Phenotypical divergence between self-reported and clinically ascertained autism.

While allowing for rapid recruitment of large samples, online psychiatric and neurodevelopmental research relies heavily on participants' self-report of neuropsychiatric symptoms, foregoing the rigorous clinical characterization of laboratory settings. Autism spectrum disorder (ASD) research is one example where the clinical validity of such an approach remains elusive. Here, we compared participants characterized online via self-reports against in-person participants evaluated by clinicians. Despite having comparable self-reported autism symptoms, the online high-trait group reported significantly more social anxiety and avoidant behavior than in-person ASD subjects. Within the in-person sample, there was no relationship between self-rated and clinician-rated autism symptoms, suggesting these approaches may capture different aspects of ASD. The online high-trait and in-person ASD participants also differed in their behavior in well-validated social decision-making tasks: the in-person group perceived having less social control and acted less affiliative towards virtual characters. Our study aimed to draw comparisons at three levels: methodological platform (online versus in-person), symptom measurement (self- versus clinician-report), and social behavior. We identified a lack of agreement between self- and clinician-rated measures of symptoms and divergent social tendencies in groups ascertained by each method, highlighting the need for differentiation between in-person versus online samples in autism research.

Examining the latent structure and correlates of sensory reactivity in autism: a multi-site integrative data analysis by the autism sensory research consortium.

BACKGROUND: Differences in responding to sensory stimuli, including sensory hyperreactivity (HYPER), hyporeactivity (HYPO), and sensory seeking (SEEK) have been observed in autistic individuals across sensory modalities, but few studies have examined the structure of these "supra-modal" traits in the autistic population. METHODS: Leveraging a combined sample of 3868 autistic youth drawn from 12 distinct data sources (ages 3-18 years and representing the full range of cognitive ability), the current study used modern psychometric and meta-analytic techniques to interrogate the latent structure and correlates of caregiver-reported HYPER, HYPO, and SEEK within and across sensory modalities. Bifactor statistical indices were used to both evaluate the strength of a "general response pattern" factor for each supra-modal construct and determine the added value of "modality-specific response pattern" scores (e.g., Visual HYPER). Bayesian random-effects integrative data analysis models were used to examine the clinical and demographic correlates of all interpretable HYPER, HYPO, and SEEK (sub)constructs. RESULTS: All modality-specific HYPER subconstructs could be reliably and validly measured, whereas certain modality-specific HYPO and SEEK subconstructs were psychometrically inadequate when measured using existing items. Bifactor analyses supported the validity of a supra-modal HYPER construct (ωH = .800) but not a supra-modal HYPO construct (ωH = .653), and supra-modal SEEK models suggested a more limited version of the construct that excluded some sensory modalities (ωH = .800; 4/7 modalities). Modality-specific subscales demonstrated significant added value for all response patterns. Meta-analytic correlations varied by construct, although sensory features tended to correlate most with other domains of core autism features and co-occurring psychiatric symptoms (with general HYPER and speech HYPO demonstrating the largest numbers of practically significant correlations). LIMITATIONS: Conclusions may not be generalizable beyond the specific pool of items used in the current study, which was limited to caregiver report of observable behaviors and excluded multisensory items that reflect many "real-world" sensory experiences. CONCLUSION: Of the three sensory response patterns, only HYPER demonstrated sufficient evidence for valid interpretation at the supra-modal level, whereas supra-modal HYPO/SEEK constructs demonstrated substantial psychometric limitations. For clinicians and researchers seeking to characterize sensory reactivity in autism, modality-specific response pattern scores may represent viable alternatives that overcome many of these limitations.

Examining the Latent Structure and Correlates of Sensory Reactivity in Autism: A Multi-site Integrative Data Analysis by the Autism Sensory Research Consortium.

