Le numéro de mai 2011 de Pediatric Research propose un dossier spécial sur les troubles neuropsychiatriques et la pédopsychiatrie avec plusieurs articles consacrés à l’autisme, à la théorie de l’esprit et aux cognitions sociales.

Le numéro est consultable sur le site de l’éditeur.

1. Chen R, Jiao Y, Herskovits EH. Structural MRI in autism spectrum disorder. Pediatr Res ;2011 (May) ;69(5 Pt 2):63R-68R.

Magnetic resonance (MR) examination provides a powerful tool for investigating brain structural changes in children with autism spectrum disorder (ASD). We review recent advances in the understanding of structural MR correlates of ASD. We summarize findings from studies based on voxel-based morphometry, surface-based morphometry, tensor-based morphometry, and diffusion-tensor imaging. Finally, we discuss diagnostic models of ASD based on MR-derived features.

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2. Constantino JN. The quantitative nature of autistic social impairment. Pediatr Res ;2011 (May) ;69(5 Pt 2):55R-62R.

Autism, like intellectual disability, represents the severe end of a continuous distribution of developmental impairments that occur in nature, that are highly inherited, and that are orthogonally related to other parameters of development. A paradigm shift in understanding the core social abnormality of autism as a quantitative trait rather than as a categorically defined condition has key implications for diagnostic classification, the measurement of change over time, the search for underlying genetic and neurobiologic mechanisms, and public health efforts to identify and support affected children. Here, a recent body of research in genetics and epidemiology is presented to examine a dimensional reconceptualization of autistic social impairment-as manifested in clinical autistic syndromes, the broader autism phenotype, and normal variation in the general population. It illustrates how traditional categorical approaches to diagnosis may lead to misclassification of subjects (especially girls and mildly affected boys in multiple-incidence autism families), which can be particularly damaging to biological studies and proposes continued efforts to derive a standardized quantitative system by which to characterize this family of conditions.

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3. Frye RE, Rossignol DA. Mitochondrial dysfunction can connect the diverse medical symptoms associated with autism spectrum disorders. Pediatr Res ;2011 (May) ;69(5 Pt 2):41R-47R.

Autism spectrum disorder (ASD) is a devastating neurodevelopmental disorder. Over the past decade, evidence has emerged that some children with ASD suffer from undiagnosed comorbid medical conditions. One of the medical disorders that has been consistently associated with ASD is mitochondrial dysfunction. Individuals with mitochondrial disorders without concomitant ASD manifest dysfunction in multiple high-energy organ systems, such as the central nervous, muscular, and gastrointestinal (GI) systems. Interestingly, these are the identical organ systems affected in a significant number of children with ASD. This finding increases the possibility that mitochondrial dysfunction may be one of the keys that explains the many diverse symptoms observed in some children with ASD. This article will review the importance of mitochondria in human health and disease, the evidence for mitochondrial dysfunction in ASD, the potential role of mitochondrial dysfunction in the comorbid medical conditions associated with ASD, and how mitochondrial dysfunction can bridge the gap for understanding how these seemingly disparate medical conditions are related. We also review the limitations of this evidence and other possible explanations for these findings. This new understanding of ASD should provide researchers a pathway for understanding the etiopathogenesis of ASD and clinicians the potential to develop medical therapies.

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4. Gressens P, Ferriero DM. 21st century research in pediatric psychiatry. Pediatr Res ;2011 (May) ;69(5 Pt 2):1R-2R.

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5. Huang LT. The link between perinatal glucocorticoids exposure and psychiatric disorders. Pediatr Res ;2011 (May) ;69(5 Pt 2):19R-25R.

The perinatal period is particularly sensitive to a variety of insults during which stress-regulating systems can be permanently altered and psychopathologies ensue. The programming of physiological, endocrinological, and behavioral functions by perinatal adversities is mediated by altered levels of glucocorticoids or the hypothalamic-pituitary-adrenal axis activity in either the mother or offspring. In this article, I review the integrated data from human studies and from animal models that suggest the programming effects of perinatal glucocorticoids exposure. Finally, the concept of developmental origins of psychiatric disorders is discussed.

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6. Johnson S, Marlow N. Preterm birth and childhood psychiatric disorders. Pediatr Res ;2011 (May) ;69(5 Pt 2):11R-18R.

Epidemiologic studies have, for many years, identified preterm birth as a significant risk factor for psychiatric disorders. There has been a recent resurgence of interest in neurobehavioral outcomes after preterm birth. In this article, we review clinical cohort studies of the prevalence, etiology, and risk factors for psychiatric sequelae in ex-preterm children. Studies using diagnostic psychiatric evaluations are few in number but typically report a 3- to 4-fold increased risk for disorders in middle childhood. Our review of studies reveals a « preterm behavioral phenotype » characterized by an increased risk for symptoms and disorders associated with inattention, anxiety, and social difficulties. The most contemporary studies have also reported a markedly increased prevalence of autism spectrum disorders (ASD) in preterm populations. Our examination of the correlates and comorbidities of psychiatric disorders is indicative of a different causative pathway that may be associated with altered brain development after preterm birth. Despite the low population attributable risk, the frequency of these symptoms and disorders means that psychiatric screening is likely to be beneficial in this vulnerable population.

