Pubmed du 18/02/16

Pubmed du jour

2016-02-18 12:03:50

1. Accordino RE, Kidd C, Politte LC, Henry CA, McDougle CJ. {{Psychopharmacological Interventions in Autism Spectrum Disorder}}. {Expert Opin Pharmacother};2016 (Feb 18)
INTRODUCTION: Individuals with autism spectrum disorder (ASD) commonly present for treatment of emotional and behavioral disturbances associated with ASD’s « core » symptoms. Psychotropic medications are widely utilized in alleviating associated emotional and behavioral symptoms. Areas covered: Emotional and behavioral disturbances associated with ASD include irritability/severely disruptive behavior, which comprises the heaviest symptom burden; hyperactivity and other Attention-Deficit-Hyperactivity-Disorder (ADHD)-type symptoms; repetitive/stereotyped behaviors; and social withdrawal. Existing evidence for medications for each of these symptom clusters will be examined in this review. Expert opinion: Psychopharmacological treatment of core and associated symptoms in ASD is challenging, in large part because of the heterogeneity in the presentation of ASD. Furthermore, children and adolescents with ASD are more vulnerable to the side effects of psychopharmacological intervention than their age-matched, typically developing counterparts. Currently, risperidone and aripiprazole are the only medications that have been (relatively) reliably shown to help treat certain symptom clusters associated with ASD, namely severely disruptive behavior and hyperactivity. Recent studies have begun to look at medications with mechanisms that are novel in the treatment of ASD and that may address underlying pathophysiology and/or core symptoms such as glutamate-modulating agents. Overall, randomized, placebo-controlled studies of medications for the treatment of ASD are scarce.

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2. Caracci MO, Avila ME, De Ferrari GV. {{Synaptic Wnt/GSK3beta Signaling Hub in Autism}}. {Neural Plast};2016;2016:9603751.

Hundreds of genes have been associated with autism spectrum disorders (ASDs) and the interaction of weak and de novo variants derive from distinct autistic phenotypes thus making up the « spectrum. » The convergence of these variants in networks of genes associated with synaptic function warrants the study of cell signaling pathways involved in the regulation of the synapse. The Wnt/beta-catenin signaling pathway plays a central role in the development and regulation of the central nervous system and several genes belonging to the cascade have been genetically associated with ASDs. In the present paper, we review basic information regarding the role of Wnt/beta-catenin signaling in excitatory/inhibitory balance (E/I balance) through the regulation of pre- and postsynaptic compartments. Furthermore, we integrate information supporting the role of the glycogen synthase kinase 3beta (GSK3beta) in the onset/development of ASDs through direct modulation of Wnt/beta-catenin signaling. Finally, given GSK3beta activity as key modulator of synaptic plasticity, we explore the potential of this kinase as a therapeutic target for ASD.

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3. Cawkwell P, Lawler A, Maneta E, Coffey BJ. {{Staying Up at Night: Overlapping Bipolar and Obsessive-Compulsive Disorder Symptoms in an Adolescent with Autism Spectrum Disorder}}. {J Child Adolesc Psychopharmacol};2016 (Feb);26(1):74-77.

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4. Chown N, Hughes L. {{History and First Descriptions of Autism: Asperger Versus Kanner Revisited}}. {J Autism Dev Disord};2016 (Feb 17)
When reading Michael Fitzgerald’s chapter entitled ‘Autism: Asperger’s Syndrome-History and First Descriptions’ in ‘Asperger’s Disorder’ edited by Rausch, Johnson and Casanova, a while ago, one of us was struck by his contention that Kanner was guilty of plagiarism as well as non-attribution of Asperger’s 1938 paper ‘Das psychisch abnorme kind’ (Fitzgerald in Asperger’s disorder. Informa Healthcare, New York, 2008) published in a Vienna weekly. Steve Silberman has discovered evidence that Kanner rescued Asperger’s chief diagnostician from the Nazis in 1944 so must have been aware of Asperger’s work and conclusions. Fitzgerald was on the right track but it appears that Kanner may have plagiarised Asperger’s ideas rather than his 1938 paper.

