1. Burrows CA, Usher LV, Becker-Haimes EM, McMahon CM, Mundy PC, Jensen-Doss A, Henderson HA. {{Profiles and Correlates of Parent-Child Agreement on Social Anxiety Symptoms in Youth with Autism Spectrum Disorder}}. {J Autism Dev Disord}. 2018.
This study characterized patterns and correlates of parent-youth agreement on social anxiety in youth with and without autism spectrum disorder (ASD). Participants (279 verbally-fluent youth aged 8-16 years, NASD = 144, NTD = 135) completed the SASC-R. Youth with ASD exhibited higher social anxiety across informants. While TD youth endorsed higher anxiety than did parents, self- and parent-reports did not differ in youth with ASD. For children with ASD, higher parent-youth agreement was associated with lower lifetime ASD symptoms and higher adaptive skills. For TD youth, agreement on high anxiety was associated with lowest adaptive skills. Demographic factors (age, verbal IQ, gender) did not relate to agreement for either group. In ASD, parent-child agreement on youth anxiety, either high or low, was associated with better outcomes.
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2. Friedman L, Sterling A, Barton-Hulsey A. {{Gaze avoidance and perseverative language in fragile X syndrome and autism spectrum disorder: brief report}}. {Dev Neurorehabil}. 2018: 1-4.
Gaze avoidance and perseverative language impact pragmatics in autism spectrum disorder (ASD) and fragile X syndrome (FXS). We examined these features during conversation samples in boys with ASD (n = 10) and boys with FXS and ASD (FXS+ASD; n = 10). Both groups had similar high rates of gaze avoidance and topic and conversation device perseverations, yet these features were not correlated with one another. Boys with FXS+ASD produced a higher proportion of single utterance perseverations. Results from this study highlight the need for future research to identify potential mechanisms influencing the presence of language perseverations and gaze avoidance.
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3. Guisso DR, Saadeh FS, Saab D, El Deek J, Chamseddine S, El Hassan HA, Majari G, Boustany RM. {{Association of Autism with Maternal Infections, Perinatal and Other Risk Factors: A Case-Control Study}}. {J Autism Dev Disord}. 2018.
This case-control study explores the association between pregnancy/birth complications and other factors with Autism Spectrum Disorder (ASD) in Lebanese subjects aged 2-18 years. Researchers interviewed 136 ASD cases from the American University of Beirut Medical Center Special Kids Clinic, and 178 controls selected by systematic digit dialing in the Greater-Beirut area. Male gender (Adjusted Odds Ratio [95% CI]: 3.9 [2.2-7.0]); postpartum feeding difficulties (2.5 [1.2-5.4]); maternal infections/complications during pregnancy (2.9 [1.5-5.5], 2.1 [1.1-3.9]); consanguinity (2.5 [1.0-6.0]); family history of psychiatric disorders (2.2 [1.1-4.4]) were risk factors for ASD. Being born first/second (0.52 [0.28-0.95]) and maternal psychological support during pregnancy (0.49 [0.27-0.89]) were negatively associated with ASD. Identifying ASD correlates is crucial for instigating timely screening and subsequent early intervention.
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4. Morales DR, Slattery J, Evans S, Kurz X. {{Antidepressant use during pregnancy and risk of autism spectrum disorder and attention deficit hyperactivity disorder: systematic review of observational studies and methodological considerations}}. {BMC medicine}. 2018; 16(1): 6.
