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Objective: There are few well-evaluated uncomplicated community-based interventions for childhood aggression. Based on experience with provision and evaluation of community-based anger management programs under two funding models (research funding and government funding), this poster aims to examine the strengths and difficulties of providing community-based anger management programs under the different funding models. Methods: Community-based family-focused anger management programs for children 7-to 11- years old and their families have been provided in the Hamilton, Ontario community over the past 4 years. The programs include (i) caregiver/parent psycho-education/skill building group sessions, (ii) a children’s cognitive-behavioural therapy based group program and (iii) an individual family-based component. Program funding from 2002- early 2005 was provided through research grants, and since has been provided through the Ontario Ministry of Children and Youth. Issues related to participant recruitment (e.g., demand, screening, incentives, maintenance) and program provision (e.g., format, staffing, evaluation, budget) are examined across funding models. Results: Total participation to date includes 148 children/families in 13 groups for research-funded programming and 39 children/families in 6 groups for government-funded programming. There have been no differences with participant demand across funding models. However, funding differences have contributed to changes related to participant recruitment as well as program format, staffing, budget and evaluation. For example, group leader hiring under government funding requires involvement of the hospital administration and is much more complicated. Conclusion: Stable program funding for community-based programs through government sources is not superior for all aspects of participant recruitment and program provision.
Objectives: Explore the prevalence of mathematical disabilities (MD) in school-aged children with attention-deficit hyper-activity disorder (ADHD) and examine effects of age, gender, ADHD sub-type on the comorbidity. Methods: Participants were 476 school-age children with confirmed DSM-IV diagnosis of ADHD. The assessment included semi-structured parent and teacher interviews and standardized measures of intelligence, academic attainment and language abilities. Based on the presence or absence of concurrent learning disorders, we compared the emerging four groups: ADHD-only, ADHD + MD, ADHD + reading disabilities (RD), and ADHD + MD + RD. Results: Overall prevalence of comorbid ADHD + MD was 18.1%. Age, sex, ADHD subtypes, or concomitant conduct disorder did not affect the frequency of MD. Children with concurrent ADHD and learning disorders attained lower IQ, language and academic scores than those with ADHD alone. Children with ADHD + MD + RD were more seriously impaired and demonstrated greater deficits in receptive and expressive language. Conclusion: Mathematical disabilities are relatively common in school-age children with ADHD and are frequently associated with Reading Disabilities. Children with ADHD+ MD + RD are more severely impaired. These deficits can not simply be explained as consequence of ADHD and might have unique biological underpinnings with implications for intervention and remediation.
Objective: Although there is now reasonably good agreement on the diagnosis of autism, there is still much controversy on the utility and accuracy of differentiating autism from the other types of Autism Spectrum Disorders (ASD) such as Asperger syndrome (AS) and PDDNOS. Methods: Recent epidemiological data show wide variation in rates of these three types of ASD across different studies and between epidemiologic and clinical studies. Results: We will present new data on the structure of the ASD phenotype based on factor analysis and how that data can be used to improve the differentiation of autism from AS and PDDNOS, especially if information on language skills is included in the diagnostic assessment. Conclusion: Finally the utility of the differentiation will be presented in terms of long term follow up data of ASD children from the preschool years to late adolescence.
Objective: Autism Spectrum Disorders have strong genetic basis as indicated by twin and family studies and ongoing molecular genetic studies are unravelling progressively the genetic mechanisms involved. However, these data do not rule out an etiologic role for environmental risk factors. Methods: There have also been some concerns about the interpretation of recent trends towards increased prevalence estimates for population rates of autism spectrum disorders. Results: We will review what is known about these trends and whether or not they might index environmental factors which might be associated with the risk of ASD with or without gene interactions. Conclusion: A review of recent environmental hypotheses in the risk of PDD’s does not however provide strong clues about environmental pathways to autism.