Pubmed du 29/08/13

Pubmed du jour

2013-08-29 12:03:50

1. {{Partnership Working with Family Carers of People with a Learning Disability and People with AutismPartnership Working with Family Carers of People with a Learning Disability and People with Autism}}. {Nurs Stand}. 2013; 27(52): 28.

Establishing sound working relationships between service users, family carers and paid staff is one of the most crucial aspects to delivering good support.

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2. Ajamian M, Rajadhyaksha AM, Alaedini A. {{Autism and Lyme disease–reply}}. {JAMA}. 2013; 310(8): 857.

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3. Andrea S, Jacena LM, Patrick A, Rawi N, Tasleem C, John O, Randi H, David H. {{Electrocortical changes associated with minocycline treatment in fragile X syndrome}}. {J Psychopharmacol}. 2013.

Minocycline normalizes synaptic connections and behavior in the knockout mouse model of fragile X syndrome (FXS). Human-targeted treatment trials with minocycline have shown benefits in behavioral measures and parent reports. Event-related potentials (ERPs) may provide a sensitive method of monitoring treatment response and changes in coordinated brain activity. Measurement of electrocortical changes due to minocycline was done in a double-blind, placebo-controlled crossover treatment trial in children with FXS. Children with FXS (Meanage 10.5 years) were randomized to minocycline or placebo treatment for 3 months then changed to the other treatment for 3 months. The minocycline dosage ranged from 25-100 mg daily, based on weight. Twelve individuals with FXS (eight male, four female) completed ERP studies using a passive auditory oddball paradigm. Current source density (CSD) and ERP analysis at baseline showed high-amplitude, long-latency components over temporal regions. After 3 months of treatment with minocycline, the temporal N1 and P2 amplitudes were significantly reduced compared with placebo. There was a significant amplitude increase of the central P2 component on minocycline. Electrocortical habituation to auditory stimuli improved with minocycline treatment. Our study demonstrated improvements of the ERP in children with FXS treated with minocycline, and the potential feasibility and sensitivity of ERPs as a cognitive biomarker in FXS treatment trials.

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4. Bransfield RC, Kuhn M. {{Autism and Lyme disease}}. {JAMA}. 2013; 310(8): 856-7.

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5. Bruno JL, Shelly EW, Quintin EM, Rostami M, Patnaik S, Spielman D, Mayer D, Gu M, Lightbody AA, Reiss AL. {{Aberrant basal ganglia metabolism in fragile X syndrome: a magnetic resonance spectroscopy study}}. {J Neurodev Disord}. 2013; 5(1): 20.

BACKGROUND: The profile of cognitive and behavioral variation observed in individuals with fragile X syndrome (FXS), the most common known cause of inherited intellectual impairment, suggests aberrant functioning of specific brain systems. Research investigating animal models of FXS, characterized by limited or lack of fragile X mental retardation protein, (FMRP), has linked brain dysfunction to deficits in the cholinergic and glutamatergic systems. Thus, we sought to examine in vivo levels of neurometabolites related to cholinergic and glutamatergic functioning in males and females with FXS. METHODS: The study participants included 18 adolescents and young adults with FXS, and a comparison group of 18 individuals without FXS matched for age, sex and general intellectual functioning. Proton magnetic resonance spectroscopy (MRS) was used to assess neurometabolite levels in the caudate nucleus, a region known to be greatly enlarged and involved in abnormal brain circuitry in individuals with FXS. A general linear model framework was used to compare group differences in metabolite concentration. RESULTS: We observed a decrease in choline (P = 0.027) and in glutamate + glutamine (P = 0.032) in the caudate nucleus of individuals with FXS, relative to individuals in the comparison group. CONCLUSIONS: This study provides evidence of metabolite differences in the caudate nucleus, a brain region of potential importance to our understanding of the neural deficits underlying FXS. These metabolic differences may be related to aberrant receptor signaling seen in animal models. Furthermore, identification of the specific neurometabolites involved in FXS dysfunction could provide critical biomarkers for the design and efficacy tracking of disease-specific pharmacological treatments.

