Claire Davidson, Shahela Islam, Enrico Venturini, Anja Lowit, Christopher Gillberg, Helen Minnis
Background
Children with Disinhibited Social Engagement Disorder (DSED) have specific difficulties with indiscriminate sociability, yet little is known about their broader social competencies as DSED tends not to be identified within samples in the wider ‘maltreatment literature.’
Aim
To systematically review the literature to determine the social competencies of children with DSED.
Methods
A comprehensive search following PRISMA guidelines was undertaken using PsycINFO, Medline, Embase, and Cumulative Index to Nursing & Allied Health.
Results
From a total of 553 articles, 16 studies were selected and critically evaluated. Children with DSED were consistently reported to have poorer social competencies than non-maltreated peers and environmental controls. Greater peer problems were consistently found, and they may present with poor self-esteem/concept related to social acceptance. Findings regarding social interaction/communication skills were mixed.
Limitations
50% of studies were of moderate quality due to sampling and possible confounding variables.
Conclusion
Children with DSED present with social relationship problems, beyond the core symptoms of the disorder, but the relative impact of co-occurring neurodevelopmental conditions is not yet clear. In addition, pragmatic language and communication skills require further research.
背景患有抑制性社交参与障碍（Disinhibited Social Engagement Disorder，DSED）的儿童在不加区分的社交方面有特殊的困难，但人们对他们更广泛的社交能力知之甚少，因为在更广泛的 "虐待文献 "中，DSED往往不会在样本中被识别出来。 目的 系统回顾文献以确定 DSED 儿童的社交能力。 方法 按照 PRISMA 指南，使用 PsycINFO、Medline、Embase 和 Cumulative Index to Nursing & Allied Health 进行全面检索。 结果 从总共 553 篇文章中筛选出 16 项研究并对其进行了严格评估。据报道，患有 DSED 的儿童的社交能力一直低于未接受治疗的同龄人和环境对照组。他们的同伴问题也越来越多，而且他们的自尊心/与社会接纳有关的观念也可能很差。有关社会交往/沟通技能的研究结果不一。 局限性 由于抽样和可能的混杂变量，50%的研究质量中等。 结论 DSED 患儿除患有该障碍的核心症状外，还存在社会关系问题，但并发神经发育疾病的相对影响尚不明确。此外，实用语言和沟通技能也需要进一步研究。
{"title":"Social competencies of children with disinhibited social engagement disorder: A systematic review","authors":"Claire Davidson, Shahela Islam, Enrico Venturini, Anja Lowit, Christopher Gillberg, Helen Minnis","doi":"10.1002/jcv2.12226","DOIUrl":"https://doi.org/10.1002/jcv2.12226","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Children with Disinhibited Social Engagement Disorder (DSED) have specific difficulties with indiscriminate sociability, yet little is known about their broader social competencies as DSED tends not to be identified within samples in the wider ‘maltreatment literature.’</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>To systematically review the literature to determine the social competencies of children with DSED.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A comprehensive search following PRISMA guidelines was undertaken using PsycINFO, Medline, Embase, and Cumulative Index to Nursing & Allied Health.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>From a total of 553 articles, 16 studies were selected and critically evaluated. Children with DSED were consistently reported to have poorer social competencies than non-maltreated peers and environmental controls. Greater peer problems were consistently found, and they may present with poor self-esteem/concept related to social acceptance. Findings regarding social interaction/communication skills were mixed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Limitations</h3>\u0000 \u0000 <p>50% of studies were of moderate quality due to sampling and possible confounding variables.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Children with DSED present with social relationship problems, beyond the core symptoms of the disorder, but the relative impact of co-occurring neurodevelopmental conditions is not yet clear. In addition, pragmatic language and communication skills require further research.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12226","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142170184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ivan Voronin, Isabelle Ouellet-Morin, Amélie Petitclerc, Geneviève Morneau-Vaillancourt, Mara Brendgen, Ginette Dione, Frank Vitaro, Michel Boivin
Background
Hyperactivity and inattention, the symptoms of ADHD, are marked by high levels of heritability and intergenerational transmission. Two distinct pathways of genetic intergenerational transmission are distinguished: direct genetic transmission when parental genetic variants are passed to the child's genome and genetic nurture when the parental genetic background contributes to the child's outcomes through rearing environment. This study assessed genetic contributions to hyperactivity and inattention in childhood through these transmission pathways.