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5. Cotter M, Archibald AD, McClaren BJ, Burgess T, Francis D, Hills L, Martyn M, Oertel R, Slater H, Cohen J, Metcalfe SA. {{Clinical audit of genetic testing and referral patterns for fragile X and associated conditions}}. {Am J Med Genet A};2016 (Feb 18)
An audit was conducted of laboratory/clinical databases of genetic tests performed between January 2003 and December 2009, and for 2014, as well as referrals to the clinical service and a specialist multidisciplinary clinic, to determine genetic testing request patterns for fragile X syndrome and associated conditions and referrals for genetic counseling/multidisciplinary management in Victoria, Australia. An expanded allele (full mutation, premutation or intermediate) was found in 3.7% of tests. Pediatricians requested approximately 70% of test samples, although fewer general practitioners and more obstetricians/gynecologists ordered tests in 2014. Median age at testing for individuals with a full mutation seeking a diagnosis without a fragile X family history was 4.3 years (males) and 9.4 years (females); these ages were lower when pediatricians ordered the tests (2.1 years and 6.1 years, respectively). Individuals with a premutation were generally tested at a later age (median age: males, 33.2 years; females, 36.4 years). Logistic regression showed that a family history of ID (OR 3.28 P = 0.005, CI 1.77-5.98) was the only indication to independently increase the likelihood of a test-positive (FM or PM) result. Following testing, approximately 25% of full mutation or premutation individuals may not have attended clinical services providing genetic counseling or multidisciplinary management for these families. The apparent delay in fragile X syndrome diagnosis and lack of appropriate referrals for some may result in less than optimal management for these families. These findings suggest continued need for awareness and education of health professionals around diagnosis and familial implications of fragile X syndrome and associated conditions. (c) 2016 Wiley Periodicals, Inc.

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6. Crespi B, Leach E, Dinsdale N, Mokkonen M, Hurd P. {{Imagination in human social cognition, autism, and psychotic-affective conditions}}. {Cognition};2016 (Feb 18);150:181-199.

Complex human social cognition has evolved in concert with risks for psychiatric disorders. Recently, autism and psychotic-affective conditions (mainly schizophrenia, bipolar disorder, and depression) have been posited as psychological ‘opposites’ with regard to social-cognitive phenotypes. Imagination, considered as ‘forming new ideas, mental images, or concepts’, represents a central facet of human social evolution and cognition. Previous studies have documented reduced imagination in autism, and increased imagination in association with psychotic-affective conditions, yet these sets of findings have yet to be considered together, or evaluated in the context of the diametric model. We first review studies of the components, manifestations, and neural correlates of imagination in autism and psychotic-affective conditions. Next, we use data on dimensional autism in healthy populations to test the hypotheses that: (1) imagination represents the facet of autism that best accounts for its strongly male-biased sex ratio, and (2) higher genetic risk of schizophrenia is associated with higher imagination, in accordance with the predictions of the diametric model. The first hypothesis was supported by a systematic review and meta-analysis showing that Imagination exhibits the strongest male bias of all Autism Quotient (AQ) subscales, in non-clinical populations. The second hypothesis was supported, for males, by associations between schizophrenia genetic risk scores, derived from a set of single-nucleotide polymorphisms, and the AQ Imagination subscale. Considered together, these findings indicate that imagination, especially social imagination as embodied in the default mode human brain network, mediates risk and diametric dimensional phenotypes of autism and psychotic-affective conditions.

