Pubmed du 12/11/19

mardi 12 novembre 2019

1. Chandrasekhar T, Copeland JN, Spanos M, Sikich L. Autism, Psychosis, or Both ? Unraveling Complex Patient Presentations. Child Adolesc Psychiatr Clin N Am ;2020 (Jan) ;29(1):103-113.

Autism spectrum disorders (ASDs) and schizophrenia spectrum disorders co-occur at elevated rates. Although these conditions are diagnostically distinct, they share multiple clinical features and genetic risk factors. This article describes the epidemiologic features and clinical manifestations of psychosis in individuals with ASDs, while also discussing shared genetic risk factors and affected brain regions. Components of a diagnostic assessment, including a thorough developmental, behavioral, medical, and psychiatric history, will be reviewed. The authors highlight the manifestations of catatonia in this population and note the shared features between catatonia and ASDs. Finally, treatment approaches and areas for future study are suggested.

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2. Hegarty JP, Lazzeroni LC, Raman MM, Pegoraro LFL, Monterrey JC, Cleveland SC, Hallmayer JF, Wolke ON, Phillips JM, Reiss AL, Hardan AY. Genetic and Environmental Influences on Lobar Brain Structures in Twins With Autism. Cereb Cortex ;2019 (Nov 11)

This investigation examined whether the variation of cerebral structure is associated with genetic or environmental factors in children with autism spectrum disorder (ASD) compared with typically developing (TD) controls. T1-weighted magnetic resonance imaging scans were obtained from twin pairs (aged 6-15 years) in which at least one twin was diagnosed with ASD or both were TD. Good quality data were available from 30 ASD, 18 discordant, and 34 TD pairs (n = 164). Structural measures (volume, cortical thickness, and surface area) were generated with FreeSurfer, and ACE modeling was completed. Lobar structures were primarily genetically mediated in TD twins (a2 = 0.60-0.89), except thickness of the temporal (a2 = 0.33 [0.04, 0.63]) and occipital lobes (c2 = 0.61 [0.45, 0.77]). Lobar structures were also predominantly genetically mediated in twins with ASD (a2 = 0.70-1.00) ; however, thickness of the frontal (c2 = 0.81 [0.71, 0.92]), temporal (c2 = 0.77 [0.60, 0.93]), and parietal lobes (c2 = 0.87 [0.77, 0.97]), and frontal gray matter (GM) volume (c2 = 0.79 [0.63, 0.95]), were associated with environmental factors. Conversely, occipital thickness (a2 = 0.93 [0.75, 1.11]) did not exhibit the environmental contributions that were found in controls. Differences in GM volume were associated with social communication impairments for the frontal (r = 0.52 [0.18, 0.75]), temporal (r = 0.61 [0.30, 0.80]), and parietal lobes (r = 0.53 [0.19, 0.76]). To our knowledge, this is the first investigation to suggest that environmental factors influence GM to a larger extent in children with ASD, especially in the frontal lobe.

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3. Liao X, Li Y. Economic burdens on parents of children with autism : a literature review. CNS Spectr ;2019 (Nov 11):1-7.

This review aims to summarize evidence from published articles regarding the economic burdens on parents of children diagnosed with autism to elaborate on current research status, discern key findings and provide suggestions for future studies. A total of 1024 records were identified through our systematic literature research, and 33 studies were included in the review. The 33 included studies reported findings from 10 different countries around the world. These articles (published from 2003 to 2017) used a variety of research methods, including quantitative (n = 26), qualitative (n = 4), and mixed (n = 3) study designs. In summary, parents of autistic children were susceptible to adverse employment impacts and increased financial burdens, especially mothers. More attention should be given to the development of appropriate medical resource allocation and the alleviation of economic burdens on parents of children with autism.

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4. Matsumura K, Baba M, Nagayasu K, Yamamoto K, Kondo M, Kitagawa K, Takemoto T, Seiriki K, Kasai A, Ago Y, Hayata-Takano A, Shintani N, Kuriu T, Iguchi T, Sato M, Takuma K, Hashimoto R, Hashimoto H, Nakazawa T. Autism-associated protein kinase D2 regulates embryonic cortical neuron development. Biochem Biophys Res Commun ;2019 (Nov 12) ;519(3):626-632.

Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental disorder, characterized by impaired social interaction, repetitive behavior and restricted interests. Although the molecular etiology of ASD remains largely unknown, recent studies have suggested that de novo mutations are significantly involved in the risk of ASD. We and others recently identified spontaneous de novo mutations in PKD2, a protein kinase D family member, in sporadic ASD cases. However, the biological significance of the de novo PKD2 mutations and the role of PKD2 in brain development remain unclear. Here, we performed functional analysis of PKD2 in cortical neuron development using in utero electroporation. PKD2 is highly expressed in cortical neural stem cells in the developing cortex and regulates cortical neuron development, including the neuronal differentiation of neural stem cells and migration of newborn neurons. Importantly, we determined that the ASD-associated de novo mutations impair the kinase activity of PKD2, suggesting that the de novo PKD2 mutations can be a risk factor for the disease by loss of function of PKD2. Our current findings provide novel insight into the molecular and cellular pathogenesis of ASD.

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5. Neupane KG. Autism Spectrum Disorder : The Parental Experience. J Psychosoc Nurs Ment Health Serv ;2019 (Nov 11):1-6.