Methods
The sample included 415 families from the Quebec Newborn Twin Study. Twins' hyperactivity and inattention were assessed in early childhood by parents and in primary school by teachers. The polygenic scores for ADHD (ADHD-PGS) and educational attainment (EA-PGS) were computed from twins' and parents' genotypes. A model of intergenerational transmission was developed to estimate (1) the contributions of parents' and children's PGS to the twins' ADHD symptoms and (2) whether these variances were explained by genetic transmission and/or genetic nurture.
Results
ADHD-PGS explained up to 1.6% of the variance of hyperactivity and inattention in early childhood and primary school. EA-PGS predicted ADHD symptoms at both ages, explaining up to 1.6% of the variance in early childhood and up to 5.5% in primary school. Genetic transmission was the only significant transmission pathway of both PGS. The genetic nurture channeled through EA-PGS explained up to 3.2% of the variance of inattention in primary school but this association was non-significant.
Conclusions
Genetic propensities to ADHD and education predicted ADHD symptoms in childhood, especially in primary school. Its intergenerational transmission was driven primarily by genetic variants passed to the child, rather than by environmentally mediated parental genetic effects. The model developed in this study can be leveraged in future research to investigate genetic transmission and genetic nurture while accounting for parental assortative mating.
{"title":"Intergenerational transmission of genetic risk for hyperactivity and inattention. Direct genetic transmission or genetic nurture?","authors":"Ivan Voronin, Isabelle Ouellet-Morin, Amélie Petitclerc, Geneviève Morneau-Vaillancourt, Mara Brendgen, Ginette Dione, Frank Vitaro, Michel Boivin","doi":"10.1002/jcv2.12222","DOIUrl":"10.1002/jcv2.12222","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Hyperactivity and inattention, the symptoms of ADHD, are marked by high levels of heritability and intergenerational transmission. Two distinct pathways of genetic intergenerational transmission are distinguished: direct genetic transmission when parental genetic variants are passed to the child's genome and genetic nurture when the parental genetic background contributes to the child's outcomes through rearing environment. This study assessed genetic contributions to hyperactivity and inattention in childhood through these transmission pathways.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The sample included 415 families from the Quebec Newborn Twin Study. Twins' hyperactivity and inattention were assessed in early childhood by parents and in primary school by teachers. The polygenic scores for ADHD (ADHD-PGS) and educational attainment (EA-PGS) were computed from twins' and parents' genotypes. A model of intergenerational transmission was developed to estimate (1) the contributions of parents' and children's PGS to the twins' ADHD symptoms and (2) whether these variances were explained by genetic transmission and/or genetic nurture.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>ADHD-PGS explained up to 1.6% of the variance of hyperactivity and inattention in early childhood and primary school. EA-PGS predicted ADHD symptoms at both ages, explaining up to 1.6% of the variance in early childhood and up to 5.5% in primary school. Genetic transmission was the only significant transmission pathway of both PGS. The genetic nurture channeled through EA-PGS explained up to 3.2% of the variance of inattention in primary school but this association was non-significant.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Genetic propensities to ADHD and education predicted ADHD symptoms in childhood, especially in primary school. Its intergenerational transmission was driven primarily by genetic variants passed to the child, rather than by environmentally mediated parental genetic effects. The model developed in this study can be leveraged in future research to investigate genetic transmission and genetic nurture while accounting for parental assortative mating.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12222","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140079988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The March 2024 issue of JCPP Advances features two neuroimaging studies that investigate links between early environmental risk factors for mental health problems, brain development and psychopathology in children and young adults. The papers provide new insights into how adverse environments and negative experiences in childhood increase risk for depression and mental health problems, and how this may or may not be mediated, or moderated, by individual differences in the brain.
