1. Amihaesei IC, Stefanachi E. {{Autism, an overwhelming condition: history, etiopathogenesis, types, diagnosis, therapy and prognosis}}. {Revista medico-chirurgicala a Societatii de Medici si Naturalisti din Iasi}. 2013 Jul-Sep;117(3):654-61.
Autism is defined as a neurologic developmental disorder affecting brain and behavior, becoming usually apparent before 3 years of age, with stable evolution and no remission. No neurologic morphologic abnormality was associated with the disease. Several types of disease being described, autism is part of a larger spectrum known as autism spectrum disorders (ASD), or pervasive developmental disorders (PDD). The disease was first described long before it was defined and it has received its modern name. Main cause in the development of autism is considered to be genetic, up to 90 %. However, environmental factors could be incriminated, sometimes. The five types included in ASD are: Asperger syndrome, pervasive developmental disorder-not otherwise specified (PDD-NOS), typical autism, Rett syndrome and childhood disintegrative disorder (CDD). The classical triad of symptoms includes: social interaction impairments, communication impairments and repetitive, stereotype behavior. Diagnosis is based on interview of the parents and specialized observation of the suspected children. Main tools used in therapy are the family and the educational system. Well established, specialized programs of therapy were developed in time. Prognosis of autism is severe, since no cure is possible; nevertheless spontaneous recoveries do occur, in some cases.
2. Baghdadli A, Pry R, Michelon C, Rattaz C. {{Impact of autism in adolescents on parental quality of life}}. {Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation}. 2014 Feb 7.
PURPOSE: To study the impact of autism spectrum disorders (ASDs) on parental quality of life (QoL) at adolescence using the parental-developmental disorders-quality of life scale (Par-DD-QoL). METHODS: One hundred and fifty-two mothers of adolescents with ASD completed Par-DD-QoL. This scale assesses the following dimensions: emotional, daily disturbance and global QoL. This cross-sectional study uses a subset of data collected at the final time of a follow-up study (EpiTED cohort). RESULTS: A polytomic regression identified an increase in aberrant behavior scores as the major independent risk factor for parental QoL. The identified protective factors were the increase in daily living, communication and object cognition scores and a higher number of siblings. CONCLUSIONS: Those results suggest that there is a negative effect of externalizing behaviors and a protective effect of adaptive skills, communication and object cognition on parental QoL. Study limitations and implications are discussed.
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3. Findling RL, Mankoski R, Timko K, Lears K, McCartney T, McQuade RD, Eudicone JM, Amatniek J, Marcus RN, Sheehan JJ. {{A randomized controlled trial investigating the safety and efficacy of aripiprazole in the long-term maintenance treatment of pediatric patients with irritability associated with autistic disorder}}. {The Journal of clinical psychiatry}. 2014 Jan;75(1):22-30.
OBJECTIVE: To evaluate the efficacy and safety of aripiprazole versus placebo in preventing relapse of irritability symptoms associated with autistic disorder in pediatric patients. METHOD: This multicenter, double-blind, randomized, placebo-controlled, relapse-prevention trial enrolled patients (6-17 years) who met the current Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DMS-IV-TR) criteria for autistic disorder and who also had serious behavioral problems (ie, tantrums, aggression, self-injurious behavior, or a combination of these behavioral problems) between March 2011 and June 2012. In phase 1, single-blind aripiprazole was flexibly dosed (2-15 mg/d) for 13-26 weeks. Patients with a stable response (>/= 25% decrease in Aberrant Behavior Checklist-irritability subscale score and a rating of « much improved » or « very much improved » on the Clinical Global Impressions-Improvement scale) for 12 consecutive weeks were randomized into phase 2 to continue aripiprazole or switch to placebo. Treatment was continued until relapse or up to 16 weeks. The primary end point was time from randomization to relapse. RESULTS: Eighty-five patients were randomized in phase 2. The difference in time to relapse between aripiprazole and placebo was not statistically significant (P = .097). Kaplan-Meier relapse rates at week 16 were 35% for aripiprazole and 52% for placebo (hazard ratio [HR] = 0.57; number needed to treat [NNT] = 6). The most common adverse events during phase 1 were weight increase (25.2%), somnolence (14.8%), and vomiting (14.2%); and, during phase 2 (aripiprazole vs placebo), they were upper respiratory tract infection (10.3% vs 2.3%), constipation (5.1% vs 0%), and movement disorder (5.1% vs 0%). CONCLUSIONS: In this study, there was no statistically significant difference between aripiprazole and placebo in time to relapse during maintenance therapy. However, the HR and NNT suggest some patients will benefit from maintenance treatment. Patients receiving aripiprazole should be periodically reassessed to determine the continued need for treatment. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT01227668.