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7. Dawson G. {{Why It’s Important to Continue Universal Autism Screening While Research Fully Examines Its Impact}}. {JAMA Pediatr};2016 (Feb 16)

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8. de Vries PJ. {{Thinking globally to meet local needs: autism spectrum disorders in Africa and other low-resource environments}}. {Curr Opin Neurol};2016 (Feb 16)
PURPOSE OF REVIEW: Most people with autism spectrum disorders (ASDs) live in low and middle-income countries, yet almost everything we know about ASD comes from high-income countries. Here we review recent research from Africa, with some references to research in other low-resource environments. We examine publications on screening and diagnosis, intervention, clinical presentation of ASD, cultural perspectives, and neuroscience and technology. RECENT FINDINGS: Open-access screening and diagnostic tools represent a positive, but nontrivial, future goal. Recent efforts at ‘low intensity’ community-based interventions are encouraging, but many significant scalability challenges remain. Proposals that ASD in Africa is more severe and overrepresented in high socioeconomic families are likely to be attributable to ascertainment biases and the absence of standardized phenotyping tools. Cultural perspectives and innovative use of technology and neuroscience have the potential to generate novel strategies of global relevance, but research priorities have to be determined by local needs. SUMMARY: To have a real impact on clinical services, training, and research in local communities, clinician-scientists should start by thinking globally. ASD research in Africa and other low-resource environments remains limited and of questionable quality and highlights the need to build high-quality research capacity in these low-resource environments.

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9. Dolan BK, Van Hecke AV, Carson AM, Karst JS, Stevens S, Schohl KA, Potts S, Kahne J, Linneman N, Remmel R, Hummel E. {{Brief Report: Assessment of Intervention Effects on In Vivo Peer Interactions in Adolescents with Autism Spectrum Disorder (ASD)}}. {J Autism Dev Disord};2016 (Feb 17)
This study aimed to evaluate the effectiveness of a randomized controlled trial of a social skills intervention, the Program for the Education and Enrichment of Relational Skills (PEERS: Laugeson et al. in J Autism Dev Disord 39(4): 596-606, 2009), by coding digitally recorded social interactions between adolescent participants with ASD and a typically developing adolescent confederate. Adolescent participants engaged in a 10-min peer interaction at pre- and post-treatment. Interactions were coded using the Contextual Assessment of Social Skills (Ratto et al. in J Autism Dev Disord 41(9): 1277-1286, 2010). Participants who completed PEERS demonstrated significantly improved vocal expressiveness, as well as a trend toward improved overall quality of rapport, whereas participants in the waitlist group exhibited worse performance on these domains. The degree of this change was related to knowledge gained in PEERS.

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10. Faja S, Dawson G, Sullivan K, Meltzoff AN, Estes A, Bernier R. {{Executive function predicts the development of play skills for verbal preschoolers with autism spectrum disorders}}. {Autism Res};2016 (Feb 18)
Executive function and play skills develop in early childhood and are linked to cognitive and language ability. The present study examined these abilities longitudinally in two groups with autism spectrum disorder-a group with higher initial language (n = 30) and a group with lower initial language ability (n = 36). Among the lower language group, concurrent nonverbal cognitive ability contributed most to individual differences in executive function and play skills. For the higher language group, executive function during preschool significantly predicted play ability at age 6 over and above intelligence, but early play did not predict later executive function. These results suggested that factors related to the development of play and executive function differ for subgroups of children with different language abilities and that early executive function skills may be critical in order for verbal children with autism to develop play. Autism Res 2016. (c) 2016 International Society for Autism Research, Wiley Periodicals, Inc.

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11. Gokcen E, Frederickson N, Petrides KV. {{Theory of Mind and Executive Control Deficits in Typically Developing Adults and Adolescents with High Levels of Autism Traits}}. {J Autism Dev Disord};2016 (Feb 17)
Autism spectrum disorder (ASD) is characterised by profound difficulties in empathic processing and executive control. Whilst the links between these processes have been frequently investigated in populations with autism, few studies have examined them at the subclinical level. In addition, the contribution of alexithymia, a trait characterised by impaired interoceptive awareness and empathy, and elevated in those with ASD, is currently unclear. The present two-part study employed a comprehensive battery of tasks to examine these processes. Findings support the notion that executive function and theory of mind are related abilities. They also suggest that individuals with elevated levels of autism-like traits experience a partially similar pattern of social and executive function difficulties to those diagnosed with ASD, and that these impairments are not explained by co-occurring alexithymia.

