1. Beretich GR. {{Reversal of autistic symptoms by removal of low-relative tryptophan foods: Case report}}. {Med Hypotheses};2009 (May 27)
2. Gerrard S, Rugg G. {{Sensory Impairments and Autism: A Re-Examination of Causal Modelling}}. {J Autism Dev Disord};2009 (Jun 2)
Sensory impairments are widely reported in autism, but remain largely unexplained by existing models. This article examines Kanner’s causal reasoning and identifies unsupported assumptions implicit in later empirical work. Our analysis supports a heterogeneous causal model for autistic characteristics. We propose that the development of a standardised framework for analysing autistic characteristics would facilitate the identification of sub-groups and the location of biological markers for genetic variation. We also support a neuroconstructivist model proposing that peripheral sensory abnormalities disrupt compilation of complex skills; impact on synaptogenesis, synaptic pruning and myelination; and subsequently manifest themselves as autistic behaviours. This model explains some of the structural and functional brain abnormalities and many of the perceptual, cognitive and attentional features found in autism.
3. Koegel RL, Shirotova L, Koegel LK. {{Brief Report: Using Individualized Orienting Cues to Facilitate First-Word Acquisition in Non-Responders with Autism}}. {J Autism Dev Disord};2009 (Jun 2)
Though considerable progress has been made in developing techniques for improving the acquisition of expressive verbal communication in children with autism, research has documented that 10-25% still fail to develop speech. One possible technique that could be significant in facilitating responding for this nonverbal subgroup of children is the use of orienting cues. Using a multiple baseline design, this study examined whether individualized orienting cues could be identified, and whether their presentation would result in verbal expressive words. The results suggest that using individualized orienting cues can increase correct responding to verbal models as well as subsequent word use. Theoretical and applied implications of orienting cues as they relate to individualized programming for children with autism are discussed.
4. Masi G, Cosenza A, Millepiedi S, Muratori F, Pari C, Salvadori F. {{Aripiprazole monotherapy in children and young adolescents with pervasive developmental disorders: a retrospective study}}. {CNS Drugs};2009;23(6):511-521.
Pervasive developmental disorders (PDDs) are severe psychiatric disorders characterized by impairment in social interactions, in verbal and non-verbal communication, and by restricted and stereotyped patterns of interest and behaviour, with onset in the first 3 years of life. The appropriate use of pharmacotherapy can improve some aberrant symptoms and behaviours and increase the person’s response to non-pharmacological interventions. To describe clinical outcomes, or symptom changes, and adverse effects during naturalistic treatment with aripiprazole monotherapy in children with PDDs and severe behavioural disorders (such as aggression against self and/or others, hostility, hyperactivity, severe impulsiveness). This retrospective naturalistic study included 34 patients (23 males and 11 females, age range 4.5-15 years, mean age 10.2 +/- 3.3 years), admitted during 2006-2007, diagnosed according to DSM-IV criteria and followed up for 4-12 months (mean 7.0 +/- 3.6 months). Outcome measures were three global measures of clinical and functional impairment and improvement from baseline: the Clinical Global Impression-Severity (CGI-S) and CGI-Improvement (CGI-I) scales; the Children’s Global Assessment Scale (C-GAS); and the Childhood Autism Rating Scale (CARS), a specific measure of PDD symptoms. The mean baseline CGI-S was 5.7 +/- 0.8 (markedly ill/severely ill). The mean final dosage of aripiprazole was 8.1 +/- 4.9 mg/day. At the endpoint, 11 patients (32.4%) were ‘much improved’ or ‘very much improved’ (CGI-I score of 1 or 2), 12 patients (35.3%) were ‘minimally improved’ (CGI-I score of 3) and 10 (29.4%) were ‘unchanged’ or ‘worsened’ (CGI-I score of 4 or 5). C-GAS and CARS scores significantly improved (p < 0.0001, effect sizes 0.59 and 0.62, respectively). Nine patients (26.5%) experienced moderate to severe agitation, which was associated with self-injurious behaviours in five of these patients, and five patients presented with sleep disorders. Twelve patients (35.3%) discontinued medication during the follow-up because of lack of efficacy or adverse effects. In these severely impaired children with PDDs, aripiprazole monotherapy was associated with a significant improvement in maladaptive behaviours in one-third of patients. Agitation and insomnia were the most frequent adverse effects. Further controlled studies in larger samples to explore possible predictors of efficacy are warranted.
