Over the past decade extensive research has examined the segregation of the human brain into large-scale functional networks. The resulting network maps, i.e. parcellations, are now commonly used for the a priori identification of functional networks. However, the use of these parcellations, particularly in developmental and clinical samples, hinges on four fundamental assumptions: (1) the various parcellations are equally able to recover the networks of interest; (2) adult-derived parcellations well represent the networks in children's brains; (3) network properties, such as within-network connectivity, are reliably measured across parcellations; and (4) parcellation selection does not impact the results with regard to individual differences in given network properties. In the present study we examined these assumptions using eight common parcellation schemes in two independent developmental samples. We found that the parcellations are equally able to capture networks of interest in both children and adults. However, networks bearing the same name across parcellations (e.g., default network) do not produce reliable within-network measures of functional connectivity. Critically, parcellation selection significantly impacted the magnitude of associations of functional connectivity with age, poverty, and cognitive ability, producing meaningful differences in interpretation of individual differences in functional connectivity based on parcellation choice. Our findings suggest that work employing parcellations may benefit from the use of multiple schemes to confirm the robustness and generalizability of results. Furthermore, researchers looking to gain insight into functional networks may benefit from employing more nuanced network identification approaches such as using densely-sampled data to produce individual-derived network parcellations. A transition towards precision neuroscience will provide new avenues in the characterization of functional brain organization across development and within clinical populations.
Objective: Childhood abuse represents one of the most potent risk factors for developing psychopathology, espe- cially in females. Evidence suggests that exposure to early-life adversity may be related to advanced maturation of emotion processing neural circuits. However, it remains unknown whether abuse is related to early circuit matura- tion and whether maturation patterns depend on the pres- ence of psychopathology.
Methods: A multisite sample of 234 girls (ages 8–18 years) completed clinical assessment, maltreatment histories, and high-resolution T1-weighted structural MRI. Girls were stratified by abuse history and internalizing disorder diag- nosis into typically developing (no abuse/no diagnosis), resilient (abuse/no diagnosis), and susceptible (abuse/ current diagnosis) groups. Machine learning models of nor- mative brain development were aggregated in a stacked generalization framework trained to predict chronological age using gray matter volume in whole-brain, emotion, and language circuit parcellations. Brain age gap estima- tions (BrainAGEs; predicted age minus true chronological age) were calculated as indices of relative circuit maturation.
Results: Childhood abuse was related to reduced Brain- AGE (delayed maturation) specific to emotion circuits. Delayed emotion circuit BrainAGE was further related to increased hyperarousal symptoms. Childhood physical neglect was associated with increased whole-brain BrainAGE (advanced maturation). Neural contributors to emotion circuit BrainAGE differed in girls with and with- out an internalizing diagnosis, especially in the lateral prefrontal, parietal, and insular cortices and the hippocampus.
Conclusions: Abuse exposure in girls is associated with a delayed structural maturation pattern specific to emotion circuitry, a potentially adaptive mechanism enhancing threat generalization. Physical neglect, on the other hand, is associated with a broader brain-wide pattern of advanced structural maturation. The differential influence of fronto- parietal cortices and the hippocampus on emotion circuit maturity in resilient girls may represent neurodeve- lopmental markers of reduced psychiatric risk following abuse.
