1. Fraser R, Angus B, Cotton S, Gentle E, Allott K, Thompson A. {{Prevalence of autism spectrum conditions in a youth mental health service}}. {Aust N Z J Psychiatry};2011 (Mar 10)
2. Guenole F, Godbout R, Nicolas A, Franco P, Claustrat B, Baleyte JM. {{Melatonin for disordered sleep in individuals with autism spectrum disorders: Systematic review and discussion}}. {Sleep Med Rev};2011 (Mar 8)
Sleep disturbance is common in autism spectrum disorders (ASD) and melatonin is widely prescribed in such cases despite a lack of guidelines. The aim of this paper is to provide a systematic review of efficacy and safety of exogenous melatonin for treating disordered sleep in individuals with ASD. We performed a Pubmed((R)) documentary search enlarged by a manual review of references, which finally supplied 12 citations (4 case reports, 3 retrospective studies, 2 open-label clinical trials, and 3 placebo-controlled trials). As a whole, we found that the literature supports the existence of a beneficial effect of melatonin on sleep in individuals with ASD, with only few and minor side effects. However, considering the small number of studies and their methodological limits, these conclusions cannot yet be regarded as evidence-based. Randomized controlled trials and long-term follow-up data are still lacking to better assess efficacy and safety of exogenous melatonin for disordered sleep in individuals with ASD.
3. Kaluzna-Czaplinska J, Michalska M, Rynkowski J. {{Homocysteine level in urine of autistic and healthy children}}. {Acta Biochim Pol};2011 (Mar 11)
Homocysteine is an amino acid, which plays several important roles in human physiology and is an important biomarker for possible deficiencies of various vitamins (vitamin B6 and B12, folic acid). In this work GC-MS method was used to determine the levels of homocysteine in the urine of autistic and healthy children. The levels of homocysteine in urine samples from 34 autistic and 21 healthy children were 2.36 +/- 1.24 and 0.76 +/- 0.31 (mmol mol(-1) creatinine), respectively. The higher level of homocysteine in autistic children may indicate deficiencies of folic acid and vitamins B6 and B12 in nutrition of these children. The results of this work were taken into consideration in the nutrition of autistic children treated in the Navicula Centre of Diagnosis and Therapy of Autism in Lodz (Poland).
4. Konyukh M, Delorme R, Chaste P, Leblond C, Lemiere N, Nygren G, Anckarsater H, Rastam M, Stahlberg O, Amsellem F, Gillberg IC, Mouren-Simeoni MC, Herbrecht E, Fauchereau F, Toro R, Gillberg C, Leboyer M, Bourgeron T. {{Variations of the Candidate SEZ6L2 Gene on Chromosome 16p11.2 in Patients with Autism Spectrum Disorders and in Human Populations}}. {PLoS One};2011;6(3):e17289.
BACKGROUND: Autism spectrum disorders (ASD) are a group of severe childhood neurodevelopmental disorders with still unknown etiology. One of the most frequently reported associations is the presence of recurrent de novo or inherited microdeletions and microduplications on chromosome 16p11.2. The analysis of rare variations of 8 candidate genes among the 27 genes located in this region suggested SEZ6L2 as a compelling candidate. METHODOLOGY/PRINCIPAL FINDINGS: We further explored the role of SEZ6L2 variations by screening its coding part in a group of 452 individuals, including 170 patients with ASD and 282 individuals from different ethnic backgrounds of the Human Genome Diversity Panel (HGDP), complementing the previously reported screening. We detected 7 previously unidentified non-synonymous variations of SEZ6L2 in ASD patients. We also identified 6 non-synonymous variations present only in HGDP. When we merged our results with the previously published, no enrichment of non-synonymous variation in SEZ6L2 was observed in the ASD group compared with controls. CONCLUSIONS/SIGNIFICANCE: Our results provide an extensive ascertainment of the genetic variability of SEZ6L2 in human populations and do not support a major role for SEZ6L2 sequence variations in the susceptibility to ASD.
5. Rice CE. {{The changing prevalence of the autism spectrum disorders}}. {Am Fam Physician};2011 (Mar 1);83(5):515.
6. Roberts TP, Cannon KM, Tavabi K, Blaskey L, Khan SY, Monroe JF, Qasmieh S, Levy SE, Edgar JC. {{Auditory Magnetic Mismatch Field Latency: A Biomarker for Language Impairment in Autism}}. {Biol Psychiatry};2011 (Mar 8)
BACKGROUND:: Auditory processing abnormalities are frequently observed in autism spectrum disorders (ASD), and these abnormalities may have sequelae in terms of clinical language impairment (LI). The present study assessed associations between language impairment and the amplitude and latency of the superior temporal gyrus magnetic mismatch field (MMF) in response to changes in an auditory stream of tones or vowels. METHODS:: Fifty-one children with ASD, and 27 neurotypical control subjects, all aged 6 to 15 years, underwent neuropsychological evaluation, including tests of language function, as well as magnetoencephalographic recording during presentation of tones and vowels. The MMF was identified in the difference waveform obtained from subtraction of responses to standard from deviant stimuli. RESULTS:: Magnetic mismatch field latency was significantly prolonged (p < .001) in children with ASD, compared with neurotypical control subjects. Furthermore, this delay was most pronounced ( approximately 50 msec) in children with concomitant LI, with significant differences in latency between children with ASD with LI and those without (p < .01). Receiver operator characteristic analysis indicated a sensitivity of 82.4% and specificity of 71.2% for diagnosing LI based on MMF latency. CONCLUSIONS:: Neural correlates of auditory change detection (the MMF) are significantly delayed in children with ASD, and especially those with concomitant LI, suggesting a neurobiological basis as well as a clinical biomarker for LI in ASD.
7. Zeiner P, Gjevik E, Weidle B. {{Response to atomoxetine in boys with high-functioning Autism Spectrum Disorders and Attention Deficit/Hyperactivity Disorder}}. {Acta Paediatr};2011 (Mar 10)
Aim: To study efficacy and tolerability of atomoxetine in high functioning boys with Autism Spectrum Disorders (ASD) and comorbid Attention Deficit/Hyperactivity Disorder (AD/HD). Methods: Fourteen boys (age 7 – 17) participated in a 10 weeks open-label study. Atomoxetine doses were 0.5 mg/kg/day in week 1 and 1.2 – 1.4 mg/kg/day in weeks 2 – 10. Changes in AD/HD symptoms were measured by the AD/HD Rating Scale, and in global improvements by the Clinical Global Improvement Scale. Both measures were used to assess of drug response. Assessments were done at baseline and at weeks 2, 4, 6, and 10. Teacher ratings were done at baseline and 10 weeks. Results: There were significant reductions of AD/HD symptoms rated by parents (p < .005) and by teachers (p < .05). One participant was rated as « Much improved », five as « Moderately improved », seven as « Minimally improved », and one as « Unchanged or worse ». Seven subjects were classified as clinical responders. The most common adverse events were nausea and headache. Two participants discontinued treatment. Conclusion: Seven out of 14 boys with high functioning ASD and comorbid AD/HD showed significant reductions in AD/HD symptoms and were classified as responders to atomoxetine. Most children tolerated the drug well.
