1. Bellani M, Calderoni S, Muratori F, Brambilla P. {{Brain anatomy of autism spectrum disorders I. Focus on corpus callosum}}. {Epidemiology and psychiatric sciences}. 2013 Mar 26:1-5.
This brief review aims to examine the structural magnetic resonance imaging (sMRI) studies on corpus callosum in autism spectrum disorders (ASD) and discuss the clinical and demographic factors involved in the interpretation of results.
Lien vers le texte intégral (Open Access ou abonnement)
2. Bushnell PJ. {{Special issue: Environmental influences and emerging mechanisms in the etiology of autism}}. {Neurotoxicology and teratology}. 2013 Mar-Apr;36:1-2.
Lien vers le texte intégral (Open Access ou abonnement)
3. De Jaegher H. {{Embodiment and sense-making in autism}}. {Frontiers in integrative neuroscience}. 2013;7:15.
In this article, I sketch an enactive account of autism. For the enactive approach to cognition, embodiment, experience, and social interaction are fundamental to understanding mind and subjectivity. Enaction defines cognition as sense-making: the way cognitive agents meaningfully connect with their world, based on their needs and goals as self-organizing, self-maintaining, embodied agents. In the social realm, the interactive coordination of embodied sense-making activities with others lets us participate in each other’s sense-making (social understanding = participatory sense-making). The enactive approach provides new concepts to overcome the problems of traditional functionalist accounts of autism, which can only give a piecemeal and disintegrated view because they consider cognition, communication, and perception separately, do not take embodied into account, and are methodologically individualistic. Applying the concepts of enaction to autism, I show: How embodiment and sense-making connect, i.e., how autistic particularities of moving, perceiving, and emoting relate to how people with autism make sense of their world. For instance, restricted interests or preference for detail will have certain sensorimotor correlates, as well as specific meaning for autistic people.That reduced flexibility in interactional coordination correlates with difficulties in participatory sense-making. At the same time, seemingly irrelevant « autistic behaviors » can be quite attuned to the interactive context. I illustrate this complexity in the case of echolalia. An enactive account of autism starts from the embodiment, experience, and social interactions of autistic people. Enaction brings together the sensorimotor, cognitive, social, experiential, and affective aspects of autism in a coherent framework based on a complex non-linear multi-causality. This foundation allows to build new bridges between autistic people and their often non-autistic context, and to improve quality of life prospects.
Lien vers le texte intégral (Open Access ou abonnement)
4. de Lacy N, King BH. {{Revisiting the relationship between autism and schizophrenia: toward an integrated neurobiology}}. {Annual review of clinical psychology}. 2013 Mar 28;9:555-87.
Schizophrenia and autism have been linked since their earliest descriptions. Both are disorders of cerebral specialization originating in the embryonic period. Genetic, molecular, and cytologic research highlights a variety of shared contributory mechanisms that may lead to patterns of abnormal connectivity arising from altered development and topology. Overt behavioral pathology likely emerges during or after neurosensitive periods in which resource demands overwhelm system resources and the individual’s ability to compensate using interregional activation fails. We are at the threshold of being able to chart autism and schizophrenia from the inside out. In so doing, the door is opened to the consideration of new therapeutics that are developed based upon molecular, synaptic, and systems targets common to both disorders.
Lien vers le texte intégral (Open Access ou abonnement)
5. Green J, Wan MW, Guiraud J, Holsgrove S, McNally J, Slonims V, Elsabbagh M, Charman T, Pickles A, Johnson M, The BT. {{Intervention for Infants at Risk of Developing Autism: A Case Series}}. {J Autism Dev Disord}. 2013 Mar 27.
Theory and evidence suggest the potential value of prodromal intervention for infants at risk of developing autism. We report an initial case series (n = 8) of a parent-mediated, video-aided and interaction-focused intervention with infant siblings of autistic probands, beginning at 8-10 months of age. We outline the theory and evidence base behind this model and present data on feasibility, acceptability and measures ranging from parent-infant social interaction, to infant atypical behaviors, attention and cognition. The intervention proves to be both feasible and acceptable to families. Measurement across domains was successful and on larger samples promise to be an effective test of whether such an intervention in infancy will modify emergent atypical developmental trajectories in infants at risk for autism.
