Pubmed du 05/09/15

Pubmed du jour

2015-09-05 12:03:50

1. Arnold B, Elliott A, Laohamroonvorapongse D, Hanna J, Norvell D, Koh J. {{Autistic children and anesthesia: is their perioperative experience different?}}. {Paediatric anaesthesia}. 2015 Sep 4.

BACKGROUND: Children with autism spectrum disorders (ASD) are an increasingly common patient population in the perioperative setting. Children with ASD present with abnormal development in social interaction, communication, and stereotyped patterns of behavior and may be more prone to elevated perioperative anxiety. The perioperative experience for these patients is complex and presents a unique challenge for clinicians. AIM: The aim of the current study was to provide a further understanding of the premedication patterns and perioperative experiences of children with ASD in comparison to children without ASD. METHODS: Using a retrospective cohort study design, medical records were evaluated for patients with and without ASD undergoing general anesthesia for dental rehabilitation from 2006-2011. The following objectives were measured and compared: (i) premedication patterns and (ii) complications, pain, anesthetic type, PACU time, and time to discharge. To compare categorical variables, the chi-square test was used. Bivariate and multivariable analyses were performed to control for potential confounding as a result of baseline differences between the two groups. RESULTS: A total of 121 ASD patients and 881 non-ASD patients were identified. When controlling for age, weight, and gender, children in the ASD group were more likely to have nonstandard premedication types (P < 0.0001), while children without ASD were more likely to have standard premedication types (P < 0.0001). No significant group differences were identified in regards to the other outcome measures. CONCLUSIONS: Other than a significant difference in the premedication type and route, we found that children with ASD seemed to have similar perioperative experiences as non-ASD subjects. It was especially interesting to find that their postoperative period did not pose any special challenges. There is much to be learned about this unique patient population, and a more in-depth prospective evaluation is warranted to help better delineate the best approach to caring for these patients.

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2. Maier S, Tebartz van Elst L, Beier D, Ebert D, Fangmeier T, Radtke M, Perlov E, Riedel A. {{Increased hippocampal volumes in adults with high functioning autism spectrum disorder and an IQ>100: A manual morphometric study}}. {Psychiatry research}. 2015 Aug 10.

Previous studies concerning the volumes of the amygdala and the hippocampus in autism spectrum disorders (ASD) show inconsistent results. We acquired magnetic resonance images of 30 individuals with ASD and individually matched controls. All participants had an IQ>100 to increase the likelihood of including non-syndromal forms of ASD. Manually defined amygdala volumes showed no significant group difference, while hippocampi were significantly enlarged in ASD. This finding is discussed with regard to the ‘intense world hypothesis’.

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3. Sabuncuoglu O, Irmak MY, Ucok Demir N, Murat D, Tumba C, Yilmaz Y. {{Sibling Death after Being Thrown from Window by Brother with Autism: Defenestration, an Emerging High-Risk Behavior}}. {Case reports in psychiatry}. 2015;2015:463694.

Children diagnosed with autistic spectrum disorders (ASD) may have serious behavioral problems such as aggression, self-injury, and violence. However, the literature on ASD either overrules any correlation between aggression and ASD or maintains the fact that the efforts to link them have so far been inconclusive. Although severe forms of violence are extremely rare in children with autism, there are a few cases reported in the literature with significant harm to siblings. We hereby report an 8-year-old boy with ASD who caused the death of his sibling by throwing her out of the window. Shared similarities of all defenestration cases indicate a pattern of high-risk behavior threatening the survival of minors. We recommend precautions against this high-risk behavior in children with ASD.

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4. Sala C, Vicidomini C, Bigi I, Mossa A, Verpelli C. {{Shank synaptic scaffold proteins: keys to understanding the pathogenesis of autism and other synaptic disorders}}. {Journal of neurochemistry}. 2015 Jul 6.