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12. Hendren RL, James SJ, Widjaja F, Lawton B, Rosenblatt A, Bent S. {{Randomized, Placebo-Controlled Trial of Methyl B12 for Children with Autism}}. {J Child Adolesc Psychopharmacol};2016 (Feb 18)
OBJECTIVE: Children with autism spectrum disorder (ASD) have been reported to have reduced ability to methylate DNA and elevated markers of oxidative stress. We sought to determine if methyl B12, a key metabolic cofactor for cellular methylation reactions and antioxidant defense, could improve symptoms of ASD. METHODS: A total of 57 children with ASD were randomly assigned to 8 weeks of treatment with methyl B12 (75 mug/kg) or saline placebo every 3 days in a subcutaneous injection. The primary outcome measure was overall improvement in symptoms of ASD as measured by the Clinical Global Impressions-Improvement (CGI-I) score. Secondary outcome measures included changes in the Aberrant Behavior Checklist (ABC) and the Social Responsiveness Scale (SRS). Laboratory measures of methionine methylation and antioxidant glutathione metabolism were assessed at baseline and 8 weeks. RESULTS: A total of 50 children (mean age 5.3 years, 79% male) completed the study. The primary outcome measure – the clinician rated CGI-I score – was statistically significantly better (lower) in the methyl B12 group (2.4) than in the placebo group (3.1) (0.7 greater improvement in the methyl B12 group, 95% CI 1.2-0.2, p = 0.005). Clinical improvement among children treated with methyl B12 was positively correlated with increases in plasma methionine (p = 0.05), decreases in S-adenosyl-l-homocysteine (SAH) (p = 0.007) and improvements in the ratio of S-adenosylmethionine (SAM) to SAH (p = 0.007), indicating an improvement in cellular methylation capacity. No improvements were observed in the parent-rated ABC or SRS. CONCLUSIONS: Methyl B12 treatment improved clinician-rated symptoms of ASD that were correlated with improvements in measures of methionine metabolism and cellular methylation capacity. Clinical Trial Registry: Efficacy Study of Subcutaneous Methyl B12 in Children with Autism: NCT01039792 ( clinicaltrials.gov1 ).

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13. Horiuchi M, Smith L, Maezawa I, Jin LW. {{CXCR1 ablation ameliorates motor and respiratory dysfunctions and improves survival of a Rett syndrome mouse model}}. {Brain Behav Immun};2016 (Feb 13)
Rett syndrome (RTT) is a neurodevelopmental disorder caused by loss-of-function mutations in the gene encoding MeCP2, an epigenetic modulator that binds the methyl CpG dinucleotide in target genes to regulate transcription. Previously we and others reported a role of microglia in the pathophysiology of RTT. Because microglia in the Mecp2 knockout (Mecp2KO) mouse model of RTT over-produce neurotoxic mediators glutamate and reactive oxygen species, we hypothesize that blocking neuron-microglia interaction by ablation of CX3CR1, a chemokine receptor expressed in microglia/myeloid cells mediating such interaction by pairing with its neuronal ligand CX3CL1, would ameliorate the RTT-like phenotype in Mecp2KO mice. Here we report that CX3CR1 ablation prolonged the lifespan of Mecp2KO mice from a median survival of 54.5 days to 74 days, and significantly improved the body weight gain, symptomatic scores, major respiratory parameters, and motor coordination and performance. CX3CR1 ablation rectified previously identified histological abnormalities in the Mecp2KO brain such as neuronal soma size in hippocampal CA2, and the number, soma size, and process complexity of microglia. Moreover, CX3CR1 ablation enhanced the neurotrophic action of microglia in Mecp2KO mice by producing higher amount of insulin-like growth factor 1. Our data support a role of myeloid cells/microglia in RTT and suggest a novel therapeutic approach for RTT by targeting CX3CR1 with specific antagonists or genetic downregulation.

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14. Jin J. {{JAMA PATIENT PAGE. Screening for Autism Spectrum Disorder}}. {JAMA};2016 (Feb 16);315(7):718.

