14 research outputs found
Autism and the right to education in the EU: Policy mapping and scoping review of the United Kingdom, France, Poland and Spain
Introduction: Autistic people may have different educational needs that need to be met to allow them to develop their full potential. Education and disability policies remain within the competence of EU Member States, with current educational standards and provisions for autistic people implemented locally. This scoping review aims to map EU and national special education policies with the goal of scoping the level of fulfilment of the right to education of autistic people. / Methods: Four EU countries (United Kingdom, France, Poland and Spain) were included in this scoping review study. Governmental policies in the field of education, special education needs and disability law were included. Path dependency framework was used for data analysis; a net of inter-dependencies between international, EU and national policies was created. / Results and discussion: Each country created policies where the right to free education without discrimination is provided. Poland does not have an autism specific strategy, whereas the United Kingdom, France and Spain have policies specifically designed for autistic individuals. Within the United Kingdom, all countries created different autism plans, nevertheless all aim to reach the same goal—inclusive education for autistic children that leads to the development of their full potential. / Conclusion: Policy-making across Europe in the field of education has been changing through the years in favour of autistic people. Today their rights are noticed and considered, but there is still room for improvement. Results showed that approaches and policies vastly differ between countries, more Member States should be analysed in a similar manner to gain a broader and clearer view with a special focus on disability rights in Central and Eastern Europe
Atypical measures of diffusion at the gray-white matter boundary in autism spectrum disorder in adulthood
Autism spectrum disorder (ASD) is a highly complex neurodevelopmental condition that is accompanied by neuroanatomical differences on the macroscopic and microscopic level. Findings from histological, genetic, and more recently in vivo neuroimaging studies converge in suggesting that neuroanatomical abnormalities, specifically around the gray-white matter (GWM) boundary, represent a crucial feature of ASD. However, no research has yet characterized the GWM boundary in ASD based on measures of diffusion. Here, we registered diffusion tensor imaging data to the structural T1-weighted images of 92 adults with ASD and 92 matched neurotypical controls in order to examine between-group differences and group-by-sex interactions in fractional anisotropy and mean diffusivity sampled at the GWM boundary, and at different sampling depths within the superficial white and into the gray matter. As hypothesized, we observed atypical diffusion at and around the GWM boundary in ASD, with between-group differences and group-by-sex interactions depending on tissue class and sampling depth. Furthermore, we identified that altered diffusion at the GWM boundary partially (i.e., ~50%) overlapped with atypical gray-white matter tissue contrast in ASD. Our study thus replicates and extends previous work highlighting the GWM boundary as a crucial target of neuropathology in ASD, and guides future work elucidating etiological mechanisms
In Vivo Evidence of Reduced Integrity of the Gray–White Matter Boundary in Autism Spectrum Disorder
Atypical cortical organization and reduced integrity of the gray–white matter boundary have been reported by postmortem
studies in individuals with autism spectrum disorder (ASD). However, there are no in vivo studies that examine these
particular features of cortical organization in ASD. Hence, we used structural magnetic resonance imaging to examine
differences in tissue contrast between gray and white matter in 98 adults with ASD and 98 typically developing controls, to
test the hypothesis that individuals with ASD have significantly reduced tissue contrast. More specifically, we examined
contrast as a percentage between gray and white matter tissue signal intensities (GWPC) sampled at the gray–white matter
boundary, and across different cortical layers. We found that individuals with ASD had significantly reduced GWPC in
several clusters throughout the cortex (cluster, P < 0.05). As expected, these reductions were greatest when tissue intensities
were sampled close to gray–white matter interface, which indicates a less distinct gray–white matter boundary in ASD. Our
in vivo findings of reduced GWPC in ASD are therefore consistent with prior postmortem findings of a less well-defined
gray–white matter boundary in ASD. Taken together, these results indicate that GWPC might be utilized as an in vivo proxy
measure of atypical cortical microstructural organization in future studies
Neural self-representation in autistic women and association with ‘compensatory camouflaging
