1. Blood GW, Blood IM, Coniglio AD, Finke EH, Boyle MP. {{Familiarity breeds support: Speech-language pathologists’ perceptions of bullying of students with autism spectrum disorders}}. {J Commun Disord};2013 (Jan 31)
Children with autism spectrum disorders (ASD) are primary targets for bullies and victimization. Research shows school personnel may be uneducated about bullying and ways to intervene. Speech-language pathologists (SLPs) in schools often work with children with ASD and may have victims of bullying on their caseloads. These victims may feel most comfortable turning to SLPs for help during one-to-one treatment sessions to discuss these types of experiences. A nationwide survey mailed to 1000 school-based SLPs, using a vignette design technique, determined perceptions about intervention for bullying and use of specific strategies. Results revealed a majority of the SLPs (89%) responses were in « likely » or « very likely » to intervene categories for all types of bullying (physical, verbal, relational and cyber), regardless of whether the episode was observed or not. A factor analysis was conducted on a 14 item strategy scale for dealing with bullying for children with ASD. Three factors emerged, labeled « Report/Consult », « Educate the Victim », and Reassure the Victim ». SLPs providing no services to children with ASD on their caseloads demonstrated significantly lower mean scores for the likelihood of intervention and using select strategies. SLPs may play an important role in reducing and/or eliminating bullying episodes in children with ASD. Learning outcomes: Readers will be able to (a) explain four different types of bullying, (b) describe the important role of school personnel in reducing and eliminating bullying, (c) describe the perceptions and strategies selected by SLPs to deal with bullying episodes for students with ASD, and (d) outline the potential role of SLPs in assisting students with ASD who are victimized.
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2. Farmer C, Thurm A, Grant P. {{Pharmacotherapy for the Core Symptoms in Autistic Disorder: Current Status of the Research}}. {Drugs};2013 (Mar 16)
The current review covers extant literature on pharmacotherapy for core symptoms of autism. The core symptoms of autism include impairments in social interaction and communication, as well as the presence of restricted and repetitive behaviors. There are no known efficacious treatments for the core social symptoms, although effects on repetitive behaviors are indicated with some data. While studies of fenfluramine, secretin, opiates, and mood stabilizers generally find no effect, mixed results suggest more research is needed on antidepressants and atypical antipsychotics. Newer lines of research, including cholinergic and glutamatergic agents and oxytocin, will be of considerable interest in the future. However, research on the treatment of core symptoms is plagued by limitations in study design, statistical power, and other issues inherent to the study of treatments for autism (e.g., heterogeneity of the disorder) that continue to prevent the elucidation of efficacious treatments.
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3. Golubchik P, Sever J, Weizman A. {{Reboxetine treatment for autistic spectrum disorder of pediatric patients with depressive and inattentive/hyperactive symptoms: an open-label trial}}. {Clin Neuropharmacol};2013 (Mar);36(2):37-41.
BACKGROUND: Reboxetine is a norepinephrine reuptake inhibitor that may be useful in treating pediatric depression as well as attention-deficit/hyperactivity disorder (ADHD). Both are often comorbid with autistic spectrum disorder (ASD). We evaluated the effectiveness of reboxetine treatment in pediatric patients with ASD with symptoms of depression and ADHD. METHOD: Eleven adolescent patients with ASD (9 boys and 2 girls, aged 12.2 +/- 3.6 years) with depressive and ADHD symptoms were treated with reboxetine (maximal dose, 4 mg/d) in an open-label trial during a 12-week period. The severity of depressive and ADHD symptoms was assessed by the Child Depression Rating Scale (CDRS) and Attention-Deficit/Hyperactivity Disorder Rating Scale (ADHD-RS), respectively. RESULTS: Significant, but modest, decreases in the severity of depressive symptoms (CDRS before vs after scores: 65.5 +/- 10.8 vs 58.3 +/- 8.2; paired t test, 3.1; df, 10; P =0.01) and ADHD symptoms (Attention Deficit/Hyperactivity Disorder Rating Scale before vs after: 36.4 +/- 5 vs 32.8 +/- 5; paired-t test, 2.94; df, 10; P = 0.015) were obtained after reboxetine treatment. The patients (n = 5) with high baseline scores of CDRS (T score >75) showed a trend toward larger response to reboxetine than those (n = 6) with low (T score <75) basal CDRS scores (Delta, 12.8 +/- 5.4 vs 2.3 +/- 5.2; P = 0.07).A significant positive correlation was found between the changes in the total scores of the depression and the ADHD severity (Spearman correlation r = 0.65 [95% confidence interval, 0.09-0.9]; n = 11; P = 0.029). Most of the patients (approximately 90%) reported tolerable adverse effects. CONCLUSIONS: Reboxetine treatment may reduce, modestly but significantly, depressive and ADHD symptoms in adolescents with ASD. High rate of adverse effects requires close monitoring.
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4. Napolioni V, Ober-Reynolds B, Szelinger S, Corneveaux JJ, Pawlowski T, Ober-Reynolds S, Kirwan J, Persico AM, Melmed RD, Craig DW, Smith CJ, Huentelman MJ. {{Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder}}. {J Neuroinflammation};2013 (Mar 14);10(1):38.