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15. Klusek J, McGrath SE, Abbeduto L, Roberts JE. {{Pragmatic Language Features of Mothers With the FMR1 Premutation Are Associated With the Language Outcomes of Adolescents and Young Adults With Fragile X Syndrome}}. {J Speech Lang Hear Res};2016 (Feb 18):1-13.

Purpose: Pragmatic language difficulties have been documented as part of the FMR1 premutation phenotype, yet the interplay between these features in mothers and the language outcomes of their children with fragile X syndrome is unknown. This study aimed to determine whether pragmatic language difficulties in mothers with the FMR1 premutation are related to the language development of their children. Method: Twenty-seven mothers with the FMR1 premutation and their adolescent/young adult sons with fragile X syndrome participated. Maternal pragmatic language violations were rated from conversational samples using the Pragmatic Rating Scale (Landa et al., 1992). Children completed standardized assessments of vocabulary, syntax, and reading. Results: Maternal pragmatic language difficulties were significantly associated with poorer child receptive vocabulary and expressive syntax skills, with medium effect sizes. Conclusions: This work contributes to knowledge of the FMR1 premutation phenotype and its consequences at the family level, with the goal of identifying modifiable aspects of the child’s language-learning environment that may promote the selection of treatments targeting the specific needs of families affected by fragile X. Findings contribute to our understanding of the multifaceted environment in which children with fragile X syndrome learn language and highlight the importance of family-centered intervention practices for this group.

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16. Krakovich TM, McGrew JH, Yu Y, Ruble LA. {{Stress in Parents of Children with Autism Spectrum Disorder: An Exploration of Demands and Resources}}. {J Autism Dev Disord};2016 (Feb 17)
We applied the ABCX model of stress and coping to assess the association between child and family demands, school-based resources (i.e., parent-teacher alliance and COMPASS, a consultation intervention), and two measures of parent stress: perceptions of the demands of raising a child (Child domain) and reactions to those demands (Parent domain). Data were analyzed from seventy-nine parents of children ages 3-9 with ASD participating in two randomized controlled trials of COMPASS. Stronger parent-teacher alliance correlated with decreased Parent domain stress and participation in COMPASS correlated with decreased Child domain stress after controlling for baseline stress. The study indicates that school-based resources can help reduce parent stress.

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17. Lewis C, Vigo L, Novak L, Klein EJ. {{Listening to Parents: A Qualitative Look at the Dental and Oral Care Experiences of Children with Autism Spectrum Disorder}}. {Pediatr Dent};2015;37(7):98-104.

PURPOSE: Children with autism spectrum disorder (ASD) experience various barriers to optimal dental and oral care. The purpose of this study was to conduct focus groups of parents of children with autism spectrum disorder and subsequent qualitative analysis of the interviews in order to better understand problems in dental and oral care encountered by children with ASD. METHODS: Four focus groups, comprised of parents of children with ASD, ranging in age from three to 17 years old, were assembled. We took a semi-structured approach, facilitating discussion about home oral hygiene and professional dental care. Audiotapes were transcribed and independently coded by four investigators who then jointly identified themes. RESULTS: There were three overarching, interrelated themes: (1) There is variability between children with ASD in how they tolerate dental and oral care and in what facilitates such care. (2) Parents want more extensive dental care for their children with ASD. (3) Each child’s dental and oral care should be individualized based on parents’ input about the unique characteristics and needs of their child. CONCLUSIONS: There is no « one size fits all » approach to dental and oral care for children with autism spectrum disorder. Parents are valuable partners in informing the unique dental and oral care needs of their child with ASD.