The volume of subcortical structures represents a reliable, quantitative, and objective phenotype that captures genetic effects, environmental effects such as trauma, and disease effects such as posttraumatic stress disorder (PTSD). Trauma and PTSD represent potent exposures that may interact with genetic markers to influence brain structure and function. Genetic variants, associated with subcortical volumes in two large normative discovery samples, were used to compute polygenic scores (PGS) for the volume of seven subcortical structures. These were applied to a target sample enriched for childhood trauma and PTSD. Subcortical volume PGS from the discovery sample were strongly associated in our trauma/PTSD enriched sample (n = 7580) with respective subcortical volumes of the hippocampus (p = 1.10 × 10−20), thalamus (p = 7.46 × 10−10), caudate (p = 1.97 × 10−18), putamen (p = 1.7 × 10−12), and nucleus accumbens (p = 1.99 × 10−7). We found a significant association between the hippocampal volume PGS and hippocampal volume in control subjects from our sample, but was absent in individuals with PTSD (GxE; (beta = −0.10, p = 0.027)). This significant GxE (PGS × PTSD) relationship persisted (p < 1 × 10−19) in four out of five threshold peaks (0.024, 0.133, 0.487, 0.730, and 0.889) used to calculate hippocampal volume PGSs. We detected similar GxE (G × ChildTrauma) relationships in the amygdala for exposure to childhood trauma (rs4702973; p = 2.16 × 10−7) or PTSD (rs10861272; p = 1.78 × 10−6) in the CHST11 gene. The hippocampus and amygdala are pivotal brain structures in mediating PTSD symptomatology. Trauma exposure and PTSD modulate the effect of polygenic markers on hippocampal volume (GxE) and the amygdala volume PGS is associated with PTSD risk, which supports the role of amygdala volume as a risk factor for PTSD.
Altered aversive learning represents a potential mechanism through which childhood trauma (CT) might influence risk for psychopathology. This study examines the temporal dynamics of neural activation and patterns of functional connectivity during aversive learning in children with and without exposure to CT involving interpersonal violence and evaluates whether these neural patterns mediate the association of CT with psychopathology in a longitudinal design.
Children from low-socioeconomic status (SES) households on average exhibit lower academic achievement than their higher-SES peers. We investigated a novel hypothesis that differences in early-developing sensory networks—specifically the ventral visual stream (VVS), which is involved in processing visual stimuli—contribute to SES-related disparities in executive functions (EF) and academic outcomes. We used fMRI to investigate SES-related differences in neural function in children (6–8 years, n = 62) during two attentional tasks involving attention to visual information: cued attention and memory-guided attention. Recruitment of VVS during both tasks was associated with EF and academic achievement, and SES-related differences in VVS activation during cued attention were marginally explained by differences in cognitive stimulation. VVS activation during cued attention mediated SES-related differences in academic achievement. Finally, the link between VVS activation during both tasks and academic achievement was mediated by differences in EF. We extend previous work by highlighting that: (i) early-developing visual processing regions play a role in supporting complex attentional processes, (ii) childhood SES is associated with VVS function, which is explained in part by SES-related differences in cognitive stimulation and (iii) provide preliminary evidence that individual differences in VVS function may play a role in the emergence of the income-achievement gap.
IMPORTANCE Childhood adversity (CA) is a powerful determinant of long-term physical and mental health that is associated with elevated risk for chronic disease and psychopathology. However, the degree to which CA contributes to mortality as a preventable driver of ill-health and death is unknown.
OBJECTIVE To estimate the contribution of CA to health behaviors, including smoking and sedentary behavior, as well as the annual mortality attributable to CA in the US through influences on leading causes of death (eg, cardiovascular disease).
EVIDENCE REVIEW For this systematic review, the PsycINFO and MEDLINE databases were searched on November 15, 2019. The databases were searched for publications from inception (1806 for PsycINFO, 1946 for MEDLINE) to November 15, 2019. Meta-analyses of the associations between CA and morbidity outcomes were included. The population attributable fraction (PAF) was calculated from these associations along with the estimated US prevalence of CA. The PAF was then applied to the number of annual deaths associated with each cause of death to estimate the number of deaths that are attributable to CA. Additionally, the PAF was applied to the incidence of health behaviors to derive the number of cases attributable to CA. Exposure to 1 or more experiences of adversity before the age of 18 years was analyzed, including abuse, neglect, family violence, and economic adversity.
FINDINGS A total of 19 meta-analyses with 20 654 832 participants were reviewed. Childhood adversity accounted for approximately 439 072 deaths annually in the US, or 15% of the total US mortality in 2019 (2 854 838 deaths), through associations with leading causes of death (including heart disease, cancer, and suicide). In addition, CA was associated with millions of cases of unhealthy behaviors and disease markers, including more than 22 million cases of sexually transmitted infections, 21 million cases of illicit drug use, 19 million cases of elevated inflammation, and more than 10 million cases each of smoking and physical inactivity. The greatest proportion of outcomes attributable to CA were for suicide attempts and sexually transmitted infections, for which adversity accounted for up to 38% and 33%, respectively.