Lien vers le texte intégral (Open Access ou abonnement)
6. Kral TV, Eriksen WT, Souders MC, Pinto-Martin JA. {{Eating Behaviors, Diet Quality, and Gastrointestinal Symptoms in Children With Autism Spectrum Disorders: A Brief Review}}. {Journal of pediatric nursing}. 2013 Mar 23.
Children with autism spectrum disorders (ASD) and their caregivers face unique challenges in the children’s daily eating routines and food intake patterns. The aim of this brief review is to describe eating behaviors of children with ASD, including increased food neophobia and food selectivity, and review findings on children’s diet quality, and gastrointestinal (GI) symptoms. Advancing knowledge about the interrelationships between these nutrition-related domains in children with ASD is expected to have important implications for clinical nursing practice and caregiver care.
Lien vers le texte intégral (Open Access ou abonnement)
7. Mandell DS. {{Adults with Autism-A New Minority}}. {Journal of general internal medicine}. 2013 Mar 27.
Lien vers le texte intégral (Open Access ou abonnement)
8. Miller EJ. {{Surveillance for behavioral health problems and developmental disabilities in pediatric primary care}}. {North Carolina medical journal}. 2013 Jan-Feb;74(1):63-4.
9. Miyahara M. {{Meta review of systematic and meta analytic reviews on movement differences, effect of movement based interventions, and the underlying neural mechanisms in autism spectrum disorder}}. {Frontiers in integrative neuroscience}. 2013;7:16.
Purposes: To identify and appraise evidence from published systematic and meta analytic reviews on (1) movement differences of individuals with autism spectrum disorders (ASD); (2) the effects of movement based interventions for ASD; (3) hypothesized underlying neural mechanisms for the movement characteristics. Methods: A meta review of published systematic and meta analytic reviews on movement differences, structural, and functional brain anomalies in ASD and the effects of movement based interventions for individuals with ASD between 1806 and October 2012. The methodological quality of the identified systematic and meta analytic reviews was independently assessed by two assessors with the assessment of multiple systematic reviews (AMSTAR). Results: The search yielded a total of 12 reviews that met the inclusion/exclusion criteria. The methodological quality of the reviews varied, but the review conclusions were similar. Although individuals with ASD generally perform less well than age-matched controls in developmental movement tasks, there are few exceptions whose movement abilities are intact. Most movement based interventions report their efficacies. However, all existing studies employ the research design that is inherently incapable of providing strong evidence, and they often fail to report the extent of psychosocial interactions within the movement interventions. The hypothesized neural mechanisms are still under development and speculative in nature. Conclusions: It is premature to designate movement disturbance as a core symptom of ASD. The effects of movement based interventions on the present ASD core symptoms need to be further validated by stronger evidence and verified theoretical mechanisms linking ASD with movement disorders.
Lien vers le texte intégral (Open Access ou abonnement)
10. Moran MF, Foley JT, Parker ME, Weiss MJ. {{Two-legged hopping in autism spectrum disorders}}. {Frontiers in integrative neuroscience}. 2013;7:14.
Sensory processing deficits are common within autism spectrum disorders (ASD). Deficits have a heterogeneous dispersion across the spectrum and multimodal processing tasks are thought to magnify integration difficulties. Two-legged hopping in place in sync with an auditory cue (2.3, 3.0 Hz) was studied in a group of six individuals with expressive language impaired ASD (ELI-ASD) and an age-matched control group. Vertical ground reaction force data were collected and discrete Fourier transforms were utilized to determine dominant hopping cadence. Effective leg stiffness was computed through a mass-spring model representation. The ELI-ASD group were unsuccessful in matching their hopping cadence (2.21 +/- 0.30 hops.s(-1), 2.35 +/- 0.41 hops.s(-1)) to either auditory cue with greater deviations at the 3.0 Hz cue. In contrast, the control group was able to match hopping cadence (2.35 +/- 0.06 hops.s(-1), 3.02 +/- 0.10 hops.s(-1)) to either cue via an adjustment of effective leg stiffness. The ELI-ASD group demonstrated a varied response with an interquartile range (IQR) in excess of 0.5 hops.s(-1) as compared to the control group with an IQR < 0.03 hops.s(-1). Several sensorimotor mechanisms could explain the inability of participants with ELI-ASD to modulate motor output to match an external auditory cue. These results suggest that a multimodal gross motor task can (1) discriminate performance among a group of individuals with severe autism, and (2) could be a useful quantitative tool for evaluating motor performance in individuals with ASD individuals.
