Pubmed du 20/11/19

mercredi 20 novembre 2019

1. Ben-Reuven L, Reiner O. Dynamics of cortical progenitors and production of subcerebral neurons are altered in embryos of a maternal inflammation model for autism. Mol Psychiatry ;2019 (Nov 18)

The broad impairments in cognitive and neurologic functioning found in Autism Spectrum Disorder (ASD) patients are thought to originate during early prenatal developmental stages. Indeed, postmortem and imaging studies in ASD patients detected white-matter abnormalities, as well as prefrontal and temporal cortex deficits, evident from early childhood. Here, we used Maternal Immune Activation (MIA), a mouse model for ASD, in which the offsprings exhibit Autistic-like behaviors as well as cortical abnormalities. However, the dynamics that influence the number and the identity of newly born cortical neurons following maternal inflammation remains unknown. Our study shows early changes in the duration of the S-phase of PAX6(+) progenitors, leading to an increased proportion of neurogenic divisions and a reciprocal decrease in the proliferative divisions. In two different time points of maternal inflammation, MIA resulted in an overproduction of CTIP2(+) cortical neurons, which remained overrepresented at the end of gestation and in postnatal mice. Interestingly, MIA-resistant IL6-KO mice did not exhibit these changes. Lastly, we propose that elevated levels of the transcription factor PAX6 following MIA supports the overproduction of CTIP2(+) neurons. Taken together, our data reveals a possible link between maternal immune activation and the excess of cortical neurons found in the cortex of ASD patients.

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2. Beversdorf DQ, Stevens HE, Margolis KG, Van de Water J. Prenatal stress and maternal immune dysregulation in autism spectrum disorders- potential points for intervention. Curr Pharm Des ;2019 (Nov 18)

BACKGROUND : Genetics are a major etiological contributor to autism spectrum disorder (ASD). Environmental factors, however, also appear to contribute. ASD pathophysiology due to gene x environment is also beginning to be explored. One reason to focus on environmental factors is that they may allow opportunities for intervention or prevention. METHODS AND RESULTS : Herein, we review two such factors that have been associated with a significant proportion of ASD risk, prenatal stress exposure and maternal immune dysregulation. Maternal stress susceptibility appears to interact with prenatal stress exposure to affect offspring neurodevelopment. We also explore how maternal stress may interact with the microbiome in the neurodevelopmental setting. Additionally, understanding of the impact of maternal immune dysfunction on ASD has recently been advanced by recognition of specific fetal brain proteins targeted by maternal autoantibodies, and identification of unique mid-gestational maternal immune profiles. This might also be interrelated with maternal stress exposure. Animal models have been developed to explore pathophysiology targeting each of these factors. CONCLUSIONS : We are beginning to understand the behavioral, pharmacopathological, and epigenetic effects related to these interactions, and we are beginning to explore potential mitigating factors. Continued growth in understanding of these mechanisms may ultimately allow for the identification of multiple potential targets for prevention or intervention for this subset of environmental-associated ASD cases.

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3. Bochynska A, Vulchanova M, Vulchanov V, Landau B. Spatial language difficulties reflect the structure of intact spatial representation : Evidence from high-functioning autism. Cogn Psychol ;2019 (Nov 16) ;116:101249.

Previous studies have shown that the basic properties of the visual representation of space are reflected in spatial language. This close relationship between linguistic and non-linguistic spatial systems has been observed both in typical development and in some developmental disorders. Here we provide novel evidence for structural parallels along with a degree of autonomy between these two systems among individuals with Autism Spectrum Disorder, a developmental disorder with uneven cognitive and linguistic profiles. In four experiments, we investigated language and memory for locations organized around an axis-based reference system. Crucially, we also recorded participants’ eye movements during the tasks in order to provide new insights into the online processes underlying spatial thinking. Twenty-three intellectually high-functioning individuals with autism (HFA) and 23 typically developing controls (TD), all native speakers of Norwegian matched on chronological age and cognitive abilities, participated in the studies. The results revealed a well-preserved axial reference system in HFA and weakness in the representation of direction within the axis, which was especially evident in spatial language. Performance on the non-linguistic tasks did not differ between HFA and control participants, and we observed clear structural parallels between spatial language and spatial representation in both groups. However, there were some subtle differences in the use of spatial language in HFA compared to TD, suggesting that despite the structural parallels, some aspects of spatial language in HFA deviated from the typical pattern. These findings provide novel insights into the prominence of the axial reference systems in non-linguistic spatial representations and spatial language, as well as the possibility that the two systems are, to some degree, autonomous.