CONCLUSIONS AND RELEVANCE The results of this systematic review suggest that CA is a leading contributor to morbidity and mortality in the US and may be considered a preventable determinant of mortality. The prevention of CA and the intervention on pathways that link these e
Stressful life events (SLEs) are strongly associated with the emergence of adolescent anxiety and depression, but the underlying mechanisms remain poorly understood, especially at the within-persons level. We investigated how adolescent social communication (i.e., frequency of calls and texts) following SLEs relates to changes in internalizing symptoms in a multitimescale, intensive, year-long study (N = 30; n = 355 monthly observations; n ≈ 5,000 experiencesampling observations). Within-persons increases in SLEs were associated with receiving more calls than usual at both the month and moment levels and making more calls at the month level. Increased calls were prospectively associated with worsening internalizing symptoms at the month level only, suggesting that SLEs rapidly influence phone communication patterns, but these communication changes may have a more protracted, cumulative influence on internalizing symptoms. Finally, increased incoming calls prospectively mediated the association between SLEs and anxiety at the month level. We identify adolescent social communication fluctuations as a potential mechanism conferring risk for stress-related internalizing psychopathology
We review the three prevailing approaches—specificity, cumulative risk, and dimensional models—to conceptualizing the developmental consequences of early-life adversity and address fundamental problems with the characterization of these frameworks in a recent Perspectives on Psychological Science piece by Smith and Pollak. We respond to concerns raised by Smith and Pollak about dimensional models of early experience and highlight the value of these models for studying the developmental consequences of early-life adversity. Basic dimensions of adversity proposed in existing models include threat/harshness, deprivation, and unpredictability. These models identify core dimensions of early experience that cut across the categorical exposures that have been the focus of specificity and cumulative risk approaches (e.g., abuse, institutional rearing, chronic poverty); delineate aspects of early experience that are likely to influence brain and behavioral development; afford hypotheses about adaptive and maladaptive responses to different dimensions of adversity; and articulate specific mechanisms through which these dimensions exert their influences, conceptualizing experience-driven plasticity within an evolutionary-developmental framework. In doing so, dimensional models advance specific falsifiable hypotheses, grounded in neurodevelopmental and evolutionary principles, that are supported by accumulating evidence and provide fertile ground for empirical studies on early-life adversity.
Childhood exposure to violence is strongly associated with psychopathology. High resting respiratory sinus arrhythmia (RSA) is associated with lower levels of psychopathology in children exposed to violence. High RSA may help to protect against psychopathology by facilitating fear extinction learning, allowing more flexible autonomic responses to learned threat and safety cues. In this study, 165 youth (79 female, aged 9–17; 86 exposed to violence) completed assessments of violence exposure, RSA, and psychopathology, and a fear extinction learning task; 134 participants returned and completed psychopathology assessments 2 years later. Resting RSA moderated the longitudinal association of violence exposure with post-traumatic stress disorder (PTSD) symptoms and externalizing psychopathology, such that the association was weaker among youths with higher RSA. Higher skin conductance responses (SCR) during extinction learning to the threat cue (CS+) was associated with higher internalizing symptoms at follow-up and greater SCR to the safety cue (CS–) was associated with higher PTSD, internalizing, and externalizing symptoms, as well as the p-factor, controlling for baseline symptoms. Findings suggest that higher RSA may protect against emergence of psychopathology among children exposed to violence. Moreover, difficulty extinguishing learned threat responses and elevated autonomic responses to safety cues may be associated with risk for future psychopathology.
COVID-19 presents significant social, economic, and medical challenges. Because COVID-19 has already begun to precipitate huge increases in mental health problems, clinical psychological science must assert a leadership role in guiding a national response to this secondary crisis. In this article, COVID-19 is conceptualized as a unique, compounding, multidimensional stressor that will create a vast need for intervention and necessitate new paradigms for mental health service delivery and training. Urgent challenge areas across developmental periods are discussed, followed by a review of psychological symptoms that likely will increase in prevalence and require innovative solutions in both science and practice. Implications for new research directions, clinical approaches, and policy issues are discussed to highlight the opportunities for clinical psychological science to emerge as an updated, contemporary field capable of addressing the burden of mental illness and distress in the wake of COVID-19 and beyond.
