Journal of Child Psychology and Psychiatry最新文献

Background: Children of maltreated mothers are at increased risk for adverse physical and psychological health. Both prenatal and postnatal alterations in offspring biological stress systems have been proposed as mechanisms contributing to such transmission. The aim of the current study was to assess whether maternal postnatal care of the infant moderated any effect of maternal childhood maltreatment on infant cortisol output during a mild stressor at 4 months of age.

Methods: Participants included 181 mother-infant dyads, screened at recruitment to result in 57.4% reporting one or more forms of childhood maltreatment. Mothers were assessed for quality of caregiving, and infants were assessed for infant salivary cortisol output during the Still-Face Paradigm at infant age 4 months. Maternal childhood maltreatment was assessed using the Maltreatment and Abuse Chronology of Exposure (MACE) self-report scales.

Results: Greater severity of maternal childhood neglect interacted with higher levels of maternal disoriented caregiving to predict higher infant cortisol output over the course of the Still-Face Paradigm. In contrast, maternal childhood abuse interacted with higher levels of maternal negative-intrusion to predict lower infant cortisol output. Greater maternal role confusion was linked to greater infant cortisol output regardless of maternal maltreatment history.

Conclusions: Maternal caregiving may moderate the effects of risk factors existing prior to the infant's birth. Disoriented caregiving in the context of maternal childhood neglect and negative-intrusive behavior in the context of maternal childhood abuse were associated with opposite directions of effect on infant stress hormone output. The results suggest that interventions addressing risks from both prenatal and postnatal periods may be most effective in mitigating intergenerational effects of maltreatment.

Background: Naturalistic developmental behavioural interventions (NDBI) may improve social communication in toddlers/pre-school aged children with autism spectrum disorder (ASD). Here, we study efficacy of the low-intensity, complex NDBI 'Frankfurt Early Intervention Program for ASD' (A-FFIP) over 1 year by a confirmatory phase-III, prospective, randomised, controlled, parallel-group study with two treatment arms over four centres.

Methods: Main inclusion criteria: ASD (DSM-5), age 24-66 months, developmental quotient >30.

Intervention: Manualised A-FFIP intervention. Control intervention: Early intervention as usual (EIAU).

Primary outcome: Change in core ASD symptoms from baseline (T2) to immediate intervention endpoint at 12 months (T6) based on the blindly rated Brief Observation for Communication Change (BOSCC) total score.

Statistical analysis: Mixed model for repeated measures with covariates baseline BOSCC-total, chronological age and centre.

Results: Between July 2018 and October 2021, N = 134 children with ASD were randomly allocated to intervention (A-FFIP: n = 68, EIAU: n = 66). Groups did not differ at baseline, with a mean age of 49 (SD 10) months, a mean developmental age of 23.3 (SD 13.6) months and 26 (19.4%) females. The SARS-CoV-2 pandemic interfered severely with trial procedures. Intention-to-treat analysis in the primary analysis set, with at least one postbaseline BOSCC measure (A-FFIP n = 64, EIAU n = 60), did not find differences in the primary outcome by group (adjusted ES -0.06, 95% CI to -0.24 to 0.11). SARS-CoV2-related lockdown led to less improvement across groups. Secondary outcomes showed stronger improvements in parent-rated repetitive behaviour as well as parent- and teacher-rated executive functions for A-FFIP versus EIAU. Adverse events were comparable between groups.

Conclusions: The manualised NDBI program A-FFIP, which allows individually targeting six core basic abilities and five developmental domains related to longitudinal development in ASD, did not improve social communication, cognitive or behavioural outcomes beyond EIAU after 1 year, but may improve repetitive behaviour and executive function.

Background: Sex differences have been identified in young adults along the psychosis continuum, but studies in children and adolescents are scarce. This study aimed to evaluate possible sex differences in clinical characteristics and outcomes in children and adolescents with clinical high risk for psychosis (CHR).

Methods: A naturalistic longitudinal cohort study assessed sociodemographics, CHR symptoms, functioning, and mood at baseline and at 18 months' follow-up in 221 CHR participants (154 females and 67 males) and 159 controls (93 females and 66 males). Regression analyses were performed to test baseline differences, and multinominal regression was used to test the implication of sex in outcome.

Results: Despite initial pairwise differences in attenuated positive symptoms, regression analyses failed to show sex differences in CHR symptoms when control group was added to the analyses. The interaction between sex and group significantly predicted depressive symptoms (B = -2.907, p = .040, 95% CI: [-5.681, -0.133]) and caffeine use lifetime (OR = 0.36, 95% CI: [0.138, 0.924], p = .034). A significant interaction between age and sex showed that the older the age in females, the greater the probability of non-remission of CHR at follow-up, as compared to males (B = 0.338, IC 95%: [0.123, 0.933], p = .036), but no relevant associations with sex were found in psychosis outcome.

