1. Gilbert SJ, Meuwese JD, Towgood KJ, Frith CD, Burgess PW. {{Abnormal functional specialization within medial prefrontal cortex in high-functioning autism: a multi-voxel similarity analysis}}. {Brain};2009 (Apr);132(Pt 4):869-878.
Multi-voxel pattern analyses have proved successful in ‘decoding’ mental states from fMRI data, but have not been used to examine brain differences associated with atypical populations. We investigated a group of 16 (14 males) high-functioning participants with autism spectrum disorder (ASD) and 16 non-autistic control participants (12 males) performing two tasks (spatial/verbal) previously shown to activate medial rostral prefrontal cortex (mrPFC). Each task manipulated: (i) attention towards perceptual versus self-generated information and (ii) reflection on another person’s mental state (‘mentalizing’versus ‘non-mentalizing’) in a 2 x 2 design. Behavioral performance and group-level fMRI results were similar between groups. However, multi-voxel similarity analyses revealed strong differences. In control participants, the spatial distribution of activity generalized significantly between task contexts (spatial/verbal) when examining the same function (attention/mentalizing) but not when comparing different functions. This pattern was disrupted in the ASD group, indicating abnormal functional specialization within mrPFC, and demonstrating the applicability of multi-voxel pattern analysis to investigations of atypical populations.
2. Johnson S, Marlow N. {{Positive screening results on the modified checklist for autism in toddlers: implications for very preterm populations}}. {J Pediatr};2009 (Apr);154(4):478-480.
3. Kenworthy L, Black DO, Harrison B, Della Rosa A, Wallace GL. {{Are Executive Control Functions Related to Autism Symptoms in High-Functioning Children?}}. {Child Neuropsychol};2009 (Jan 27):1-16.
Background: Linking autism symptoms to cognitive abilities can expand phenotypic descriptions and facilitate investigations into the etiology and treatment of this multiplex disorder. Executive dysfunction is one of several potential cognitive phenotypes in autism. Method: Archival clinical data on 89 children diagnosed with Autism Spectrum Disorders and administered a large neuropsychological battery were evaluated for relationships between executive functioning and autism symptoms. Results: Significant relationships between both laboratory tasks and behavior rating scales of executive functions and autism symptoms were identified. Multiple regression analyses revealed that measures of semantic fluency, divided auditory attention, and behavioral regulation were significantly correlated with autism symptoms, even after accounting for the variance from correlated « nuisance variables, » such as vocabulary and age. Conclusions: Executive dysfunction is related to all three clusters of behavioral symptoms in Autism Spectrum Disorders.
4. Kuban KC, O’Shea TM, Allred EN, Tager-Flusberg H, Goldstein DJ, Leviton A. {{Positive screening on the Modified Checklist for Autism in Toddlers (M-CHAT) in extremely low gestational age newborns}}. {J Pediatr};2009 (Apr);154(4):535-540 e531.
OBJECTIVE: To test the hypothesis that children born preterm are more likely to screen positive on the M-CHAT for an autism spectrum disorder. STUDY DESIGN: We compared the M-CHAT positive rate of those with cerebral palsy, cognitive impairment, and vision and hearing impairments to those without such deficits. RESULTS: Relative to children who could walk, the odds for screening positive on the M-CHAT were increased 23-fold for those unable to sit or stand independently and more than 7-fold for those requiring assistance to walk. Compared with children without a diagnosis of cerebral palsy, those with quadriparesis were 13 times more likely to screen positive, and those with hemiparesis were 4 times more likely to screen positive. Children with major vision or hearing impairments were 8 times more likely to screen positive than those without such impairments. Relative to those with a Mental Development Index (MDI) of >70, the odds for screening positive were increased 13-fold for those with an MDI of <55 and more than 4-fold for those with an MDI of 55 to 69. CONCLUSIONS: Major motor, cognitive, visual, and hearing impairments appear to account for more than half of the positive M-CHAT screens in extremely low gestational age newborns. Even after those with such impairments were eliminated, 10% of children–nearly double the expected rate–screened positive.