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7. Korkmaz B. Theory of mind and neurodevelopmental disorders of childhood. Pediatr Res ;2011 (May) ;69(5 Pt 2):101R-108R.

To a large extent, the human infant is socialized through the acquisition of a specific cognitive mechanism known as theory of mind (ToM), a term which is currently used to explain a related set of intellectual abilities that enable us to understand that others have beliefs, desires, plans, hopes, information, and intentions that may differ from our own. Various neurodevelopmental disorders, such as autism spectrum disorders, attention deficit hyperactivity disorder, developmental language disorders, and schizophrenia, as well as acquired disorders of the right brain (and traumatic brain injury) impair ToM. ToM is a composite function, which involves memory, joint attention, complex perceptual recognition (such as face and gaze processing), language, executive functions (such as tracking of intentions and goals and moral reasoning), emotion processing-recognition, empathy, and imitation. Hence, ToM development is dependent on the maturation of several brain systems and is shaped by parenting, social relations, training, and education ; thus, it is an example of the dense interaction that occurs between brain development and (social) environment.

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8. Lampis V, Maziade M, Battaglia M. Animal models of human anxiety disorders : reappraisal from a developmental psychopathology vantage point. Pediatr Res ;2011 (May) ;69(5 Pt 2):77R-84R.

We are witnessing a tremendous expansion of strategies and techniques that derive from basic and preclinical science to study the fine genetic, epigenetic, and proteomic regulation of behavior in the laboratory animal. In this endeavor, animal models of psychiatric illness are becoming the almost exclusive domain of basic researchers, with lesser involvement of clinician researchers in their conceptual design, and transfer into practice of new paradigms. From the side of human behavioral research, the growing interest in gene-environment interplay and the fostering of valid endophenotypes are among the few substantial innovations in the effort of linking common mental disorders to cutting-edge clinical research questions. We argue that it is time for cross-fertilization between these camps. In this article, we a) observe that the « translational divide » can-and should-be crossed by having investigators from both the basic and the clinical sides cowork on simpler, valid « endophenotypes » of neurodevelopmental relevance ; b) emphasize the importance of unambiguous physiological readouts, more than behavioral equivalents of human symptoms/syndromes, for animal research ; c) indicate and discuss how this could be fostered and implemented in a developmental framework of reference for some common anxiety disorders and ultimately lead to better animal models of human mental disorders.

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9. Marco EJ, Hinkley LB, Hill SS, Nagarajan SS. Sensory processing in autism : a review of neurophysiologic findings. Pediatr Res ;2011 (May) ;69(5 Pt 2):48R-54R.

Atypical sensory-based behaviors are a ubiquitous feature of autism spectrum disorders (ASDs). In this article, we review the neural underpinnings of sensory processing in autism by reviewing the literature on neurophysiological responses to auditory, tactile, and visual stimuli in autistic individuals. We review studies of unimodal sensory processing and multisensory integration that use a variety of neuroimaging techniques, including electroencephalography (EEG), magnetoencephalography (MEG), and functional MRI. We then explore the impact of covert and overt attention on sensory processing. With additional characterization, neurophysiologic profiles of sensory processing in ASD may serve as valuable biomarkers for diagnosis and monitoring of therapeutic interventions for autism and reveal potential strategies and target brain regions for therapeutic interventions.

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10. Meyer U, Feldon J, Dammann O. Schizophrenia and autism : both shared and disorder-specific pathogenesis via perinatal inflammation ?. Pediatr Res ;2011 (May) ;69(5 Pt 2):26R-33R.

Prenatal exposure to infection and subsequent inflammatory responses have been implicated in the etiology of schizophrenia and autism. In this review, we summarize current evidence from human and animal studies supporting the hypothesis that the pathogenesis of these two disorders is linked via exposure to inflammation at early stages of development. Moreover, we propose a hypothetical model in which inflammatory mechanisms may account for multiple shared and disorder-specific pathological characteristics of both entities. In essence, our model suggests that acute neuroinflammation during early fetal development may be relevant for the induction of psychopathological and neuropathological features shared by schizophrenia and autism, whereas postacute latent and persistent inflammation may contribute to schizophrenia- and autism-specific phenotypes, respectively.

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11. Monk C, Fitelson EM, Werner E. Mood disorders and their pharmacological treatment during pregnancy : is the future child affected ?. Pediatr Res ;2011 (May) ;69(5 Pt 2):3R-10R.

