Mental Disorder During Adolescence:Evidence of Arrested Personality Development

The experience of a mental disorder may affect the development of personality in multiple ways, but empirical evidence regarding psychopathology effects on personality development that persist after remission of the disorder is limited and inconsistent. In the longitudinal cohort TRacking Adolescents' Individual Lives Survey (TRAILS), mental disorders during adolescence were assessed using the Composite International Diagnostic Interview and parent-reported effortful control, fearfulness, and frustration at age 11 and age 19 through the Early Adolescent Temperament Questionnaire. We found that adolescent mental disorders had small effects on personality change. Internalizing disorders predicted increases of fearfulness and frustration but hardly affected effortful control; externalizing disorders were unrelated to frustration and fearfulness but predicted a decrease of effortful control. Whereas fearfulness and frustration partially caught up after disorder remission, virtually all delay in effortful control was still present 2.9 years later, suggesting scarring effects

The association of developmental trajectories of adolescent mental health with early-adult functioning

BACKGROUND: Mental health problems during adolescence may create a problematic start into adulthood for affected individuals. Usually, categorical indicators of adolescent mental health issues (yes/no psychiatric disorder) are used in studies into long-term functional outcomes. This however does not take into account the full spectrum of mental health, nor does it consider the trajectory of mental health problem development over time. The aim of this study was twofold: (1) to identify distinct developmental trajectories of (co-occurring) internalizing and externalizing mental health symptoms over the course of adolescence (ages 11-19), and (2) to document the associations between these adolescent trajectories and economic, social, and health outcomes in young adulthood (age 22), unadjusted and adjusted for childhood functioning, putative confounders and current mental health. METHODS: Data were used from the Dutch TRAILS cohort study (subsample n = 1524, 47.3% males). Self-reported INT and EXT symptoms using the Youth/Adult Self Report were assessed four times (ages 11y, 13y, 16y, 19y). Adolescent mental health trajectories were estimated using Parallel-Processes Latent Class Growth Analyses. Self-reported economic, social, and health outcomes and parent-reported current mental health (using Adult Behaviour Checklist) were assessed at age 22. Multiple logistic regression analyses were performed to test associations between trajectories and outcomes. RESULTS: Four distinct trajectory classes were identified: (1) a normative class with decreasing-low INT+EXT symptoms (n = 460), (2) continuous moderately-high INT+EXT (n = 298), (3) continuous moderate, INT>EXT (n = 414), and (4) decreasing moderate, EXT>INT (n = 352). Compared to the normative class, the other three trajectories generally predicted less optimal early-adult outcomes, with the strongest effects observed for individuals with continuous moderate-high levels of both INT and EXT symptoms throughout adolescence. The associations largely remained after adjustment for pre-adolescent functioning, selected confounders and current mental health. CONCLUSIONS: Both adolescent trajectories and current mental health had substantial independent effects on early-adult functioning

Does the cognitive architecture of simplex and multiplex ASD families differ?

Contains fulltext : 167741.pdf (publisher's version ) (Open Access)Children with an autism spectrum disorder (ASD) and their unaffected siblings from 54 simplex (SPX, one individual in the family affected) and 59 multiplex (MPX, two or more individuals affected) families, and 124 controls were assessed on intelligence, social cognition and executive functions. SPX and MPX ASD probands displayed similar cognitive profiles, but within-family contrasts were highest in SPX families, suggesting SPX-MPX stratification may help parse etiological heterogeneity of ASD. Unaffected siblings (regardless SPX or MPX) were mostly unimpaired, suggesting that cognitive problems may be part of the defining features of ASD, rather than being an endophenotypic trait. Except for affective prosody, which appeared to be the most sensitive cognitive marker for detecting familial risk for ASD

Identifying Unique Versus Shared Pre- and Perinatal Risk Factors for ASD and ADHD Using a Simplex-Multiplex Stratification

Contains fulltext : 167866.pdf (publisher's version ) (Open Access)Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) frequently co-occur. Besides shared genetic factors, pre- and perinatal risk factors (PPFs) may determine if ASD, ADHD, or the combination of both disorders becomes manifest. This study aimed to test shared and unique involvement of PPFs for ASD and ADHD, using an approach that stratifies the sample into affected/unaffected offspring and single-incidence (SPX) versus multi-incidence (MPX) families. Pre- perinatal data based on retrospective parent-report were collected in 288 children (71 % males) from 31 SPX and 59 MPX ASD families, 476 children (65 % males) from 31 SPX and 171 MPX ADHD families, and 408 control children (42 % males). Except for large family size and more firstborns amongst affected offspring, no shared PFFs were identified for ASD and ADHD. PPFs predominantly related to ASD (maternal infections and suboptimal condition at birth) were more often reported in affected than unaffected siblings. PPFs associated with ADHD (low parental age, maternal diseases, smoking and stress) were shared between affected and unaffected siblings. Firstborn-ship was more frequent in SPX than MPX ASD probands. Our results suggest that the co-morbidity of ASD and ADHD is not likely explained by shared PPFs. Instead, PPFs might play a crucial role in the developmental pathways leading up to either disorder. PPFs in ADHD appear to index an increased shared risk, whereas in ASD PPFs possibly have a more determining role in the disorder. SPX-MPX stratification detected possible etiological differences in ASD families, but provided no deeper insight in the role of PPFs in ADHD

A Causal and Mediation Analysis of the Comorbidity Between Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD)

Contains fulltext : 173171.pdf (publisher's version ) (Open Access

How 'core' are motor timing difficulties in ADHD? A latent class comparison of pure and comorbid ADHD classes

