1. Barbosa IG, Rodrigues DH, Rocha NP, Sousa LF, Vieira EL, Simoes ESAC, Kummer A, Teixeira AL. {{Plasma levels of alarmin IL-33 are unchanged in autism spectrum disorder: A preliminary study}}. {J Neuroimmunol}. 2015; 278: 69-72.
The pathogenesis of autism spectrum disorder (ASD) is unknown, and the immune system has been appointed to play an important role. The interleukin 33 (IL-33), a member of the IL-1, may act as an alarmin. This study aimed to evaluate plasma levels of IL-33, sST2, and IL-1beta in 30 patients with ASD in comparison with 18 controls matched by gender, age and maternal age at childbirth. Patients did not differ from controls in IL-33, sST2, and IL-1beta plasma levels. Alarmin levels were not correlated with age, and neither was influenced by clinical parameters. Our results undermine the role of IL-33/ST2 in ASD.
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2. Bird PD. {{The treatment of autism with low-dose phenytoin: a case report}}. {J Med Case Rep}. 2015; 9(1): 8.
INTRODUCTION: The drug treatment of autism spectrum disorders is often poorly tolerated and has traditionally targeted associated conditions (such as inattention or irritability) that frequently coexist, with limited benefit for the core social deficits. Here, I describe the novel use of a low dose of the anti-epileptic phenytoin to enhance social functioning in a patient with an autism spectrum disorder. CASE PRESENTATION: I present the case of a 19-year-old Caucasian man with autism spectrum disorder treated with stimulant medication since early childhood. He experienced long-standing difficulties in establishing and maintaining relationships and reading social cues, and was socially isolated. Within 10 minutes of a single sublingual low dose of phenytoin there was an immediate observable improvement in his eye contact and integration of both verbal and non-verbal communication. This enhanced social functioning associated with his adherence to the low-dose phenytoin therapy was maintained for over 18 months of follow-up. These clinical observations were supported by ratings using the Autism-Spectrum Quotient and the Depression, Anxiety and Stress Scales, recorded pre-treatment and after seven months on 5mg phenytoin. CONCLUSION: This case report provides the first potential evidence that a low dose of phenytoin, a widely used and well tolerated anti-epileptic medication, may be capable of modifying the core social cognitive deficits associated with autism spectrum disorders. While acknowledging this is a single case study, the lack of availability of safe and effective treatments to address the important core deficits associated with autism spectrum disorders makes this case noteworthy.
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3. Havercamp SM, Scott HM. {{National health surveillance of adults with disabilities, adults with intellectual and developmental disabilities, and adults with no disabilities}}. {Disabil Health J}. 2014.
BACKGROUND: People with disabilities experience worse health and poorer access to health care compared to people without disability. Large-scale health surveillance efforts have largely excluded adults with intellectual and developmental disability. This study expands knowledge of health status, health risks and preventative health care in a representative US sample comparing the health of adults with no disability to adults with intellectual and developmental disability and to adults with other types of disability. OBJECTIVES: The purposes of this study were (1) to identify disparities between adults with intellectual and developmental disability and adults with no disability and (2) compare this pattern of disparities to the pattern between adults with other types of disability and adults without disability. METHODS: This study compares health status, health risks and preventative health care in a national sample across three groups of adults: No Disability, Disability, and Intellectual and Developmental Disability. Data sources were the 2010 Behavior Risk Factor Surveillance Survey and the National Core Indicators Consumer Survey. RESULTS: Adults with disability and with intellectual and developmental disability were more likely to report being in poor health compared to adults without disability. Disability and intellectual and developmental disability conferred unique health risks and health care utilization patterns. CONCLUSIONS: Significant disparities in health and health care utilization were found for adults with disability and developmental disability relative to adults without disability. Disability training for health care providers and health promotion research that identifies disability as a demographic group is needed.
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4. Hock R, Kinsman A, Ortaglia A. {{Examining treatment adherence among parents of children with autism spectrum disorder}}. {Disabil Health J}. 2014.