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6. Cave SMF. {{Autism in Children}}. {Int J Pharm Compd}. 2001; 5(1): 18-9.

Abstract not available.

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7. Cook JL, Blakemore SJ, Press C. {{Atypical basic movement kinematics in autism spectrum conditions}}. {Brain}. 2013; 136(Pt 9): 2816-24.

Individuals with autism spectrum conditions have difficulties in understanding and responding appropriately to others. Additionally, they demonstrate impaired perception of biological motion and problems with motor control. Here we investigated whether individuals with autism move with an atypical kinematic profile, which might help to explain perceptual and motor impairments, and in principle may contribute to some of their higher level social problems. We recorded trajectory, velocity, acceleration and jerk while adult participants with autism and a matched control group conducted horizontal sinusoidal arm movements. Additionally, participants with autism took part in a biological motion perception task in which they classified observed movements as ‘natural’ or ‘unnatural’. Results show that individuals with autism moved with atypical kinematics; they did not minimize jerk to the same extent as the matched typical control group, and moved with greater acceleration and velocity. The degree to which kinematics were atypical was correlated with a bias towards perceiving biological motion as ‘unnatural’ and with the severity of autism symptoms as measured by the Autism Diagnostic Observation Schedule. We suggest that fundamental differences in movement kinematics in autism might help to explain their problems with motor control. Additionally, developmental experience of their own atypical kinematic profiles may lead to disrupted perception of others’ actions.

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8. Coskun MA, Loveland KA, Pearson DA, Papanicolaou AC, Sheth BR. {{Interaction of Finger Representations in the Cortex of Individuals with Autism: A Functional Window into Cortical Inhibition}}. {Autism Res}. 2013.

An established neural biomarker of autism spectrum disorder (ASD) has the potential to provide novel biological and pharmacological targets for treatment. Lower level of inhibition in brain circuits is a leading biomarker candidate. A physiological investigation of the functional levels of inhibition in the cortex of individuals with autism can provide a strong test of the hypothesis. The amplitude of cortical response to the stimulation of adjacent fingers is controlled by the level of cortical inhibition and provides just such a test. Using magnetoencephalography, we recorded the response of the somatosensory cortex to the passive tactile stimulation of the thumb (D1), and index finger (D2), and to the simultaneous stimulation of both fingers combined (D1,D2) of the dominant (right) hand of young subjects with and without autism. For each participant, we measured the response to the stimulation of both fingers combined (D1,D2) relative to the post hoc sum of the responses to the stimulation of each finger alone (D1+D2) in multiple different ways and linearly regressed the ASD and neurotypical (NT) groups’ responses. The resulting slopes were then compared: Smaller slope values imply attenuated response to paired finger stimulation, and enhanced levels of inhibition. The short-latency M40 and mid-latency M80 response slopes of the group with autism obtained in different ways were either significantly smaller, or statistically indistinguishable from NT. The result does not support reduced inhibition in the somatosensory cortex of individuals with autism, contrary to the seminal hypothesis of reduced inhibition. Implications are discussed including refinements of current theory. Autism Res 2013, : -. (c) 2013 International Society for Autism Research, Wiley Periodicals, Inc.

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9. Dansie LE, Phommahaxay K, Okusanya AG, Uwadia J, Huang M, Rotschafer SE, Razak KA, Ethell DW, Ethell IM. {{Long-lasting effects of minocycline on behavior in young but not adult Fragile X mice}}. {Neuroscience}. 2013; 246: 186-98.