Lien vers le texte intégral (Open Access ou abonnement)
11. Shimmura C, Suzuki K, Iwata Y, Tsuchiya KJ, Ohno K, Matsuzaki H, Iwata K, Kameno Y, Takahashi T, Wakuda T, Nakamura K, Hashimoto K, Mori N. {{Enzymes in the glutamate-glutamine cycle in the anterior cingulate cortex in postmortem brain of subjects with autism}}. {Molecular autism}. 2013 Mar 26;4(1):6.
BACKGROUND: Accumulating evidence suggests that dysfunction in the glutamatergic system may underlie the pathophysiology of autism. The anterior cingulate cortex (ACC) has been implicated in autism as well as in glutamatergic neurotransmission. We hypothesized that alterations in the glutamate-glutamine cycle in the ACC might play a role in the pathophysiology of autism. METHODS: We performed Western blot analyses for the protein expression levels of enzymes in the glutamate-glutamine cycle, including glutamine synthetase, kidney-type glutaminase, liver-type glutaminase, and glutamate dehydrogenases 1 and 2, in the ACC of postmortem brain of individuals with autism (n = 7) and control subjects (n = 13). RESULTS: We found that the protein levels of kidney-type glutaminase, but not those of the other enzymes measured, in the ACC were significantly lower in subjects with autism than in controls. CONCLUSION: The results suggest that reduced expression of kidney-type glutaminase may account for putative alterations in glutamatergic neurotransmission in the ACC in autism.
Lien vers le texte intégral (Open Access ou abonnement)
12. Stevenson JL, Gernsbacher MA. {{Abstract spatial reasoning as an autistic strength}}. {PLoS One}. 2013;8(3):e59329.
Autistic individuals typically excel on spatial tests that measure abstract reasoning, such as the Block Design subtest on intelligence test batteries and the Raven’s Progressive Matrices nonverbal test of intelligence. Such well-replicated findings suggest that abstract spatial processing is a relative and perhaps absolute strength of autistic individuals. However, previous studies have not systematically varied reasoning level – concrete vs. abstract – and test domain – spatial vs. numerical vs. verbal, which the current study did. Autistic participants (N = 72) and non-autistic participants (N = 72) completed a battery of 12 tests that varied by reasoning level (concrete vs. abstract) and domain (spatial vs. numerical vs. verbal). Autistic participants outperformed non-autistic participants on abstract spatial tests. Non-autistic participants did not outperform autistic participants on any of the three domains (spatial, numerical, and verbal) or at either of the two reasoning levels (concrete and abstract), suggesting similarity in abilities between autistic and non-autistic individuals, with abstract spatial reasoning as an autistic strength.
Lien vers le texte intégral (Open Access ou abonnement)
13. Wang H, Doering LC. {{Reversing autism by targeting downstream mTOR signaling}}. {Frontiers in cellular neuroscience}. 2013;7:28.
Lien vers le texte intégral (Open Access ou abonnement)
14. Zhou SS, Zhou YM, Li D, Ma Q. {{Early infant exposure to excess multivitamin: a risk factor for autism?}}. {Autism research and treatment}. 2013;2013:963697.
Autism, a neurodevelopmental disorder that affects boys more than girls, is often associated with altered levels of monoamines (serotonin and catecholamines), especially elevated serotonin levels. The monoamines act as both neurotransmitters and signaling molecules in the gastrointestinal and immune systems. The evidence related to monoamine metabolism may be summarized as follows: (i) monoamine neurotransmitters are enzymatically degraded/inactivated by three mechanisms: oxidative deamination, methylation, and sulfation. The latter two are limited by the supply of methyl groups and sulfate, respectively. (ii) A decrease in methylation- and sulfation-mediated monoamine inactivation can be compensated by an increase in the oxidative deamination catalyzed by monoamine oxidase, an X-linked enzyme exhibiting higher activity in females than in males. (iii) Vitamins can, on one hand, facilitate the synthesis of monoamine neurotransmitters and, on the other hand, inhibit their inactivation by competing for methylation and sulfation. Therefore, we postulate that excess multivitamin feeding in early infancy, which has become very popular over the past few decades, may be a potential risk factor for disturbed monoamine metabolism. In this paper, we will focus on the relationship between excess multivitamin exposure and the inactivation/degradation of monoamine neurotransmitters and its possible role in the development of autism.
