Chez, Michael; Buchanan, Cathleen; Bagan, Bradley; Hammer, Michael; McCarthy, Karla; Ovrutskaya, Irina; Nowinski, Caralynn; Cohen, Zamia
doi: 10.1023/A:1005443119324pmid: 10832772
Recent anecdotal reports have touted the gastrointestinal (GI) hormone secretin as a treatment modality for autism, though there is little clinical evidence or literature to support its viability. We undertook a two-part clinical trial to investigate these claims. Fifty-six patients (49 boys, 7 girls, mean age = 6.4 years, SD = 2.7) enrolled in an open-label trial of secretin, during which they received one injection of the hormone (2 IU/kg). All subjects were evaluated by their parents at baseline and follow-up visits (3–6 weeks later, M = 3.7, SD = 1.4 weeks) with Childhood Autism Rating Scales (CARS). Thirty-four patients were labeled with Pervasive Developmental Disorder Not Otherwise Specified, and 22 met diagnostic criteria for Autistic Disorder. Forty-five patients were concurrently on other drug treatments. At follow-up, some reported minimal but potentially significant improvements including changes in GI symptoms, expressive and/or receptive language function, and improved awareness and social interactions. No adverse effects were reported or observed. Subsequently, 17 of the most responsive patients from Study 1 began a double-blind trial that also included 8 newly enrolled patients. Patients in this second study were alternatively entered into one of two groups and received injections of secretin or placebo with crossover at 4 weeks. Patients from Study 1 entered into Study 2 at an average of 6.5 (SD = 0.8) weeks after beginning Study 1. Results of both inquiries indicate that although treatment with secretin was reported to cause transient changes in speech and behavior in some children, overall it produced few clinically meaningful changes when compared to children given placebo injections.
Arnold, L.; Aman, Michael; Martin, Andres; Collier-Crespin, Angie; Vitiello, Benedetto; Tierney, Elaine; Asarnow, Robert; Bell-Bradshaw, Felicia; Freeman, Betty; Gates-Ulanet, Patricia; Klin, Ami; McCracken, James; McDougle, Christopher; McGough, James; Posey, David;
Davidovitch, Michael; Glick, Lilach; Holtzman, Gabriela; Tirosh, Emanuel; Safir, Marilyn
doi: 10.1023/A:1005403421141pmid: 10832775
Developmental regression among children with autism is a common phenomenon of unknown origin. The purpose of this study was to identify the differences between children with autism who reportedly regressed with those who did not regress. A representative group of 39 mothers were interviewed (40 children—1 pair of twin girls) about familial, pregnancy, perinatal, as well as medical history and developmental milestones. The study focused on mothers' perceptions of developmental regression. Nineteen children (47.5 %) regressed in verbal and non-verbal communication and social but not in motor abilities. Mean age of regression was 24 months, with 11 children who regressed before and 8 after this age. No significant differences were reported by mothers of children who did or did not regress. More mothers of children who regressed, than those of children who did not, expressed guilt feelings regarding the development of autism, and almost all of them had an “explanation” for the possible mechanisms that might have influenced their children's developmental course. In conclusion, developmental regression in our population appears to be a typical event in the natural course of autism. There is little difference between those children who regressed and those who did not regress in maternal perceptions and reports of development, family, and medical history.
Zwaigenbaum, L.; Szatmari, P.; Mahoney, W.; Bryson, S.; Bartolucci, G.; MacLean, J.
doi: 10.1023/A:1005455505211pmid: 10832776
Childhood Disintegrative Disorder (CDD) is grouped with autism as a subtype of Pervasive Developmental Disorder (PDD) in ICD-10 and DSM-IV. This is the first report of autism and CDD cosegregating within a sibship. J. P. and M. P. are half-brothers with the same mother. J. P. is an 18-year-old with impairments in communication, social reciprocity, and stereotypies and was diagnosed with autism. M. P. is a 7-year-old who developed normally to 2 years 4 months. He then underwent a profound regression, becoming nonverbal and socially withdrawn, and lost adaptive skills. Investigations did not reveal any neurodegenerative process. M. P. was diagnosed with CDD. The rarity of the two conditions suggests a shared transmissible mechanism. The implications for autism/PDD genetic studies are discussed.
