a multidimensional category. Further research is needed to investigate the unique and/or common causative factors of each symptom dimension, their underlying (and interacting) neural mechanisms and the related neuropsychological processes, as well as their long-term developmental trajectories to adulthood. Possibly, differential interventions could be developed and delivered to children and adolescents who have oppositional defiant disorder, with corresponding implications for service planning.

Further molecular genetic and neurobiological research improving our understanding of the developmental trajectories of functional brain networks underlying symptoms is necessary to refine the diagnostic validity of PBD, ODD and other categorical diagnoses, to clarify the unique and shared pathways of child psychiatric disorders, and to guide the development of new treatment strategies. In that context, prospective longitudinal studies on epidemiological samples are clearly needed, because studies using clinical samples may be biased by referral patterns.

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