Abstract

The extensive scientific literature on child maltreatment (CM) has provided strong evidence of the globally negative effects of abuse, neglect, and emotional maltreatment on healthy development and of the remarkable resilience of individuals who manage to prosper even in the face of these adverse experiences.1,2 Yet, after many decades of CM research, the underlying mechanisms by which risk and resilience are conferred are just beginning to be understood. In recent years, there has been an acceleration of progress in this area, owing largely to advances in developmental cognitive neuroscience methodologies that are allowing researchers an unprecedented opportunity to understand the manner by which these experiences get “under the skin”3 to affect the development of neurobiological systems.4–6 These findings (from animal and human studies) document structural and functional changes in the developing brain associated with CM7,8 and yield strong support for the role of CM in subsequent psychopathology, in childhood and across the lifespan.9 Edmiston et al. followed this recent trend of neuroscientific investigations of CM but broke new ground in four important ways. First, by examining adolescents, Edmiston et al. revealed linkages between the neurobiological effects of CM previously observed in children and adults. Specifically, Edmiston et al. showed that gray matter (GM) volume is decreased across several cortical, striatal, and limbic regions in adolescents reporting prior CM. The results cited in Edmiston et al. demonstrate GM volume decreases in both adults and children. However, whereas volumetric hippocampal reductions are the most frequent finding in previous research with adults with CM, this pattern is absent in children with CM, raising the question of whether it emerges in adolescence. Edmiston et al. suggested that such volumetric hippocampal reductions are present in some adolescents. Second, whereas prior neuroscience researchers have treated CM as a unitary construct (without distinguishing subtypes or severity of CM) or have focused on a single type of CM (e.g., physical abuse), Edmiston et al. examined differences on measures of brain morphometry according to CM subtypes. For example, the above noted decreased hippocampal volume in the CM sample was primarily observed in those reporting emotional neglect. Similarly, the authors noted other regional effects that were common across CM subtypes (specifically, GM reductions in rostral prefrontal cortex [PFC]) and provided logical (albeit speculative) hypotheses about how these differences might explain parallel differences in previously reported behavioral sequelae of specific CM subtypes. Third, Edmiston et al. examined gender dimorphic CM effects on brain morphometry. Specifically, the regions most impacted in males with prior CM appear to be more strongly associated with impulse control, including the caudate and rostral PFC. In contrast, the females showed alterations in multiple areas associated with emotion reactivity and regulation, including the amygdala, orbitofrontal cortex, subgenual cingulate cortex, insula, and hippocampus. Similar to the results for CM subtypes, the gender analyses provide evidence of concordance between previously observed behavioral phenomena (specifically, differential vulnerability to psychopathology) and underlying neurobiological effects. Fourth, and perhaps the most noteworthy characteristic of the study, the sample consisted of individuals who did not meet criteria for a mental health disorder. The morphometric differences that were noted and were associated with particular CM subtypes existed among individuals who appeared behaviorally unscathed by their experiences of prior adversity. As Edmiston et al. noted, these results might be evidence of future vulnerabilities and/or evidence of adaptations that have allowed compensatory processes to facilitate healthy development in the face of adversity. Additional work in this area is particularly important to meeting the needs of this population because understanding future risk in the absence of behavioral difficulties would greatly assist in the development of screening and prevention programs. Furthermore, knowledge about compensatory processes that help to support resiliency could be leveraged in the development of treatment programs to mitigate CM effects.

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