BACKGROUND: Antidepressant exposure during pregnancy has been associated with an increased risk of autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) in several observational studies. We performed a systematic review of these studies to highlight the effect that important methodological limitations have on such analyses and to consider approaches to the conduct, reporting and interpretation of future studies. METHODS: A review of MEDLINE and EMBASE identified case-control, cohort and sibling studies assessing the risk of ASD and ADHD with antidepressant use during pregnancy. Approaches to confounding adjustment were described. Crude and adjusted effect estimates for comparisons between antidepressant exposure during pregnancy vs. all unexposed women were first meta-analysed using a generic inverse variance method of analysis, followed by effect estimates for alternative pre-selected comparison groups. RESULTS: A total of 15 studies measuring ASD as an outcome (involving 3,585,686 children and 40,585 cases) and seven studies measuring ADHD as an outcome (involving 2,765,723 patients and 52,313 cases) were identified. Variation in confounding adjustment existed between studies. Updated effect estimates for the association between maternal antidepressant exposure during pregnancy vs. all unexposed women remained statistically significant for ASD (adjusted random-effects risk ratio [RaRR] 1.53, 95% confidence interval [CI] 1.31-1.78). Similar significant associations were observed using pre-pregnancy maternal antidepressant exposure (RaRR 1.48, 95% CI 1.29-1.71) and paternal antidepressant exposure during pregnancy (1.29, 95% CI 1.08-1.53), but analyses restricted to using women with a history of affective disorder (1.18, 95% CI 0.91-1.52) and sibling studies (0.96, 95% CI 0.65-1.42) were not statistically significant. Corresponding associations for risk of ADHD with exposure were: RaRR 1.38, 95% CI 1.13-1.69 (during pregnancy), RaRR 1.38, 95% CI 1.14-1.69 (during pre-pregnancy), RaRR 1.71, 95% CI 1.31-2.23 (paternal exposure), RaRR 0.98, 95% CI 0.77-1.24 (women with a history of affective disorder) and RaRR 0.88, 95% CI 0.70-1.11 (sibling studies). CONCLUSIONS: Existing observational studies measuring the risk of ASD and ADHD with antidepressant exposure are heterogeneous in their design. Classical comparisons between exposed and unexposed women during pregnancy are at high risk of residual confounding. Alternative comparisons and sibling designs may aid the interpretation of causality and their utility requires further evaluation, including understanding potential limitations of undertaking meta-analyses with such data.
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5. Riva V, Cantiani C, Mornati G, Gallo M, Villa L, Mani E, Saviozzi I, Marino C, Molteni M. {{Distinct ERP profiles for auditory processing in infants at-risk for autism and language impairment}}. {Sci Rep}. 2018; 8(1): 715.
Early identification of autism spectrum disorder (ASD) is crucial for the formulation of effective intervention programs. Language deficits may be a hallmark feature of ASD and language delay observed in ASD shows striking similarities to that observed in children with language impairment (LI). Auditory processing deficits are seen in both LI and ASD, however, they have not previously been compared directly using Event-Related Potentials (ERPs) in the two at-risk populations. This study aims to characterize infants at-risk for ASD (HR-ASD) at the electrophysiological level and to compare them with infants at-risk for LI (HR-LI) and controls, to find specific markers with predictive value. At 12-month-old, auditory processing in HR-ASD, HR-LI and controls was characterized via ERP oddball paradigm. All infants were then evaluated at 20 months, to investigate the associations between auditory processing and language/ASD-related outcomes. In both HR-ASD and HR-LI, mismatch response latency was delayed compared to controls, whereas only HR-ASD showed overall larger P3 amplitude compared to controls. Interestingly, these ERP measures correlated with later expressive vocabulary and M-CHAT critical items in the whole sample. These results may support the use of objective measurement of auditory processing to delineate pathophysiological mechanisms in ASD, as compared to LI.
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6. Sikela JM, Searles Quick VB. {{Genomic trade-offs: are autism and schizophrenia the steep price of the human brain?}}. {Human genetics}. 2018.
Evolution often deals in genomic trade-offs: changes in the genome that are beneficial overall persist even though they also produce disease in a subset of individuals. Here, we explore the possibility that such trade-offs have occurred as part of the evolution of the human brain. Specifically, we provide support for the possibility that the same key genes that have been major contributors to the rapid evolutionary expansion of the human brain and its exceptional cognitive capacity also, in different combinations, are significant contributors to autism and schizophrenia. Furthermore, the model proposes that one of the primary genes behind this trade-off may not technically be « a gene » or « genes » but rather are the highly duplicated sequences that encode the Olduvai protein domain family (formerly called DUF1220). This is not an entirely new idea. Others have proposed that the same genes involved in schizophrenia were also critical to the rapid expansion of the human brain, a view that has been expressed as « the same ‘genes’ that drive us mad have made us human ». What is new is that a « gene », or more precisely a protein domain family, has been found that may satisfy these requirements.