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4. Capkova Z, Capkova P, Srovnal J, Staffova K, Becvarova V, Trkova M, Adamova K, Santava A, Curtisova V, Hajduch M, Prochazka M. Differences in the importance of microcephaly, dysmorphism, and epilepsy in the detection of pathogenic CNVs in ID and ASD patients. PeerJ ;2019 ;7:e7979.

Background : Autism spectrum disorders (ASD) and intellectual disabilities (ID) are heterogeneous and complex developmental diseases with significant genetic backgrounds and overlaps of genetic susceptibility loci. Copy number variants (CNVs) are known to be frequent causes of these impairments. However, the clinical heterogeneity of both disorders causes the diagnostic efficacy of CNV analysis to be modest. This could be resolved by stratifying patients according to their clinical features. Aim : First, we sought to assess the significance of particular clinical features for the detection of pathogenic CNVs in separate groups of ID and ASD patients and determine whether and how these groups differ from each other in the significance of these variables. Second, we aimed to create a statistical model showing how particular clinical features affect the probability of pathogenic CNV findings. Method : We tested a cohort of 204 patients with ID (N = 90) and ASD (N = 114) for the presence of pathogenic CNVs. We stratified both groups according to their clinical features. Fisher’s exact test was used to determine the significance of these variables for pathogenic CNV findings. Logistic regression was used to create a statistical model of pathogenic CNV findings. Results : The frequency of pathogenic CNV was significantly higher in the ID group than in the ASD group : 18 (19.78%) versus 8 (7%) (p < 0.004). Microcephaly showed a significant association with pathogenic findings in ID patients (p < 0.01) according to Fisher’s exact test, whereas epilepsy showed a significant association with pathogenic findings in ASD patients (p < 0.01). The probability of pathogenic CNV findings when epilepsy occurred in ASD patients was more than two times higher than if epilepsy co-occurred with ID (29.6%/14.0%). Facial dysmorphism was a significant variable for detecting pathogenic CNVs in both groups (ID p = 0.05, ASD p = 0.01). However, dysmorphism increased the probability of pathogenic CNV detection in the ID group nearly twofold compared to the ASD group (44.4%/23.7%). The presence of macrocephaly in the ASD group showed a 25% probability of pathogenic CNV findings by logistic regression, but this was insignificant according to Fisher’s exact test. The probability of detecting pathogenic CNVs decreases up to 1% in the absence of dysmorphism, macrocephaly, and epilepsy in the ASD group. Conclusion : Dysmorphism, microcephaly, and epilepsy increase the probability of pathogenic CNV findings in ID and ASD patients. The significance of each feature as a predictor for pathogenic CNV detection differs depending on whether the patient has only ASD or ID. The probability of pathogenic CNV findings without dysmorphism, macrocephaly, or epilepsy in ASD patients is low. Therefore the efficacy of CNV analysis is limited in these patients.

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5. Duan W, Wang K, Duan Y, Chu X, Ma R, Hu P, Xiong B. Integrated Transcriptome Analyses Revealed Key Target Genes in Mouse Models of Autism. Autism Res ;2019 (Nov 19)

Genetic mutations are the major pathogenic factor of Autism Spectrum Disorder (ASD). In recent years, more and more ASD risk genes have been revealed, among which there are a group of transcriptional regulators. Considering the similarity of the core clinical phenotypes, it is possible that these different factors may regulate the expression levels of certain key targets. Identification of these targets could facilitate the understanding of the etiology and developing of novel diagnostic and therapeutic methods. Therefore, we performed integrated transcriptome analyses of RNA-Seq and microarray data in multiple ASD mouse models and identified a number of common downstream genes in various brain regions, many of which are related to the structure and function of the synapse components or drug addiction. We then established protein-protein interaction networks of the overlapped targets and isolated the hub genes by 11 algorithms based on the topological structure of the networks, including Sdc4, Vegfa, and Cp in the Cortex-Adult subgroup, Gria1 in the Cortex-Juvenile subgroup, and Kdr, S1pr1, Ubc, Grm2, Grin2b, Nrxn1, Pdyn, Grin3a, Itgam, Grin2a, Gabra2, and Camk4 in the Hippocampus-Adult subgroup, many of which have been associated with ASD in previous studies. Finally, we cross compared our results with human brain transcriptional data sets and verified several key candidates, which may play important role in the pathology process of ASD, including SDC4, CP, S1PR1, UBC, PDYN, GRIN2A, GABRA2, and CAMK4. In summary, by integrated bioinformatics analysis, we have identified a series of potentially important molecules for future ASD research. Autism Res 2019. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY : Abnormal transcriptional regulation accounts for a significant portion of Autism Spectrum Disorder. In this study, we performed transcriptome analyses of mouse models to identify common downstream targets of transcriptional regulators involved in ASD. We identified several recurrent target genes that are close related to the common pathological process of ASD, including SDC4, CP, S1PR1, UBC, PDYN, GRM2, NRXN1, GRIN3A, ITGAM, GRIN2A, GABRA2, and CAMK4. These results provide potentially important targets for understanding the molecular mechanism of ASD.

