1. {{A majority of parents accept newborn screening for fragile X}}. {Am J Med Genet A}. 2011 Sep;155(9):x-xi.
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2. Buckley AW, Sassower K, Rodriguez AJ, Jennison K, Wingert K, Buckley J, et al. {{An open label trial of donepezil for enhancement of rapid eye movement sleep in young children with autism spectrum disorders}}. {J Child Adolesc Psychopharmacol}. 2011 Aug;21(4):353-7.
Abstract Background: Rapid eye movement (REM) sleep is greatest in the developing brain, is driven by acetylcholine, and may represent a protected time for neuroplasticity. Recently published data from our lab observed that children with autism spent significantly less time in this state during a single night recording than did typically developing children and those with developmental delay without autism. The objective of this study was to determine whether or not donepezil can increase the REM % in children with diagnosed autism spectrum disorder (ASD) found to have REM % values of at least two standard deviations below expected for age. Methods: Five subjects found to have an ASD (ages 2.5-6.9 years) and demonstrated deficits in REM sleep compared with within-lab controls were enrolled in a dose finding study of donepezil. Each subject was examined by polysomnography for REM sleep augmentation after drug administration. Results: REM sleep as a percentage of Total Sleep Time was increased significantly and REM latency was decreased significantly after drug administration in all subjects. No other observed sleep parameter was changed significantly. Conclusions: Donepezil can increase the amount of time that children with an ASD spend in the REM sleep state. A double-blind, placebo-controlled trial is needed to assess the association between REM sleep augmentation and learning, cognition, and behavior in such children.
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3. Dager SR, Corrigan NM, Estes A, Shaw DW. {{Further Commentary on Mitochondrial Dysfunction in Autism Spectrum Disorder: Assessment and Treatment Considerations}}. {J Autism Dev Disord}. 2011 Aug 19.
The authors respond to a recent letter (Rossignol and Frye 2011) critical of their paper, « Proton magnetic resonance spectroscopy and MRI reveal no evidence for brain mitochondrial dysfunction in children with autism spectrum disorder » (Corrigan et al. 2011). Further considerations regarding the assessment of mitochondrial dysfunction in autism spectrum disorder, and related treatment considerations, are discussed.
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4. Dykens EM, Lee E, Roof E. {{Prader-Willi syndrome and autism spectrum disorders: an evolving story}}. {J Neurodev Disord}. 2011 Aug 20.
Prader-Willi syndrome (PWS) is well-known for its genetic and phenotypic complexities. Caused by a lack of paternally derived imprinted material on chromosome 15q11-q13, individuals with PWS have mild to moderate intellectual disabilities, repetitive and compulsive behaviors, skin picking, tantrums, irritability, hyperphagia, and increased risks of obesity. Many individuals also have co-occurring autism spectrum disorders (ASDs), psychosis, and mood disorders. Although the PWS 15q11-q13 region confers risks for autism, relatively few studies have assessed autism symptoms in PWS or directly compared social, behavioral, and cognitive functioning across groups with autism or PWS. This article identifies areas of phenotypic overlap and difference between PWS and ASD in core autism symptoms and in such comorbidities as psychiatric disorders, and dysregulated sleep and eating. Though future studies are needed, PWS provides a promising alternative lens into specific symptoms and comorbidities of autism.
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5. Golnik A, Scal P, Wey A, Gaillard P. {{Autism-Specific Primary Care Medical Home Intervention}}. {J Autism Dev Disord}. 2011 Aug 19.
Forty-six subjects received primary medical care within an autism-specific medical home intervention ( www.autismmedicalhome.com ) and 157 controls received standard primary medical care. Subjects and controls had autism spectrum disorder diagnoses. Thirty-four subjects (74%) and 62 controls (40%) completed pre and post surveys. Controlling for pre-survey medical home status, subjects had 250% greater odds of receipt of a medical home at the study end compared to controls (p = 0.021). Compared to controls, subjects receiving the intervention reported significantly more satisfaction (p = 0.0004), greater shared decision making (p = 0.0005) and fewer unmet needs (p = 0.067). However, subjects reported no change in family stress (p = 0.204).
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6. Laugeson EA, Frankel F, Gantman A, Dillon AR, Mogil C. {{Evidence-Based Social Skills Training for Adolescents with Autism Spectrum Disorders: The UCLA PEERS Program}}. {J Autism Dev Disord}. 2011 Aug 20.
The present study examines the efficacy and durability of the PEERS Program, a parent-assisted social skills group intervention for high-functioning adolescents with ASD. Results indicate that teens receiving PEERS significantly improved their social skills knowledge, social responsiveness, and overall social skills in the areas of social communication, social cognition, social awareness, social motivation, assertion, cooperation, and responsibility, while decreasing autistic mannerisms and increasing the frequency of peer interactions. Independent teacher ratings revealed significant improvement in social skills and assertion from pre-test to follow-up assessment. Examination of durability of improvement revealed maintenance of gains in nearly all domains with additional treatment gains at a 14-week follow-up assessment.
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7. Norris M, Lecavalier L, Edwards MC. {{The Structure of Autism Symptoms as Measured by the Autism Diagnostic Observation Schedule}}. {J Autism Dev Disord}. 2011 Aug 20.
The current study tested several competing models of the autism phenotype using data from modules 1 and 3 of the ADOS. Participants included individuals with ASDs aged 3-18 years (N = 1,409) from the AGRE database. Confirmatory factor analyses were performed on total samples and subsamples based on age and level of functioning. Three primary models were tested, including a one-factor model, the DSM-IV model, and the anticipated DSM-V model. Results indicated all models fit similarly. Module 1 ratings yielded better indices of fit across all models and higher inter-factor correlations than Model 3. Model fits were impacted by age and level of functioning. The lack of differentiation between models suggests that the structure of ASD symptoms is complex to measure statistically.