{"title":"How early environment influences the developing brain and long-term mental health","authors":"Emma Sprooten","doi":"10.1002/jcv2.12230","DOIUrl":"https://doi.org/10.1002/jcv2.12230","url":null,"abstract":"<p>The March 2024 issue of JCPP Advances features two neuroimaging studies that investigate links between early environmental risk factors for mental health problems, brain development and psychopathology in children and young adults. The papers provide new insights into how adverse environments and negative experiences in childhood increase risk for depression and mental health problems, and how this may or may not be mediated, or moderated, by individual differences in the brain.</p>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12230","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140114354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Grace R. Jacobs, Stephanie H. Ameis, Peter Szatmari, John D. Haltigan, Aristotle N. Voineskos
Background
Due to limitations of categorical definitions of mental illness, there is a need for quantitative empirical investigations of the dimensional structure of psychopathology. Using exploratory bifactor methods, this study investigated a comprehensive and representative structure of psychopathology in children to better understand how psychotic-like experiences (PLEs), autism spectrum disorder (ASD) symptoms, impulsivity, and sensitivity to reward and punishment, may be integrated into extant general factor models of psychopathology.
Methods
We used seven child-report and three parent-report instruments capturing diverse mental health symptoms in 11,185 children aged 9–10 from the Adolescent Brain Cognitive DevelopmentSM (ABCD) Study. We built on previous modeling frameworks by conducting both split sample and full sample factor analytic approaches that harnessed recent methodological advances in bifactor exploratory structural equation modeling (B-ESEM) to examine a wide range of psychopathology measures not previously integrated into a single analysis. Validity of psychopathology dimensions was examined by investigating associations with sex, age, cognition, imaging measures, and medical service usage.
Results
All four factor analytic models showed excellent fit and similar structure within informant. PLEs loaded most highly onto a general psychopathology factor, suggesting that they may reflect non-specific risk for mental illness. ASD symptoms loaded separately from attention/hyperactivity symptoms. Symptoms of impulsivity and sensitivity to reward and punishment loaded onto specific factors, distinct from externalizing and internalizing factors. All identified factors were associated with clinically relevant risk factors, providing preliminary evidence for their construct validity.
Conclusion
By integrating diverse child-report and parent-report psychopathology measures for children in the ABCD sample, we deliver data on the quantitative structure of psychopathology for an exceptionally large set of measurements and discuss implications for the field.
{"title":"Bifactor models of psychopathology using multi-informant and multi-instrument dimensional measures in the ABCD study","authors":"Grace R. Jacobs, Stephanie H. Ameis, Peter Szatmari, John D. Haltigan, Aristotle N. Voineskos","doi":"10.1002/jcv2.12228","DOIUrl":"10.1002/jcv2.12228","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Due to limitations of categorical definitions of mental illness, there is a need for quantitative empirical investigations of the dimensional structure of psychopathology. Using exploratory bifactor methods, this study investigated a comprehensive and representative structure of psychopathology in children to better understand how psychotic-like experiences (PLEs), autism spectrum disorder (ASD) symptoms, impulsivity, and sensitivity to reward and punishment, may be integrated into extant general factor models of psychopathology.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used seven child-report and three parent-report instruments capturing diverse mental health symptoms in 11,185 children aged 9–10 from the Adolescent Brain Cognitive Development<sup>SM</sup> (ABCD) Study. We built on previous modeling frameworks by conducting both split sample and full sample factor analytic approaches that harnessed recent methodological advances in bifactor exploratory structural equation modeling (B-ESEM) to examine a wide range of psychopathology measures not previously integrated into a single analysis. Validity of psychopathology dimensions was examined by investigating associations with sex, age, cognition, imaging measures, and medical service usage.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>All four factor analytic models showed excellent fit and similar structure within informant. PLEs loaded most highly onto a general psychopathology factor, suggesting that they may reflect non-specific risk for mental illness. ASD symptoms loaded separately from attention/hyperactivity symptoms. Symptoms of impulsivity and sensitivity to reward and punishment loaded onto specific factors, distinct from externalizing and internalizing factors. All identified factors were associated with clinically relevant risk factors, providing preliminary evidence for their construct validity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>By integrating diverse child-report and parent-report psychopathology measures for children in the ABCD sample, we deliver data on the quantitative structure of psychopathology for an exceptionally large set of measurements and discuss implications for the field.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12228","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140429640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tracey Chau, Jeggan Tiego, Louise E. Brown, Olivia J. Mellahn, Beth P. Johnson, Aurina Arnatkeviciute, Ben D. Fulcher, Natasha Matthews, Mark A. Bellgrove
Background
Autistic traits are often reported to be elevated in children diagnosed with attention-deficit/hyperactivity disorder (ADHD). However, the distribution of subclinical autistic traits in children with ADHD has not yet been established; knowing this may have important implications for diagnostic and intervention processes. The present study proposes a preliminary model of the distribution of parent-reported ADHD and subclinical autistic traits in two independent samples of Australian children with and without an ADHD diagnosis.