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6. Geier DA, Kern JK, Geier MR. Down Syndrome as a Genetic Model to Evaluate the Role of Oxidative Stress and Transsulfuration Abnormities in Autism Spectrum Disorder : A Ten-Year Longitudinal Cohort Study. Dev Neurobiol ;2019 (Nov 19)

Autism spectrum disorder (ASD) is a neurodevelopmental disorder in which evidence reveals oxidative stress and transsulfuration pathway abnormalities. Down Syndrome (DS) is a genetic disorder characterized by similar oxidative stress and transsulfuration pathway abnormalities. This hypothesis-testing longitudinal cohort study determined whether transsulfuration abnormalities and oxidative stress are important susceptibility factors in ASD etiology by evaluating the rate of ASD diagnoses in DS as compared to the general population. The Independent Healthcare Research Database (IHRD) was analyzed for healthcare records prospectively generated in Florida Medicaid. A cohort of 101,736 persons (born : 1990-1999) with >/= 10 outpatient office visits and continuously followed for 120-months after birth were examined. There were 942 children in the DS cohort (ICD-9 code : 758.0) and 100,749 children the undiagnosed cohort (no DS diagnosis). ASD diagnoses were defined as autistic disorder (ICD-9 code : 299.00) or Asperger’s disorder/pervasive developmental disorder - not otherwise specified (PDD-NOS) (ICD-9 code : 299.80). ASDs were diagnosed in 5.31% of the DS cohort and 1.34% in the undiagnosed cohort. The risk ratio of being diagnosed with an ASD in the DS cohort as compared to the undiagnosed cohort was 3.97-fold significantly increased with a risk difference of 3.97%. Among children diagnosed with DS, less than 6% were also diagnosed with an ASD. Among children diagnosed with an ASD, less than 5% were also diagnosed with DS. Children diagnosed with DS are apparently more susceptible to ASD diagnosis relative to the general population suggesting oxidative stress and transsulfuration pathway abnormalities are important susceptibility factors in ASD.

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7. Lim J, Ryu J, Kang S, Noh HJ, Kim CH. Autism-like behaviors in male mice with a Pcdh19 deletion. Mol Brain ;2019 (Nov 20) ;12(1):95.

Mutations in protocadherin 19 (PCDH19), which is on the X-chromosome, cause the brain disease Epilepsy in Females with Mental Retardation (EFMR). EFMR is also often associated with autism-like symptoms. In mice and humans, epilepsy occurs only in heterozygous females who have a mixture of PCDH19 wild-type (WT) and mutant cells caused by random X-inactivation ; it does not occur in hemizygous PCDH19 mutant males. This unique inheritance pattern strongly suggests the underlying disease mechanism operates via interference between WT and mutant cells rather than being a result of complete loss of PCDH19 functions. Although it remains unclear whether the other symptoms of EFMR also conform to this unique genotype-phenotype relationship, PCDH19 mutant males were recently reported to demonstrate autism-like symptoms. We, therefore, used a Pcdh19 knockout (KO) mouse model to ask whether a complete lack of PCDH19 causes autism-like behaviors. Consistent with the autism observed in EFMR females, we found Pcdh19 heterozygous KO female mice (with mosaic expression of PCDH19) show defects in sociability in the 3-chamber test. Surprisingly, hemizygous Pcdh19 KO male mice (without any PCDH19 expression) exhibit impaired sociability in the 3-chamber test and reduced social interactions in the reciprocal social interaction test. We also observed that, compared to WT mice, mutant mice display more repetitive behaviors, including self-grooming and rearing. These findings indicate that hemizygous Pcdh19 KO male mice show autism-like phenotypes.

