Psychiatry and developmental psychopathology: Unifying themes and future directions

Abstract

In the past 35 years, developmental psychopathology has grown into a flourishing discipline that shares a scientific agenda with contemporary psychiatry. In this editorial, which introduces the special issue, we describe the history of developmental psychopathology, including core principles that bridge allied disciplines. These include (1) emphasis on interdisciplinary research, (2) elucidation of multicausal pathways to seemingly single disorders (phenocopies), (3) description of divergent multifinal outcomes from common etiological start points (pathoplasticity), and (4) research conducted across multiple levels of analysis spanning genes to environments. Next, we discuss neurodevelopmental models of psychopathology, and provide selected examples. We emphasize differential neuromaturation of subcortical and cortical neural networks and connectivity, and how both acute and protracted environmental insults can compromise neural structure and function. To date, developmental psychopathology has placed greater emphasis than psychiatry on neuromaturational models of mental illness. However, this gap is closing rapidly as advances in technology render etiopathophysiologies of psychopathology more interrogable. We end with suggestions for future interdisciplinary research, including the need to evaluate measurement invariance across development, and to construct more valid assessment methods where indicated.

Keywords: Developmental psychopathology; Equifinality; Interdisciplinary; Multifinality; Neurodevelopment; Psychiatry.

Fig. 1.

Progression from unidisciplinary to multidisciplinary to interdisciplinary to transdisciplinary science. At each step, disciplines become more integrated and interdependent. Psychiatry and developmental psychopathology have entered a transdisciplinary era [35,41].

Fig. 2.

Relations between numbers of syndrome-relevant GWAS single nucleotide polymorphisms (SNPs) and proportions of phenotypic variation explained for schizophrenia (SCZ), celiac disease, myocardial infarction (MI), rheumatoid arthritis (RA), and type II diabetes (T2D). Shaded regions represent posterior probability densities, derived from approximate Bayesian polygenic analysis (ABPA). Collectively, 8332 SNPs explain 50% of population based phenotypic variation in schizophrenia liability. Reproduced with permission from “Genome-wide association analysis identifies 13 new risk loci for schizophrenia”, by S. Ripke et al. [62], Nature Genetics, 45: 1150–9.

Fig. 3.

Etiological complexity of well characterized externalizing progression for many affected males. Low tonic striatal activity and blunted striatal reactivity while anticipating incentives arise from accrual of and complex interactions among genetic influences (heritable SNPs and CNVs, de novo mutations, epigenetic effects), impinging exogenous risk exposures (TBI, hypoxia), and neurohormone regulation. Any single research study can address very few of these influences. For simplicity of presentation, other neural systems that modulate striatal function are omitted [31]. Striatal dysfunction imbues an irritable, anhedonic mood state, which in turn elicits a temperamental/behavioral bias toward reward seeking to upregulate aversive mood. Genetic, neural, and temperamental vulnerabilities are expressed syndromally as ADHD, which predisposes to externalizing progression specifically in high risk environments [87].

Fig. 4.

A neurodevelopmental model of externalizing progression for many affected males. Early in life, impulsivity (ADHD) derives largely from subcortically-mediated neural vulnerability (top panel, left). Progression to more severe externalizing conduct occurs in conjunction with deficient in cortical neuromaturation, which gives rise to self- and emotion regulation deficits (top panel, right). Environmental risk factors potentiate this progression (see text). The bottom panel shows relative contributions of subcortical and cortical dysfunction to overall impairment across development.