Background Differences in responding to sensory stimuli, including sensory hyperreactivity (HYPER), hyporeactivity (HYPO), and sensory seeking (SEEK) have been observed in autistic individuals across sensory modalities, but few studies have examined the structure of these "supra-modal" traits in the autistic population. Methods Leveraging a combined sample of 3,868 autistic youth drawn from 12 distinct data sources (ages 3-18 years and representing the full range of cognitive ability), the current study used modern psychometric and meta-analytic techniques to interrogate the latent structure and correlates of caregiver-reported HYPER, HYPO, and SEEK within and across sensory modalities. Bifactor statistical indices were used to both evaluate the strength of a "general response pattern" factor for each supra-modal construct and determine the added value of "modality-specific response pattern" scores (e.g., Visual HYPER). Bayesian random-effects integrative data analysis models were used to examine the clinical and demographic correlates of all interpretable HYPER, HYPO and SEEK (sub)constructs. Results All modality-specific HYPER subconstructs could be reliably and validly measured, whereas certain modality-specific HYPO and SEEK subconstructs were psychometrically inadequate when measured using existing items. Bifactor analyses unambiguously supported the validity of a supra-modal HYPER construct (ω H = .800), whereas a coherent supra-modal HYPO construct was not supported (ω H = .611), and supra-modal SEEK models suggested a more limited version of the construct that excluded some sensory modalities (ω H = .799; 4/7 modalities). Within each sensory construct, modality-specific subscales demonstrated substantial added value beyond the supra-modal score. Meta-analytic correlations varied by construct, although sensory features tended to correlate most strongly with other domains of core autism features and co-occurring psychiatric symptoms. Certain subconstructs within the HYPO and SEEK domains were also associated with lower adaptive behavior scores. Limitations: Conclusions may not be generalizable beyond the specific pool of items used in the current study, which was limited to parent-report of observable behaviors and excluded multisensory items that reflect many "real-world" sensory experiences. Conclusion Psychometric issues may limit the degree to which some measures of supra-modal HYPO/SEEK can be interpreted. Depending on the research question at hand, modality-specific response pattern scores may represent a valid alternative method of characterizing sensory reactivity in autism.

Distinct Symptom Network Structure and Shared Central Social Communication Symptomatology in Autism and Schizophrenia: A Bayesian Network Analysis.

Autism (ASD) and schizophrenia spectrum disorders (SCZ) are neurodevelopmental conditions with overlapping and interrelated symptoms. A network analysis approach that represents clinical conditions as a set of "nodes" (symptoms) connected by "edges" (relations among symptoms) was used to compare symptom organization in the two conditions. Gaussian graphical models were estimated using Bayesian methods to model separate symptom networks for adults with confirmed ASD or SCZ diagnoses. Though overall symptom organization differed by diagnostic group, both symptom networks demonstrated high centrality of social communication difficulties. Autism-relevant restricted and repetitive behaviors and schizophrenia-related cognitive-perceptual symptoms were uniquely central to the ASD and SCZ networks, respectively. Results offer recommendations to improve differential diagnosis and highlight potential treatment targets in ASD and SCZ.

Electrophysiological Studies of Reception of Facial Communication in Autism Spectrum Disorder and Schizophrenia.

Autism spectrum disorder (ASD) and schizophrenia spectrum disorders (SZ) are characterized by difficulty with social cognition and atypical reception of facial communication - a key area in the Research Domain Criteria framework. To identify areas of overlap and dissociation between ASD and SZ, we review studies of event-related potentials (ERP) to faces across ASD and SZ populations, focusing on ERPs implicated in social perception: P100, N170, N250, and P300. There were many inconsistent findings across studies; however, replication was strongest for delayed N170 latency in ASD and attenuated N170 amplitude in SZ. These results highlight the challenges of replicating research findings in heterogeneous clinical populations and the need for transdiagnostic research that continuously quantifies behavior and neural activity across neurodevelopmental disorders.

Predictability modulates neural response to eye contact in ASD.