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18. Mei Y, Monteiro P, Zhou Y, Kim JA, Gao X, Fu Z, Feng G. {{Adult restoration of Shank3 expression rescues selective autistic-like phenotypes}}. {Nature};2016 (Feb 17)
Because autism spectrum disorders are neurodevelopmental disorders and patients typically display symptoms before the age of three, one of the key questions in autism research is whether the pathology is reversible in adults. Here we investigate the developmental requirement of Shank3 in mice, a prominent monogenic autism gene that is estimated to contribute to approximately 1% of all autism spectrum disorder cases. SHANK3 is a postsynaptic scaffold protein that regulates synaptic development, function and plasticity by orchestrating the assembly of postsynaptic density macromolecular signalling complex. Disruptions of the Shank3 gene in mouse models have resulted in synaptic defects and autistic-like behaviours including anxiety, social interaction deficits, and repetitive behaviour. We generated a novel Shank3 conditional knock-in mouse model, and show that re-expression of the Shank3 gene in adult mice led to improvements in synaptic protein composition, spine density and neural function in the striatum. We also provide behavioural evidence that certain behavioural abnormalities including social interaction deficit and repetitive grooming behaviour could be rescued, while anxiety and motor coordination deficit could not be recovered in adulthood. Together, these results reveal the profound effect of post-developmental activation of Shank3 expression on neural function, and demonstrate a certain degree of continued plasticity in the adult diseased brain.

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19. Montgomery CB, Allison C, Lai MC, Cassidy S, Langdon PE, Baron-Cohen S. {{Do Adults with High Functioning Autism or Asperger Syndrome Differ in Empathy and Emotion Recognition?}}. {J Autism Dev Disord};2016 (Feb 16)
The present study examined whether adults with high functioning autism (HFA) showed greater difficulties in (1) their self-reported ability to empathise with others and/or (2) their ability to read mental states in others’ eyes than adults with Asperger syndrome (AS). The Empathy Quotient (EQ) and ‘Reading the Mind in the Eyes’ Test (Eyes Test) were compared in 43 adults with AS and 43 adults with HFA. No significant difference was observed on EQ score between groups, while adults with AS performed significantly better on the Eyes Test than those with HFA. This suggests that adults with HFA may need more support, particularly in mentalizing and complex emotion recognition, and raises questions about the existence of subgroups within autism spectrum conditions.

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20. Ngamsamut N, Hongkaew Y, Vanwong N, Srisawasdi P, Puangpetch A, Chamkrachchangpada B, Tan-Kam T, Limsila P, Sukasem C. {{9-Hydroxyrisperidone-induced Hyperprolactinaemia in Thai Children and Adolescents with Autism Spectrum Disorder}}. {Basic Clin Pharmacol Toxicol};2016 (Feb 16)
Although our previous study revealed an association between prolactin level and risperidone dosage, data regarding the plasma concentration of risperidone are lacking. Therefore, this study aimed to investigate any association between plasma drug concentrations of risperidone, 9-hydroxyrisperidone and serum prolactin level in Thai children and adolescents with autism spectrum disorders (ASD). The individuals for this study were 103 children and adolescents with ASD (90 males and 13 females). In the 12th hour after the last risperidone dose, blood samples were collected for analysis. Serum prolactin, plasma risperidone and 9-hydroxyrisperidone levels were measured. Patients’ clinical data were collected from medical records – age, weight, height, body mass index, dose of risperidone and duration of treatment. Serum prolactin level was significantly positively correlated with plasma 9-hydroxyrisperidone level (rs = 0.355, P < 0.001). The median concentration of 9-hydroxyrisperidone in individuals with hyperprolactinaemia (7.59 ng/ml; IQR 4.86-15.55) was significantly higher than non-hyperprolactinaemic individuals (5.18 ng/ml; IQR 2.10-8.99) after risperidone treatment (P = 0.006). By multivariate analysis, high prolactin level was correlated to high 9-hydroxyrisperidone level (P = 0.010). The results of this study showed that serum prolactin levels, especially in autistic individuals with hyperprolactinaemia during risperidone treatment, were significantly correlated with the level of 9-hydroxyrisperidone. These results suggest that hyperprolactinaemia may develop during risperidone treatment. This article is protected by copyright. All rights reserved. Lien vers le texte intégral (Open Access ou abonnement)

21. Parkinson J. {{Gender Dysphoria and Autism Spectrum Disorders: A Note of Caution}}. {LGBT Health};2016 (Feb 16)

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22. Powell CM. {{Autism Screening or Smoke Screen and Mirrors?}}. {JAMA Neurol};2016 (Feb 16)

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23. Riquelme I, Hatem SM, Montoya P. {{Abnormal Pressure Pain, Touch Sensitivity, Proprioception, and Manual Dexterity in Children with Autism Spectrum Disorders}}. {Neural Plast};2016;2016:1723401.

