The autism spectrum is characterized by genetic and behavioral heterogeneity. However, it is still unknown whether there is a universal pattern of cognitive impairment in autism spectrum disorder (ASD) and whether multiple cognitive impairments are needed to explain the full range of behavioral symptoms. This study aimed to determine whether three widely acknowledged cognitive abnormalities (Theory of Mind (ToM) impairment, Executive Function (EF) impairment, and the presence of a Local Processing Bias (LB)) are universal and fractionable in autism, and whether the relationship between cognition and behavior is dependent on the method of behavioral assessment. Thirty‐one high‐functioning children with ASD and thirty‐seven children with neurotypical development (NTD), comparable in age, gender and Intelligence Quotient (IQ), completed several tasks tapping into ToM, EF, and LB, and autistic symptomatology was assessed through parental and teacher questionnaires, parental interview and direct observation. We found that ToM and EF deficits differentiated the groups and some ToM and EF tasks were related to each other. ToM and EF were together able to correctly classify more than three‐quarters of the children into cases and controls, despite relating to none of the specific behavioral measures. Only a small subgroup of individuals displayed a LB, which was unrelated to ToM and EF, and did not aid diagnostic classification, most likely contributing to non‐diagnostic symptoms in a subgroup. Despite the characteristic heterogeneity of the autism spectrum, it remains a possibility therefore that a single cognitive cause may underlie the range of diagnostic symptoms in all individuals with autism. Autism Res 2016, 9: 1328–1339. © 2016 International Society for Autism Research, Wiley Periodicals, Inc.

The relation between autism spectrum disorders (ASD) and schizophrenia is a subject of intense debate and research due to evidence of common neurobiological pathways in the two disorders. The objective of this study was to explore whether deficits in prepulse inhibition (PPI) of the startle reflex, as usually seen in schizophrenic patients, can be replicated in a group of children with ASD in comparison with a group of matched neuro-typically developed (NTD) controls. An additional aim was to explore possible psychophysiological subgroups within our ASD sample. In a case-control design, 35 ASD patients and 40 matched NTD controls were tested in a psychophysiological test battery. The PPI of the acoustic startle reflex was analyzed in 18 ASD subjects and 34 NTD controls. Habituation and sensitization were analyzed in 23 ASD subjects and 39 NTD controls. In trials with less intense prestimuli (76 dB), patients with ASD did not display the drop in percentage PPI normally found in healthy controls. In addition, ASD patients showed significantly increased sensitization compared with NTD controls. Combined, our results may reflect the hypersensitivity to sensory information in children with ASD. The relation to PPI deficits observed in schizophrenia is not apparent. Future research should study the developmental course of PPI deficits in ASD patients in a longitudinal design.

Automatic detection of deviant sounds in the environment, such as upcoming traffic, is often affected in children with autism spectrum disorders (ASD). Mismatch negativity (MMN) is a way to quantify automatic deviancy detection, using electroencephalography. In this study, auditory MMN was assessed in 35 children with ASD and 38 matched control children, revealing significantly reduced MMN in the ASD group. This may indicate that children with ASD are less able to automatically detect environmentally deviant stimuli.

Acoustic atypicalities in speech production are argued to be potential markers of clinical features in autism spectrum disorder (ASD). A recent meta-analysis highlighted shortcomings in the field, in particular small sample sizes and study heterogeneity. We showcase a cumulative (i.e., explicitly building on previous studies both conceptually and statistically) yet self-correcting (i.e., critically assessing the impact of cumulative statistical techniques) approach to prosody in ASD to overcome these issues. We relied on the recommendations contained in the meta-analysis to build and analyze a cross-linguistic corpus of multiple speech productions in 77 autistic and 72 neurotypical children and adolescents (>1000 recordings in Danish and US English). We used meta-analytically informed and skeptical priors, with informed priors leading to more generalizable inference. We replicated findings of a minimal cross-linguistically reliable distinctive acoustic profile for ASD (higher pitch and longer pauses) with moderate effect sizes. We identified novel reliable differences between the two groups for normalized amplitude quotient, maxima dispersion quotient, and creakiness. However, the differences were small, and there is likely no one acoustic profile characterizing all autistic individuals. We identified reliable relations of acoustic features with individual differences (age, gender), and clinical features (speech rate and ADOS subscores). Besides cumulatively building our understanding of acoustic atypicalities in ASD, the study shows how to use systematic reviews and meta-analyses to guide the design and analysis of follow-up studies. We indicate future directions: larger and more diverse cross-linguistic datasets, focus on heterogeneity, selfcritical cumulative approaches, and open science. Lay SummaryAutistic individuals are reported to speak in distinctive ways. Distinctive vocal production can affect social interactions and social development and could represent a noninvasive way to support the assessment of autism spectrum disorder (ASD). We systematically checked whether acoustic atypicalities highlighted in previous articles could be actually found across multiple recordings and two languages. We find a minimal acoustic profile of ASD: higher pitch, longer pauses, increased hoarseness and creakiness of the voice. However, there is much individual variability (by age, sex, language, and clinical characteristics). This suggests that the search for one common "autistic voice" might be naive and more finegrained approaches are needed.