BACKGROUND: Deficits in establishing and maintaining eye-contact are early and persistent vulnerabilities of autism spectrum disorder (ASD), and the neural bases of these deficits remain elusive. A promising hypothesis is that social features of autism may reflect difficulties in making predictions about the social world under conditions of uncertainty. However, no research in ASD has examined how predictability impacts the neural processing of eye-contact in naturalistic interpersonal interactions. METHOD: We used eye tracking to facilitate an interactive social simulation wherein onscreen faces would establish eye-contact when the participant looked at them. In Experiment One, receipt of eye-contact was unpredictable; in Experiment Two, receipt of eye-contact was predictable. Neural response to eye-contact was measured via the N170 and P300 event-related potentials (ERPs). Experiment One included 23 ASD and 46 typically developing (TD) adult participants. Experiment Two included 25 ASD and 43 TD adult participants. RESULTS: When receipt of eye-contact was unpredictable, individuals with ASD showed increased N170 and increased, but non-specific, P300 responses. The magnitude of the N170 responses correlated with measures of sensory and anxiety symptomology, such that increased response to eye-contact was associated with increased symptomology. However, when receipt of eye-contact was predictable, individuals with ASD, relative to controls, exhibited slower N170s and no differences in the amplitude of N170 or P300. LIMITATIONS: Our ASD sample was composed of adults with IQ > 70 and included only four autistic women. Thus, further research is needed to evaluate how these results generalize across the spectrum of age, sex, and cognitive ability. Additionally, as analyses were exploratory, some findings failed to survive false-discovery rate adjustment. CONCLUSIONS: Neural response to eye-contact in ASD ranged from attenuated to hypersensitive depending on the predictability of the social context. These findings suggest that the vulnerabilities in eye-contact during social interactions in ASD may arise from differences in anticipation and expectation of eye-contact in addition to the perception of gaze alone.

An open-label study evaluating the safety, behavioral, and electrophysiological outcomes of low-dose ketamine in children with ADNP syndrome.

Activity-dependent neuroprotective protein (ADNP) syndrome is a rare genetic condition associated with intellectual disability and autism spectrum disorder. Preclinical evidence suggests that low-dose ketamine may induce expression of ADNP and that neuroprotective effects of ketamine may be mediated by ADNP. The goal of the proposed research was to evaluate the safety, tolerability, and behavioral outcomes of low-dose ketamine in children with ADNP syndrome. We also sought to explore the feasibility of using electrophysiological markers of auditory steady-state response and computerized eye tracking to assess biomarker sensitivity to treatment. This study utilized a single-dose (0.5 mg/kg), open-label design, with ketamine infused intravenously over 40 min. Ten children with ADNP syndrome ages 6 to 12 years were enrolled. Ketamine was generally well tolerated, and there were no serious adverse events. The most common adverse events were elation/silliness (50%), fatigue (40%), and increased aggression (40%). Using parent-report instruments to assess treatment effects, ketamine was associated with nominally significant improvement in a wide array of domains, including social behavior, attention deficit and hyperactivity, restricted and repetitive behaviors, and sensory sensitivities, a week after administration. Results derived from clinician-rated assessments aligned with findings from the parent reports. Overall, nominal improvement was evident based on the Clinical Global Impressions - Improvement scale, in addition to clinician-based scales reflecting key domains of social communication, attention deficit and hyperactivity, restricted and repetitive behaviors, speech, thinking, and learning, activities of daily living, and sensory sensitivities. Results also highlight the potential utility of electrophysiological measurement of auditory steady-state response and eye-tracking to index change with ketamine treatment. Findings are intended to be hypothesis generating and provide preliminary support for the safety and efficacy of ketamine in ADNP syndrome in addition to identifying useful endpoints for a ketamine clinical development program. However, results must be interpreted with caution given limitations of this study, most importantly the small sample size and absence of a placebo-control group.

Disrupted computations of social control in individuals with obsessive-compulsive and misophonia symptoms.