BACKGROUND: Children with Autism Spectrum Disorder (ASD) participate in a variety of treatments, including medication, behavioral, alternative and developmental treatments. Parent adherence to these treatments is crucial for positive child outcomes. OBJECTIVE: The current study: 1) Explored patterns of parent adherence across the full range of treatments that are prescribed to children with ASD and, 2) Examined whether parent demographics, parent treatment attitudes, and child ASD severity contribute to parents’ adherence across ASD treatments. METHOD: Questionnaires were distributed to parents of children with ASD in a southeastern state. Parents (N = 274) were included if they were parenting a child with ASD who was receiving treatment for ASD symptoms. Paired t-tests and multiple linear regression were used to assess the study aims. RESULTS: Adherence to medication treatment was significantly greater than adherence to behavioral, developmental, or alternative treatments (adjusted p-values 0.0006, 0.0030, 0.0006 respectively). Perceived family burden of a treatment was associated with lower adherence to medication, developmental, and alternative treatments. Finally, greater ASD severity was associated with lower adherence to alternative treatments. CONCLUSION: Overall, the independent variables accounted for more variance in adherence to medication and alternative treatments than in behavioral and developmental treatments. Parents’ adherence to ASD treatment differs significantly by treatment type and is influenced by parental perceptions of the burden of treatment on the family. These findings highlight the importance of understanding and addressing the impact of ASD treatment regimens on family life.
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5. Niederhofer H. {{Is the vigilance regulation model of affective disorders and ADHD also appropriate for other psychiatric disorders (schizophrenia, autism) and is it associated with glutamate?}}. {Med Hypotheses}. 2014.
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6. Wegiel J, Flory M, Kuchna I, Nowicki K, Ma S, Imaki H, Frackowiak J, Kolecka B, Wierzba-Bobrowicz T, London E, Wisniewski T, Hof PR, Brown W. {{Neuronal nucleus and cytoplasm volume deficit in children with autism and volume increase in adolescents and adults}}. {Acta Neuropathol Commun}. 2015; 3(1): 2.
IntroductionCharacterization of the type and topography of structural changes and their alterations throughout the lifespan of individuals with autism is essential for understanding the mechanisms contributing to the autistic phenotype. The aim of this stereological study of neurons in 16 brain structures of 14 autistic and 14 control subjects from 4 to 64 years of age was to establish the course of neuronal nuclear and cytoplasmic volume changes throughout the lifespan of individuals with autism.ResultsOur data indicate that a deficit of neuronal soma volume in children with autism is associated with deficits in the volume of the neuronal nucleus and cytoplasm. The significant deficits of neuronal nuclear and cytoplasmic volumes in 13 of 16 examined subcortical structures, archicortex, cerebellum, and brainstem in 4- to 8-year-old autistic children suggest a global nature of brain developmental abnormalities, but with region-specific differences in the severity of neuronal pathology. The observed increase in nuclear volumes in 8 of 16 structures in the autistic teenagers/young adults and decrease in nuclear volumes in 14 of 16 regions in the age-matched control subjects reveal opposite trajectories throughout the lifespan. The deficit in neuronal nuclear volumes, ranging from 7% to 42% in the 16 examined regions in children with autism, and in neuronal cytoplasmic volumes from 1% to 31%, as well as the broader range of interindividual differences for the nuclear than the cytoplasmic volume deficits, suggest a partial distinction between nuclear and cytoplasmic pathology.ConclusionsThe most severe deficit of both neuronal nucleus and cytoplasm volume in 4-to 8-year-old autistic children appears to be a reflection of early developmental alterations that may have a major contribution to the autistic phenotype. The broad range of functions of the affected structures implies that their developmental and age-associated abnormalities contribute not only to the diagnostic features of autism but also to the broad spectrum of clinical alterations associated with autism. Lack of clinical improvement in autistic teenagers and adults indicates that the observed increase in neuron nucleus and cytoplasm volume close to control level does not normalize brain function.