Methods
Factor mixture modelling was applied to Autism Quotient and Conners' Parent Rating Scale – Revised responses from parents of Australian children aged 6–15 years who participated in one of two independent studies.
Results
A 2-factor, 2-class factor mixture model with class varying factor variances and intercepts demonstrated the best fit to the data in both discovery and replication samples. The factors corresponded to the latent constructs of ‘autism’ and ‘ADHD’, respectively. Class 1 was characterised by low levels of both ADHD and autistic traits. Class 2 was characterised by high levels of ADHD traits and low-to-moderate levels of autistic traits. The classes were largely separated along diagnostic boundaries. The largest effect size for differences between classes on the Autism Quotient was on the Social Communication subscale.
Conclusions
Our findings support the conceptualisation of ADHD as a continuum, whilst confirming the utility of current categorical diagnostic criteria. Results suggest that subclinical autistic traits, particularly in the social communication domain, are unevenly distributed across children with clinically significant levels of ADHD traits. These traits might be profitably screened for in assessments of children with high ADHD symptoms and may also represent useful targets for intervention.
{"title":"The distribution of parent-reported attention-deficit/hyperactivity disorder and subclinical autistic traits in children with and without an ADHD diagnosis","authors":"Tracey Chau, Jeggan Tiego, Louise E. Brown, Olivia J. Mellahn, Beth P. Johnson, Aurina Arnatkeviciute, Ben D. Fulcher, Natasha Matthews, Mark A. Bellgrove","doi":"10.1002/jcv2.12223","DOIUrl":"10.1002/jcv2.12223","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Autistic traits are often reported to be elevated in children diagnosed with attention-deficit/hyperactivity disorder (ADHD). However, the distribution of subclinical autistic traits in children with ADHD has not yet been established; knowing this may have important implications for diagnostic and intervention processes. The present study proposes a preliminary model of the distribution of parent-reported ADHD and subclinical autistic traits in two independent samples of Australian children with and without an ADHD diagnosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Factor mixture modelling was applied to Autism Quotient and Conners' Parent Rating Scale – Revised responses from parents of Australian children aged 6–15 years who participated in one of two independent studies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A 2-factor, 2-class factor mixture model with class varying factor variances and intercepts demonstrated the best fit to the data in both discovery and replication samples. The factors corresponded to the latent constructs of ‘autism’ and ‘ADHD’, respectively. Class 1 was characterised by low levels of both ADHD and autistic traits. Class 2 was characterised by high levels of ADHD traits and low-to-moderate levels of autistic traits. The classes were largely separated along diagnostic boundaries. The largest effect size for differences between classes on the Autism Quotient was on the Social Communication subscale.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our findings support the conceptualisation of ADHD as a continuum, whilst confirming the utility of current categorical diagnostic criteria. Results suggest that subclinical autistic traits, particularly in the social communication domain, are unevenly distributed across children with clinically significant levels of ADHD traits. These traits might be profitably screened for in assessments of children with high ADHD symptoms and may also represent useful targets for intervention.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12223","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140433946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the excitement about genomics, it is easy to lose sight of one of the most important findings from behavioural genetics: At least half of the variance of psychopathology is caused by environmental effects that are not shared by children growing up in the same family, which includes error of measurement. However, a 30-year search for the systematic causes of nonshared environment in a line-up of the usual suspects, especially parenting, has not identified the culprits.