Misophonia is a disorder in which certain sounds produced by other people lead to intense negative reactions. It remains unknown how misophonia relates to other psychiatric conditions or impairments. To identify latent constructs underlying symptoms, we conducted a factor analysis consisting of items from questionnaires assessing symptoms of misophonia and other psychiatric conditions. One thousand forty-two participants completed the questionnaires and a social exchange task in which they either could ("controllable") or could not ("uncontrollable") influence future monetary offers from other people. Misophonia and obsessive-compulsive (OC) symptoms loaded onto the same factor. Compared with individuals with low Miso-OC factor scores, individuals with high scores reported higher perceived controllability of their social interactions during the uncontrollable condition and stronger aversion to social norm violations in the uncontrollable compared with the controllable condition. Together, these results suggest misophonia, and OC symptoms share a latent psychiatric dimension characterized by aberrant computations of social controllability.

Brief Report: Assessment of a Caregiver-Implemented Intervention for Improving Social Communication Skills in Toddlers and Young Children with Autism.

As early identification of autism improves, there is a critical need for interventions to support the development of social communication skills in toddlers. Caregiver coaching and parental involvement is crucial for improving outcomes and providing children with adequate hours of planned active engagement. This pilot study assessed a 4-week intervention for individual caregiver-child dyads. Eight toddlers 21- to 45-months of age participated. Standardized assessments were collected at four study visits to assess autism symptomatology, language development, and both caregiver knowledge and engagement. Results demonstrated the feasibility of the intervention. Social communication, receptive and expressive language all improved as measured by direct assessment. Caregiver knowledge and caregivers' subjective feelings of engagement with their toddlers also improved.

Neural Markers of Auditory Response and Habituation in Phelan-McDermid Syndrome.

Phelan-McDermid Syndrome (PMS) is a rare genetic disorder caused by deletion or sequence variation in the SHANK3 gene at terminal chromosome 22 that confers high likelihood of comorbid autism spectrum disorder (ASD). Whereas individuals with idiopathic ASD (iASD) can demonstrate diverse patterns of sensory differences, PMS is mainly characterized by sensory hyporesponsiveness. This study used electrophysiology and a passive auditory habituation paradigm to test for neural markers of hyporesponsiveness. EEG was recorded from 15 individuals with PMS, 15 with iASD, and 16 with neurotypical development (NT) while a series of four consecutive 1,000 Hz tones was repeatedly presented. We found intact N1, P2, and N2 event-related potentials (ERPs) and habituation to simple auditory stimuli, both in individuals with iASD and in those with PMS. Both iASD and PMS groups showed robust responses to the initial tone and decaying responses to each subsequent tone, at levels comparable to the NT control group. However, in PMS greater initial N1 amplitude and habituation were associated with auditory hypersensitivity, and P2 habituation correlated with ASD symptomatology. Additionally, further classification of the PMS cohort into genetic groupings revealed dissociation of initial P2 amplitude and habituation of N1 based on whether the deletions included additional genes beyond solely SHANK3 and those not thought to contribute to phenotype. These results provide preliminary insight into early auditory processing in PMS and suggest that while neural response and habituation is generally preserved in PMS, genotypic and phenotypic characteristics may drive some variability. These initial findings provide early evidence that the robust pattern of behavioral hyporesponsiveness in PMS may be due, at least in audition, to higher order factors.

Autism spectrum disorder and schizophrenia: An updated conceptual review.

