1. Chown N. {{‘History and First Descriptions’ of Autism: A response to Michael Fitzgerald}}. {J Autism Dev Disord};2012 (Apr 18)
Letter to the editor in response to Michael Fitzgerald’s controversial allegation that one of the two pioneers of autism-Leo Kanner-may have been influenced by an earlier paper by the other autism pioneer-Hans Asperger-without acknowledging the debt, and that Kanner may even have been guilty of plagiarising Asperger. In correspondence, Professor Fitzgerald has suggested that I « consider doing my take on the matter ». This is it.
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2. Churches O, Baron-Cohen S, Ring H. {{The psychophysiology of narrower face processing in autism spectrum conditions}}. {Neuroreport};2012 (Apr 18);23(6):395-399.
Faces are encountered across a huge range of visual conditions, including differences in light, distance and visibility. To accurately detect all faces under all these conditions, the face detection system must be suitably generalized. However, in autism spectrum conditions (ASCs), the typical generalization of perceptual learning is narrower. Here, we tested the generalization of the face detection system in a sample of adults with ASCs and a matched control group without ASCs. We recorded electroencephalography while participants viewed images of actual faces, face-like objects and non-face-like objects. Analysis of the N170 event-related potential component, which is related to the early stages of face detection, showed that the two participant groups were comparable in the activation of the N170 to actual faces and face-like objects, but that the typical control group showed an increased N170 for non-face-like objects over the group with ASCs. This indicates that the face detection system is less generalized (narrower) in ASCs than in typical development. We propose that the reduced social interest characteristic of ASCs is associated with a narrower face detection system that is less reliable in detecting all the faces in the environment.
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3. Geier DA, Kern JK, King PG, Sykes LK, Geier MR. {{An evaluation of the role and treatment of elevated male hormones in autism spectrum disorders}}. {Acta Neurobiol Exp (Wars)};2012;72(1):1-17.
Autism, Asperger’s syndrome (AS), and pervasive developmental disorder – not otherwise specified (PDD-NOS) compose the overall diagnostic category of autism spectrum disorder (ASD). Subjects diagnosed with an ASD have a male:female ratio of 4:1, and among subjects diagnosed with AS the male:female ratio is as high as 9:1. The purpose of this study was to examine evidence of the association between hyperandrogenism and autistic traits (ATs) among subjects diagnosed with an ASD, and to evaluate the effectiveness of anti-androgen therapy as a means to help treat ATs in subjects diagnosed with an ASD. Evidence of hyperandrogenism in subjects diagnosed with an ASD is supported by multiple studies in the areas of psychological framework, brain pathology, tissue culture, and pre- and postnatal androgen levels. Data from subjects diagnosed with other conditions associated with elevated androgens reveals many of these individuals have ATs. Finally, in a placebo-controlled trial of testosterone administration to neurotypical subjects, testosterone was found to increase ATs. In addition, a controlled trial of human transsexuals revealed a significant increase in ATs in female-to-male transsexuals and a decrease in ATs in male-to-female transsexuals. Data from multiple animals and human clinical trials suggest that antiandrogen medications have the ability to significantly reduce ATs in patients diagnosed with an ASD. In light of the robust association between hyperandrogenism and ASD, it is recommended subjects diagnosed with an ASD should undergo routine screening for elevated androgens, and appropriate treatment should be initiated for those with elevated androgens.
4. Lord C, Luyster R, Guthrie W, Pickles A. {{Patterns of Developmental Trajectories in Toddlers With Autism Spectrum Disorder}}. {J Consult Clin Psychol};2012 (Apr 16)
Objective: Our objective was to follow toddlers referred for risk of autism, using standardized observational measures administered frequently from age 18 months to age 36 months. Method: Sixty-five children who were consecutive referrals and 13 children from other research projects were seen approximately every 2 months, from age 18 months to age 36 months, for standardized assessments and clinical judgments by the same examiner and every 6 months by an examiner blind to previous scores. Results: Thirty children never received an autism spectrum disorder (ASD) diagnosis; 48 children (all referrals) received at least 1 diagnosis of ASD. The best trajectory typology, using Autism Diagnostic Observation Schedule (ADOS) scores, revealed 4 trajectory classes with high probabilities for fit to the most likely class: severe persistent (21%), worsening (21%), improving (19%), and nonspectrum (40%). Classes differed by trajectories in verbal and nonverbal mental ages; never-ever ASD groups differed on Autism Diagnostic Interview-Revised (ADI-R) domain scores and clinician judgments, but improving-worsening trajectory groups did not. Conclusions: The results replicated the findings from studies of infants whose siblings have autism and infants whose siblings do not have autism, suggesting variability in early trajectories and supporting the need for early identification, regular monitoring, and standardized assessments of young children suspected of having ASD. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
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5. Martin-Du Pan RC. {{L’ocytocine: hormone de l’amour, de la confiance et du lien conjugal et social.}}. {Rev Med Suisse};2012 (Mar 21);8(333):627-630.