Contains fulltext : 167849.pdf (publisher's version ) (Open Access)Children with attention-deficit/hyperactivity disorder (ADHD) have motor timing difficulties. This study examined whether affected motor timing accuracy and variability are specific for ADHD, or that comorbidity with autism spectrum disorders (ASD) contributes to these motor timing difficulties. An 80-trial motor timing task measuring accuracy (mu), variability (sigma) and infrequent long response times (tau) in estimating a 1-s interval was administered to 283 children and adolescents (8-17 years) from both a clinic and population based sample. They were divided into four latent classes based on the SCQ and CPRS-R:L data. These classes were: without behavioral problems 'Normal-class' (n = 154), with only ADHD symptoms 'ADHD-class' (n = 49), and two classes with both ASD and ADHD symptoms; ADHD(+ASD)-class (n = 39) and ASD(+ADHD)-class (n = 41). The pure ADHD-class did not deviate from the Normal class on any of the motor timing measures (mean RTs 916 and 925 ms, respectively). The comorbid ADHD(+ASD) and ASD(+ADHD) classes were significantly less accurate (more time underestimations) compared to the Normal class (mean RTs 847 and 870 ms, respectively). Variability in motor timing was reduced in the younger children in the ADHD(+ASD) class, which may reflect a tendency to rush the tedious task. Only patients with more severe behavioral symptoms show motor timing deficiencies. This cannot merely be explained by high ADHD severity with ASD playing no role, as ADHD symptom severity in the pure ADHD-class and the ASD(+ADHD) class was highly similar, with the former class showing no motor timing deficits

Why employees and managers engage in unethical practices

The scope of this paper is to investigate the reasons as to why employees and managers in the workplace engage willingly in unethical practices. The paper begins by exploring the concept of ethics in the corporate world. It further highlights the different forms of unethical practices in the various companies in the contemporary world. The various theories that explore the issue of unethical practices in the workplace are highlighted and how they relate to the occurrence of unethical demeanor. The social contract theory and the psychological theories are highlighted in the paper. The study further delves in exploring the various types of reasons as depicted in different forms of literature in the world. The reasons include the pressure for performance at work, the effect of groupthink in the workplace, pressure from management, management control, demographic factors, and psychological traps, broken window theory. The paper also recommends the executive techniques that can be used to curb the psychological traps in the corporations. The paper also explores the broken window theory as a cause for unethical practices in the workplace. In conclusion, the paper comes up with recommendations for corporations

The co-occurrence of autism spectrum disorder and attention-deficit/hyperactivity disorder symptoms in parents of children with ASD or ASD with ADHD

Background: Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) share about 50-72% of their genetic factors, which is the most likely explanation for their frequent co-occurrence within the same patient or family. An additional or alternative explanation for the co-occurrence may be (cross-)assortative mating, e.g., the tendency to choose a partner that is similar or dissimilar to oneself. Another issue is that of parent-of-origin effect which refers to the possibility of parents differing in the relative quantity of risk factors they transmit to the offspring. The current study sets out to examine (cross-)assortative mating and (cross-)parent-of-origin effects of ASD and ADHD in parents of children with either ASD or ASD with ADHD diagnosis. Methods: In total, 121 families were recruited in an ongoing autism-ADHD family genetics project. Participating families consisted of parents and at least one child aged between 2 and 20 years, with either autistic disorder, Asperger disorder or PDD-NOS, and one or more biological siblings. All children and parents were carefully screened for the presence of ASD and ADHD. Results: No correlations were found between maternal and paternal ASD and ADHD symptoms. Parental ASD and ADHD symptoms were predictive for similar symptoms in the offspring, but with maternal hyperactive-impulsive symptoms, but not paternal symptoms, predicting similar symptoms in daughters. ASD pathology in the parents was not predictive for ADHD pathology in the offspring, but mother's ADHD pathology was predictive for offspring ASD pathology even when corrected for maternal ASD pathology. Conclusions: Cross-assortative mating for ASD and ADHD does not form an explanation for the frequent co-occurrence of these disorders within families. Given that parental ADHD is predictive of offspring' ASD but not vice versa, risk factors underlying ASD may overlap to a larger degree with risk factors underlying ADHD than vice versa. However, future research is needed to clarify this issue. Keywords: Assortative mating, parent-of-origin effect, autism spectrum disorder, attention-deficit/hyperactivity disorder

Examining the intertwined development of prosocial skills and ASD symptoms in adolescence

Autism spectrum disorder (ASD) and reduced prosocial behaviour are strongly intertwined. However, social interactions with peers may be increasingly practiced over the course of development and may instigate a reduction in ASD symptoms and vice versa. We, therefore, sought to determine if, during adolescence, possible improvements in prosocial behaviours and ASD symptoms may benefit one another over time. Participants were 2773 adolescents from the Tracking Adolescents' Individual Lives Survey (TRAILS) cohorts. Measurements took place over three waves (mean ages: 11.1, 13.4, and 16.2 years). Longitudinal associations between teacher-rated classroom prosocial skills and parent-rated ASD symptoms were examined using the random intercept cross-lagged panel model (RI-CLPM). In addition to estimating the stable, between-person associations, the dynamical effects between prosocial skills and ASD symptoms over time were estimated at the within-person level. At the between-person level, prosocial skills and ASD symptoms were substantially negatively correlated. At the within-person level, a small and unexpected positive cross-lagged effect from wave 1 ASD symptoms on wave 2 prosocial skills was observed. We added to the existing literature by showing that, in addition to replicating the already firmly established between-person association between low prosocial skills and ASD, within-person gains in prosocial skills do not lead to subsequent reduction of ASD symptoms, and reductions in ASD symptoms do not lead to subsequent enhancement of prosocial skills. We, therefore, conclude from our findings that the inverse association between autistic symptoms and prosocial skills in adolescence is highly stable