Nearly half the US population will meet criteria for a neuropsychiatric disorder at some point in their lives, and 1 in 17 has a seriously debilitating illness. Although not all affected adults had an identified disorder as a child, increasingly these psychopathologies are conceptualized as the late-stage culmination of aberrant developmental processes shaped by a complex interplay of genes and experience, including experiences in utero. Decades of studies with pregnant animals demonstrate that stress-elicited perturbations in maternal biology affect offspring neurodevelopment. Studies of stress in pregnant women largely mirror these findings. Pregnant women with anxiety and/or depression experience greater life stress, and illness-related alterations in their neurobiology, with a potential to impact fetal neurobehavioral development via associated changes in the intrauterine environment and/or pharmacologic interventions. This article critically reviews findings on child development (including fetal neurobehavior) related to maternal depression, anxiety, and pharmacological treatments, primarily selective serotonin reuptake inhibitors (SSRIs). The hypothesis under review is that, in addition to genetics and characteristics of the postnatal environment, the familial transmission of risk for neuropsychiatric disorders involves a « third path »-prenatal exposure to psychiatric illness and its treatment.

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12. Patterson PH. Modeling autistic features in animals. Pediatr Res ;2011 (May) ;69(5 Pt 2):34R-40R.

A variety of features of autism can be simulated in rodents, including the core behavioral hallmarks of stereotyped and repetitive behaviors, and deficits in social interaction and communication. Other behaviors frequently found in autism spectrum disorders (ASDs) such as neophobia, enhanced anxiety, abnormal pain sensitivity and eye blink conditioning, disturbed sleep patterns, seizures, and deficits in sensorimotor gating are also present in some of the animal models. Neuropathology and some characteristic neurochemical changes that are frequently seen in autism, and alterations in the immune status in the brain and periphery are also found in some of the models. Several known environmental risk factors for autism have been successfully established in rodents, including maternal infection and maternal valproate administration. Also under investigation are a number of mouse models based on genetic variants associated with autism or on syndromic disorders with autistic features. This review briefly summarizes recent developments in this field, highlighting models with face and/or construct validity, and noting the potential for investigation of pathogenesis, and early progress toward clinical testing of potential therapeutics. Wherever possible, reference is made to reviews rather than to primary articles.

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13. Purper-Ouakil D, Ramoz N, Lepagnol-Bestel AM, Gorwood P, Simonneau M. Neurobiology of attention deficit/hyperactivity disorder. Pediatr Res ;2011 (May) ;69(5 Pt 2):69R-76R.

Attention deficit/hyperactivity disorder (ADHD), a prevalent neurodevelopmental disorder, has been associated with various structural and functional CNS abnormalities but findings about neurobiological mechanisms linking genes to brain phenotypes are just beginning to emerge. Despite the high heritability of the disorder and its main symptom dimensions, common individual genetic variants are likely to account for a small proportion of the phenotype’s variance. Recent findings have drawn attention to the involvement of rare genetic variants in the pathophysiology of ADHD, some being shared with other neurodevelopmental disorders. Traditionally, neurobiological research on ADHD has focused on catecholaminergic pathways, the main target of pharmacological treatments. However, more distal and basic neuronal processes in relation with cell architecture and function might also play a role, possibly accounting for the coexistence of both diffuse and specific alterations of brain structure and activation patterns. This article aims to provide an overview of recent findings in the rapidly evolving field of ADHD neurobiology with a focus on novel strategies regarding pathophysiological analyses.

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14. Skuse DH, Gallagher L. Genetic influences on social cognition. Pediatr Res ;2011 (May) ;69(5 Pt 2):85R-91R.

Human social behavior develops under the influence of genetic, environmental, and cultural factors. Social cognition comprises our ability to understand and respond appropriately to other people’s social approaches or responses. The concept embraces self-knowledge and theory of mind, or the ability to think about emotions and behavior from the perspective of another person. The neuropeptides oxytocin (OT) and vasopressin (AVP) are now known to play an important role, affecting individual differences in parenting behavior, social recognition, and affiliative behaviors. The processes of social cognition are also supported by reward circuitry, underpinned by the dopaminergic neurotransmitter system. Reward processes build social relationships, in parenting and pair-bonding, and influence social interactions that require trust, or display altruism. The impact of emotional regulation upon social behavior, including mood and anxiety, is also mediated through the serotonergic system. Variation in activity of serotonergic networks in the brain influences emotional responsivity, including subjective feelings, physiological responses, emotional expressions, and the tendency to become engaged in action as a consequence of a feeling state. Genetic variation in the receptors associated with OT, AVP, dopamine, and serotonin has been intensively studied in humans and animal models. Recent findings are building an increasingly coherent picture of regulatory mechanisms.

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15. Zahir FR, Brown CJ. Epigenetic impacts on neurodevelopment : pathophysiological mechanisms and genetic modes of action. Pediatr Res ;2011 (May) ;69(5 Pt 2):92R-100R.

Disruptions of genes that are involved in epigenetic functions are known to be causative for several mental retardation/intellectual disability (MR/ID) syndromes. Recent work has highlighted genes with epigenetic functions as being implicated in autism spectrum disorders (ASDs) and schizophrenia (SCZ). The gene-environment interaction is an important factor of pathogenicity for these complex disorders. Epigenetic modifications offer a mechanism by which we can explain how the environment interacts with, and is able to dynamically regulate, the genome. This review aims to provide an overview of the role of epigenetic deregulation in the etiopathology for neurodevelopment disease.

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