Neurodiversity and Autism - A Critical Examination of a Popular Concept Abstract: Neurodiversity refers to the natural diversity of human beings and thus emphasizes the natural range of differences between people. As simple, convincing, and popular as this assumption is, the interpretations, conclusions, and implications of this statement are just as varied. This article focuses on the scientific basis of the concept, on the one hand, and on autism and divergence, on the other. It outlines the implications regarding biological determinism, identity, and the effects on diagnosis and therapy, and examines and critically reflects on the demands arising from the concept. The author concludes that the claim of "neurological difference" posited in the context of neurodiversity - which asserts a fundamental, innate distinctiveness and, at the same time, a specific mode of functioning, as well as the determination of a person´s identity by these factors - has not been sufficiently substantiated by empirical research. Clinical evidence regarding the etiology, heterogeneity, course, and changeability of the diagnoses encompassed by this concept is not compatible with the assumed determinism regarding a person´s identity. Neurodiversity is an important approach to reducing stigmatization and promoting acceptance of difference, but diversity should not be limited by new stereotypes, and in-group-out-group processes are not helpful regarding acceptance, openness, and tolerance. Diagnoses instrumentalized in the sense of identity formation, stabilization, and justification for otherness do not imply an appreciative attitude toward those whose deficits, limited behavioral and developmental possibilities, suffering, and impairments are described by the diagnoses.

Neurodiversity refers to the natural diversity of human beings and thus emphasizes the natural range of differences between people. As simple, convincing, and popular as this assumption is, the interpretations, conclusions, and implications of this statement are just as varied. This article focuses on the scientific basis of the concept, on the one hand, and on autism and divergence, on the other. It outlines the implications regarding biological determinism, identity, and the effects on diagnosis and therapy, and examines and critically reflects on the demands arising from the concept. The author concludes that the claim of "neurological difference" posited in the context of neurodiversity - which asserts a fundamental, innate distinctiveness and, at the same time, a specific mode of functioning, as well as the determination of a persons identity by these factors - has not been sufficiently substantiated by empirical research. Clinical evidence regarding the etiology, heterogeneity, course, and changeability of the diagnoses encompassed by this concept is not compatible with the assumed determinism regarding a persons identity. Neurodiversity is an important approach to reducing stigmatization and promoting acceptance of difference, but diversity should not be limited by new stereotypes, and in-group-out-group processes are not helpful regarding acceptance, openness, and tolerance. Diagnoses instrumentalized in the sense of identity formation, stabilization, and justification for otherness do not imply an appreciative attitude toward those whose deficits, limited behavioral and developmental possibilities, suffering, and impairments are described by the diagnoses.

Functional near-infrared spectroscopy (fNIRS) has become a well-established tool for neuroscience research and been suggested as a potential biomarker during clinical assessment in individuals with mental disorders. Biomarker need to be objective indications of biological processes which can be measured accurately and reproducibly. Despite various applications in clinical research, test-retest reliability of the fNIRS signal has not yet been evaluated sufficiently. To assess reliability of the fNIRS signal during tasks of executive functions, a group of 34 healthy subjects (13 male, 21 female) were tested twice for inhibitory control and working memory. On a group level results show a specific activation pattern throughout the two sessions, reflecting a task-related frontal network associated with the assessed cognitive functions. On the individual level the retest reliability of the activation patterns were considerably lower and differed strongly between participants. In conclusion, the interpretation of fNIRS signal on a single subject level is partially hampered by its low reliability. More studies are needed to optimize the retest reliability of fNIRS and to be applied on a routine basis in developmental research.