Schreck, Kimberly; Mulick, James
doi: 10.1023/A:1005407622050pmid: 10832777
This research evaluated parent reports of sleep behaviors of four groups of children: those with Autism or Pervasive Developmental Disorders, those with General Mental Retardation alone, those attending Special Education classes (with no MR diagnosis), and a control group of similar aged children without a developmental diagnosis. Diagnostic classification and demographic information were determined through parent report, report of classroom registration, and the Gilliam Autism Rating Scale (Gilliam, 1995). To evaluate sleeping behavior the study used a 28-item, five-factor scale (Behavioral Evaluation of Disorders of Sleep/BEDS; Schreck, 1997/1998) constructed from the diagnostic criteria for childhood sleep disorders found in the International Classification of Sleep Disorders: Diagnostic and Coding Manual (ICSD, American Sleep Disorders Association, 1990). Findings suggest that reports of parents with children with autistic characteristics exhibit expected quantities of sleep, but parent perception of their sleep difficulties and sleep quality is different for children with autism than for children in all other study groups.
Harris, Sandra; Handleman, Jan
doi: 10.1023/A:1005459606120pmid: 10832778
The predictive power of age and IQ at time of admission to an intensive treatment program using applied behavior analysis were examined in a 4- to 6-year follow-up of educational placement. Twenty-seven children with autistic disorder who were between the ages of 31 and 65 months and had IQs on the Stanford Binet between 35 and 109 at time of admission to the Douglass Developmental Disabilities Center were followed up 4 to 6 years after they left the preschool. The results showed that having a higher IQ at intake (M = 78) and being of younger age (M = 42 months) were both predictive of being in a regular education class after discharge, whereas having a lower IQ (M = 46) and being older at intake (M = 54 months) were closely related to placement in a special education classroom. The results are interpreted as pointing to the need for very early intervention for children with Autistic Disorder. It is also emphasized that older children and those with lower IQs in the present study showed measurable gains in IQ from treatment. The data should not be taken to suggest that children older than 4 years of age do not merit high quality treatment.
doi: 10.1023/A:1005411722958pmid: 10832779
While professionals commonly advocate sharing information about autism spectrum disorders with siblings, no guidelines currently exist that describe what types of information might be relevant for siblings at different ages. To address this issue, the interviewing method described by Bibace and Walsh (1979, 1980), which measures cognitive sophistication in thinking about illness, was adapted to examine perspectives on autism spectrum disorders. Sixty-three siblings of individuals with autism or related disorders were interviewed using this measure. Parents were given the same interview as their child, and asked to predict their child's responses. Children's reasoning became more mature with age, but developed at a delayed rate compared to norms for illness concepts. Although accurate in estimating their child's understanding of the definition and cause of their sibling' s; diagnosis, parents tended to overestimate their child's understanding of the disorder's impact.
Showing 1 to 10 of 16 Articles
doi: 10.1023/A:1005451304303pmid: 10832774
Assessment of autistic disorder (autism) symptoms, primary and secondary, poses more challenging problems than ordinarily found in multisite randomized clinical trial (RCT) assessments. For example, subjects may be uncommunicative and extremely heterogeneous in problem presentation, and current pharmacological treatments are not likely to alter most core features of autism. The Autism Research Units on Pediatric Psychopharmacology (RUPP Autism Network) resolved some of these problems during the design of a risperidone RCT in children/adolescents. The inappropriateness of the usual anchors for a Clinical Global Impression of Severity (CGI-S) was resolved by defining uncomplicated autism without secondary symptoms as a CGI-S of 3, mildly ill. The communication problems, compromising use of the patient as an informant, were addressed by several strategies, including careful questioning of care providers, rating scales, laboratory tests, and physical exams. The broad subject heterogeneity requires outcome measures sensitive to individual change over a wide spectrum of treatment response and side effects. The problems of neuropsychologically testing nonverbal, lower functioning, sometimes noncompliant subjects requires careful instrument selection/adaptation and flexible administration techniques. The problems of assessing low-end IQs, neglected by most standardized test developers, was resolved by an algorithm of test hierarchy. Scarcity of other autism-adapted cognitive and neuropsychological tests and lack of standardization required development of a new, specially adapted battery. Reliability on the Autism Diagnostic Interview (currently the most valid diagnostic instrument) and other clinician instruments required extensive cross-site training (in-person, videotape, and teleconference sessions). Definition of a treatment responder required focus on individually relevant target symptoms, synthesis of possible modest improvements in many domains, and acceptance of attainable though imperfect goals. The assessment strategy developed is implemented in a RCT of risperidone (McDougle et al., 2000) for which the design and other methodological challenges are described elsewhere (Scahill et al., 2000). Some of these problems and solutions are partially shared with RCTs of other treatments and other disorders.