In 2018, one in every 59 children was diagnosed in the United States with autism spectrum disorder (ASD). ASD is a developmental disability, which is a biologically based neurodevelopmental disorder that affects a child’s social interaction and communication skills. ASD includes repetitive patterns and restrictive behaviors, which could last a lifetime. Limited awareness of disease condition, less effective coping strategies, and inadequate guidance lead to increased stress levels among parents of children with ASD. Parents experience peaks and troughs of social, emotional, and financial challenges as they go through a pre-diagnosis phase, diagnosis phase, and post-diagnosis phase. The shortage of health care providers and fragmentation of care in the health care delivery system delays early diagnosis and management of ASD. Primary care providers along with the U.S. physician workforce for patients with ASD are strongly encouraged to review their practices on early screening and diagnosis and have clearly planned out care for every child with a family-centered approach. [Journal of Psychosocial Nursing and Mental Health Services, x(x), xx-xx.].

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6. Okumura T, Kumazaki H, Singh AK, Touhara K, Okamoto M. Individuals With Autism Spectrum Disorder Show Altered Event-Related Potentials in the Late Stages of Olfactory Processing. Chem Senses ;2019 (Nov 11)

Atypical sensory reactivities are pervasive among people with autism spectrum disorder (ASD). With respect to olfaction, most previous studies have used psychophysical or questionnaire-based methodologies ; thus, the neural basis of olfactory processing in ASD remains unclear. This study aimed to determine the stages of olfactory processing that are altered in ASD. Fourteen young adults with high-functioning ASD (mean age, 21 years ; 3 females) were compared with 19 age-matched typically developing (TD) controls (mean age, 21 years ; 4 females). Olfactory event-related potentials (OERPs) for 2-phenylethyl alcohol-a rose-like odor-were measured with 64 scalp electrodes while participants performed a simple odor detection task. Significant group differences in OERPs were found in 3 time windows 542 ms after the stimulus onset. The cortical source activities in these time windows, estimated using standardized low-resolution brain electromagnetic tomography, were significantly higher in ASD than in TD in and around the posterior cingulate cortex, which is known to play a crucial role in modality-general cognitive processing. Supplemental Bayesian analysis provided substantial evidence for an alteration in the later stages of olfactory processing, whereas conclusive evidence was not provided for the earlier stages. These results suggest that olfactory processing in ASD is altered at least at the later, modality-general processing stage.

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7. Schiavi S, Iezzi D, Manduca A, Leone S, Melancia F, Carbone C, Petrella M, Mannaioni G, Masi A, Trezza V. Reward-Related Behavioral, Neurochemical and Electrophysiological Changes in a Rat Model of Autism Based on Prenatal Exposure to Valproic Acid. Front Cell Neurosci ;2019 ;13:479.

Prenatal exposure to the antiepileptic drug valproic acid (VPA) induces autism spectrum disorder (ASD) in humans and autistic-like behaviors in rodents, which makes it a good model to study the neural underpinnings of ASD. Rats prenatally exposed to VPA show profound deficits in the social domain. The altered social behavior displayed by VPA-exposed rats may be due to either a deficit in social reward processing or to a more general inability to properly understand and respond to social signals. To address this issue, we performed behavioral, electrophysiological and neurochemical experiments and tested the involvement of the brain reward system in the social dysfunctions displayed by rats prenatally exposed to VPA (500 mg/kg). We found that, compared to control animals, VPA-exposed rats showed reduced play responsiveness together with impaired sociability in the three-chamber test and altered social discrimination abilities. In addition, VPA-exposed rats showed altered expression of dopamine receptors together with inherent hyperexcitability of medium spiny neurons (MSNs) in the nucleus accumbens (NAc). However, when tested for socially-induced conditioned place preference, locomotor response to amphetamine and sucrose preference, control and VPA-exposed rats performed similarly, indicating normal responses to social, drug and food rewards. On the basis of the results obtained, we hypothesize that social dysfunctions displayed by VPA-exposed rats are more likely caused by alterations in cognitive aspects of the social interaction, such as the interpretation and reciprocation of social stimuli and/or the ability to adjust the social behavior of the individual to the changing circumstances in the social and physical environment, rather than to inability to enjoy the pleasurable aspects of the social interaction. The observed neurochemical and electrophysiological alterations in the NAc may contribute to the inability of VPA-exposed rats to process and respond to social cues, or, alternatively, represent a compensatory mechanism towards VPA-induced neurodevelopmental insults.

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8. van Heijst BF, Deserno MK, Rhebergen D, Geurts HM. Autism and depression are connected : A report of two complimentary network studies. Autism ;2019 (Nov 10):1362361319872373.

Autism and depression often co-occur. Through network analysis, we seek to gain a better understanding of this co-occurrence by investigating whether (1) autism and depression share overlapping groups of symptoms and/or (2) are connected through a bridge of mastery or worry symptoms. This is addressed in two complimentary studies : (1) Study 1 focusing on depressed (N = 258) and non-depressed adults (N = 117), aged 60-90 years ; (2) Study 2 focusing on autistic (N = 173) and non-autistic adults (N = 70), aged 31-89 years. Self-report questionnaire data were collected on autistic traits (AQ-28), depression symptoms (Study 1 : Inventory of Depressive Symptomatology Self Report ; Study 2 : Symptom Checklist 90-Revised depression subscale), worry (Worry Scale-R) and mastery (the Pearlin Mastery Scale). For both studies, data were analysed by creating glasso networks and subsequent centrality analyses to identify the most influential variables in the respective networks. Both depressed and autistic adults are highly similar in the perceived amount of worries and lack of control. While caution is needed when interpreting the pattern of findings given the bootstrapping results, findings from both studies indicate that overlapping symptoms do not fully explain the co-occurrence of autism and depression and the perception of having control over your life, that is, mastery seems a relevant factor in connecting autism and depression.

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