BACKGROUND:Autism spectrum disorder (ASD) is a persistent neu - rodevelopmental condition characterized by impaired social communication and the presence of restricted, repetitive patterns of behavior, typically manifesting in early childhood. The rising prevalence of ASD has been discussed in relation to increased media consumption. METHODS:A selective literature search was conducted in the Medline database on the topics of media consumption and mental disorders, particularly autism, in preschool children. Seven systematic reviews and meta-analyses and 36 original studies were included in the analysis. RESULTS:The findings across studies consistently demonstrated that media consumption in preschool children was associated with deficits in language and cognitive development (adjusted odds ratio [aOR] 1.67-2.28) and was a risk factor for the development of emotional, behavioral, and developmental disorders (aOR: 1.34-3.06). Symptoms consistent with ASD were also found to be associated with increased media consumption (OR 1.97, 95% confidence interval [1.30; 3.00]). However, these observed effects were consistently identified in the context of multiple other risk factors for mental health problems-such as low socioeconomic status, a family history of mental disorders, or parental stress-which mediated these effects, either directly or indirectly. Intervention studies showed that reducing media consumption, combined with an increase in constructive parent-child interactions, led to a reduction in symptom severity. CONCLUSION:In the context of additional risk factors, increased media consumption in young children is associated with atypical or delayed development. The extent of developmental disorders can be reduced through targeted support for parents. When risk factors are present, it is therefore essential to educate parents and implement preventive measures to promote the long-term healthy development of children.

Background. Dropout from healthcare interventions can negatively affect patients and healthcare providers through impaired trust in the healthcare system and ineffective use of resources. Research on this topic is still largely missing on refugees and asylum seekers. The current study aimed to characterize predictors for dropout in the Mental Health in Refugees and Asylum Seekers (MEHIRA) study, one of the largest multicentered controlled trials investigating the effectiveness and cost-effectiveness of a nationwide stepped and collaborative care model. Methods. Predictors were multiply imputed and selected for descriptive modelling using backward elimination. The final variable set was entered into logistic regression. Results. The overall dropout rate was 41,7%. Dropout was higher in participants in group therapy ( p = 0.001; OR = 10.7), with larger satisfaction with social relationships ( p = 0.017; OR = 1.87), with difficulties in maintaining personal relationships ( p = 0.005; OR = 4.27), and with higher depressive symptoms ( p = 0.029; OR = 1.05). Participants living in refugee accommodation ( p = 0.040; OR = 0.45), with a change in social status ( p = 0.008; OR = 0.67) and with conduct ( p = 0.020; OR = 0.24) and emotional problems ( p = 0.013; OR = 0.31) were significantly less likely to drop out of treatment. Conclusion. Overall, the outcomes of this study suggest that predictors assessing social relationships, social status, and living conditions should be considered as topics of psychological treatment to increase adherence and as predictors for future research studies (including treatment type).

This perspective article compares and contrasts the conceptualization of Autism Spectrum Disorder (ASD) in ICD-11 and DSM-5. By guiding the user through the ICD-11 text, it is argued that, in contrast to DSM-5, ICD-11 allows a high variety in symptom combinations, which results in an operationalization of ASD that is in favor of an extreme diverse picture, yet possibly at the expense of precision, including unforeseeable effects on clinical practice, care, and research. The clinical utility is questionable as this conceptualization can hardly be differentiated from other mental disorders and autism-like traits. It moves away from an observable, behavioral, and neurodevelopmental disorder to a disorder of inner experience that can hardly be measured objectively. It contains many vague and subjective concepts that lead to non-falsifiable diagnoses. This bears a large danger of false positive diagnoses, of further increased prevalence rates, limitations of access to ASD-specific services and of increasing the non-specificity of treatments. For research, the hypothesis is that the specificity of ASD will be reduced and this will additional increase the already high heterogeneity with the effect that replication of studies will be hampered. This could limit our understanding of etiology and biological pathways of ASD and bears the risk that precision medicine, i.e., a targeted approach for individual treatment strategies based on precise diagnostic markers, is more far from becoming reality. Thus, a more precise, quantitative description and more objective measurement of symptoms are suggested that define the clinical ASD phenotype. Identification of core ASD subtypes/endophenotypes and a precise description of symptoms is the necessary next step to advance diagnostic classification systems. Therefore, employing a more finely grained, objective, clinical symptom characterization which is more relatable to neurobehavioral concepts is of central significance.