Oxytocin, an octapeptide synthesized in the hypothalamus, stimulates milk election and uterine contractions. In the brain this hormone acts as a neuropeptide. It could inhibit through the GABAergic system the activity of limbic amygdala, which is involved in the response to fear. Oxytocin could also induce the protective behaviour of the mother towards its offspring through the dopaminergic system. In mankind, oxytocin plays a role in trust, empathy, generosity, stress and sexuality. Clinical studies are testing potential benefits of oxytocin administration in autism, depression and social phobia. Results are still preliminary.
6. Williams K, Wray JA, Wheeler DM. {{Intravenous secretin for autism spectrum disorders (ASD)}}. {Cochrane Database Syst Rev};2012;4:CD003495.
BACKGROUND: In 1998 secretin, a gastrointestinal hormone, was suggested as an effective treatment for autism spectrum disorders (ASD) based on anecdotal evidence. OBJECTIVES: To assess whether intravenous secretin improves the core features of ASD, other aspects of behaviour or function such as self-injurious behaviour, and the quality of life of affected individuals and their carers. We also assessed whether secretin causes harm. This is an updated version of our review of this topic originally published in 2005. SEARCH METHODS: We searched CENTRAL (2010 Issue 1), MEDLINE (1950 to January 2010) , EMBASE (1980 to 2010 Week 2), PsycINFO (1806 to 2010 Week 2), CINAHL (1938 to January 2010), ERIC (1966 to January 2010), Sociological Abstracts (1952 to January 2010). Sociofile and HealthStar were searched in March 2005 when this review was first published, but were not available for this update. Records were limited to studies published since 1998 as this is when secretin was first proposed as a possible treatment for ASD. We searched reference lists of trials and reviews; we also contacted experts and trialists to find unpublished studies. SELECTION CRITERIA: Randomised controlled trials of intravenous secretin compared to a placebo treatment in children or adults diagnosed with ASD, where at least one standardised outcome measure was reported. DATA COLLECTION AND ANALYSIS: Sixteen studies met the inclusion criteria but for two of these, conducted by Repligen, the only available multisite data were reported in press releases. All outcome data from the other 14 trials were continuous. Where trials used cross-over designs, we conducted analysis on results from the first treatment phase. Where mean change from baseline was reported, we used this in preference to post-treatment scores for meta-analyses or forest plots. Meta-analysis was able to be attempted for only one outcome (Childhood Autism Rating Scale). Insufficient data were available to conduct sensitivity or subgroup analyses to assess the impact of study quality, clinical differences in the intervention or clinically relevant differences between groups, such as age or presence of gastrointestinal symptoms. MAIN RESULTS: Over 900 children were recruited for the secretin trials. Twenty-five established standardised outcome measures were reported to assess core features of ASD, communication, behaviour, visuospatial skills, affect and adverse events. One standardised measure of global impression was also used. No more than four studies used any one outcome measure similarly. When duration from the start of the intervention to outcome assessment was known, outcomes were reported at between three and six weeks. Meta-analysis of data was not possible but there is now consistency of findings, with RCTs of the efficacy of secretin in autism not showing improvements for core features of ASD. AUTHORS’ CONCLUSIONS: There is no evidence that single or multiple dose intravenous secretin is effective and as such currently it should not be recommended or administered as a treatment for ASD. Further experimental assessment of secretin’s effectiveness for ASD can only be justified if there is new high-quality and replicated scientific evidence that either finds that secretin has a role in neurotransmission in a way that could benefit all children with ASD or identifies important subgroups of children with ASD who could benefit from secretin because of a proven link between the action of secretin and the known cause of their ASD, or the type of problems they are experiencing.