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4. Mazzone L, Postorino V, Valeri G, Vicari S. {{Catatonia in Patients with Autism: Prevalence and Management}}. {CNS drugs}. 2014 Feb 7.
Although recent studies have shown that catatonia can occur in patients with autism spectrum disorders (ASDs), the overlap of the behavioral features between these disorders raises many diagnostic challenges. In fact, in clinical practice it is common to misinterpret catatonic symptoms, including mutism, stereotypic speech, repetitive behaviors, echolalia, posturing, mannerisms, purposeless agitation and rigidity, as features of ASDs. The current medical treatment algorithm for catatonia in ASDs recommends the use of benzodiazepines. Electroconvulsive therapy (ECT) is indicated when patients are unresponsive, or insufficiently responsive, to benzodiazepines. Other pharmacological options are also described for the treatment of catatonic patients resistant to benzodiazepines and ECT, and there is evidence for the effectiveness of a psychological treatment, co-occurring with medical treatments, in order to support the management of these patients. In this article we provide a summary of studies exploring catatonia in ASDs and our clinical experience in the management and treatment of this syndrome through the presentation of three brief case studies. Moreover, we review the mechanisms underlying symptoms of catatonia in ASDs, as well as the diagnostic challenges, providing an outline for the management and treatment of this syndrome in this clinical population.
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5. Nielsen JA, Zielinski BA, Fletcher PT, Alexander AL, Lange N, Bigler ED, Lainhart JE, Anderson JS. {{Abnormal lateralization of functional connectivity between language and default mode regions in autism}}. {Molecular autism}. 2014 Feb 6;5(1):8.
BACKGROUND: Lateralization of brain structure and function occurs in typical development, and abnormal lateralization is present in various neuropsychiatric disorders. Autism is characterized by a lack of left lateralization in structure and function of regions involved in language, such as Broca and Wernicke areas. METHODS: Using functional connectivity magnetic resonance imaging from a large publicly available sample (n = 964), we tested whether abnormal functional lateralization in autism exists preferentially in language regions or in a more diffuse pattern across networks of lateralized brain regions. RESULTS: The autism group exhibited significantly reduced left lateralization in a few connections involving language regions and regions from the default mode network, but results were not significant throughout left- and right-lateralized networks. There is a trend that suggests the lack of left lateralization in a connection involving Wernicke area and the posterior cingulate cortex associates with more severe autism. CONCLUSIONS: Abnormal language lateralization in autism may be due to abnormal language development rather than to a deficit in hemispheric specialization of the entire brain.
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6. Tyzio R, Nardou R, Ferrari DC, Tsintsadze T, Shahrokhi A, Eftekhari S, Khalilov I, Tsintsadze V, Brouchoud C, Chazal G, Lemonnier E, Lozovaya N, Burnashev N, Ben-Ari Y. {{Oxytocin-mediated GABA inhibition during delivery attenuates autism pathogenesis in rodent offspring}}. {Science (New York, NY)}. 2014 Feb 7;343(6171):675-9.
We report that the oxytocin-mediated neuroprotective gamma-aminobutyric acid (GABA) excitatory-inhibitory shift during delivery is abolished in the valproate and fragile X rodent models of autism. During delivery and subsequently, hippocampal neurons in these models have elevated intracellular chloride levels, increased excitatory GABA, enhanced glutamatergic activity, and elevated gamma oscillations. Maternal pretreatment with bumetanide restored in offspring control electrophysiological and behavioral phenotypes. Conversely, blocking oxytocin signaling in naive mothers produced offspring having electrophysiological and behavioral autistic-like features. Our results suggest a chronic deficient chloride regulation in these rodent models of autism and stress the importance of oxytocin-mediated GABAergic inhibition during the delivery process. Our data validate the amelioration observed with bumetanide and oxytocin and point to common pathways in a drug-induced and a genetic rodent model of autism.
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7. Williams DM, Bowler DM. {{Autism spectrum disorder: fractionable or coherent?}}. {Autism}. 2014 Jan;18(1):2-5.
8. Zimmerman AW, Connors SL. {{Neuroscience. Could autism be treated prenatally?}}. {Science (New York, NY)}. 2014 Feb 7;343(6171):620-1.
