Explore the vast range of titles available.

The past decade has evinced a boom of computer-based approaches to aid movement assessment in early infancy. Increasing interests have been dedicated to develop AI driven approaches to complement the classic Prechtl general movements assessment (GMA). This study proposes a novel machine learning algorithm to detect an age-specific movement pattern, the fidgety movements (FMs), in a prospectively collected sample of typically developing infants. Participants were recorded using a passive, single camera RGB video stream. The dataset of 2800 five-second snippets was annotated by two well-trained and experienced GMA assessors, with excellent inter- and intra-rater reliabilities. Using OpenPose, the infant full pose was recovered from the video stream in the form of a 25-points skeleton. This skeleton was used as input vector for a shallow multilayer neural network (SMNN). An ablation study was performed to justify the network’s architecture and hyperparameters. We show for the first time that the SMNN is sufficient to discriminate fidgety from non-fidgety movements in a sample of age-specific typical movements with a classification accuracy of 88%. The computer-based solutions will complement original GMA to consistently perform accurate and efficient screening and diagnosis that may become universally accessible in daily clinical practice in the future.

Environmental adversities constitute potent risk factors for psychiatric disorders. Evidence suggests the brain adapts to adversity, possibly in an adversity-type and region-specific manner. However, the long-term effects of adversity on brain structure and the association of individual neurobiological heterogeneity with behavior have yet to be elucidated. Here we estimated normative models of structural brain development based on a lifespan adversity profile in a longitudinal at-risk cohort aged 25 years ( n  = 169). This revealed widespread morphometric changes in the brain, with partially adversity-specific features. This pattern was replicated at the age of 33 years ( n  = 114) and in an independent sample at 22 years ( n  = 115). At the individual level, greater volume contractions relative to the model were predictive of future anxiety. We show a stable neurobiological signature of adversity that persists into adulthood and emphasize the importance of considering individual-level rather than group-level predictions to explain emerging psychopathology. In a birth cohort, Holz et al. found widespread structural brain changes at the age of 25 years as a function of adversity. This pattern was replicated at the age of 33 years and in another cohort. Individual-level volume reductions on top of this pattern predicted anxiety.

Chronic peer victimization has long-term impacts on mental health; however, the biological mediators of this adverse relationship are unknown. We sought to determine whether adolescent brain development is involved in mediating the effect of peer victimization on psychopathology. We included participants (n = 682) from the longitudinal IMAGEN study with both peer victimization and neuroimaging data. Latent profile analysis identified groups of adolescents with different experiential patterns of victimization. We then associated the victimization trajectories and brain volume changes with depression, generalized anxiety, and hyperactivity symptoms at age 19. Repeated measures ANOVA revealed time-by-victimization interactions on left putamen volume (F = 4.38, p = 0.037). Changes in left putamen volume were negatively associated with generalized anxiety (t = −2.32, p = 0.020). Notably, peer victimization was indirectly associated with generalized anxiety via decreases in putamen volume (95% CI = 0.004–0.109). This was also true for the left caudate (95% CI = 0.002–0.099). These data suggest that the experience of chronic peer victimization during adolescence might induce psychopathology-relevant deviations from normative brain development. Early peer victimization interventions could prevent such pathological changes.

Mental disorders represent an increasing personal and financial burden and yet treatment development has stagnated in recent decades. Current disease classifications do not reflect psychobiological mechanisms of psychopathology, nor the complex interplay of genetic and environmental factors, likely contributing to this stagnation. Ten years ago, the longitudinal IMAGEN study was designed to comprehensively incorporate neuroimaging, genetics, and environmental factors to investigate the neural basis of reinforcement-related behavior in normal adolescent development and psychopathology. In this article, we describe how insights into the psychobiological mechanisms of clinically relevant symptoms obtained by innovative integrative methodologies applied in IMAGEN have informed our current and future research aims. These aims include the identification of symptom groups that are based on shared psychobiological mechanisms and the development of markers that predict disease course and treatment response in clinical groups. These improvements in precision medicine will be achieved, in part, by employing novel methodological tools that refine the biological systems we target. We will also implement our approach in low- and medium-income countries to understand how distinct environmental, socioeconomic, and cultural conditions influence the development of psychopathology. Together, IMAGEN and related initiatives strive to reduce the burden of mental disorders by developing precision medicine approaches globally.

Diagnosing autism spectrum disorders (ASD) is a complicated, time-consuming process which is particularly challenging in older individuals. One of the most widely used behavioral diagnostic tools is the Autism Diagnostic Observation Schedule (ADOS). Previous work using machine learning techniques suggested that ASD detection in children can be achieved with substantially fewer items than the original ADOS. Here, we expand on this work with a specific focus on adolescents and adults as assessed with the ADOS Module 4. We used a machine learning algorithm (support vector machine) to examine whether ASD detection can be improved by identifying a subset of behavioral features from the ADOS Module 4 in a routine clinical sample of N = 673 high-functioning adolescents and adults with ASD (n = 385) and individuals with suspected ASD but other best-estimate or no psychiatric diagnoses (n = 288). We identified reduced subsets of 5 behavioral features for the whole sample as well as age subgroups (adolescents vs. adults) that showed good specificity and sensitivity and reached performance close to that of the existing ADOS algorithm and the full ADOS, with no significant differences in overall performance. These results may help to improve the complicated diagnostic process of ASD by encouraging future efforts to develop novel diagnostic instruments for ASD detection based on the identified constructs as well as aiding clinicians in the difficult question of differential diagnosis.