Shank/ProSAP proteins are essential to synaptic formation, development, and function. Mutations in the family of SHANK genes are strongly associated with autism spectrum disorders (ASD) and other neurodevelopmental and neuropsychiatric disorders, such as intellectual disability (ID), and schizophrenia. Thus, the term ‘Shankopathies’ identifies a number of neuronal diseases caused by alteration of Shank protein expression leading to abnormal synaptic development. With this review we want to summarize the major genetic, molecular, behavior and electrophysiological studies that provide new clues into the function of Shanks and pave the way for the discovery of new therapeutic drugs targeted to treat patients with SHANK mutations and also patients affected by other neurodevelopmental and neuropsychiatric disorders. Shank/ProSAP proteins are essential to synaptic formation, development, and function. Mutations in the family of SHANK genes are strongly associated with autism spectrum disorders (ASD) and other neurodevelopmental and neuropsychiatric disorders, such as intellectual disability (ID), and schizophrenia (SCZ). With this review we want to summarize the major genetic, molecular, behavior and electrophysiological studies that provide new clues into the function of Shanks and pave the way for the discovery of new therapeutic drugs targeted to treat patients with SHANK mutations.

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5. Say GN, Karabekiroglu K, Babadagi Z, Yuce M. {{Maternal stress and perinatal features in autism & attention deficit/ hyperactivity disorder}}. {Pediatrics international : official journal of the Japan Pediatric Society}. 2015 Sep 4.

BACKGROUND: We aimed to explore the shared and non-shared perinatal risk factors for autism spectrum disorders (ASD) and attention deficit/hyperactivity disorder (ADHD) in a clinical sample. Additionally, we aimed to compare these groups regarding pre/postpartum maternal stress and the duration of breastfeeding. METHODS: Children aged 3-18 years old with ASD (n = 100) were compared with age and gender matched children with ADHD (n = 100) and age and gender matched healthy controls (n = 80). RESULTS: This study revealed prematurity of the neonate and maternal stress/depressive mood in pregnancy as common risk factors shared by ASD and ADHD. The results suggested that postpartum maternal depressive mood may be more specific to ASD while shorter duration of breastfeeding may be related to ADHD. CONCLUSIONS: The results of this study revealed that ASD and ADHD may share some perinatal features in common. Identification of perinatal factors for ASD and ADHD carries clinical implications in terms of primary prevention.

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6. Tonacci A, Billeci L, Tartarisco G, Ruta L, Muratori F, Pioggia G, Gangemi S. {{Olfaction in autism spectrum disorders: A systematic review}}. {Child neuropsychology : a journal on normal and abnormal development in childhood and adolescence}. 2015 Sep 4:1-25.

Olfactory function is a well-known early biomarker for neurodegeneration and neural functioning in the adult population, being supported by a number of brain structures that could be dysfunctioning in neurodegenerative processes. Evidence has suggested that atypical sensory and, particularly, olfactory processing is present in several neurodevelopmental conditions, including autism spectrum disorders (ASDs). In this paper, we present data obtained by a systematic literature review, conducted according to PRISMA guidelines, regarding the possible association between olfaction and ASDs, and analyze them critically in order to evaluate the occurrence of olfactory impairment in ASDs, as well as the possible usefulness of olfactory evaluation in such conditions. The results obtained in this analysis suggested a possible involvement of olfactory impairment in ASDs, underlining the importance of olfactory evaluation in the clinical assessment of ASDs. This assessment could be potentially included as a complementary evaluation in the diagnostic protocol of the condition. Methods for study selection and inclusion criteria were specified in advance and documented in PROSPERO protocol #CRD42014013939.

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7. Wang L, Almeida LE, Spornick NA, Kenyon N, Kamimura S, Khaibullina A, Nouraie M, Quezado ZM. {{Modulation of social deficits and repetitive behaviors in a mouse model of autism: the role of the nicotinic cholinergic system}}. {Psychopharmacology}. 2015 Sep 4.

RATIONALE: Accumulating evidence implicates the nicotinic cholinergic system in autism spectrum disorder (ASD) pathobiology. Neuropathologic studies suggest that nicotinic acetylcholine (ACh) receptor (nAChR) subtypes are altered in brain of autistic individuals. In addition, strategies that increase ACh, the neurotransmitter for nicotinic and muscarinic receptors, appear to improve cognitive deficits in neuropsychiatric disorders and ASD. OBJECTIVE: The aim of this study is to examine the role of the nicotinic cholinergic system on social and repetitive behavior abnormalities and exploratory physical activity in a well-studied model of autism, the BTBR T+ Itpr3 tf /J (BTBR) mouse. METHODS: Using a protocol known to up-regulate expression of brain nAChR subtypes, we measured behavior outcomes before and after BTBR and C57BL/6J (B6) mice were treated (4 weeks) with vehicle or nicotine (50, 100, 200, or 400 mug/ml). RESULTS: Increasing nicotine doses were associated with decreases in water intake, increases in plasma cotinine levels, and at the higher dose (400 mug/ml) with weight loss in BTBR mice. At lower (50, 100 mug/ml) but not higher (200, 400 mug/ml) doses, nicotine increased social interactions in BTBR and B6 mice and at higher, but not lower doses, it decreased repetitive behavior in BTBR. In the open-field test, nicotine at 200 and 400 mug/ml, but not 100 mug/ml compared with vehicle, decreased overall physical activity in BTBR mice. CONCLUSIONS: These findings support the hypotheses that the nicotinic cholinergic system modulates social and repetitive behaviors and may be a therapeutic target to treat behavior deficits in ASD. Further, the BTBR mouse may be valuable for investigations of the role of nAChRs in social deficits and repetitive behavior.