Fragile X Syndrome (FXS) is the most common single-gene inherited form of intellectual disability with behaviors characteristic of autism. People with FXS display childhood seizures, hyperactivity, anxiety, developmental delay, attention deficits, and visual-spatial memory impairment, as well as a propensity for obsessive-compulsive disorder. Several of these aberrant behaviors and FXS-associated synaptic irregularities also occur in « fragile X mental retardation gene » knock-out (Fmr1 KO) mice. We previously reported that minocycline promotes the maturation of dendritic spines – postsynaptic sites for excitatory synapses – in the developing hippocampus of Fmr1 KO mice, which may underlie the beneficial effects of minocycline on anxiolytic behavior in young Fmr1 KO mice. In this study, we compared the effectiveness of minocycline treatment in young and adult Fmr1 KO mice, and determined the dependence of behavioral improvements on short-term versus long-term minocycline administration. We found that 4- and 8-week-long treatments significantly reduced locomotor activity in both young and adult Fmr1 KO mice. Some behavioral improvements persisted in young mice post-treatment, but in adults the beneficial effects were lost soon after minocycline treatment was stopped. We also show, for the first time, that minocycline treatment partially attenuates the number and severity of audiogenic seizures in Fmr1 KO mice. This report provides further evidence that minocycline treatment has immediate and long-lasting benefits on FXS-associated behaviors in the Fmr1 KO mouse model.

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10. de Magistris L, Picardi A, Siniscalco D, Riccio MP, Sapone A, Cariello R, Abbadessa S, Medici N, Lammers KM, Schiraldi C, Iardino P, Marotta R, Tolone C, Fasano A, Pascotto A, Bravaccio C. {{Antibodies against Food Antigens in Patients with Autistic Spectrum Disorders}}. {Biomed Res Int}. 2013; 2013: 729349.

Purpose. Immune system of some autistic patients could be abnormally triggered by gluten/casein assumption. The prevalence of antibodies to gliadin and milk proteins in autistic children with paired/impaired intestinal permeability and under dietary regimen either regular or restricted is reported. Methods. 162 ASDs and 44 healthy children were investigated for intestinal permeability, tissue-transglutaminase (tTG), anti-endomysium antibodies (EMA)-IgA, and total mucosal IgA to exclude celiac disease; HLA-DQ2/-DQ8 haplotypes; total systemic antibodies (IgA, IgG, and IgE); specific systemic antibodies: alpha -gliadin (AGA-IgA and IgG), deamidated-gliadin-peptide (DGP-IgA and IgG), total specific gliadin IgG (all fractions: alpha , beta , gamma , and omega ), beta -lactoglobulin IgG, alpha -lactalbumin IgG, casein IgG; and milk IgE, casein IgE, gluten IgE, -lactoglobulin IgE, and alpha -lactalbumin IgE. Results. AGA-IgG and DPG-IgG titers resulted to be higher in ASDs compared to controls and are only partially influenced by diet regimen. Casein IgG titers resulted to be more frequently and significantly higher in ASDs than in controls. Intestinal permeability was increased in 25.6% of ASDs compared to 2.3% of healthy children. Systemic antibodies production was not influenced by paired/impaired intestinal permeability. Conclusions. Immune system of a subgroup of ASDs is triggered by gluten and casein; this could be related either to AGA, DPG, and Casein IgG elevated production or to impaired intestinal barrier function.

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11. Delli K, Reichart PA, Bornstein MM, Livas C. {{Management of children with autism spectrum disorder in the dental setting: Concerns, behavioural approaches and recommendations}}. {Med Oral Patol Oral Cir Bucal}. 2013.

Objectives: This article reviews the present literature on the issues encountered while coping with children with autistic spectrum disorder from the dental perspective. The autistic patient profile and external factors affecting the oral health status of this patient population are discussed upon the existing body of evidence. Material and Methods: The MEDLINE database was searched using the terms ‘Autistic Disorder’, ‘Behaviour Control/methods’, ‘Child’, ‘Dental care for disabled’, ‘Education’, ‘Oral Health’, and ‘Pediatric Dentistry’ to locate related articles published up to January 2013. Results: Most of the relevant studies indicate poor oral hygiene whereas they are inconclusive regarding the caries incidence in autistic individuals. Undergraduate dental education appears to determine the competence of dental professionals to treat developmentally disabled children and account partly for compromised access to dental care. Dental management of an autistic child requires in-depth understanding of the background of the autism and available behavioural guidance theories. The dental professional should be flexible to modify the treatment approach according to the individual patient needs.