Conclusions: No sex-related differences in CHR symptoms were observed in a CHR children and adolescent population. Outcomes related to non-remission of CHR state in older females could reflect the greater prevalence of psychosis-like experiences in adolescent females. These results invite us to reconsider the usefulness of the current CHR criteria in young populations, especially if we do not take into account a gender perspective and how age might affect it.

Background: Placental malperfusion, categorised into maternal vascular malperfusion (MVM) and foetal vascular malperfusion (FVM), is a main placental pathology known to affect placental functioning and offspring outcomes. The aim of this review is to evaluate the association between exposure to placental malperfusion and offspring neurodevelopment from birth to 18 years of age.

Methods: Following the registered protocol on Prospero, Medline, Cochrane, CINHAL, Embase and PsycINFO databases were searched systematically from inception to 01/11/2023. Included were publications examining exposure to placental malperfusion detected on histopathological examination and clinically measured neurodevelopmental outcomes. Publications on multi-pregnancies or animals, exposure to malformations, surgical or medical interventions, review and opinion articles, or those not translated to English, were excluded. Grey literature search and forward and backward citation chaining were performed. The Joanna Briggs Institute's checklists were used for quality assessment. Three studies were pooled using percentages of adjusted associations.

Results: Nine observational studies fulfilled the eligibility criteria. The included neurodevelopmental outcomes were assessed from 5 days to 8 years when age of assessment is reported. Four publications showed an association between exposure to MVM and poor neurodevelopment at 10-40 months and 8 years, however, no association was observed when examining preterm infants up to 24 months. Conversely, in the six studies examining exposure to FVM, FVM association with neurodevelopmental disorders was reported in two studies looking at preterm infants assessed at 24 months and 8 years and better neurodevelopmental scores in other two studies at 10-40 months.

Conclusions: The pattern of association between MVM and FVM with neurodevelopmental outcomes varied among the included studies. Clinical and methodological heterogeneities and poor reporting of relevant populations' characteristics hindered full understanding of the results. Methodologically rigorous research is required to help utilise histopathological findings of placental malperfusion in predicting offspring's neurodevelopmental outcomes.

Background: Humans are inevitably exposed to multiple physical and social environmental risk factors, potentially contributing to psychiatric problems and cognitive deficits; however, the combined effects of prenatal air pollution and psychosocial environments on youth remain unclear. This longitudinal study aimed to examine how prenatal ozone exposure interacts with psychosocial environments at 9-10 years to affect adolescent limbic system development, cognition, and psychotic-like experiences (PLEs) at 11-13 years.

Methods: We analyzed data from 6,778 participants in the Adolescent Brain Cognitive Development (ABCD) Study® at two time points (baseline: 9-10 years and 2-year follow-up). Prenatal ozone exposure was calculated as a 9-month average of daily exposure estimates based on birth year and address. Social environmental factors included school environment and neighborhood safety at both time points. Structural MRI measures included bilateral amygdala and hippocampus volumes at both time points. Behavioral data consisted of cognition and PLEs scores at both time points. Moderation and moderated mediation models with cluster-robust standard errors were constructed to examine the effects, controlling for covariates.

Results: Children who were prenatally exposed to greater ozone and had a more unfavorable school environment exhibited a smaller increase in left hippocampal volume, leading to poorer cognition and more PLEs. Moreover, children who were prenatally exposed to greater ozone and lived in a more unsafe neighborhood had a larger increase in right amygdala volume.

Conclusions: This longitudinal study is the first to demonstrate the combined effects of prenatal ozone pollutant and adverse social environments in childhood on youth psychotic-like experiences and cognition, highlighting the limbic system as an important neural mechanism underlying the effects.

Background: Despite the higher prevalence of childhood traumatic experiences and post-traumatic stress disorder (PTSD) in autistic adults, research on trauma-related psychopathology and autistic traits in young people is lacking. This study examined if high autistic traits in childhood predispose individuals to traumatic experiences, the development of PTSD and general psychopathology, and greater functional impairment by age 18, in both the general population and a subsample of trauma-exposed young people.

Methods: Data were utilised from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative cohort of 2,232 same-sex twins born in 1994-1995 across England and Wales. Participants were a subset of children whose parents completed the Childhood Autism Spectrum Test (CAST), during assessments at ages 8, 9 and/or 12 years (N = 1,504). We tested associations between autistic traits in childhood and age-18 reports of lifetime trauma exposure, lifetime PTSD diagnosis, general psychopathology ('p-factor') and NEET status ('not in employment, education or training'). Analyses were conducted controlling for sex, family socioeconomic status (SES), intelligence quotient (IQ) and accounting for family clustering.

