1. Besag FM. {{Current controversies in the relationships between autism and epilepsy}}. {Epilepsy Behav};2015 (Jun);47:143-146.
The controversies that have arisen in endeavoring to establish the nature of the relationships between autism and epilepsy might be summarized in a few simple questions, most of which do not yet have clear, complete answers. Does epilepsy cause autism? Does autism cause epilepsy? Are there underlying brain mechanisms that predispose to both conditions? What is the role of genetics in this regard? What is the importance of prenatal, perinatal, and postnatal environmental factors? Do any of the proposed relationships between autism and epilepsy provide insight into useful management or treatment? Is the prognosis of either autism or epilepsy different when the other condition is also present? What is the role of additional comorbidities, such as intellectual impairment or attention deficit hyperactivity disorder, in the relationship between the two conditions and in influencing treatment choices? From the evidence currently available, it would appear that epilepsy can rarely be the cause of autistic features but is not the cause of autism in most cases. There is currently no credible mechanism for suggesting that autism might cause epilepsy. There is strong evidence for an underlying predisposition for both conditions, particularly arising from genetic investigations. However, many issues remain unresolved. Considering the amount of research that has been published in this area, it is surprising that so few definitive answers have been established. The papers in this issue’s special section provide additional insights into the relationships between autism and epilepsy; while they do not provide answers to all the questions, they represent considerable progress in this area and, at the very least, give some strong indication of what research might, in the future, provide such answers.
Lien vers le texte intégral (Open Access ou abonnement)
2. Campbell SB, Leezenbaum NB, Schmidt EN, Day TN, Brownell CA. {{Concern for Another’s Distress in Toddlers at High and Low Genetic Risk for Autism Spectrum Disorder}}. {J Autism Dev Disord};2015 (Jun 21)
We examined concern for others in 22-month-old toddlers with an older sibling with autism spectrum disorder (ASD) and low risk typically-developing toddlers with older siblings. Responses to a crying infant and an adult social partner who pretended to hurt her finger were coded. Children with a later diagnosis of ASD showed limited empathic concern in either context compared to low risk toddlers. High risk toddlers without a later diagnosis fell between the ASD and low risk groups. During the crying baby probe the low risk and high risk toddlers without a diagnosis engaged their parent more often than the toddlers with ASD. Low levels of empathic concern and engagement with parents may signal emerging ASD in toddlerhood.
Lien vers le texte intégral (Open Access ou abonnement)
3. Costanzo V, Chericoni N, Amendola FA, Casula L, Muratori F, Scattoni ML, Apicella F. {{Early detection of autism spectrum disorders: From retrospective home video studies to prospective ‘high risk’ sibling studies}}. {Neurosci Biobehav Rev};2015 (Jun 17)
In the autism spectrum disorders (ASD) field of research there is scientific consensus on the importance of early identification (and subsequently, of timely treatment) for a better prognosis. For this reason, early diagnosis represents a common challenge for clinicians and an area of great interest for researchers. In the past decades, many studies have focused on identifying subclinical signs of ASD with different types of experimental designs and methods, both retrospectively and prospectively. The purpose of this narrative review is to present changes in methodology, from an historical point of view, highlighting the strengths and weaknesses of different research designs. Conclusions are drawn taking into account potentialities of prospective designs for the study of early predictors of ASD.
Lien vers le texte intégral (Open Access ou abonnement)
4. Goepfert E, Mule C, von Hahn E, Visco Z, Siegel M. {{Family System Interventions for Families of Children with Autism Spectrum Disorder}}. {Child Adolesc Psychiatr Clin N Am};2015 (Jul);24(3):571-583.
The increasing prevalence of autism spectrum disorder (ASD), the severity of impairment, and its impact on systems are a source of ever-growing concern. This article (1) describes briefly the spectrum of ASD and its treatments; (2) discusses the impact that ASD has on the individual, family, and external environment; and (3) discusses the application of family therapy principles in order to meet the needs of children and families affected by ASD. Illustrative case examples are presented.
Lien vers le texte intégral (Open Access ou abonnement)
5. Kennedy DP, Paul LK, Adolphs R. {{Brain Connectivity in Autism: The Significance of Null Findings}}. {Biol Psychiatry};2015 (Jul 15);78(2):81-82.
Lien vers le texte intégral (Open Access ou abonnement)
6. McKenna PE, Glass A, Rajendran G, Corley M. {{Strange Words: Autistic Traits and the Processing of Non-Literal Language}}. {J Autism Dev Disord};2015 (Jun 21)
Previous investigations into metonymy comprehension in ASD have confounded metonymy with anaphora, and outcome with process. Here we show how these confounds may be avoided, using data from non-diagnosed participants classified using Autism Quotient. Participants read sentences containing target words with novel or established metonymic senses (e.g., Finland, Vietnam) in literal- or figurative-supporting contexts. Participants took longer to read target words in figurative contexts, especially where the metonymic sense was novel. Importantly, participants with higher AQs took longer still to read novel metonyms. This suggests a focus for further exploration, in terms of potential differences between individuals diagnosed with ASD and their neurotypical counterparts, and more generally in terms of the processes by which comprehension is achieved.
Lien vers le texte intégral (Open Access ou abonnement)
7. Pedersen LH. {{Prenatal Antidepressant Exposure and Childhood Autism Spectrum Disorders: Cause for Concern?}}. {Paediatr Drugs};2015 (Jun 20)
There is empirical evidence for a role for serotonin in autism . In experimental animals, early life exposure to serotonergic antidepressants or maternal stress affects brain development, with subsequent changes in serotonin tone in adult animals. Recently, antidepressant exposure during pregnancy has been associated with autism in epidemiological studies. At least part of the association is potentially explained by maternal depression or factors associated with depression. Importantly, even if there is no causal relation between prenatal antidepressant exposure and autism, use of antidepressants during pregnancy is a marker of potential problems later in life across five independent study populations, and exposed children may need special attention regardless of the underlying mechanism. Future studies need to disentangle the effects of maternal depression and antidepressant use during pregnancy while adjusting for the postnatal environment. One promising strategy is to use results from basic science to guide the inclusion of potential biological intermediates in advanced epidemiological studies.