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12. Grodberg D, Weinger PM, Halpern D, Parides M, Kolevzon A, Buxbaum JD. {{The Autism Mental Status Exam: Sensitivity and Specificity Using DSM-5 Criteria for Autism Spectrum Disorder in Verbally Fluent Adults}}. {J Autism Dev Disord}. 2013.

The phenotypic heterogeneity of adults suspected of autism spectrum disorder (ASD) requires a standardized diagnostic approach that is feasible in all clinical settings. The autism mental status exam (AMSE) is an eight-item observational assessment that structures the observation and documentation of social, communicative and behavioral signs and symptoms of ASD. Previous findings indicate high classification accuracy when compared to the autism diagnostic observation schedule in a non-stratified population of high-risk patients suspected of having ASD. This protocol investigates the sensitivity and specificity of AMSE scores using DSM-5 criteria for ASD in a sample of high-risk verbally fluent adults. Findings indicate an optimized sensitivity of 0.91 and a specificity of 0.93 for this group. Because of its high clinical utility, the AMSE holds promise as a diagnostic assessment tool that can support one’s clinical diagnosis of ASD in high-risk adults.

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13. Hansel K. {{Rethinking insurance coverage of « experimental » Applied Behavioral Analysis therapy and its usefulness in combating autism spectrum disorder}}. {J Leg Med}. 2013; 34(2): 215-33.

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14. King EC, Toney SR. {{Topical Secretin for the Treatment of Autism}}. {Int J Pharm Compd}. 2001; 5(6): 436-7.

Abstract not available.

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15. Neuhaus E, Bernier R, Beauchaine TP. {{Brief Report: Social Skills, Internalizing and Externalizing Symptoms, and Respiratory Sinus Arrhythmia in Autism}}. {J Autism Dev Disord}. 2013.

Theoretical and empirical models describe respiratory sinus arrhythmia (RSA) as a peripheral biomarker of emotion regulation and social competence. Recent findings also link RSA to individual differences in social functioning within autism spectrum disorder (ASD). However, associations between RSA and symptoms of internalizing/externalizing psychopathology in ASD have not been explored. We assessed RSA, social functioning, and internalizing/externalizing symptoms among boys with and without ASD. Compared with controls, participants with ASD evidenced reduced parasympathetic cardiac control, which correlated with social behavior. Symptoms were associated with deficiencies in RSA, over-and-above the contribution of social functioning. These findings yield a more nuanced understanding of parasympathetic function in ASD, and suggest a role for integrative intervention strategies that address socioemotional difficulties.

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16. Tyson K, Kelley E, Fein D, Orinstein A, Troyb E, Barton M, Eigsti IM, Naigles L, Schultz RT, Stevens M, Helt M, Rosenthal M. {{Language and Verbal Memory in Individuals with a History of Autism Spectrum Disorders Who Have Achieved Optimal Outcomes}}. {J Autism Dev Disord}. 2013.

Some individuals who lose their autism spectrum disorder diagnosis may continue to display subtle weaknesses in language. We examined language and verbal memory in 44 individuals with high-functioning autism (HFA), 34 individuals with « optimal outcomes » (OO) and 34 individuals with typical development (TD). The OO group scored in the average range or above on all measures and showed few differences from the TD group. The HFA group performed within the average range but showed significantly lower mean performance than the other groups on multiple language measures, even when controlling for verbal IQ. Results also indicate that OO individuals show strong language abilities in all areas tested, but that their language may show greater reliance on verbal memory.

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