Children with autism spectrum disorders (ASD) often display an abnormal reactivity to tactile stimuli, altered pain perception, and lower motor skills than healthy children. Nevertheless, these motor and sensory deficits have been mostly assessed by using clinical observation and self-report questionnaires. The present study aims to explore somatosensory and motor function in children with ASD by using standardized and objective testing procedures. Methods. Tactile and pressure pain thresholds in hands and lips, stereognosis, proprioception, and fine motor performance of the upper limbs were assessed in high-functioning children with ASD (n = 27) and compared with typically developing peers (n = 30). Results. Children with ASD showed increased pain sensitivity, increased touch sensitivity in C-tactile afferents innervated areas, and diminished fine motor performance and proprioception compared to healthy children. No group differences were observed for stereognosis. Conclusion. Increased pain sensitivity and increased touch sensitivity in areas classically related to affective touch (C-tactile afferents innervated areas) may explain typical avoiding behaviors associated with hypersensitivity. Both sensory and motor impairments should be assessed and treated in children with ASD.

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24. Rommelse NN, Hartman CA. {{Review: changing (shared) heritability of ASD and ADHD across the lifespan}}. {Eur Child Adolesc Psychiatry};2016 (Feb 16)

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25. Silverstein M, Radesky J. {{Embrace the Complexity: The US Preventive Services Task Force Recommendation on Screening for Autism Spectrum Disorder}}. {JAMA};2016 (Feb 16);315(7):661-662.

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26. Siu AL, Bibbins-Domingo K, Grossman DC, Baumann LC, Davidson KW, Ebell M, Garcia FA, Gillman M, Herzstein J, Kemper AR, Krist AH, Kurth AE, Owens DK, Phillips WR, Phipps MG, Pignone MP. {{Screening for Autism Spectrum Disorder in Young Children: US Preventive Services Task Force Recommendation Statement}}. {JAMA};2016 (Feb 16);315(7):691-696.

DESCRIPTION: New US Preventive Services Task Force (USPSTF) recommendation on screening for autism spectrum disorder (ASD) in young children. METHODS: The USPSTF reviewed the evidence on the accuracy, benefits, and potential harms of brief, formal screening instruments for ASD administered during routine primary care visits and the benefits and potential harms of early behavioral treatment for young children identified with ASD through screening. POPULATION: This recommendation applies to children aged 18 to 30 months who have not been diagnosed with ASD or developmental delay and for whom no concerns of ASD have been raised by parents, other caregivers, or health care professionals. RECOMMENDATION: The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for ASD in young children for whom no concerns of ASD have been raised by their parents or a clinician. (I statement).

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27. Stubbs G, Henley K, Green J. {{Autism: Will vitamin D supplementation during pregnancy and early childhood reduce the recurrence rate of autism in newborn siblings?}}. {Med Hypotheses};2016 (Mar);88:74-78.

BACKGROUND: Vitamin D deficiency is widespread in the world including the vulnerable group of pregnant women. Vitamin D deficiency during pregnancy is hypothesized to contribute to the cause of autism. Further, it is hypothesized that vitamin D supplementation during pregnancy and early childhood will reduce the recurrence rate of autism in newborn siblings. METHODS: To investigate the hypothesis an open label prospective study was performed prescribing vitamin D during pregnancy to mothers of children with autism at a dose of 5000IU/day. The newborn siblings were at high risk for the recurrence of autism. The newborn infants were also prescribed vitamin D, 1000IU/day to their third birthday. The newborn siblings were followed for three years and during that time, were assessed for autism on two separate occasions: at 18months and 36months of age. The results were compared to the reported recurrence rates in siblings of autistic children in the literature. RESULTS: The final outcome was 1 out of 19 (5%) developed autism in contrast to the recurrence rate of approximately 20% in the literature. We did not have a control group, nor was there blinding. CONCLUSIONS: The results are promising, however, this is a preliminary study with very small numbers and was uncontrolled. Further study with larger numbers is indicated. The ethics of prescribing a low dosage of vitamin D such as 400IU D3/day to a control group of mothers in comparison to a large dose such as 5000IU D3/day are problematic in our opinion.