Abstract Background Autistic-like traits (ALT) are prevalent across the general population and might be linked to some facets of a broader autism spectrum disorder (ASD) phenotype. Recent studies suggest an association of these traits with both genetic and brain structural markers in non-autistic individuals, showing similar spatial location of findings observed in ASD and thus suggesting a potential neurobiological continuum. Methods In this study, we first tested an association of ALTs (assessed with the AQ questionnaire) with cortical complexity, a cortical surface marker of early neurodevelopment, and then the association with disrupted functional connectivity. We analysed structural T1-weighted and resting-state functional MRI scans in 250 psychiatrically healthy individuals without a history of early developmental disorders, in a first step using the CAT12 toolbox for cortical complexity analysis and in a second step we used regional cortical complexity findings to apply the CONN toolbox for seed-based functional connectivity analysis. Results Our findings show a significant negative correlation of both AQ total and AQ attention switching subscores with left superior temporal sulcus (STS) cortical folding complexity, with the former being significantly correlated with STS to left lateral occipital cortex connectivity, while the latter showed significant positive correlation of STS to left inferior/middle frontal gyrus connectivity (n = 233; all p < 0.05, FWE cluster-level corrected). Additional analyses also revealed a significant correlation of AQ attention to detail subscores with STS to left lateral occipital cortex connectivity. Limitations Phenotyping might affect association results (e.g. choice of inventories); in addition, our study was limited to subclinical expressions of autistic-like traits. Conclusions Our findings provide further evidence for biological correlates of ALT even in the absence of clinical ASD, while establishing a link between structural variation of early developmental origin and functional connectivity.

BACKGROUND:Predictors of symptom improvement are an essential starting point for tailoring psychological treatments to each individual and, in turn, increasing treatment efficacy overall. However, such research regarding refugees/asylum seekers from Arabic-/Farsi-speaking countries is lacking. The current study aimed to characterize predictors for symptom improvement in the Mental Health in Refugees and Asylum Seekers (MEHIRA) study, one of the most extensive multicentered controlled trials on a nationwide stepped and collaborative care model compared to routine German mental health care. METHODS:Variables characterizing symptom change were chosen using backward elimination and inserted into logistic regression models for two depression endpoints, namely the Patient Health Questionnaire-9 (PHQ-9) and the Montgomery Asberg Depression Rating Scale (MADRS). RESULTS:Six variables were found to be at least marginally significantly associated with symptom decrease in both outcomes: baseline depressive symptom load, comorbid post-traumatic stress disorder, identifying as a refugee, years of schooling, physical health, and post-migration social status difference. Additionally, psychological health and resilience were marginally significant for one of the models. LIMITATIONS:Some predictor constructs - such as social support - were not adequately measured to replicate previous findings. Additionally, the study was underpowered for symptom change prediction of individual treatments beyond the group intervention. CONCLUSIONS:These outcomes indicate that trauma-related elements as well as content on refugee identity and post-migration social status changes should be included in depression interventions for refugees. Further, recommendations for future outcome prediction studies are made.

Adolescent refugees and asylum seekers (ARAS) are highly vulnerable to mental health problems. Stepped care models (SCM) and culturally sensitive therapies offer promising treatment approaches to effectively provide necessary medical and psychological support. To our knowledge, we were the first to investigate whether a culturally sensitive SCM will reduce symptoms of depression and PTSD in ARAS more effectively and efficiently than treatment as usual (TAU). We conducted a multicentric, randomized, controlled and rater-blinded trial across Germany with ARAS between the ages of 14 to 21 years. Participants ( N = 158) were stratified by their level of depressive symptom severity and then equally randomized to either SCM or TAU. Depending on their severity level, SCM participants were allocated to tailored interventions. Symptom changes were assessed for depression (PHQ) and PTSD (CATS) at four time points, with the primary end point at post-intervention after 12 weeks. Based on an intention-to-treat sample, we used a linear mixed model approach for the main statistical analyses. Further evaluations included cost–utility analyses, sensitivity analyses, follow-up-analyses, response and remission rates and subgroup analysis. We found a significant reduction of PHQ ( d = 0.52) and CATS ( d = 0.27) scores in both groups. However, there was no significant difference between SCM and TAU. Cost–utility analyses indicated that SCM generated greater cost–utility when measured as quality-adjusted life years compared to TAU. Subgroup analysis revealed different effects for the SCM interventions depending on the outcome measure. Although culturally sensitive, SCMs did not prove to be more effective in symptom change and represent a more cost-effective treatment alternative for mentally burdened ARAS. Our research contributes to the optimization of clinical productivity and the improvement of therapeutic care for ARAS. Disorder-specific interventions should be further investigated.