PubMed · 16586156
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Fred Volkmar. 2006. Ask the editor.. https://doi.org/10.1007/s10803-006-0083-4
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The importance of early developmental and behavioral treatment for children with autism is increasingly recognized. Little is known, however, about early intervention policies that may affect service delivery to these children. The current study describes states' policies for providing early intervention services to children with Autistic Spectrum Disorders under the Individuals with Disabilities Education Act Part C and examines how Part C policies are associated with the proportion of school-age children diagnosed with autism served under IDEA. Results indicate few consistencies among states in policies and practices regarding the identification and care of infants and toddlers with autism. The implications of state variation for policy makers are discussed.
The identification of autism susceptibility genes has been hampered by phenotypic heterogeneity of autism, among other factors. However, the use of endophenotypes has shown preliminary success in reducing heterogeneity and identifying potential autism-related susceptibility regions. To further explore the utility of using language-related endophenotypes, we performed linkage analysis on multiplex autism families stratified according to delayed expressive speech and also assessed the extent to which parental phenotype information would aid in identifying regions of linkage. A whole genome scan using a multipoint non-parametric linkage approach was performed in 133 families, stratifying the sample by phrase speech delay and word delay (WD). None of the regions reached suggested genome-wide or replication significance thresholds. However, several loci on chromosomes 1, 2, 4, 6, 7, 8, 9, 10, 12, 15, and 19 yielded nominally higher linkage signals in the delayed groups. The results did not support reported linkage findings for loci on chromosomes 7 or 13 that were a result of stratification based on the language delay endophenotype. In addition, inclusion of information on parental history of language delay did not appreciably affect the linkage results. The nominal increase in NPL scores across several regions using language delay endophenotypes for stratification suggests that this strategy may be useful in attenuating heterogeneity. However, the inconsistencies in regions identified across studies highlight the importance of increasing sample sizes to provide adequate power to test replications in independent samples.
We examined autistic behavior in a cross-sectional sample of 179 children with fragile X syndrome (FXS) and a longitudinal subset of 116 children using the Childhood Autism Rating Scale (CARS) to (a) determine a prevalence of autistic behavior in FXS, (b) examine the stability of autistic ratings over time, and (c) assess the association between the fragile X mental retardation protein (FMRP) and autistic behavior. Approximately 21% of the sample of 129 children (25.9% of boys) scored at or above the cutoff for autism. CARS scores increased slowly, yet significantly, over time, and low levels of FMRP were associated with higher mean levels of autistic behavior as measured by the CARS.