OBJECTIVE: Converging lines of evidence point to the existence of immune dysfunction in autism spectrum disorder (ASD), which could directly affect several key neurodevelopmental processes. Previous studies have shown higher cytokine levels in patients with autism compared with matched controls or subjects with other developmental disorders. In the current study, we used plasma-cytokine profiling for 25 discordant sibling pairs to evaluate whether these alterations occur within families with ASD. METHODS: Plasma-cytokine profiling was conducted using an array-based multiplex sandwich ELISA for simultaneous quantitative measurement of 40 unique targets. We also analyzed the correlations between cytokine levels and clinically relevant quantitative traits (Vineland Adaptive Behavior Scale in Autism (VABS) composite score, Social Responsiveness Scale (SRS) total T score, head circumference, and full intelligence quotient (IQ)). In addition, because of the high phenotypic heterogeneity of ASD, we defined four subgroups of subjects (those who were non-verbal, those with gastrointestinal issues, those with regressive autism, and those with a history of allergies), which encompass common and/or recurrent endophenotypes in ASD, and tested the cytokine levels in each group. RESULTS: None of the measured parameters showed significant differences between children with ASD and their related typically developing siblings. However, specific target levels did correlate with quantitative clinical traits, and these were significantly different when the ASD subgroups were analyzed. It is notable that these differences seem to be attributable to a predisposing immunogenetic background, as no other significant differences were noticed between discordant sibling pairs. Interleukin-1beta appears to be the cytokine most involved in quantitative traits and clinical subgroups of ASD. CONCLUSIONS: In the present study, we found a lack of significant differences in plasma-cytokine levels between children with ASD and in their related non-autistic siblings. Thus, our results support the evidence that the immune profiles of children with autism do not differ from their typically developing siblings. However, the significant association of cytokine levels with the quantitative traits and the clinical subgroups analyzed suggests that altered immune responses may affect core feature of ASD.
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5. Terrett G, Rendell PG, Raponi-Saunders S, Henry JD, Bailey PE, Altgassen M. {{Episodic Future Thinking in Children with Autism Spectrum Disorder}}. {J Autism Dev Disord};2013 (Mar 16)
The capacity to imagine oneself experiencing future events has important implications for effective daily living but investigation of this ability in autism spectrum disorder (ASD) is limited. This study investigated future thinking in 30 children with high functioning ASD (IQ > 85) and 30 typically developing children. They completed the Adapted Autobiographical Interview, a measure which required participants to describe personal past events (indexing episodic memory) and plausible future events (indexing episodic future thinking). The results showed that there are ASD-related deficits in future thinking, and also provided preliminary evidence regarding cognitive mechanisms that may (and may not) contribute to these difficulties. The theoretical and practical implications of these results are discussed.
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6. Wilson CE, Gillan N, Spain D, Robertson D, Roberts G, Murphy CM, Maltezos S, Zinkstok J, Johnston K, Dardani C, Ohlsen C, Deeley PQ, Craig M, Mendez MA, Happe F, Murphy DG. {{Comparison of ICD-10R, DSM-IV-TR and DSM-5 in an Adult Autism Spectrum Disorder Diagnostic Clinic}}. {J Autism Dev Disord};2013 (Mar 16)
An Autism Spectrum Disorder (ASD) diagnosis is often used to access services. We investigated whether ASD diagnostic outcome varied when DSM-5 was used compared to ICD-10R and DSM-IV-TR in a clinical sample of 150 intellectually able adults. Of those diagnosed with an ASD using ICD-10R, 56 % met DSM-5 ASD criteria. A further 19 % met DSM-5 (draft) criteria for Social Communication Disorder. Of those diagnosed with Autistic Disorder/Asperger Syndrome on DSM-IV-TR, 78 % met DSM-5 ASD criteria. Sensitivity of DSM-5 was significantly increased by reducing the number of criteria required for a DSM-5 diagnosis, or by rating ‘uncertain’ criteria as ‘present’, without sacrificing specificity. Reduced rates of ASD diagnosis may mean some ASD individuals will be unable to access clinical services.
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7. Xu H, Rosales-Reynoso MA, Barros-Nunez P, Peprah E. {{DNA repair/replication transcripts are down regulated in patients with Fragile X syndrome}}. {BMC Res Notes};2013 (Mar 11);6(1):90.
BACKGROUND: Fragile X syndrome (FXS) and its associated disorders are caused by the expansion of the CGG repeat in the 5′ untranslated region of the fragile X mental retardation 1 (FMR1) gene, with disease classification based on the number of CGG repeats. The mechanisms of repeat expansion are dependent on the presence of cis elements and the absence of trans factors both of which are not mutually exclusive and contribute to repeat instability. Expansions associated with trans factors are due to the haploinsuffient or reduced expression of several DNA repair/metabolizing proteins. The reduction of expression in trans factors has been primarily conducted in animal models without substantial examination of many of these expansion mechanism and trans factors in humans. RESULTS: To understand the trans factors and pathways associated with trinucleotide repeat expansion we have analyzed two microarray datasets which characterized the transcript expression in patients with FXS and in controls. CONCLUSION: We observed significant down regulation of DNA damage/repair pathway transcripts. This observation was consistent in both datasets, which used different populations. Within these datasets, several transcripts overlapped in the direction of association and fold change. Further characterization of these genes will be critical to understand their role in trinucleotide repeat instability in FXS.