Recent studies proposed a general psychopathology factor underlying common comorbidities among psychiatric disorders. However, its neurobiological mechanisms and generalizability remain elusive. In this study, we used a large longitudinal neuroimaging cohort from adolescence to young adulthood (IMAGEN) to define a neuropsychopathological (NP) factor across externalizing and internalizing symptoms using multitask connectomes. We demonstrate that this NP factor might represent a unified, genetically determined, delayed development of the prefrontal cortex that further leads to poor executive function. We also show this NP factor to be reproducible in multiple developmental periods, from preadolescence to early adulthood, and generalizable to the resting-state connectome and clinical samples (the ADHD-200 Sample and the STRATIFY & ESTRA Project). In conclusion, we identify a reproducible and general neural basis underlying symptoms of multiple mental health disorders, bridging multidimensional evidence from behavioral, neuroimaging and genetic substrates. These findings may help to develop new therapeutic interventions for psychiatric comorbidities. Evidence from large longitudinal neuroimaging cohorts, which include genetic and behavioral data, suggest a common neural basis for symptoms seen across multiple psychiatric disorders.

Autism Spectrum Disorder (ASD) is often characterized by deficits in emotion regulation and empathic abilities, potentially linked to alterations in prefrontal brain regions. This randomized, controlled clinical trial examines the efficacy of slow cortical potential neurofeedback training, specifically targeting these prefrontal areas, in improving emotion regulation and empathy among children and adolescents with ASD. The study involved 41 participants, with 21 undergoing slow cortical potential training and 20 receiving treatment as usual. All participants were allowed to continue usual care in progress, if it was kept stable. Emotional processing was evaluated using an adapted and extended version of the Multifaceted Empathy Test, alongside electroencephalography assessments focusing on event-related potentials, including N170, LPP, and P300 components. The main findings indicate a significant group × time interaction in P300 latency, with shorter latencies in the SCP neurofeedback group and longer latencies in controls, though post hoc tests were not significant. A trend toward reduced P300 amplitude in the experimental group suggests possible modulation of attentional processing. Additionally, changes in a late component of LPP amplitude were linked to reaction time in processing positive emotions, with increases associated with slower responses and decreases with faster responses. These results suggest slow cortical potential neurofeedback training may influence cognitive efficiency and emotional processing in autistic individuals. While promising, further research is needed to confirm these findings and optimize neurofeedback protocols for this population.

The causes of aggressive behavior in children with autism are poorly understood, which limits treatment options. Therefore, this study used behavioral testing and parent reports of 60 children with autism to investigate the interplay of emotion misinterpretation and hostile attribution bias in the prediction of different aggressive behaviors. Further, the additional impact of dysfunctional emotion regulation was examined. Path analyses indicated that hostile attribution bias increased verbal and covert aggression but not physical aggression and bullying. Dysfunctional emotion regulation had an additional impact on bullying, verbal aggression, and covert aggression. Emotion recognition was positively associated with hostile attribution bias. These findings provide a first insight into a complex interplay of socio-emotional variables; longitudinal studies are needed to examine causal relationships.

Autism spectrum disorders (ASD) are associated with high services use, but European data on costs are scarce. Utilisation and annual costs of 385 individuals with ASD (aged 4–67 years; 18.2% females; 37.4% IQ < 85) from German outpatient clinics were assessed. Average annual costs per person were 3287 EUR, with psychiatric inpatient care (19.8%), pharmacotherapy (11.1%), and occupational therapy (11.1%) being the largest cost components. Females incurred higher costs than males (4864 EUR vs. 2936 EUR). In a regression model, female sex (Cost Ratio: 1.65), lower IQ (1.90), and Asperger syndrome (1.54) were associated with higher costs. In conclusion, ASD-related health costs are comparable to those of schizophrenia, thus underlining its public health relevance. Higher costs in females demand further research.

Imaging genetics offers the possibility of detecting associations between genotype and brain structure as well as function, with effect sizes potentially exceeding correlations between genotype and behavior. However, study results are often limited due to small sample sizes and methodological differences, thus reducing the reliability of findings. The IMAGEN cohort with 2000 young adolescents assessed from the age of 14 onwards tries to eliminate some of these limitations by offering a longitudinal approach and sufficient sample size for analyzing gene-environment interactions on brain structure and function. Here, we give a systematic review of IMAGEN publications since the start of the consortium. We then focus on the specific phenotype ‘drug use’ to illustrate the potential of the IMAGEN approach. We describe findings with respect to frontocortical, limbic and striatal brain volume, functional activation elicited by reward anticipation, behavioral inhibition, and affective faces, and their respective associations with drug intake. In addition to describing its strengths, we also discuss limitations of the IMAGEN study. Because of the longitudinal design and related attrition, analyses are underpowered for (epi-) genome-wide approaches due to the limited sample size. Estimating the generalizability of results requires replications in independent samples. However, such densely phenotyped longitudinal studies are still rare and alternative internal cross-validation methods (e.g., leave-one out, split-half) are also warranted. In conclusion, the IMAGEN cohort is a unique, very well characterized longitudinal sample, which helped to elucidate neurobiological mechanisms involved in complex behavior and offers the possibility to further disentangle genotype × phenotype interactions.