Method
I briefly review this research, but primarily consider the conceptual framework of the search for ‘missing’ nonshared environmental effects.
Results
The search has focused on exogenous events like parenting, but nonshared environment might not be caused by anything we would call an event. Instead, it might reflect endogenous processes such as noisy biological systems (such as somatic mutations and epigenetics) or, at a psychological level, idiosyncratic subjective perceptions of past and present experiences, which could be called nonshared environmental experience to distinguish it from exogenous events. Although real, nonshared environment might be random in the philosophy of science sense of being unpredictable, even though it can have stable effects that predict subsequent behaviour.
Conclusion
I wade into the weeds of randomness and suggest that this so-called ‘gloomy prospect’ might not be so gloomy.
{"title":"Nonshared environment: Real but random","authors":"Robert Plomin","doi":"10.1002/jcv2.12229","DOIUrl":"10.1002/jcv2.12229","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>In the excitement about genomics, it is easy to lose sight of one of the most important findings from behavioural genetics: At least half of the variance of psychopathology is caused by environmental effects that are not shared by children growing up in the same family, which includes error of measurement. However, a 30-year search for the systematic causes of nonshared environment in a line-up of the usual suspects, especially parenting, has not identified the culprits.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>I briefly review this research, but primarily consider the conceptual framework of the search for ‘missing’ nonshared environmental effects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The search has focused on exogenous events like parenting, but nonshared environment might not be caused by anything we would call an event. Instead, it might reflect endogenous processes such as noisy biological systems (such as somatic mutations and epigenetics) or, at a psychological level, idiosyncratic subjective perceptions of past and present experiences, which could be called nonshared environmental <i>experience</i> to distinguish it from exogenous events. Although real, nonshared environment might be random in the philosophy of science sense of being unpredictable, even though it can have stable effects that predict subsequent behaviour.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>I wade into the weeds of randomness and suggest that this so-called ‘gloomy prospect’ might not be so gloomy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12229","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140440287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jaclyn Gunderson, Frank Symons, Nidhi Kohli, Rebecca Grzadzinski, Casey Burrows, Annette Estes, Stephen Dager, Joseph Piven, Jason Wolff, IBIS Network
Background
Empirical evidence regarding the development of sensory responsivity in young children at high likelihood to develop autism spectrum disorder (ASD) remains relatively limited. It is unclear how sensory responsivity behaviors may change over time and impact later developmental outcomes. The goals of this study were to (a) characterize developmental trajectories of sensory responsivity across infancy (∼12 months), toddlerhood (∼24 months), and school age (6–11 years) in children at high and low familial likelihood for ASD; and (b) determine if sensory responsivity in infancy predicts adaptive and cognitive functioning at school age among children with ASD.
Methods
Generalized linear mixed effects models were used to examine scores from the Sensory Experiences Questionnaire in three groups of children including high-likelihood children later diagnosed with ASD (HL-ASD; n = 30), high-likelihood children without ASD (HL-Neg; n = 150), and low-likelihood control children not meeting ASD diagnostic criteria (LL-Neg; n = 94). Hierarchical linear regression was then used to examine the association between sensory responsivity scores in infancy and functional adaptive and cognitive outcomes at school age for children at high likelihood of ASD.
Results
Development of sensory responsivity from infancy to later childhood is best estimated by the effects of chronological age and Group for Sensory Seeking and Hypo responsivity and the additional effect of the interaction of Group and chronological age for Total and Hyper responsivity. Early elevated Hypo responsivity and Sensory Seeking scores are negatively associated with later adaptive behavior but not cognitive level.