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8. McWilliams A, Reilly C, Gupta J, Hadji-Michael M, Srinivasan R, Heyman I. Autism spectrum disorder in children and young people with non-epileptic seizures. Seizure ;2019 (Nov 6) ;73:51-55.

PURPOSE : Non-epileptic seizures are paroxysmal events which to an observer resemble epileptic seizures. Proposed risk factors incorporate biopsychosocial aspects including factors in the affected individual. Unexpectedly high rates of autism spectrum disorder (ASD) occurred in the clinical population reported here. Although elevated levels of psychiatric co-morbidity are known to be present in patients with NES, ASD has only been previously described in a single case report. METHODS : This case series captures rates of ASD in 59 children and young people who were referred to a specialist paediatric mental health service at Great Ormond Street Hospital, London, UK for assessment and treatment of non-epileptic seizures between 2012 and 2016. RESULTS : 10/59 (16.9%) of the children and young people with non-epileptic seizures also had ASD, with 5/10 (50%) of these undiagnosed with ASD before referral. Children and young people with ASD were significantly more likely to have tics or attention-deficit hyperactivity disorder than those without ASD. CONCLUSION : ASD may be a common co-morbidity in non-epileptic seizures. Careful clinical assessment with consideration of ASD traits is therefore important in the non-epileptic seizures population. It is beneficial to diagnose ASD early as its presence is likely to require a modified approach to assessment and treatment of non-epileptic seizures. Study of the development of non-epileptic seizures in ASD may suggest hypotheses for the pathogenesis of non-epileptic seizures in the wider population.

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9. Mellema C, Treacher A, Nguyen K, Montillo A. Multiple Deep Learning Architectures Achieve Superior Performance Diagnosing Autism Spectrum Disorder Using Features Previously Extracted from Structural and Functional MRI. Proc IEEE Int Symp Biomed Imaging ;2019 (Apr) ;2019:1891-1895.

The diagnosis of Autism Spectrum Disorder (ASD) is a subjective process requiring clinical expertise in neurodevelopmental disorders. Since such expertise is not available at many clinics, automated diagnosis using machine learning (ML) algorithms would be of great value to both clinicians and the imaging community to increase the diagnoses’ availability and reproducibility while reducing subjectivity. This research systematically compares the performance of classifiers using over 900 subjects from the IMPAC database [1], using the database’s derived anatomical and functional features to diagnose a subject as autistic or healthy. In total 12 classifiers are compared from 3 categories including : 6 nonlinear shallow ML models, 3 linear shallow models, and 3 deep learning models. When evaluated with an AUC ROC performance metric, results include : (1) amongst the shallow learning methods, linear models outperformed nonlinear models, agreeing with [2]. (2) Deep learning models outperformed shallow ML models. (3) The best model was a dense feedforward network, achieving 0.80 AUC which compares to the recently reported 0.79+/-0.01 AUC average of the top 10 methods from the IMPAC challenge [3]. These results demonstrate that even when using features derived from imaging data, deep learning methods can provide additional predictive accuracy over classical methods.

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10. Morin-Parent F, Champigny C, Lacroix A, Corbin F, Lepage JF. Hyperexcitability and impaired intracortical inhibition in patients with fragile-X syndrome. Transl Psychiatry ;2019 (Nov 20) ;9(1):312.

Fragile-X syndrome (FXS) is characterized by neurological and psychiatric problems symptomatic of cortical hyperexcitability. Recent animal studies identified deficient gamma-aminobutyricacid (GABA) inhibition as a key mechanism for hyperexcitability in FXS, but the GABA system remains largely unexplored in humans with the disorder. The primary objective of this study was to assess GABA-mediated inhibition and its relationship with hyperexcitability in patients with FXS. Transcranial magnetic stimulation (TMS) was used to assess cortical and corticospinal inhibitory and excitatory mechanisms in 18 patients with a molecular diagnosis of FXS and 18 healthy controls. GABA-mediated inhibition was measured with short-interval intracortical inhibition (GABAA), long-interval intracortical inhibition (GABAB), and the corticospinal silent period (GABAA+B). Net intracortical facilitation involving glutamate was assessed with intracortical facilitation, and corticospinal excitability was measured with the resting motor threshold. Results showed that FXS patients had significantly reduced short-interval intracortical inhibition, increased long-interval intracortical inhibition, and increased intracortical facilitation compared to healthy controls. In the FXS group, reduced short-interval intracortical inhibition was associated with heightened intracortical facilitation. Taken together, these results suggest that reduced GABAA inhibition is a plausible mechanism underlying cortical hyperexcitability in patients with FXS. These findings closely match those observed in animal models, supporting the translational validity of these markers for clinical research.