The COVID-19 pandemic has introduced novel stressors into the lives of youth. Identifying factors that protect against the onset of psychopathology in the face of these stressors is critical. We examine a wide range of factors that may protect youth from developing psychopathology during the pandemic. We assessed pandemic-related stressors, internalizing and externalizing psychopathology, and potential protective factors by combining two longitudinal samples of children and adolescents (N = 224, 7–10 and 13–15 years) assessed prior to the pandemic, during the stay-at-home orders, and six months later. We evaluated how family behaviors during the stay-at-home orders were related to changes in psychopathology during the pandemic, identified factors that moderate the association of pandemic-related stressors with psychopathology, and determined whether associations varied by age. Internalizing and externalizing psychopathology increased substantially during the pandemic. Higher exposure to pandemic-related stressors was associated with increases in internalizing and externalizing symptoms early in the pandemic and six months later. Having a structured routine, less passive screen time, lower exposure to news media about the pandemic, and to a lesser extent more time in nature and getting adequate sleep were associated with reduced psychopathology. The association between pandemic-related stressors and psychopathology was reduced for youths with limited passive screen time and was absent for children, but not adolescents, with lower news media consumption related to the pandemic. We provide insight into simple, practical steps families can take to promote resilience against mental health problems in youth during the COVID-19 pandemic and protect against psychopathology following pandemic-related stressors.
IMPORTANCE Many studies have demonstrated an association between early-life adversity (ELA) and executive functioning in children and adolescents. However, the aggregate magnitude of this association is unknown in the context of threat and deprivation types of adversity and various executive functioning domains.
OBJECTIVE To test the hypothesis that experiences of deprivation are more strongly associated with reduced executive functioning compared with experiences of threat during childhood and adolescence.
DATA SOURCES Embase, ERIC, MEDLINE, and PsycInfo databases were searched from inception to December 31, 2020. Both forward and reverse snowball citation searches were performed to identify additional articles.
STUDY SELECTION Articles were selected for inclusion if they (1) had a child and/or adolescent sample, (2) included measures of ELA, (3) measured executive functioning, (4) evaluated the association between adversity and executive functioning, (5) were published in a peer-reviewed journal, and (6) were published in the English language. No temporal or geographic limits were set. A 2-reviewer, blinded screening process was conducted.
DATA EXTRACTION AND SYNTHESIS PRISMA guidelines were used to guide data extraction and article diagnostics (for heterogeneity, small study bias, and p-hacking). Article quality was assessed, and data extraction was performed by multiple independent observers. A 3-level meta-analytic model with a restricted maximum likelihood method was used. Moderator analyses were conducted to explore heterogeneity.
MAIN OUTCOMES AND MEASURES Primary outcomes included measures of the 3 domains of executive functioning: cognitive flexibility, inhibitory control, and working memory.
RESULTS A total of 91 articles were included, representing 82 unique cohorts and 31 188 unique individuals. Deprivation, compared with threat, was associated with significantly lower inhibitory control (F1,90 = 5.69; P = .02) and working memory (F1,54 = 5.78; P = .02). No significant difference was observed for cognitive flexibility (F1,36 = 2.38; P = .12). The pooled effect size of the association of inhibitory control with deprivation was stronger (Hedges g = −0.43; 95% CI, −0.57 to −0.29) compared with threat (Hedges g = −0.27; 95% CI, −0.46 to −0.08). The pooled effect size of the association of working memory with deprivation was stronger (Hedges g = −0.54; 95% CI, −0.75 to −0.33) compared with threat (Hedges g = −0.28; 95% CI, −0.51 to −0.05).
CONCLUSIONS AND RELEVANCE Experiences of both threat and deprivation in childhood and adolescence were associated with reduced executive functioning, but the association was stronger for exposure to deprivation. Efforts to address the consequences of ELA for development should consider the associations between specific dimensions of adversity and specific developmental outcomes.