Prior work has revealed sex/gender-dependent autistic characteristics across behavioural and neural/biological domains. It remains unclear whether and how neural sex/gender differences are related to behavioural sex/gender differences in autism. Here, we examined whether atypical neural responses during mentalizing and self-representation are sex/gender-dependent in autistic adults and explored whether ‘camouflaging’ (acting as if behaviourally neurotypical) is associated with sex/gender-dependent neural responses. In total, N = 119 adults (33 typically developing males, 29 autistic males, 29 typically developing females and 28 autistic females) participated in a task-related functional magnetic resonance imaging paradigm to assess neural activation within right temporo-parietal junction and ventromedial prefrontal cortex during mentalizing and self-representation. Camouflaging in autism was quantified as the discrepancy between extrinsic behaviour in social–interpersonal contexts and intrinsic status. While autistic men showed hypoactive right temporo-parietal junction mentalizing and ventromedial prefrontal cortex self-representation responses compared to typically developing men, such neural responses in autistic women were not different from typically developing women. In autistic women only, increasing camouflaging was associated with heightened ventromedial prefrontal cortex self-representation response. There is a lack of impaired neural self-representation and mentalizing in autistic women compared to typically developing women. Camouflaging is heightened in autistic women and may relate to neural self-representation response. These results reveal brain-behaviour relations that help explain sex/gender-heterogeneity in social brain function in autism
Business Ethics: The Promise of Neuroscience
Recent advances in cognitive neuroscience research portend well for furthering understanding of many of the fundamental questions in the field of business ethics, both normative and empirical. This article provides an overview of neuroscience methodology and brain structures, and explores the areas in which neuroscience research has contributed findings of value to business ethics, as well as suggesting areas for future research. Neuroscience research is especially capable of providing insight into individual reactions to ethical issues, while also raising challenging normative questions about the nature of moral responsibility, autonomy, intent, and free will. This article also provides a brief summary of the papers included in this special issue, attesting to the richness of scholarly inquiry linking neuroscience and business ethics. We conclude that neuroscience offers considerable promise to the field of business ethics, but we caution against overpromise
Association Between the Probability of Autism Spectrum Disorder and Normative Sex-Related Phenotypic Diversity in Brain Structure
IMPORTANCE Autism spectrum disorder (ASD) is 2 to 5 times more common in male
individuals than in female individuals. While the male preponderant prevalence of ASD might
partially be explained by sex differences in clinical symptoms, etiological models suggest that
the biological male phenotype carries a higher intrinsic risk for ASD than the female
phenotype. To our knowledge, this hypothesis has never been tested directly, and the
neurobiological mechanisms that modulate ASD risk in male individuals and female
individuals remain elusive.
OBJECTIVES To examine the probability of ASD as a function of normative sex-related
phenotypic diversity in brain structure and to identify the patterns of sex-related
neuroanatomical variability associated with low or high probability of ASD.
DESIGN, SETTING, AND PARTICIPANTS This study examined a cross-sectional sample of 98
right-handed, high-functioning adults with ASD and 98 matched neurotypical control
individuals aged 18 to 42 years. A multivariate probabilistic classification approach was used
to develop a predictive model of biological sex based on cortical thickness measures assessed
via magnetic resonance imaging in neurotypical controls. This normative model was
subsequently applied to individuals with ASD. The study dates were June 2005 to October
2009, and this analysis was conducted between June 2015 and July 2016.
MAIN OUTCOMES AND MEASURES Sample and population ASD probability estimates as a
function of normative sex-related diversity in brain structure, as well as neuroanatomical
patterns associated with ASD probability in male individuals and female individuals.
RESULTS Among the 98 individuals with ASD, 49 were male and 49 female, with a mean (SD)
age of 26.88 (7.18) years. Among the 98 controls, 51 were male and 47 female, with a mean
(SD) age of 27.39 (6.44) years. The sample probability of ASD did not increase significantly
with predictive probabilities for the male neuroanatomical brain phenotype. For example,
biological female individuals with a more male-typic pattern of brain anatomy were equally
likely to have ASD than biological female individuals with a characteristically female brain
phenotype (P = .40 vs .55, respectively; χ 2
1 = 1.11; P > .05; difference in P values, −.15; 95% CI,
−.10 to .40). This finding translates to an estimated variability in population prevalence from
0.3% to 0.6%, respectively. Moreover, the patterns of sex-related neuroanatomical variability
associated with ASD probability were sex specific (eg, in inferior temporal regions, where ASD
has different neurobiological underpinnings in male individuals and female individuals).
CONCLUSIONS AND RELEVANCE These findings imply that the male neuroanatomical
phenotype does not carry a higher intrinsic risk for ASD than the female neurophenotype and
provide important novel insights into the neurobiological mechanisms mediating sex
differences in ASD prevalence