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11. Pretzsch CM, Voinescu B, Lythgoe D, Horder J, Mendez MA, Wichers R, Ajram L, Ivin G, Heasman M, Edden RAE, Williams S, Murphy DGM, Daly E, McAlonan GM. Effects of cannabidivarin (CBDV) on brain excitation and inhibition systems in adults with and without Autism Spectrum Disorder (ASD) : a single dose trial during magnetic resonance spectroscopy. Transl Psychiatry ;2019 (Nov 20) ;9(1):313.

Autism spectrum disorder (ASD) is a high cost neurodevelopmental condition ; and there are currently no effective pharmacological treatments for its core symptoms. This has led some families and researchers to trial alternative remedies - including the non-intoxicating Cannabis sativa-derived compound cannabidivarin (CBDV). However, how CBDV affects the human brain is unknown. Previous (pre)clinical evidence suggests that CBDV may modulate brain excitatory-inhibitory systems, which are implicated in ASD. Hence, our main aim was to test, for the first time, if CBDV shifts glutamate and/or GABA metabolites - markers of the brain’s primary excitatory and inhibitory system - in both the ’typical’ and autistic brain. Our subsidiary aim was to determine whether, within ASD, brain responsivity to CBDV challenge is related to baseline biological phenotype. We tested this using a repeated-measures, double-blind, randomized-order, cross-over design. We used magnetic resonance spectroscopy (MRS) to compare glutamate (Glx = glutamate + glutamine) and GABA + (GABA + macromolecules) levels following placebo (baseline) and 600 mg CBDV in 34 healthy men with (n = 17) and without (n = 17) ASD. Data acquisition from regions previously reliably linked to ASD (dorsomedial prefrontal cortex, DMPFC ; left basal ganglia, BG) commenced 2 h (peak plasma levels) after placebo/CBDV administration. Where CBDV significantly shifted metabolite levels, we examined the relationship of this change with baseline metabolite levels. Test sessions were at least 13 days apart to ensure CBDV wash-out. CBDV significantly increased Glx in the BG of both groups. However, this impact was not uniform across individuals. In the ASD group, and not in the typically developing controls, the ’shift’ in Glx correlated negatively with baseline Glx concentration. In contrast, CBDV had no significant impact on Glx in the DMPFC, or on GABA+ in either voxel in either group. Our findings suggest that, as measured by MRS, CBDV modulates the glutamate-GABA system in the BG but not in frontal regions. Moreover, there is individual variation in response depending on baseline biochemistry. Future studies should examine the effect of CBDV on behaviour and if the response to an acute dose of CBDV could predict a potential clinical treatment response in ASD.

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12. Ros-Demarize R, Bradley C, Kanne SM, Warren Z, Boan A, Lajonchere C, Park J, Carpenter LA. ASD Symptoms in Toddlers and Preschoolers : An Examination of Sex Differences. Autism Res ;2019 (Nov 20)

Although considerable work has documented higher prevalence rates of autism spectrum disorder (ASD) in boys, fewer studies have focused on sex differences within samples of young children at-risk for ASD. This study examined sex differences in ASD symptom domains and ASD screening outcomes among toddlers (18-35 months) and preschoolers (36-72 months) with ASD-related concerns. Participants included 480 children between 18 and 72 months evaluated by university-based ASD specialty clinics. Results revealed significant sex differences in severity of social communication (SC) deficits across age groups. Within the toddler group, girls diagnosed with ASD displayed greater SC deficits according to standardized observation and clinician severity ratings. Within the preschool group, girls diagnosed with ASD were rated by parents as having more severe SC deficits, but these differences were not corroborated by standardized observations or clinician ratings. No sex differences emerged for severity of restricted repetitive behaviors (RRBs) for either age group. Across the entire referred sample, boys and girls did not differ in terms of scores on commonly used screening instruments. Importantly, results suggest that two of the most commonly used ASD screeners (i.e., Modified-Checklist for Autism in Toddlers-Revised with Follow-up and Social Communication Questionnaire ) may underidentify RRBs in toddler and preschool-aged girls as screening scores were only influenced by severity of SC deficits. Greater SC deficits in young girls with ASD along with its impact on screening status suggests greater attention be placed on the under-identification of ASD in girls as well as current screening measures’ ability to tap into the topography of ASD symptoms across genders. Autism Res 2019. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY : In this study, we found that young girls diagnosed with autism spectrum disorder tend to have greater social communication deficits than young boys and that these differences vary by age. Specifically, toddler-aged girls receive higher clinician ratings of social communication deficits when compared to boys, while preschool-aged girls receive higher parent ratings of social communication deficits. For girls, current screening tools seem to be more highly influenced by severity of social communication deficits than by restricted repetitive behaviors.