The ability to identify and label one’s emotions is associated with effective emotion regulation, rendering emotional awareness important for mental health. We evaluated how emotional awareness was related to psychopathology and whether low emotional awareness was a transdiagnostic mechanism explaining the increase in psychopathology during the transition to adolescence and as a function of childhood trauma—specifically, violence exposure. In Study 1, children and adolescents (N = 120, age range = 7–19 years) reported on emotional awareness and psychopathology. Emotional awareness was negatively associated with psychopathology (p-factor) and worsened across age in females but not males. In Study 2 (N = 262, age range = 8–16 years), we replicated these findings and demonstrated longitudinally that low emotional awareness mediated increases in p-factor as a function of age in females and violence exposure. These findings indicate that low emotional awareness may be a transdiagnostic mechanism linking adolescent development, sex, and trauma with the emergence of psychopathology.
Adolescence is a period of increased vulnerability for internalizing problems,
particularly following exposure to stressful life events. We examine how patterns of emotion regulation and brain structure and function predict internalizing problems during the COVID-19 pandemic, as well as moderate the association between pandemic-related stressors andvinternalizing problems.
Data are from a longitudinal sample (N=145, aged 10-15) strategically assessed at three crucial timepoints: prior to the pandemic, early during the stay-at-home order period, and again six months later. We examined associations of neural structure and function during an emotional processing task prior to the pandemic, use of emotion regulation strategies prior to and during the pandemic, and pandemic-related stressors with internalizing problems.
Greater exposure to pandemic-related stressors was associated with higher levels of internalizing symptoms both early (ß = .437, p<.001) and later (ß = .225, p = .004) in the pandemic. Youth who reported more frequent use of maladaptive emotion regulation strategies, including rumination (ß = .204,p = .026) and expressive suppression (ß = .177, p = .023), also had higherinternalizing problems. Higher left amygdala activation to neutral relative to fearful faces prior tothe pandemic was associated with greater internalizing symptoms (ß =-.229, p = .007), and astrongerrelation between pandemic-related stressors and internalizing problems (ß = -.186, p = .014).
Pandemic-related stressors are strongly associated with internalizing problems in adolescents, and individual differences in emotional reactivity and regulation and their underlying neural mechanisms contribute to stress-related vulnerability. Interventions that reduce pandemic-related stressors and foster adaptive emotion regulation skills may protect against adolescent psychopathology during this period of heightened exposure to stress.
The ability to regulate emotions is key to goal attainment and well-being. Although much has been discovered about neurodevelopment and the acquisition of emotion regulation, very little of this work has leveraged information encoded in whole-brain networks. Here we employed a network neuroscience framework to parse the neural underpinnings of emotion regulation skill acquisition, while accounting for age, in a sample of children and adolescents (N = 70, 34 female, aged 8–17 years). Focusing on three key network metrics—network differentiation, modularity, and community number differences between active regulation and a passive emotional baseline—we found that the control network, the default mode network, and limbic network were each related to emotion regulation ability while controlling for age. Greater network differentiation in the control and limbic networks was related to better emotion regulation ability. With regards to network community structure (modularity and community number), more communities and more crosstalk between modules (i.e., less modularity) in the control network were associated with better regulatory ability. By contrast, less crosstalk (i.e., greater modularity) between modules in the default mode network was associated with better regulatory ability. Together, these findings highlight whole-brain connectome features that support the acquisition of emotion regulation in youth.
Spanking remains common around the world, despite evidence linking corporal punishment to detrimental child outcomes. This study tested whether children (Mage = 11.60) who were spanked (N = 40) exhibited altered neural function in response to stimuli that suggest the presence of an environmental threat compared to children who were not spanked (N = 107). Children who were spanked exhibited greater activation in multiple regions of the medial and lateral prefrontal cortex (PFC), including dorsal anterior cingulate cortex, dorsomedial PFC, bilateral frontal pole, and left middle frontal gyrus in response to fearful relative to neutral faces compared to children who were not spanked. These findings suggest that spanking may alter neural responses to environmental threats in a manner similar to more severe forms of maltreatment.
The association between low socioeconomic status (SES) in childhood and increased risk for psychopathology is well established, but the mechanisms explaining this relationship are poorly understood. Here, we investigate the potential role of difficulties in executive functioning (EF) as a mechanism linking childhood and adolescent SES with externalizing and internalizing psychopathology.