Conclusion
Overall, higher degrees of Sensory Seeking and Hypo sensory responsivity are detectable in autistic children's behavioral repertoires by 12 months of age and associate with reduced adaptive functioning in middle childhood. These results point to the potential importance of early detection and treatment implications of early sensory behaviors.
{"title":"Longitudinal analysis of sensory responsivity from infancy to school age in children at high and low familial likelihood for autism","authors":"Jaclyn Gunderson, Frank Symons, Nidhi Kohli, Rebecca Grzadzinski, Casey Burrows, Annette Estes, Stephen Dager, Joseph Piven, Jason Wolff, IBIS Network","doi":"10.1002/jcv2.12227","DOIUrl":"10.1002/jcv2.12227","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Empirical evidence regarding the development of sensory responsivity in young children at high likelihood to develop autism spectrum disorder (ASD) remains relatively limited. It is unclear how sensory responsivity behaviors may change over time and impact later developmental outcomes. The goals of this study were to (a) characterize developmental trajectories of sensory responsivity across infancy (∼12 months), toddlerhood (∼24 months), and school age (6–11 years) in children at high and low familial likelihood for ASD; and (b) determine if sensory responsivity in infancy predicts adaptive and cognitive functioning at school age among children with ASD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Generalized linear mixed effects models were used to examine scores from the Sensory Experiences Questionnaire in three groups of children including high-likelihood children later diagnosed with ASD (HL-ASD; <i>n</i> = 30), high-likelihood children without ASD (HL-Neg; <i>n</i> = 150), and low-likelihood control children not meeting ASD diagnostic criteria (LL-Neg; <i>n</i> = 94). Hierarchical linear regression was then used to examine the association between sensory responsivity scores in infancy and functional adaptive and cognitive outcomes at school age for children at high likelihood of ASD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Development of sensory responsivity from infancy to later childhood is best estimated by the effects of chronological age and Group for Sensory Seeking and Hypo responsivity and the additional effect of the interaction of Group and chronological age for Total and Hyper responsivity. Early elevated Hypo responsivity and Sensory Seeking scores are negatively associated with later adaptive behavior but not cognitive level.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Overall, higher degrees of Sensory Seeking and Hypo sensory responsivity are detectable in autistic children's behavioral repertoires by 12 months of age and associate with reduced adaptive functioning in middle childhood. These results point to the potential importance of early detection and treatment implications of early sensory behaviors.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12227","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140441944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Andreas Påhlsson-Notini, Shengxin Liu, Magnus Tideman, Antti Latvala, Eva Serlachius, Henrik Larsson, Tatja Hirvikoski, Mark J. Taylor, Ralf Kuja-Halkola, Paul Lichtenstein, Agnieszka Butwicka
Background
Evidence for substance use-related problems in individuals with mild intellectual disability is sparse and mainly limited to selected psychiatric populations. We evaluated the risk of substance use-related problems in individuals with mild intellectual disability compared to the general population. Additionally, we have performed secondary sibling comparison analyses to account for familial confounding.
Methods
We conducted a population-based cohort study of individuals born in Sweden between 1973 and 2003. A total of 18,307 individuals with mild intellectual disability were compared to 915,350 reference individuals from the general population and 18,996 full siblings of individuals with mild intellectual disability. Information on mild intellectual disability and substance use-related problems was obtained from several Swedish national and regional school and healthcare registers. Substance use-related problems were measured via corresponding diagnostic and legal codes and included alcohol use disorder, drug use disorder, alcohol-related somatic disease, conviction for a substance-related crime, and substance-related death.
Results
Individuals with mild intellectual disability had a higher risk of any substance use-related problem compared to the general population (HR, 1.81; 95% CI, 1.72–1.91), both in males (HR, 1.76; 95% CI, 1.65–1.89) and females (HR, 1.89; 95% CI, 1.74–2.05). The risks of substance use-related problems were particularly elevated among individuals with mild intellectual disability and psychiatric comorbidities (HR, 2.21–8.24). The associations were attenuated in the sibling comparison models.
Conclusions
Individuals with mild intellectual disability, especially those with psychiatric comorbidity, are at an elevated risk of substance use-related problems. Familial factors shared by full siblings contribute considerably to the association between mild intellectual disability and substance use-related problems.