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28. Tsang T, Gillespie-Lynch K, Hutman T. {{Theory of Mind Indexes the Broader Autism Phenotype in Siblings of Children with Autism at School Age}}. {Autism Res Treat};2016;2016:6309189.

Subclinical variants of the social-communicative challenges and rigidity that define autism spectrum disorder (ASD) are known as the broader autism phenotype (BAP). The BAP has been conceptualized categorically (as specific to a subset of relatives of individuals with ASD) and dimensionally (as continuously distributed within the general population). The current study examined the compatibility of these two approaches by assessing associations among autism symptoms and social-communicative skills in young school-age children with ASD, children who have a sibling with ASD, and children without a sibling with ASD. Autism symptoms were associated with reduced Theory of Mind (ToM), adaptive skills, cognitive empathy, and language skills across the full sample. Reduced ToM was a core aspect of the BAP in the current sample regardless of whether the BAP was defined categorically (in terms of siblings of children with ASD who exhibited atypical developmental) or dimensionally (in terms of associations with autism symptoms across the entire sample). Early language skills predicted school-age ToM. Findings support the compatibility of categorical and dimensional approaches to the BAP, highlight reduced ToM as a core aspect of the school-age BAP, and suggest that narrative-based approaches to promoting ToM may be beneficial for siblings of children with ASD.

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29. Turkoglu S, Turkoglu G. {{Comorbid Gender Dysphoria in a Preadolescent Boy With Fragile X Syndrome}}. {Arch Sex Behav};2016 (Feb 16)

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30. Veenstra-VanderWeele J, McGuire K. {{Rigid, Inflexible Approach Results in No Recommendation for Autism Screening}}. {JAMA Psychiatry};2016 (Feb 16)

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31. Venker CE, Haebig E, Edwards J, Saffran JR, Ellis Weismer S. {{Brief Report: Early Lexical Comprehension in Young Children with ASD: Comparing Eye-Gaze Methodology and Parent Report}}. {J Autism Dev Disord};2016 (Feb 16)
Lexical comprehension is commonly measured by parent report, but it may be difficult for parents of children with ASD to accurately judge their child’s comprehension. We compared parent report to an eye-gaze measure of lexical comprehension in which participants observed pairs of images on a screen, along with accompanying speech that named one of the two images. Twenty-two toddlers with ASD participated. Trials were included if the target word was reported as unknown. Children spent significantly more time looking at the target after it was named than before (d = 0.66). These results provide evidence that eye-gaze measures can reveal emerging lexical knowledge in young children with ASD that may otherwise be overlooked.

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32. Webb SJ, Neuhaus E, Faja S. {{Face Perception and Learning in Autism Spectrum Disorders}}. {Q J Exp Psychol (Hove)};2016 (Feb 17):1-44.

Autism Spectrum Disorder (ASD) is characterized by impairment in social communication and restricted and repetitive interests (American Psychiatric Association, 2013). While not included in the diagnostic characterization, aspects of face processing and learning have shown disruptions at all stages of development in ASD, although the exact nature and extent of the impairment varies by age and level of functioning of the ASD sample as well as by task demands. In this review, we examine the nature of face attention, perception, and learning in individuals with ASD focusing on 3 broad age ranges (early development, middle childhood, and adolescence/adulthood). We propose that early delays in basic face processing contribute to the atypical trajectory of social communicative skills in individuals with ASD and contribute to poor social learning throughout development. Face learning is a life-long necessity, as the social world of individual only broadens with age, and thus addressing both the source of the impairment in ASD as well as the trajectory of ability throughout the lifespan, through targeted treatments, may serve to positively impact the lives of individuals who struggle with social understanding and information.

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