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. 2019 Dec:1:277-312.
doi: 10.1146/annurev-devpsych-121318-084950. Epub 2019 Dec 12.

Childhood Adversity and Neural Development: A Systematic Review

Katie A McLaughlin  1 , David Weissman  1 , Debbie Bitrán  2
Affiliations

Childhood Adversity and Neural Development: A Systematic Review

Katie A McLaughlin et al. Annu Rev Dev Psychol. 2019 Dec.

Abstract

An extensive literature on childhood adversity and neurodevelopment has emerged over the past decade. We evaluate two conceptual models of adversity and neurodevelopment-the dimensional model of adversity and stress acceleration model-in a systematic review of 109 studies using MRI-based measures of neural structure and function in children and adolescents. Consistent with the dimensional model, children exposed to threat had reduced amygdala, medial prefrontal cortex (mPFC), and hippocampal volume and heightened amygdala activation to threat in a majority of studies; these patterns were not observed consistently in children exposed to deprivation. In contrast, reduced volume and altered function in frontoparietal regions were observed consistently in children exposed to deprivation but not children exposed to threat. Evidence for accelerated development in amygdala-mPFC circuits was limited but emerged in other metrics of neurodevelopment. Progress in charting neurodevelopmental consequences of adversity requires larger samples, longitudinal designs, and more precise assessments of adversity.

Keywords: adverse childhood experiences; amygdala; early-life stress; hippocampus; neurodevelopment.

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Figures

Figure 1:
Figure 1:
Pie charts represent the proportion of studies that find positive (orange), negative (blue), or null (gray) associations between each adversity type and (a) amygdala volume, (b) amygdala activation, (c) medial prefrontal cortex (mPFC) structure, and (d) amygdala-mPFC connectivity. Studies of mPFC structure include those that used measures of cortical thickness, volume, or surface area. Amygdala activation refers to studies that contrasted negative emotional stimuli with neutral emotional stimuli. For two of the five studies of the relation between deprivation and amygdala activation, fearful faces were contrasted against the implicit baseline of the intertrial interval instead of a neutral stimulus. Studies of amygdala-mPFC connectivity summarized in panel d include studies measuring either fractional anisotropy of the uncinate fasciculus or seed-based resting-state functional connectivity of the amygdala.
Figure 2:
Figure 2:
Pie charts represent the proportion of studies that support the stress acceleration hypothesis (orange), compared to patterns more consistent with developmental delay (blue) and null findings (gray) with regards to three measures of amygdala-medial prefrontal cortex (mPFC) connectivity across adversity types. Uncinate fasciculus (UF) fractional anisotropy (FA) typically increases across development, so higher FA would be consistent with accelerated development, while lower FA would be consistent with developmental delay. Amygdala-mPFC resting-state functional connectivity (rs-fc) typically increases across development, so greater rs-fc would be consistent with accelerated development, while lower rs-fc would be consistent with developmental delay. Task-based functional connectivity to negative versus neutral emotional cues, as measured through psychophysiological interaction (PPI) analyses, typically decreases across development, so lower task-based functional connectivity would be consistent with accelerated development, while higher connectivity would be consistent with developmental delay.
Figure 3:
Figure 3:
Pie charts represent the proportion of studies that find positive (orange), negative (blue), or null (gray) associations between each adversity type and each measure of neural structure, function, or connectivity. Studies of (a) insula and (b) dorsal anterior cingulate cortex (dACC) activation contrasted activation to negative emotional stimuli compared to neutral emotional stimuli.
Figure 4:
Figure 4:
Pie charts represent the proportion of studies that find positive (orange), negative (blue), or null (gray) associations between each adversity type and (a) hippocampal volume, (b) hippocampal activation in response to threat cues, (c) hippocampal activation during memory tasks, and (d) hippocampus-prefrontal cortex (PFC) connectivity. In panel c, hippocampal activation data are not available (NA) for deprivation and mixed exposures. Studies of hippocampus-PFC connectivity summarized in panel d include those using either fractional anisotropy of the cingulum or seed-based resting-state functional connectivity of the hippocampus.
Figure 5:
Figure 5:
Pie charts represent the proportion of studies that find positive (orange), negative (blue), or null (gray) associations between each adversity type and (a) dorsolateral prefrontal cortex (dlPFC) structure, (b) parietal structure, and (c) frontoparietal connectivity. Studies of dlPFC and parietal structure include studies that used measures of cortical thickness, volume, or surface area. Studies of frontoparietal connectivity summarized in panel c include studies using either structural connectivity of the superior longitudinal fasciculus or the inferior fronto-occipital fasciculus or resting-state functional connectivity.
Figure 6:
Figure 6:
Pie charts represent the proportion of studies that find positive (orange), negative (blue), or null (gray) associations between each adversity type and (a) striatum activation and (b) frontostriatal connectivity. Striatum activation refers to studies that contrasted rewarding or positive emotional stimuli with neutral contrasts. For one of three studies of the relation between deprivation and striatum activation, happy faces were contrasted against the implicit baseline of the intertrial interval instead of a neutral stimulus. Studies of frontostriatal connectivity summarized in panel b include studies measuring either fractional anisotropy of one of the frontostriatal white matter tracts or seed-based resting-state functional connectivity of the striatum. Abbreviation: mPFC, medial prefrontal cortex.
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