{"title":"Substance use-related problems in mild intellectual disability: A Swedish nationwide population-based cohort study with sibling comparison","authors":"Andreas Påhlsson-Notini, Shengxin Liu, Magnus Tideman, Antti Latvala, Eva Serlachius, Henrik Larsson, Tatja Hirvikoski, Mark J. Taylor, Ralf Kuja-Halkola, Paul Lichtenstein, Agnieszka Butwicka","doi":"10.1002/jcv2.12225","DOIUrl":"10.1002/jcv2.12225","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Evidence for substance use-related problems in individuals with mild intellectual disability is sparse and mainly limited to selected psychiatric populations. We evaluated the risk of substance use-related problems in individuals with mild intellectual disability compared to the general population. Additionally, we have performed secondary sibling comparison analyses to account for familial confounding.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a population-based cohort study of individuals born in Sweden between 1973 and 2003. A total of 18,307 individuals with mild intellectual disability were compared to 915,350 reference individuals from the general population and 18,996 full siblings of individuals with mild intellectual disability. Information on mild intellectual disability and substance use-related problems was obtained from several Swedish national and regional school and healthcare registers. Substance use-related problems were measured via corresponding diagnostic and legal codes and included alcohol use disorder, drug use disorder, alcohol-related somatic disease, conviction for a substance-related crime, and substance-related death.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Individuals with mild intellectual disability had a higher risk of any substance use-related problem compared to the general population (HR, 1.81; 95% CI, 1.72–1.91), both in males (HR, 1.76; 95% CI, 1.65–1.89) and females (HR, 1.89; 95% CI, 1.74–2.05). The risks of substance use-related problems were particularly elevated among individuals with mild intellectual disability and psychiatric comorbidities (HR, 2.21–8.24). The associations were attenuated in the sibling comparison models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Individuals with mild intellectual disability, especially those with psychiatric comorbidity, are at an elevated risk of substance use-related problems. Familial factors shared by full siblings contribute considerably to the association between mild intellectual disability and substance use-related problems.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12225","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139959541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anne Dorothee Müller, Ida Christine Tholstrup Gjøde, Nikolaj Thams, Sidsel Ingversen, Mala Moszkowicz, Jens Richardt Møllegaard Jepsen, Lisbeth Juhl Mikkelsen, Signe Sofie Nielsen, Nicoline Hemager, Merete Nordentoft, Anne A. E. Thorup
Background
Children of parents with a severe mental illness have an increased risk of developing a lifetime mental illness. We aimed to compare the effects of a preventive family-based intervention, VIA Family, with treatment as usual (TAU) on these children's global functioning.
Methods
Between 2017 and 2021, we conducted a pragmatic, rater-blinded, two-arm parallel-group superiority trial in Denmark. Families with at least one child aged 6–12 years and at least one biological parent with schizophrenia spectrum disorder, bipolar disorder, or recurrent major or moderate depression were included. We randomly allocated 95 families with their 113 children to VIA Family or TAU (ratio 1:1). VIA Family was individually tailored and based on case management. The intervention included options for psychoeducation, parental support, and treatment for emerging child psychiatric symptoms. Blinded raters assessed children and their families at baseline and after 18 months. The primary outcome was the difference in change between groups at end-of-treatment in daily global functioning measured with the Children's Global Assessment Scale. Secondary outcomes were emotional and behavioral problems and days absent from school. We analyzed data blinded to allocation.
Results
At post-intervention, differences in mean change from baseline between VIA Family and TAU were non-significant (CGAS: −1.20, 95% CI = −6.61; 4.21, p = 0.66), as were the differences on the secondary and exploratory outcomes.
Conclusion
Contrary to our hypothesis, we did not find a superior effect of VIA Family compared with TAU. The short follow-up period and large sample heterogeneity might explain the null findings. Therefore, a possible long-term, preventive treatment effect has yet to be explored.
