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Journal Article
Research Support, U.S. Gov't, P.H.S.
Review
Oppositional defiant disorder and conduct disorder: a review of the past 10 years, part II.
OBJECTIVE: To review empirical findings on oppositional defiant disorder (ODD) and conduct disorder (CD).
METHOD: Selected summaries of the literature over the past decade are presented.
RESULTS: Research on ODD and CD during the past decade has addressed the complexity involved in identifying the primary risk factors and developmental pathways to disruptive behavior disorders (DBD). In some domains, research is entering an entirely new phase because of the availability of new technologies. In others, larger data sets and more complicated methodological and statistical techniques are testing increasingly complex models. Yet questions remain regarding the most useful subtyping systems, the identification of the most significant risk factors, and the relationships between risk factors from multiple domains.
CONCLUSIONS: Convincing evidence of causal linkages remains elusive. Research has questioned the notion that CD is intractable, especially when multiple domains of risk and impairment are the targets of intervention. It is apparent that there is not one single causative factor; thus it is not likely that one single modality will suffice to treat CD. Future steps will involve the restructuring of diagnostic criteria to capture adequate subtypes and indicators, clarification of the neurological underpinnings of the disorder, and refinement in the models available to explain the varied pathways to DBD.
METHOD: Selected summaries of the literature over the past decade are presented.
RESULTS: Research on ODD and CD during the past decade has addressed the complexity involved in identifying the primary risk factors and developmental pathways to disruptive behavior disorders (DBD). In some domains, research is entering an entirely new phase because of the availability of new technologies. In others, larger data sets and more complicated methodological and statistical techniques are testing increasingly complex models. Yet questions remain regarding the most useful subtyping systems, the identification of the most significant risk factors, and the relationships between risk factors from multiple domains.
CONCLUSIONS: Convincing evidence of causal linkages remains elusive. Research has questioned the notion that CD is intractable, especially when multiple domains of risk and impairment are the targets of intervention. It is apparent that there is not one single causative factor; thus it is not likely that one single modality will suffice to treat CD. Future steps will involve the restructuring of diagnostic criteria to capture adequate subtypes and indicators, clarification of the neurological underpinnings of the disorder, and refinement in the models available to explain the varied pathways to DBD.
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