Autism spectrum disorders (ASD) and schizophrenia are separate disorders, but there is evidence of conversion or comorbid overlap. The objective of this paper was to explore whether deficits in sensory gating, as seen in some schizophrenia patients, can also be found in a group of ASD children compared to neurotypically developed children. An additional aim was to investigate the possibility of subdividing our ASD sample based on these gating deficits. In a case-control design, we assessed gating of the P50 and N100 amplitude in 31 ASD children and 39 healthy matched controls (8-12 years) and screened for differences between groups and within the ASD group. We did not find disturbances in auditory P50 and N100 filtering in the group of ASD children as a whole, nor did we find abnormal P50 and N100 amplitudes. However, the P50 amplitude to the conditioning stimulus was significantly reduced in the Asperger subgroup compared to healthy controls. In contrast to what is usually reported for patients with schizophrenia, we found no evidence for sensory gating deficits in our group of ASD children taken as a whole. However, reduced P50 amplitude to conditioning stimuli was found in the Asperger group, which is similar to what has been described in some studies in schizophrenia patients. There was a positive correlation between the P50 amplitude of the conditioning stimuli and anxiety score in the pervasive developmental disorder not otherwise specified group, which indicates a relation between anxiety and sensory registration in this group.

There has been increasing interest in parent-mediated interventions (PMIs) for children with autism spectrum disorders (ASDs). The objective of this systematic review and meta-analysis was to examine the effect of PMIs compared to no PMI for children with ASD aged 2–17 years. The primary outcome was adaptive functioning rated by a parent or clinician. The secondary outcomes were long-term adaptive functioning rated by the parents, adverse events, core symptoms of ASD, disruptive behavior, parental well-being, quality of life of the child rated by the parents and anxiety. The MEDLINE, PsycInfo, Embase, and CINAHL databases were searched in March 2020. The Cochrane Risk of Bias Tool was used to rate the individual studies, and the certainty in the evidence was evaluated using GRADE. We identified 30 relevant randomized controlled trials (RCTs), including 1,934 participants. A clinically relevant effect of PMIs on parent-rated adaptive functioning was found with a low certainty of evidence [Standard mean difference (SMD): 0.28 (95% CI: −0.01, 0.57)] on Vineland Adaptive Behavior Scales (VABS), whereas no clinically relevant effect was seen for clinician-rated functional level, with a very low certainty of evidence [SMD on Clinical Global Impressions (CGI)-severity scale: SMD −0.45 [95% CI: −0.87, −0.03)]. PMIs may slightly improve clinician-rated autism core symptoms [SMD: −0.35 (95% CI: −0.71, 0.02)]. Additionally, no effect of PMIs on parent-rated core symptoms of ASD, parental well-being or adverse effects was identified, all with a low certainty of evidence. There was a moderate certainty of evidence for a clinically relevant effect on disruptive behavior [SMD: 0.55 (95% Cl: 0.36, 0.74)]. The certainty in the evidence was downgraded due to serious risk of bias, lack of blinding, and serious risk of imprecision due to few participants included in meta-analyses. The present findings suggest that clinicians may consider introducing PMIs to children with ASD, but more high-quality RCTs are needed because the effects are not well-established, and the results are likely to change with future studies. The protocol for the systematic review is registered at the Danish Health Authority website (www.sst.dk).

Several theories have attempted to characterise autism spectrum disorders (ASDs) at the cognitive level, most notably: theory of mind (ToM), executive function (EF), and a local processing bias (LB). The aim of this study was to investigate how these cognitive functions develop over time: The three cognitive domains (ToM, EF, and LB) were examined in a group of high-functioning children (age: 8-12, mean 10.85; IQ: 78-139, mean 105.48) with ASD and a matched group of children with neurotypical development (NTD) (IQ: 75-145, mean: 109.47), and several tasks were used within each domain to ensure the validity of the cognitive measures. Approximately 3 years later (mean age: 14.34), all children and their families were invited to participate in the follow-up (ASD, N = 21; NTD, N = 30). While the understanding of other's minds does improve from childhood to adolescence, ToM impairment persists in adolescents with ASD relative to their peers. Likewise, a development in EF was observed in the ASD group, while no significant improvement was seen in the NTD group, leading the ASD group to catch up in this domain. We did not detect any group differences at any time point regarding local bias processing (LB). Individual patterns of development were seen, but remarkably, ToM deficits were present in every child with ASD in whom we could detect any cognitive impairment at baseline, and a similar pattern was found at follow-up. These findings indicate that ToM is a persistent cognitive deficit in ASD.Lay Summary: This was the first study to investigate the development of three well-known cognitive functions into adolescence: While the understanding of other's minds improves from childhood to adolescence, adolescents with ASD are still impaired relative to their peers. The EFs, however, seem to improve to a neurotypical level in ASD as children enter adolescence, while local processing bias seems to differentiate the groups only in early childhood.

Acoustic atypicalities in speech production are widely documented in Autism Spectrum Disorder (ASD) and argued to be both a potential factor in atypical social development and potential markers of clinical features. A recent meta-analysis highlighted shortcomings in the field, in particular small sample sizes and study heterogeneity (Fusaroli, Lambrechts, Bang, Bowler, & Gaigg, 2017). We showcase a cumulative yet self-correcting approach to prosody in ASD to overcome these issues. We analyze a cross-linguistic corpus of multiple speech productions in 77 autistic children and adolescents and 72 TD ones (>1000 recordings in Danish and US English). We replicate findings of a minimal cross-linguistically reliable distinctive acoustic profile for ASD (higher pitch and longer pauses) with moderate effect sizes. We identified novel general reliable differences between the two groups for normalized amplitude quotient, maxima dispersion quotient and creakiness. However, all these relations are small, and there is likely no one general extensive acoustic profile characterizing all autistic individuals. We identified reliable and consistent relations of acoustic features with individual differences (age, gender), and clinical feature: speech rate and ADOS sub-scores (Communication, Social, Stereotyped). Besides cumulatively building our understanding of acoustic atypicalities in ASD, the study concretely shows how to use systematic reviews and meta-analyses to guide follow-up studies, both in their design and their statistical inferences. We indicate future directions: larger and more diverse cross-linguistic datasets, use of previous findings as statistical priors, understanding of covariance between acoustic measures, reliance on machine learning procedures, and open science.