Decline in Medicaid-Funded One-to-One Behavioral Support Use in School as Children Age
Objective: This study compared use of and associated expenditures for Medicaid-reimbursed school-based and out-of-school services for children with autism spectrum disorder (ASD) and those with other psychiatric disorders.
Methods: Philadelphia County Medicaid claims were used to identify children ages five to 17 who received behavioral health services through Medicaid any time between October 2008 and September 2009 (N=24,271). Children were categorized into four diagnostic groups: autism spectrum disorder (ASD), conduct disorder or oppositional defiant disorder (conduct-ODD), attention-deficit hyperactivity disorder (ADHD), and other psychiatric disorders. Logistic regression analysis compared use of in-school and out-of-school behavioral health services between children with ASD and children with other psychiatric disorders. Generalized linear models with gamma distribution were used to estimate differences in Medicaid expenditures for in-school and out-of-school services and total Medicaid expenditures for both service types by disorder, with adjustments for age, sex, and race-ethnicity.
Results: The most common diagnosis was ADHD (40%); 35% had other psychiatric disorders, 21% had conduct-ODD, and 4% had ASD. A significantly greater proportion of children with ASD (52%) received in-school behavioral health services (conduct-ODD, 5%; ADHD, 8%; and other psychiatric disorders, 1.7%) Per-child expenditures for both school-based and out-of-school behavioral health services were significantly higher for children with ASD than for children in the other groups.
Conclusions: Medicaid represents an important source of in-school and out-of-school care for children with ASD and their families. States that expand Medicaid under the Affordable Care Act should give careful consideration to covering school-based mental health services for children with ASD.
Phelan-McDermid syndrome (PMS), a monogenic form of autism spectrum disorder (ASD), results from deletion or mutation of the SHANK3 gene. Atypical sensory reactivity is now included in the diagnostic criteria for ASD. Examining the sensory phenotype in monogenic forms of ASD, such as PMS, may help identify underlying mechanisms of sensory reactivity. Using the Short Sensory Profile, the current study compared sensory reactivity in 24 children with PMS to 61 children with idiopathic ASD (iASD). Results suggest that children with PMS show more low energy/weak symptoms and less sensory sensitivity as compared to children with iASD. This study is the first to demonstrate differences in sensory reactivity between children with PMS and iASD, helping to refine the PMS phenotype.
Keywords: 22q13 deletion syndrome; Autism; Autism spectrum disorder; Phelan–McDermid syndrome; Sensory profile; Sensory reactivity.
Sensory reactivity is a new DSM-5 criterion for autism spectrum disorder (ASD). The current study aims to validate a clinician-administered sensory observation in ASD, the Sensory Processing Scale Assessment (SPS). The SPS and the Short Sensory Profile (SSP) parent-report were used to measure sensory reactivity in children with ASD (n = 35) and typically developing children (n = 27). Sixty-five percent of children with ASD displayed sensory reactivity symptoms on the SPS and 81.1 % on the SSP. SPS scores significantly predicted SSP scores. We next identified the five SPS tasks that best differentiated groups. Our results indicate that a combination of parent-report and at least the five most differentiating observational tasks may be most sensitive in identifying the presence of sensory reactivity issues.
Keywords: Autism spectrum disorder; New DSM-5 criterion; Sensory Processing Scale Assessment; Sensory reactivity.
There are inconsistent findings regarding parent and teacher agreement on behavioral ratings of their children with autism. One possible reason for this inconsistency is that studies have not taken autism severity into account. This study examined parent and teacher concordance of social behavior based on symptom severity for children with autism. Participants were 123 parent-teacher dyads who completed the Social Responsiveness Scale. Symptom severity was assessed using the Autism Diagnostic Observation Schedule (ADOS). Results indicated that parent and teacher ratings were statistically significantly correlated at the beginning and end of the academic year, but only for severely affected children. Teacher report of social deficits was correlated with symptom severity as measured by the ADOS; parent report was not. These findings have implications for improving assessment procedures and parent-teacher collaboration.
Keywords: Social Responsiveness Scale; autism; autism spectrum disorder; parent-teacher relationships; social behavior.
Introduction of the National Institute of Mental Health’s Research Domain Criteria and revision of diagnostic classification for Autism Spectrum Disorder in the latest diagnostic manual call for a new way of conceptualizing heterogeneous ASD features. We propose a novel conceptualization of ASD, borrowing from the schizophrenia literature in clustering ASD features along positive, negative, and cognitive dimensions. We argue that this dimensional conceptualization can offer improved ability to classify, diagnose, and treat, to apply and predict response to treatment, and to explore underlying neural and genetic alterations that may contribute to particular feature clusters. We suggest the proposed conceptualization can advance the field in a manner that may prove clinically and biologically useful for understanding and addressing heterogeneity within ASD.
Keywords: Autism spectrum disorder; Classification; Diagnosis; Heterogeneity; RDoC; Symptoms.
Background: Exposure to ambient air pollution is widespread and may be detrimental to human brain development and a potential risk factor for Autism Spectrum Disorder (ASD). We conducted a systematic review of the human evidence on the relationship between ASD and exposure to all airborne pollutants, including particulate matter air pollutants and others (e.g. pesticides and metals).
Objective: To answer the question: “is developmental exposure to air pollution associated with ASD?”
Methods: We conducted a comprehensive search of the literature, identified relevant studies using inclusion/exclusion criteria pre-specified in our protocol (registered in PROSPERO, CRD # 42015017890), evaluated the potential risk of bias for each included study and identified an appropriate subset of studies to combine in a meta-analysis. We then rated the overall quality and strength of the evidence collectively across all air pollutants.
Results: Of 1,158 total references identified, 23 human studies met our inclusion criteria (17 case-control, 4 ecological, 2 cohort). Risk of bias was generally low across studies for most domains; study limitations were related to potential confounding and accuracy of exposure assessment methods. We rated the quality of the body of evidence across all air pollutants as “moderate.” From our meta-analysis, we found statistically significant summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m3 increase in PM10 exposure (n = 6 studies) and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3 increase in PM2.5 exposure (n = 3 studies). For pollutants not included in a meta-analysis, we collectively evaluated evidence from each study in rating the strength and quality of overall evidence considering factors such as inconsistency, imprecision, and evidence of dose-response. All included studies generally showed increased risk of ASD with increasing exposure to air pollution, although not consistently across all chemical components.
Conclusion: After considering strengths and limitations of the body of research, we concluded that there is “limited evidence of toxicity” for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate. Our research supports the need for health protective public policy to reduce exposures to harmful airborne contaminants among pregnant women and children and suggests opportunities for optimizing future research.
Genetic studies of autism spectrum disorder (ASD) have established that de novo duplications and deletions contribute to risk. However, ascertainment of structural variants (SVs) has been restricted by the coarse resolution of current approaches. By applying a custom pipeline for SV discovery, genotyping, and de novo assembly to genome sequencing of 235 subjects (71 affected individuals, 26 healthy siblings, and their parents), we compiled an atlas of 29,719 SV loci (5,213/genome), comprising 11 different classes. We found a high diversity of de novo mutations, the majority of which were undetectable by previous methods. In addition, we observed complex mutation clusters where combinations of de novo SVs, nucleotide substitutions, and indels occurred as a single event. We estimate a high rate of structural mutation in humans (20%) and propose that genetic risk for ASD is attributable to an elevated frequency of gene-disrupting de novo SVs, but not an elevated rate of genome rearrangement.