1. Mostofsky SH, Powell SK, Simmonds DJ, Goldberg MC, Caffo B, Pekar JJ. {{Decreased connectivity and cerebellar activity in autism during motor task performance}}. {Brain};2009 (Apr 23)

Although motor deficits are common in autism, the neural correlates underlying the disruption of even basic motor execution are unknown. Motor deficits may be some of the earliest identifiable signs of abnormal development and increased understanding of their neural underpinnings may provide insight into autism-associated differences in parallel systems critical for control of more complex behaviour necessary for social and communicative development. Functional magnetic resonance imaging was used to examine neural activation and connectivity during sequential, appositional finger tapping in 13 children, ages 8-12 years, with high-functioning autism (HFA) and 13 typically developing (TD), age- and sex-matched peers. Both groups showed expected primary activations in cortical and subcortical regions associated with motor execution [contralateral primary sensorimotor cortex, contralateral thalamus, ipsilateral cerebellum, supplementary motor area (SMA)]; however, the TD group showed greater activation in the ipsilateral anterior cerebellum, while the HFA group showed greater activation in the SMA. Although activation differences were limited to a subset of regions, children with HFA demonstrated diffusely decreased connectivity across the motor execution network relative to control children. The between-group dissociation of cerebral and cerebellar motor activation represents the first neuroimaging data of motor dysfunction in children with autism, providing insight into potentially abnormal circuits impacting development. Decreased cerebellar activation in the HFA group may reflect difficulty shifting motor execution from cortical regions associated with effortful control to regions associated with habitual execution. Additionally, diffusely decreased connectivity may reflect poor coordination within the circuit necessary for automating patterned motor behaviour. The findings might explain impairments in motor development in autism, as well as abnormal and delayed acquisition of gestures important for socialization and communication.

2. Nilsson BM, Ekselius L. {{Acute and Maintenance Electroconvulsive Therapy for Treatment of Severely Disabling Obsessive-Compulsive Symptoms in a Patient With Asperger Syndrome}}. {J Ect};2009 (Apr 17)

We report successful treatment with electroconvulsive therapy of a comorbid condition including severe obsessive-compulsive symptoms and hypochondriacal delusions in a 38-year-old man with Asperger syndrome. His condition deteriorated into a severely disabled chronic state that was refractory to different pharmacological and psychological treatments but was completely reversed after electroconvulsive therapy. Although typical obsessive-compulsive symptoms were predominant, the case also exhibits differences compared with regular obsessive-compulsive disorder regarding onset and course that are discussed in the report.

3. Priel B. {{The transformation of sociogenic autistic defences in The Lives of Others}}. {Int J Psychoanal};2009 (Apr);90(2):387-393.

4. Sykes NH, Toma C, Wilson N, Volpi EV, Sousa I, Pagnamenta AT, Tancredi R, Battaglia A, Maestrini E, Bailey AJ, Monaco AP. {{Copy number variation and association analysis of SHANK3 as a candidate gene for autism in the IMGSAC collection}}. {Eur J Hum Genet};2009 (Apr 22)

SHANK3 is located on chromosome 22q13.3 and encodes a scaffold protein that is found in excitatory synapses opposite the pre-synaptic active zone. SHANK3 is a binding partner of neuroligins, some of whose genes contain mutations in a small subset of individuals with autism. In individuals with autism spectrum disorders (ASDs), several studies have found SHANK3 to be disrupted by deletions ranging from hundreds of kilobases to megabases, suggesting that 1% of individuals with ASDs may have these chromosomal aberrations. To further analyse the involvement of SHANK3 in ASD, we screened the International Molecular Genetic Study of Autism Consortium (IMGSAC) multiplex family sample, 330 families, for SNP association and copy number variants (CNVs) in SHANK3. A collection of 76 IMGSAC Italian probands from singleton families was also examined by multiplex ligation-dependent probe amplification for CNVs. No CNVs or SNP associations were found within the sample set, although sequencing of the gene was not performed. Our data suggest that SHANK3 deletions may be limited to lower functioning individuals with autism.European Journal of Human Genetics advance online publication, 22 April 2009; doi:10.1038/ejhg.2009.47.

5. Yerys BE, Jankowski KF, Shook D, Rosenberger LR, Barnes KA, Berl MM, Ritzl EK, Vanmeter J, Vaidya CJ, Gaillard WD. {{The fMRI success rate of children and adolescents: Typical development, epilepsy, attention deficit/hyperactivity disorder, and autism spectrum disorders}}. {Hum Brain Mapp};2009 (Apr 21)

Functional magnetic resonance imaging (fMRI) in children is increasingly used in clinical application and in developmental research; however, little is known how pediatric patient and typically developing populations successfully complete studies. We examined pediatric success rates with epilepsy, attention deficit/hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and typically developing children (TYP). We also examined the affect of age, and, for ADHD populations, medication status on success rates. We defined a successful fMRI individual run when the data were interpretable and included in group statistics. For unsuccessful runs, datasets with excessive motion or floor task performance were categorized when possible. All clinical groups scanned less successfully than controls; medication status did not affect ADHD success (epilepsy, 80%; ADHD (off methylphenidate), 77%; ADHD (on methylphenidate), 81%; ASD, 70%; TYP, 87%). Ten to 18-year-old had a significantly greater scan success rate than 4- to 6-year-old; adolescents (13- to 18-year-old) demonstrated greater scan success rates than 7- to 9-year-old. Success rate for completing an entire battery of experimental runs (n = 2-6), varied between 50-59% for patient populations and 69% for TYP (79% when excluding 4- to 6-year-old). Success rate for completing one run from a battery was greater than 90% for all groups, except for ASD (81%). These data suggest 20-30% more children should be recruited in these patient groups, but only 10-20% for TYP for research studies. Studies with 4- to 6-year-olds may require 20-40% additional participants; studies with 10- to 18-year-olds may require 10-15% additional participants. Hum Brain Mapp, 2009. (c) 2009 Wiley-Liss, Inc.