Comorbidities and Continuities as Ontogenic Processes: Toward a Developmental Spectrum model of Externalizing Psychopathology  

Oleh:

BEAUCHAINE, THEODORE. P ; MCNULTY, TIFFANY

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Development and Psychopathology vol. 25 no. 4 (Nov. 2013), page 1505–1528.
Topik: Comorbidities and continuities; ontogenic processes; developmental spectrum; model externalizing psychopathology
Fulltext: 19S0954579413000746a_Pas.pdf (617.37KB)

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Perpustakaan Pusat (Semanggi) Nomor Panggil: DD21.26 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Research on child and adolescent mental health problems has burgeoned since the inaugural issue of Development and Psychopathology was published in 1989. In the quarter century since, static models of psychopathology have been abandoned in favor of transactional models, following the agenda set by editor Dante Cicchetti and other proponents of the discipline. The transactional approach, which has been applied to autism, depression, self-injury, and delinquency, (a) specifies vulnerabilities and risk factors across multiple levels of analysis spanning genes to cultures, (b) identifies multifinal and equifinal pathways to psychopathology, and (c) transcends traditional disciplinary boundaries. However, as noted by Rutter and Sroufe (2000), specific mechanisms of continuity, discontinuity, and comorbidity of psychopathology must be identified if we wish to understand etiology fully. In this article, we present a model of early-onset externalizing behavior in which comorbidities and continuities are viewed as ontogenic processes: products of complex longitudinal transactions between interdependent individual-level vulnerabilities (e.g., genetic, epigenetic, allostatic) and equally interdependent contextual risk factors (e.g., coercive parenting, deviant peer group affiliations, neighborhood criminality). Through interactions across levels of analysis, some individuals traverse along the externalizing spectrum, beginning with heritable trait impulsivity in preschool and ending in antisociality in adulthood. In describing our model, we note that (a) the approach outlined in the DSM to subtyping externalizing disorders continues to obscure developmental pathways to antisociality, (b) molecular genetics studies will likely not identify meaningful subtypes of externalizing disorder, and (c) ontogenic trait approaches to psychopathology are much more likely to advance the discipline in upcoming years.

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