Results: Higher autistic traits in childhood were significantly associated with greater reports of lifetime trauma exposure (Odd Ratio [OR] = 1.26, 95% Confidence Intervals [CI] = 1.03; 1.54), lifetime PTSD diagnosis (OR = 1.91, 95% CI = 1.29; 2.82), general psychopathology (beta = 3.22, 95% CI = 1.84; 4.60) and NEET status (OR = 1.48, 95% CI = 1.05; 2.09) at age 18. Only the associations of autistic traits with PTSD and general psychopathology were robust to adjustment for potential confounders. Among trauma-exposed children, autistic traits were also significantly associated with lifetime PTSD diagnosis (OR = 1.75, 95% CI = 1.15; 2.68) and psychopathology (beta = 3.36, 95% CI = 0.68; 6.04) at age 18, but only the association with PTSD held when adjusted for confounders.

Conclusions: Our findings suggest a need to develop targeted assessments and evidence-based treatments for PTSD to meet the needs of children with high autistic traits. However, whether our findings extend to diagnosed autistic children requires further investigation.

Background: Children in impoverished families-especially those affected by violence-face risks to healthy development. In the years of strong economic recovery since the 1994 Genocide Against the Tutsi, the Rwandan Government has invested in early child development, social and child protection and violence prevention, but few strategies for scaling evidence-based interventions (EBIs) in these areas have been studied.

Methods: We present a Hybrid Type-2 Implementation-Effectiveness study of the PLAY Collaborative implementation strategy to engage government and other stakeholders in scaling Sugira Muryango (SM, "Strong Family") to families eligible for social protection in three rural districts. SM promotes nurturing care of children under three while reducing family violence. We assessed delivery quality (fidelity, competence) and perceptions of the PLAY Collaborative (e.g, feasibility, leadership, organisation, sustainability). An embedded trial of 538 households (778 caregivers, 555 children) tested SM effectiveness when delivered by child protection volunteers.

Results: Child protection volunteers delivered SM with high fidelity and competence that improved with time and routine supervision. The PLAY Collaborative was rated moderately to highly across implementation outcomes. The embedded trial revealed improvements in children's stimulation at home (d = 0.20, 95% CI: 0.04-0.36) as caregivers involved them more in daily activities (d = 0.37, 95% CI: 0.18-0.57) and provided more learning materials (d = 0.37, 95% CI: 0.16-0.59). SM families increased stimulating care (e.g. singing, playing; d = 0.26, 95% CI: 0.07-0.46); involved fathers more in caregiving (IRR = 1.18, 95% CI: 1.03-1.37); reduced harsh discipline (OR = 0.34, 95% CI: 0.14-0.82); and increased dietary diversity (d = 0.25, 95% CI: 0.04-0.45). SM caregivers reported improved mental health (d = -0.13, 95% CI: -0.26 to -0.01). SM households increased safe water storage (OR = 3.14, 95% CI: 1.64-6.03) and water treatment (OR = 3.56, 95% CI: 1.80-7.05) practices.

Conclusions: The PLAY Collaborative successfully overcame implementation barriers and maintained effectiveness across most outcomes while scaling delivery to N = 8,745 families, highlighting the value of systematically investigating implementation strategies while scaling an EBI as integrated into existing social and child protection systems.

Background: Sexual and gender minority (SGM) youth are more susceptible to suicidal ideation and attempts compared to their heterosexual and cisgender peers. Yet, it is unclear how interpersonal and online victimization experiences account for the elevated suicide risks in this population. This study investigates the extent of peer and cyber victimization among SGM youth and its contribution to their higher risks of suicidal ideation and attempts longitudinally.

Methods: Data were from the first three waves of the Adolescent Brain Cognitive Development (ABCD) Study (5,596 9-10-year-old youth; 2,640 [47.2%] female; 3,107 [55.5%] non-Hispanic White). Youth reported sexual and gender identities and experiences of peer (overt, relational, reputational) and cyber victimization. Suicidal ideation and attempts were assessed using youth reports of Kiddie Schedule for Affective Disorders and Schizophrenia for DSM-5. We used mixed-effects logistic regression to quantify the association between SGM identity reported at waves 1-2 (9-11 years) and suicidal ideation and attempts at wave 3 (11-12 years) and longitudinal mediation analysis to determine whether peer and cyber victimization accounted for these associations.

Results: SGM youth were at greater risk for lifetime suicidal ideation (odds ratio [OR] 4.75, 95% CI 3.74-6.03), lifetime suicide attempts (OR 5.87, 95% CI 3.72-9.28), and current suicidal ideation or attempts (OR 4.94, 95% CI 3.19-7.68) compared to non-SGM youth. SGM youth experienced elevated peer (overt: β = 0.40, 95% CI 0.31-0.49; relational: β = 0.43, 95% CI 0.34-0.53; reputational: β = 0.51, 95% CI 0.42-0.60) and cyber victimization (OR 2.35, 95% CI 1.77-3.11). Around 22%-28% of the disparities in current suicidal ideation or attempts were mediated by peer or cyber victimization.

Conclusions: SGM youth are disproportionately affected by both interpersonal and online victimization, which are subsequently associated with their elevated suicide risks. Our findings underscore the urgent need for targeted interventions to foster safer school and online environments to reduce suicide among SGM youth.