We examined whether difficulties with EF mediated the association between SES and externalizing and internalizing psychopathology in two cross-sectional samples of children and adolescents (Study 1: N = 94, ages 6–18, 51.1% male; Study 2: N = 259, ages 8–16, 54.1% male) from diverse SES backgrounds in the United States. EF was measured through behavioral tasks and parent-reported behavioral regulation (BR).
In both samples, children and adolescents from lower SES families were more likely to experience both externalizing and internalizing psychopathology than youth from more advantaged backgrounds and exhibited greater EF difficulties – they had lower performance on a task measuring inhibitory control and lower parent-rated BR. Reduced inhibitory control and BR, in turn, were associated with higher externalizing and internalizing psychopathology. In Study 1, difficulties with BR mediated the association of low-SES with both externalizing and internalizing psychopathology. In Study 2, low inhibitory control mediated the association between low-SES and externalizing psychopathology. These findings largely persisted after adjusting for exposure to violence, a form of adversity that is common in children from low-SES backgrounds.
These findings suggest that reduced EF may be an underlying mechanism through which low-SES confers risk for psychopathology in children and adolescents.
Exposure to childhood adversity is a powerful risk factor for psychopathology. Despite extensive efforts, we have not yet identified effective or scalable interventions that prevent the emergence of mental health problems in children who have experienced adversity. In this modified Delphi study, we identified intervention strategies for effectively targeting both the neurodevelopmental mechanisms linking childhood adversity and psychopathology – including heightened emotional reactivity, difficulties with emotion regulation, blunted reward processing, and social information processing biases, as well as a range of psychopathology symptoms. We iteratively synthesized information from experts in the field and relevant meta-analyses through three surveys, first with experts in intervention development, prevention, and childhood adversity (n = 32), and then within our study team (n = 8). The results produced increasing stability and good consensus on intervention strategy recommendations for specific neurodevelopmental mechanisms and symptom presentations and on strength of evidence ratings of intervention strategies targeting youth and parents. More broadly, our findings highlight how intervention decision making can be informed by meta-analyses, enhanced by aggregate group feedback, saturated before consensus, and persistently subjective or even contradictory. Ultimately, the results converged on several promising intervention strategies for prevention programming with adversity-exposed youth, which will be tested in an upcoming clinical trial.
Stressful life events (SLEs) are strongly associated with the emergence of adolescent anxiety and depression, but the underlying mechanisms remain poorly understood, especially at the within-persons level. We investigated how adolescent social communication (i.e., frequency of calls and texts) following SLEs relates to changes in internalizing symptoms in a multitimescale, intensive, year-long study (N = 30; n = 355 monthly observations; n ≈ 5,000 experience-sampling observations). Within-persons increases in SLEs were associated with receiving more calls than usual at both the month and moment levels and making more calls at the month level. Increased calls were prospectively associated with worsening internalizing symptoms at the month level only, suggesting that SLEs rapidly influence phone communication patterns, but these communication changes may have a more protracted, cumulative influence on internalizing symptoms. Finally, increased incoming calls prospectively mediated the association between SLEs and anxiety at the month level. We identify adolescent social communication fluctuations as a potential mechanism conferring risk for stress-related internalizing psychopathology.
There is a strong positive association between childhood socioeconomic status (SES) and academic achievement. This disparity may, in part, be explained by differences in early environmental experiences and language development. Cognitive stimulation—including language exposure, access to learning materials, caregiver involvement in children’s learning, and variety of experiences—varies by SES and may link SES to language development. Childhood language development in turn is associated with academic achievement. In the current longitudinal study of 101 children (60–75 months), SES was positively associated with cognitive stimulation and performance on language measures. Cognitive stimulation mediated the association between SES and children’s language. Furthermore, children’s language mediated the association between SES and academic achievement 18 months later. In addition to addressing broader inequalities in access to resources that facilitate caregivers’ abilities to provide cognitive stimulation, cognitive stimulation itself could be targeted in future interventions to mitigate SES-related disparities in language and academic achievement.