5. Kuwagata M, Ogawa T, Shioda S, Nagata T. {{Observation of fetal brain in a rat valproate-induced autism model: a developmental neurotoxicity study}}. {Int J Dev Neurosci};2009 (Jun);27(4):399-405.
Prenatal exposure to chemicals is well known to induce developmental abnormalities in the central nervous system of children. Developmental neurotoxicity (DNT) tests are important to identify neurotoxic agents and prevent neurodevelopmental disorders. We have investigated DNT, focusing on the fetal brain shortly after chemical exposure. To demonstrate a usefulness of a study focusing on the fetal brain in DNT tests, we assessed the fetal brain in a rat valproate-induced autism model. Rats were treated with sodium valproate (VPA, 800 mg/kg) orally on gestational day (GD) 9 or 11 (VPA9 or VPA11), and the fetal brains were examined on GD16 using immunohistochemistry for serotonin (5-HT), tyrosine hydroxylase (TH), and TuJ1 (neuron specific class III beta-tubulin). Hypoplasia of the cortical plate was induced in both VPA9 and VPA11 groups. Abnormal migration of TH-positive and 5-HT neurons, possibly due to the appearance of an abnormally running nerve tract in the pons, was observed only in the VPA11 group. In addition, when we compared the incidence of these abnormalities between pregnant rats mated in our own animal facility (in-house group), and rats purchased pregnant (supplier group), the supplier group was much more sensitive, especially to the pons abnormality. Shipping stress may affect the reproducibility of VPA-induced DNT. The present results demonstrate that examination of the GD16 fetal brain was useful for detecting and characterizing abnormal development of the brain after VPA exposure. Further discussion was made with reference to the findings in children with autism.
6. Turk J, Bax M, Williams C, Amin P, Eriksson M, Gillberg C. {{Autism spectrum disorder in children with and without epilepsy: impact on social functioning and communication}}. {Acta Paediatr};2009 (Apr);98(4):675-681.
AIM: To compare developmental and psychological functioning in two groups of children with autism spectrum disorder (asd), one with epilepsy and one without. METHODS: Sixty 7-17-year-old children in each group were recruited through a range of services in order to screen as representative a sample as possible. Parents were interviewed using the diagnostic interview for social and communication disorders (DISCO-11), and children were clinically examined and their medical histories assessed. RESULTS: The asd and epilepsy (asd+e) group demonstrated a substantially more even gender ratio, with a greater proportion of girls. They were more likely to have received later asd diagnoses and additional medical diagnoses. They also showed more motor difficulties, developmental delays and challenging behaviours, but were no more likely to be aloof and passive. The asd-only group experienced more abnormal fascinations with objects and used brief glances as a means of eye contact more than the asd+e group. CONCLUSION: Results support important between-group differences with diagnostic and therapeutic implications. asds often present atypically in children with seizures. However, both groups showed widely varying social and linguistic presentations.
7. Watanabe S, Yamakura S, Hirano K, Okumura Y, Aiba H. {{[Case of infantile autism with pediatric Wernicke’s encephalopathy due to severe eating disorder]}}. {No To Hattatsu};2009 (Jan);41(1):43-46.
Wernicke’s encephalopathy (WE) or thiamine deficiency is fatal if left untreated. We report a case of a 3-year-old boy with infantile autism and a severe eating disorder who developed WE after 3 weeks of starvation without thiamine supplementation. The eating disorder started when he entered preschool. He presented with unconsciousness and a cluster of seizures. Cranial magnetic resonance imaging (MRI) showed high-intensity signal changes in the basal ganglia on T2-weighted images and fluid-attenuated inversion recovery (FLAIR). Treatment with high-dose intravenous thiamine was effective. Pediatric patients with WE tends to show no typical symptoms or brain lesions on MRI as seen in adult WE patients typically along alcoholics. Brain lesions similar to those in hypoxia or mitochondrial diseases such as Leigh’s encephalopathy, are observed in patients with pediatric WE, and this makes diagnosis difficult. WE should be considered when patients with severe eating disorders present with unconsciousness and/or frequent seizures, and show basal ganglia lesions on MRI, differential diagnosis should include WE.