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8. Watanabe T, Kuroda M, Kuwabara H, Aoki Y, Iwashiro N, Tatsunobu N, Takao H, Nippashi Y, Kawakubo Y, Kunimatsu A, Kasai K, Yamasue H. {{Clinical and neural effects of six-week administration of oxytocin on core symptoms of autism}}. {Brain : a journal of neurology}. 2015 Sep 3.

Autism spectrum disorder is a prevalent neurodevelopmental disorder with no established pharmacological treatment for its core symptoms. Although previous literature has shown that single-dose administration of oxytocin temporally mitigates autistic social behaviours in experimental settings, it remains in dispute whether such potentially beneficial responses in laboratories can result in clinically positive effects in daily life situations, which are measurable only in long-term observations of individuals with the developmental disorder undergoing continual oxytocin administration. Here, to address this issue, we performed an exploratory, randomized, double-blind, placebo-controlled, crossover trial including 20 high-functional adult males with autism spectrum disorder. Data obtained from 18 participants who completed the trial showed that 6-week intranasal administration of oxytocin significantly reduced autism core symptoms specific to social reciprocity, which was clinically evaluated by Autism Diagnostic Observation Scale (P = 0.034, PFDR < 0.05, Cohen’s d = 0.78). Critically, the improvement of this clinical score was accompanied by oxytocin-induced enhancement of task-independent resting-state functional connectivity between anterior cingulate cortex and dorso-medial prefrontal cortex (rho = -0.60, P = 0.011), which was measured by functional magnetic resonance imaging. Moreover, using the same social-judgement task as used in our previous single-dose oxytocin trial, we confirmed that the current continual administration also significantly mitigated behavioural and neural responses during the task, both of which were originally impaired in autistic individuals (judgement tendency: P = 0.019, d = 0.62; eye-gaze effect: P = 0.03, d = 0.56; anterior cingulate activity: P = 0.00069, d = 0.97; dorso-medial prefrontal activity: P = 0.0014, d = 0.92; all, PFDR < 0.05). Furthermore, despite its longer administration, these effect sizes of the 6-week intervention were not larger than those seen in our previous single-dose intervention. These findings not only provide the evidence for clinically beneficial effects of continual oxytocin administration on the core social symptoms of autism spectrum disorder with suggesting its underlying biological mechanisms, but also highlight the necessity to seek optimal regimens of continual oxytocin treatment in future studies.

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9. Yu H, Liu J, Yang A, Yang G, Yang W, Lei H, Quan J, Zhang Z. {{Lack of Association Between Polymorphisms in Dopa Decarboxylase and Dopamine Receptor-1 Genes With Childhood Autism in Chinese Han Population}}. {Journal of child neurology}. 2015 Sep 3.

Genetic factors play an important role in childhood autism. This study is to determine the association of single-nucleotide polymorphisms in dopa decarboxylase (DDC) and dopamine receptor-1 (DRD1) genes with childhood autism, in a Chinese Han population. A total of 211 autistic children and 250 age- and gender-matched healthy controls were recruited. The severity of disease was determined by Children Autism Rating Scale scores. TaqMan Probe by real-time polymerase chain reaction was used to determine genotypes and allele frequencies of single-nucleotide polymorphism rs6592961 in DDC and rs251937 in DRD1. Case-control and case-only studies were respectively performed, to determine the contribution of both single-nucleotide polymorphisms to the predisposition of disease and its severity. Our results showed that there was no significant association of the genotypes and allele frequencies of both single-nucleotide polymorphisms concerning childhood autism and its severity. More studies with larger samples are needed to corroborate their predicting roles.

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