父母患有严重精神疾病的儿童终生罹患精神疾病的风险会增加。2017年至2021年期间，我们在丹麦开展了一项务实、评分者盲法、双臂平行组优效试验。试验对象包括至少有一名6-12岁儿童、至少有一名亲生父母患有精神分裂症谱系障碍、双相情感障碍或复发性重度或中度抑郁症的家庭。我们将 95 个家庭及其 113 名儿童随机分配到 VIA 家庭或 TAU（比例为 1:1）。VIA 家庭 "以个案管理为基础，为每个家庭量身定制。干预措施包括心理教育、父母支持和治疗新出现的儿童精神症状。蒙眼评定员在基线和 18 个月后对儿童及其家庭进行评估。主要结果是治疗结束时各组在儿童整体评估量表测量的日常整体功能方面的变化差异。次要结果是情绪和行为问题以及缺课天数。与我们的假设相反，我们没有发现 VIA 家庭治疗与 TAU 治疗相比有更好的效果。与我们的假设相反，我们并没有发现 VIA Family 比 TAU 更优越的效果。随访时间短和样本异质性大可能是导致结果无效的原因。因此，可能的长期预防性治疗效果还有待探索。
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Anne Dorothee Müller, I. C. T. Gjøde, Nikolaj Thams, Sidsel Ingversen, Mala Moszkowicz, J. Jepsen, L. J. Mikkelsen, S. S. Nielsen, N. Hemager, M. Nordentoft, A. Thorup
Children of parents with a severe mental illness have an increased risk of developing a lifetime mental illness. We aimed to compare the effects of a preventive family‐based intervention, VIA Family, with treatment as usual (TAU) on these children's global functioning.Between 2017 and 2021, we conducted a pragmatic, rater‐blinded, two‐arm parallel‐group superiority trial in Denmark. Families with at least one child aged 6–12 years and at least one biological parent with schizophrenia spectrum disorder, bipolar disorder, or recurrent major or moderate depression were included. We randomly allocated 95 families with their 113 children to VIA Family or TAU (ratio 1:1). VIA Family was individually tailored and based on case management. The intervention included options for psychoeducation, parental support, and treatment for emerging child psychiatric symptoms. Blinded raters assessed children and their families at baseline and after 18 months. The primary outcome was the difference in change between groups at end‐of‐treatment in daily global functioning measured with the Children's Global Assessment Scale. Secondary outcomes were emotional and behavioral problems and days absent from school. We analyzed data blinded to allocation.At post‐intervention, differences in mean change from baseline between VIA Family and TAU were non‐significant (CGAS: −1.20, 95% CI = −6.61; 4.21, p = 0.66), as were the differences on the secondary and exploratory outcomes.Contrary to our hypothesis, we did not find a superior effect of VIA Family compared with TAU. The short follow‐up period and large sample heterogeneity might explain the null findings. Therefore, a possible long‐term, preventive treatment effect has yet to be explored.
父母患有严重精神疾病的儿童终生罹患精神疾病的风险会增加。2017年至2021年期间，我们在丹麦开展了一项务实、评分者盲法、双臂平行组优效试验。试验对象包括至少有一名6-12岁儿童、至少有一名亲生父母患有精神分裂症谱系障碍、双相情感障碍或复发性重度或中度抑郁症的家庭。我们将 95 个家庭及其 113 名儿童随机分配到 VIA 家庭或 TAU（比例为 1:1）。VIA 家庭 "以个案管理为基础，为每个家庭量身定制。干预措施包括心理教育、父母支持和治疗新出现的儿童精神症状。蒙眼评定员在基线和 18 个月后对儿童及其家庭进行评估。主要结果是治疗结束时各组在儿童整体评估量表测量的日常整体功能方面的变化差异。次要结果是情绪和行为问题以及缺课天数。与我们的假设相反，我们没有发现 VIA 家庭治疗与 TAU 治疗相比有更好的效果。与我们的假设相反，我们并没有发现 VIA Family 比 TAU 更优越的效果。随访时间短和样本异质性大可能是导致结果无效的原因。因此，可能的长期预防性治疗效果还有待探索。
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