The Repetitive Behavior Scale-Revised: independent validation in individuals with autism spectrum disorders.
ABSTRACT A key feature of autism is restricted repetitive behavior (RRB). Despite the significance of RRBs, little is known about their phenomenology, assessment, and treatment. The Repetitive Behavior Scale-Revised (RBS-R) is a recently-developed questionnaire that captures the breadth of RRB in autism. To validate the RBS-R in an independent sample, we conducted a survey within the South Carolina Autism Society. A total of 320 caregivers (32%) responded. Factor analysis produced a five-factor solution that was clinically meaningful and statistically sound. The factors were labeled "Ritualistic/Sameness Behavior," "Stereotypic Behavior," "Self-injurious Behavior," "Compulsive Behavior," and "Restricted Interests." Measures of internal consistency were high for this solution, and interrater reliability data suggested that the RBS-R performs well in outpatient settings.
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ABSTRACT: Restricted repetitive behaviors (RRBs) were examined in a large group of children, adolescents and adults with ASD in order to describe age-related patterns of symptom change and association with specific contextual factors, and to examine if the patterns of change are different for the various types of RRBs. Over 700 individuals with ASD were rated on the Repetitive Behavior Scale-Revised. RRBs were less frequent and less severe among older than younger individuals, corroborating that autism symptoms abate with age. Our findings further suggest that repetitive behaviors are a heterogeneous group of behaviors, with the subtypes of RRBs having their own individual patterns across the lifespan, and in some cases, a differential association with age depending on intellectual functioning.Journal of Autism and Developmental Disorders 07/2008; 39(1):57-66. DOI:10.1007/s10803-008-0599-x · 3.34 Impact Factor
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ABSTRACT: Autism is an etiologically heterogeneous neurodevelopmental disorder for which there is no known unifying etiology or pathogenesis. Many conditions of atypical development can lead to autism, including fragile X syndrome (FXS), which is presently the most common known single-gene cause of autism. To examine whole-brain morphometric patterns that discriminate young boys with FXS from those with idiopathic autism (iAUT) as well as control participants. Cross-sectional, in vivo neuroimaging study. Academic medical centers. Young boys (n = 165; aged 1.57-4.15 years) diagnosed as having FXS or iAUT as well as typically developing and idiopathic developmentally delayed controls. Univariate voxel-based morphometric analyses, voxel-based morphometric multivariate pattern classification (linear support vector machine), and clustering analyses (self-organizing map). We found that frontal and temporal gray and white matter regions often implicated in social cognition, including the medial prefrontal cortex, orbitofrontal cortex, superior temporal region, temporal pole, amygdala, insula, and dorsal cingulum, were aberrant in FXS and iAUT as compared with controls. However, these differences were in opposite directions for FXS and iAUT relative to controls; in general, greater volume was seen in iAUT compared with controls, who in turn had greater volume than FXS. Multivariate analysis showed that the overall pattern of brain structure in iAUT generally resembled that of the controls more than FXS, both with and without AUT. Our findings demonstrate that FXS and iAUT are associated with distinct neuroanatomical patterns, further underscoring the neurobiological heterogeneity of iAUT.Archives of general psychiatry 11/2010; 68(3):295-305. DOI:10.1001/archgenpsychiatry.2010.153 · 13.75 Impact Factor
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ABSTRACT: Epidemiological data have suggested maternal infection and fever to be associated with increased risk of autism spectrum disorder (ASD). Animal studies show that gestational infections perturb fetal brain development and result in offspring with the core features of autism and have demonstrated that behavioral effects of maternal immune activation are dependent on genetic susceptibility. The goal of this study was to explore the impact of ASD-associated copy number variants (CNVs) and prenatal maternal infection on clinical severity of ASD within a dataset of prenatal history and complete genetic and phenotypic findings. We analyzed data from the Simons Simplex Collection sample including 1971 children with a diagnosis of ASD aged 4 to 18 years who underwent array comparative genomic hybridization screening. Information on infection and febrile episodes during pregnancy was collected through parent interview. ASD severity was clinically measured through parent-reported interview and questionnaires. We found significant interactive effects between the presence of CNVs and maternal infection during pregnancy on autistic symptomatology, such that individuals with CNVs and history of maternal infection demonstrated increased rates of social communicative impairments and repetitive/restricted behaviors. In contrast, no significant interactions were found between presence of CNVs and prenatal infections on cognitive and adaptive functioning of individuals with ASD. Our findings support a gene-environment interaction model of autism impairment, in that individuals with ASD-associated CNVs are more susceptible to the effects of maternal infection and febrile episodes in pregnancy on behavioral outcomes and suggest that these effects are specific to ASD rather than to global neurodevelopment.Journal of developmental and behavioral pediatrics: JDBP 01/2015; DOI:10.1097/DBP.0000000000000126 · 2.12 Impact Factor