HERE

IN THIS ISSUE

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hat is the long-term impact of early life trauma on brain development? Over the past few years, we have seen mounting evidence suggesting that the first few years of life are a vulnerable period of neurodevelopment. However, the complex relations among exposure to trauma in early life, brain development, and child psychopathology still need to be better understood. In this issue of the Journal, Suzuki and colleagues (p. 800) approached this topic by focusing on functional, rather than structural, changes in brain development. Based on previous findings, they tested 2 hypotheses: that early life stress and trauma would be associated with increased functional activation to negative emotion stimuli, i.e., fearful and sad faces, in several limbic areas; and that these effects would be exacerbated by an early life history of major depressive disorder. In this longitudinal study, children were examined annually from 3 years of age and older with a battery of diagnostic and symptom scales, and then at 7 to 12 years of age, a total of 115 children had a functional magnetic resonance imaging (fMRI) scan analyzed. The investigators described 3 major findings: increased amygdala reactivity to emotional faces in general was found not only in the children who experienced more severe trauma, but also in children exposed to a broader array of less-severe early life stressors. Children with a history of major depressive disorder showed greater hippocampal activation to sad faces associated with intensity of early life stress, and children with a history of anxiety disorders had a different pattern of interaction between early life stress and later functional activation compared with children with depression. Overall, their results shed light on the common and unique trajectories of developmental abnormalities in emotion processing associated with early life events. Suzuki and colleagues had only 1 snapshot of brain functional data to correlate with their longitudinal measurements of psychopathology in

their study. In contrast, Shaw and colleagues (p. 780) scanned 220 children 4 to 19 years old at least twice to examine the developmental trajectories of basal ganglia structures in attentiondeficit/hyperactivity disorder (ADHD). Another 320 children were scanned once, and the overall sample was evenly divided between typically developing children and children diagnosed with ADHD. Several components of ADHD, such as problems with executive functioning, motor planning, and processing of rewards, are associated with neural loops among the basal ganglia, cortex, and thalamus. Thus, Shaw and colleagues examined the development of basal ganglia from childhood to adolescence in these children, using sophisticated morphologic MRI methods, and reported 3 main findings: the ventral striatum showed progressive surface contraction in children with ADHD but not in typically developing children; multiple areas, including subregions of the caudate and putamen, showed fixed surface area reduction in ADHD that did not progress with age; and treatment with stimulants was not associated with any morphometric basal ganglia changes. These findings suggest the involvement of the basal ganglia in multiple neurocognitive processes in ADHD and highlight the importance of a longitudinal study design to assess neurodevelopmental conditions. Most studies also suggest white matter abnormalities in ADHD. However, there is significant controversy in the literature regarding the location and the nature of such changes. Van Ewijk and colleagues (p. 790) scanned a large sample of individuals with ADHD, their unaffected siblings, and healthy controls. Their diffusion tensor imaging findings suggest that there may be 2 distinct biological mechanisms behind these abnormalities: one linked to the familial risk of developing ADHD, and another with the actual symptom severity. Such mechanisms may explain the heterogeneity in the white matter literature and point the direction for future studies.

JOURNAL OF THE AMERICAN ACADEMY OF C HILD & ADOLESCENT PSYCHIATRY VOLUME 53 NUMBER 7 JULY 2014

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THERE ABSTRACT THINKING 80 Billion Dollars, Every Year ighty billion dollars: this is the estimated yearly societal cost of child abuse and neglect in the United States according to a recently released report from the Institute of Medicine.1 This staggering sum includes direct (e.g., hospitalizations, childhood mental health care, child welfare, law enforcement) and indirect (e.g., special education, early intervention, adult homelessness, lost work productivity) costs of child abuse and neglect for society. The 2013 Institute of Medicine report, a much-needed update on its 1993 original statement on child abuse, confirms the lifelong sequelae of a child’s exposure to abuse and neglect and its dramatic negative impact on brain, cognition, and social development. However, the report also brought some good news: sexual and physical abuse rates have decreased, although neglect has not. Multiple policy changes and program initiatives have improved the public child welfare system. Moreover, rigorous research on the biological consequences of child abuse and the efficacy of innovative intervention approaches has shown positive developments over the past 20 years. However, there is still much to be learned about the biology of early life adversity and how to prevent its negative consequences. Two recently published reports exemplify how to advance our knowledge in this field. Luby et al.2 examined children within the 10-year longitudinal Preschool Depression Study to investigate the effects of poverty on childhood brain development. This is the same group reporting on early life adversity and functional brain changes in this issue of the Journal (Suzuki et al.3). Poverty is often associated with psychosocial neglect, abuse, and trauma in early life. Not surprisingly, this study found that exposure to poverty during early childhood is associated with a pattern of brain abnormalities at an older age that is often found in victims of abuse and trauma, i.e., smaller white matter, cortical gray matter, and hippocampal and amygdala volumes. More important was the crucial positive influence of caregiving support and nurturing in

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hippocampal development: this underscores the key role of caregiving in protecting children from negative long-term sequelae of neglect and poverty. Thus, interventions targeting caregiving and nurturing, such as parenting education and preschool programs, might change a child’s neurodevelopmental trajectory. Along those lines, an intriguing study looked at the effects of setting up a child development account (CDA) on social and emotional development in early childhood.4 Two thousand seven hundred mostly low-income families in Oklahoma were randomized to receive support in opening a CDA around the time of their child’s birth. Four years later, having a CDA was associated with positive effects on the social and emotional development of these children. Such effects are likely due to changes in parental attitudes and behaviors toward their children: because the funds were meant only for postsecondary education, the CDAs motivated the parents, raising their expectations and increasing their support for their children’s education. Such simple, evidence-based interventions can guide us in addressing the massive personal and societal costs associated with early life adversity. Roberto B. Sassi,

MD, PhD

[email protected] Department of Psychiatry and Behavioural Neurosciences Mood Disorders Program McMaster University Hamilton, ON Canada

The author thanks Samuele Cortese MD, PhD, of the New York University Child Study Center for his edits and thoughtful suggestions. Disclosure: Dr. Sassi has received research support from the Brain and Behavior Research Foundation, Hamilton Health Sciences, the Canadian Institutes for Health Research, the March of Dimes, and the McMaster University Department of Psychiatry and Behavioural Neurosciences Alternative Funding Plan award. He has served as a consultant to and on the advisory board for Bristol-Myers Squibb and has received speaker honoraria from Bristol-Myers Squibb, Janssen, and AstraZeneca. http://dx.doi.org/10.1016/j.jaac.2014.04.016

REFERENCES 1. Institute of Medicine, National Research Council. New Directions in Child Abuse and Neglect Research. Washington, DC: National Academies Press; 2013. 2. Luby J, Belden A, Botteron K, et al. The effects of poverty on childhood brain development: the mediating effect of caregiving and stressful life events. JAMA Pediatr. 2013;167: 1135-1142.

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3. Suzuki H, Luby J, Botteron K, Dietrich R, McAvoy M, Barch D. Early life stress and trauma and enhanced limbic activation to emotionally valenced faces in depressed and healthy children. J Am Acad Child Adolesc Psychiatry. 2014;53:800-813. 4. Huang J, Sherraden M, Kim Y, Clancy M. Effects of child development accounts on early social-emotional development: an experimental test. JAMA Pediatr. 2014;168:265-271.

JOURNAL

OF THE

AMERICAN ACADEMY OF C HILD & ADOLESCENT PSYCHIATRY VOLUME 53 NUMBER 7 JULY 2014

abstract thinking: "80 billion dollars, every year".

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