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13. Semmel ES, Fox ME, Na SD, Kautiainen R, Latzman RD, King TZ. Caregiver- and Clinician-Reported Adaptive Functioning in Rett Syndrome : a Systematic Review and Evaluation of Measurement Strategies. Neuropsychol Rev ;2019 (Nov 20)

Rett syndrome is the second most common cause of intellectual disability in females worldwide. The severity of many individuals’ impairment limits the effectiveness of traditional assessment. However, clinician and parent reports of adaptive functioning may provide insight into these patients’ abilities. This review aims to synthesize the current literature assessing adaptive functioning in Rett syndrome and evaluate existing measurement tools in this population. A search was conducted on PubMed using the search term "Rett syndrome." Studies that quantitatively assessed adaptive functioning outcomes in Rett syndrome with published and normed questionnaire measures were included. Twenty-three studies met inclusion criteria. Overall results indicate that the population of people with Rett syndrome is highly impaired, both in overall adaptive functioning as well as in specific subdomains (e.g., mobility, activities of daily living). Atypical Rett syndrome groups performed better on measures of adaptive functioning relative to patients with classic Rett syndrome. Our findings identified measurement weaknesses, as many of the studies found floor effects and therefore were unable to capture meaningful variability in outcomes. Individuals with Rett syndrome are highly reliant on caregivers due to disrupted adaptive functioning abilities. Optimizing measurement of adaptive skills in Rett syndrome will facilitate the quantification of meaningful change in skills and the identification of efficacious interventions aimed at improving outcomes and quality of life.

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14. Uzun AD, Sapmaz SY, Ozturk M, Kandemir H. Hypertension Induced by Aripiprazole Use in an Autistic Child Patient. Clin Psychopharmacol Neurosci ;2019 (Nov 20) ;17(4):556-558.

Atypical antipsychotics in children and adolescents are widely used for aggression, emotional variability and psychosis treatment. Aripiprazole is also an atypical antipsychotic that increasingly used in children and adolescents with schizophrenia, autism and bipolar disorder. In this case report, a medically healthy patient with autism associated with behavioral problems is presented with the development of hypertension after the onset of aripiprazole and the return of blood pressure to normal levels after withdrawal of the drug. The purpose of this case study is to discuss and report the emergence of aripiprazole-induced hypertension as a side effect of drugs in children and adolescents.

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15. Yankowitz LD, Schultz RT, Parish-Morris J. Pre- and Paralinguistic Vocal Production in ASD : Birth Through School Age. Curr Psychiatry Rep ;2019 (Nov 20) ;21(12):126.

PURPOSE OF REVIEW : We review what is known about how pre-linguistic vocal differences in autism spectrum disorder (ASD) unfold across development and consider whether vocalization features can serve as useful diagnostic indicators. RECENT FINDINGS : Differences in the frequency and acoustic quality of several vocalization types (e.g., babbles and cries) during the first year of life are associated with later ASD diagnosis. Paralinguistic features (e.g., prosody) measured during early and middle childhood can accurately classify current ASD diagnosis using cross-validated machine learning approaches. Pre-linguistic vocalization differences in infants are promising behavioral markers of later ASD diagnosis. In older children, paralinguistic features hold promise as diagnostic indicators as well as clinical targets. Future research efforts should focus on (1) bridging the gap between basic research and practical implementations of early vocalization-based risk assessment tools, and (2) demonstrating the clinical impact of targeting atypical vocalization features during social skill interventions for older children.

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