5. Piggot J, Shirinyan D, Shemmassian S, Vazirian S, Alarcon M. {{Neural systems approaches to the neurogenetics of autism spectrum disorders}}. {Neuroscience};2009 (May 28)
utism is generally accepted as the most genetic of all the developmental neuropsychiatric syndromes. However, despite more than several decades of genetic study, the etiology of autism remains unknown, largely due to the genetic and phenotypic diversity, or heterogeneity, of this disorder, and the lack of biologically based classification systems. At the same time, in the neuroimaging literature, the body of research identifying candidate neural systems underlying aspects of autistic impairment has grown considerably, fuelled by the advent of technologies such as functional magnetic resonance imaging (fMRI). Yet the findings from these neuroimaging studies have not been incorporated to inform the collection of samples for genetic studies of autism, which are predominantly based on a diagnosis of the disorder. This article presents a review of the genetics of autism and describes the genetic approaches that have been applied, including the phenotypic strategies that have been used to address heterogeneity and optimize the power of these genetic studies. With the increasing recognition that there may be different « autisms » (Geschwind and Levitt, 2007) with unique neural mechanisms, it is argued that neural systems research, using technologies such as fMRI, currently allow for the identification of more biologically informative phenotypes for genetic studies of autism and are positioned to identify informative neuroimaging markers for « neurogenetic » studies of the disorder. To illustrate this, we describe several candidate neural systems for the social communication impairment seen in autism, and the characteristic behavioral and physiological manifestations associated with these that could be incorporated into phenotypic assessments.
6. Selkirk CG, McCarthy Veach P, Lian F, Schimmenti L, Leroy BS. {{Parents’ Perceptions of Autism Spectrum Disorder Etiology and Recurrence Risk and Effects of their Perceptions on Family Planning: Recommendations for Genetic Counselors}}. {J Genet Couns};2009 (Jun 2)
Knowledge about the etiology of Autism Spectrum Disorders (ASDs) is increasing, but causes remain elusive for most cases. Genetic counselors are positioned to help families that have children with ASDs despite uncertainty regarding etiology. To determine how genetic counselors might best provide services, an anonymous survey was conducted with 255 parents whose children were diagnosed on the autism spectrum. Questions concerned: 1) their perceptions of ASD cause(s) and 2) recurrence risk, 3) whether perceived risk affected family planning decisions, 4) whether parents had received genetic services, and 5) how genetic counselors might assist families. The most prevalent perceived cause was genetic influences (72.6%). Most parents’ recurrence risk perceptions were inaccurately high and significantly affected family planning. Only 10% had seen a genetic professional related to an ASD. Parents provided several suggestions for genetic counselor best practices. Findings indicate the importance of genetic counselor awareness of parent perceptions in order to best help families who have children with ASDs.
7. Wachtel LE, Griffin M, Reti IM. {{Electroconvulsive Therapy in a Man With Autism Experiencing Severe Depression, Catatonia, and Self-Injury}}. {J Ect};2009 (May 27)
We report the successful use of electroconvulsive therapy in a 19-year-old man with autism and mild mental retardation who developed severe depression with repeated suicide attempts, multiple symptoms of catatonia, and life-threatening repetitive self-injurious behaviors. After 3 years of failed psychotropic and behavioral interventions in inpatient settings, the patient demonstrated excellent remission of symptoms with bilateral electroconvulsive therapy.
