1. Gilger MA, Redel CA. {{Autism and the gut}}. {Pediatrics};2009 (Aug);124(2):796-798.
2. Ibrahim SH, Voigt RG, Katusic SK, Weaver AL, Barbaresi WJ. {{Incidence of gastrointestinal symptoms in children with autism: a population-based study}}. {Pediatrics};2009 (Aug);124(2):680-686.
OBJECTIVE: To determine whether children with autism have an increased incidence of gastrointestinal symptoms compared with matched control subjects in a population-based sample. DESIGN/METHODS: In a previous study including all of the residents of Olmsted County, Minnesota, aged <21 years between 1976 and 1997, we identified 124 children who fulfilled criteria on the basis of Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, for a research diagnosis of autism. Two matched control subjects were identified for each case subject. Through the Rochester Epidemiology Project, all medical diagnoses, are indexed for computerized retrieval. Gastrointestinal diagnoses before 21 years of age were grouped into 5 categories: (1) constipation; (2) diarrhea; (3) abdominal bloating, discomfort, or irritability; (4) gastroesophageal reflux or vomiting; and (5) feeding issues or food selectivity. The cumulative incidence of each category was calculated by using the Kaplan-Meier method. Cox proportional hazards models were fit to estimate the risk ratios (case subjects versus control subjects) and corresponding 95% confidence intervals. RESULTS: Subjects were followed to median ages of 18.2 (case subjects) and 18.7 (control subjects) years. Significant differences between autism case and control subjects were identified in the cumulative incidence of constipation (33.9% vs 17.6%) and feeding issues/food selectivity (24.5% vs 16.1). No significant associations were found between autism case status and overall incidence of gastrointestinal symptoms or any other gastrointestinal symptom category. CONCLUSIONS: As constipation and feeding issues/food selectivity often have a behavioral etiology, data suggest that a neurobehavioral rather than a primary organic gastrointestinal etiology may account for the higher incidence of these gastrointestinal symptoms in children with autism.
3. Shumway S, Wetherby AM. {{Communicative Acts of Children with Autism Spectrum Disorders in the Second Year of Life}}. {J Speech Lang Hear Res};2009 (Jul 27)
PURPOSE: This study examined the communicative profiles of children with autism spectrum disorders (ASD) in the second year of life. METHOD: Communicative acts were examined in 125 children 18 to 24 months of age: 50 later diagnosed with ASD; 25 with developmental delays (DD); and 50 with typical development (TD). Precise measures of rate, functions, and means of communication were obtained through systematic observation of videotaped Behavior Samples from the Communication and Symbolic Behavior Scales Developmental Profile (Wetherby & Prizant, 2002). RESULTS: Children with ASD communicated at a significantly lower rate than children with DD and TD. The ASD group used a significantly lower proportion of acts for joint attention and a significantly lower proportion of deictic gestures with a reliance on more primitive gestures compared to DD and TD. Children with ASD who did communicate for joint attention were as likely as other children to coordinate vocalizations, eye gaze, and gestures. Rate of communicative acts and joint attention were the strongest predictors of verbal outcome at age 3. CONCLUSIONS: By 18 to 24 months of age, children later diagnosed with ASD showed a unique profile of communication, with core deficits in communication rate, joint attention, and communicative gestures.
4. Umeda S, Mimura M, Kato M. {{Acquired personality traits of autism following damage to the medial prefrontal cortex}}. {Soc Neurosci};2009 (Jul 27):1-11.
Recent neuroimaging studies on « theory of mind » have demonstrated that the medial prefrontal cortex (PFC) is involved when subjects are engaged in various kinds of mentalising tasks. Although a large number of neuroimaging studies have been published, a relatively small amount of neuropsychological evidence supports involvement of the medial PFC in theory of mind reasoning. We recruited two neurological cases with damage to the medial PFC and initially performed the standard neuropsychological assessments for intelligence, memory, and executive functions. To examine theory of mind performance in these two cases, four kinds of standard and advanced tests for theory of mind were used, including first- and second-order false belief tests, the strange stories test, and the faux pas recognition test. Both patients were also requested to complete the questionnaire for the autism-spectrum quotient. Neither case showed impairment on standard theory of mind tests and only mild impairments were seen on advanced theory of mind tests. This pattern of results is basically consistent with previous studies. The most interesting finding was that both cases showed personality changes after surgical operations, leading to characteristics of autism showing a lack of social interaction in everyday life. We discuss herein the possible roles of the medial PFC and emphasize the importance of using multiple approaches to understand the mechanisms of theory of mind and medial prefrontal functions.