Autism spectrum disorder (ASD) and schizophrenia (SCZ) are separate disorders, with distinct clinical profiles and natural histories. ASD, typically diagnosed in childhood, is characterized by restricted or repetitive interests or behaviors and impaired social communication, and it tends to have a stable course. SCZ, typically diagnosed in adolescence or adulthood, is characterized by hallucinations and delusions, and tends to be associated with declining function. However, youth with ASD are three to six times more likely to develop SCZ than their neurotypical counterparts, and increasingly, research has shown that ASD and SCZ converge at several levels. We conducted a systematic review of studies since 2013 relevant to understanding this convergence, and present here a narrative synthesis of key findings, which we have organized into four broad categories: symptoms and behavior, perception and cognition, biomarkers, and genetic and environmental risk. We then discuss opportunities for future research into the phenomenology and neurobiology of overlap between ASD and SCZ. Understanding this overlap will allow for researchers, and eventually clinicians, to understand the factors that may make a child with ASD vulnerable to developing SCZ. LAY SUMMARY: Autism spectrum disorder and schizophrenia are distinct diagnoses, but people with autism and people with schizophrena share several characteristics. We review recent studies that have examined these areas of overlap, and discuss the kinds of studies we will need to better understand how these disorders are related. Understanding this will be important to help us identify which autistic children are at risk of developing schizophrenia.

Visual Evoked Potential Abnormalities in Phelan-McDermid Syndrome.

OBJECTIVE: The current study used visual evoked potentials (VEPs) to examine excitatory and inhibitory postsynaptic activity in children with Phelan-McDermid syndrome (PMS) and the association with genetic factors. PMS is caused by haploinsufficiency of SHANK3 on chromosome 22 and represents a common single-gene cause of autism spectrum disorder (ASD) and intellectual disability. METHOD: Transient VEPs were obtained from 175 children, including 31 with PMS, 79 with idiopathic ASD, 45 typically developing controls, and 20 unaffected siblings of children with PMS. Stimuli included standard and short-duration contrast-reversing checkerboard conditions, and the reliability between these 2 conditions was assessed. Test-retest reliability and correlations with deletion size were explored in the group with PMS. RESULTS: Children with PMS and, to a lesser extent, those with idiopathic ASD displayed significantly smaller amplitudes and decreased beta and gamma band activity relative to TD controls and PMS siblings. Across groups, high intraclass correlation coefficients were obtained between standard and short-duration conditions. In children with PMS, test-retest reliability was strong. Deletion size was significantly correlated with P60-N75 amplitude for both conditions. CONCLUSION: Children with PMS displayed distinct transient VEP waveform abnormalities in both time and frequency domains that might reflect underlying glutamatergic deficits that were associated with deletion size. A similar response pattern was observed in a subset of children with idiopathic ASD. VEPs offer a noninvasive measure of excitatory and inhibitory neurotransmission that holds promise for stratification and surrogate endpoints in ongoing clinical trials in PMS and ASD.

Reported autism diagnosis is associated with psychotic-like symptoms in the Adolescent Brain Cognitive Development cohort.

Although the schizophrenia (SCZ) rate is increased in autism spectrum disorder (ASD), it is difficult to identify which ASD youth will develop psychosis. We explored the relationship between ASD and emerging psychotic-like experiences (PLS) in a sample of 9127 youth aged 9-11 from the Adolescent Brain Cognitive Development (ABCD) cohort. We predicted that parent-reported ASD would be associated with PLS severity, and that ASD youth with PLS (ASD+/PLS+) would differ from ASD youth without PLS (ASD+/PLS-) and youth with PLS but not ASD (ASD-/PLS+) in cognitive function. We fit regression models that included parent-reported ASD, family history of psychosis, lifetime trauma, executive function, processing speed, working memory, age, sex, race, ethnicity, and income-to-needs ratio as predictors of Prodromal Questionnaire-Brief Child (PQ-BC) distress score, a continuous index of PLS severity. We assessed cognitive differences using regression models with ASD/PLS status and relevant covariates as predictors of NIH Toolbox measures. ASD increased raw PQ-BC distress scores by 2.47 points (95% CI 1.33-3.61), an effect at least as large as Black race (1.27 points, 95% CI 0.75-1.78), family history of psychosis (1.05 points, 95% CI 0.56-1.54), and Latinx ethnicity (0.99 points, 95% CI 0.53-1.45. We did not identify differences in cognition for ASD+/PLS+ youth relative to other groups. Our finding of association between ASD and PLS in youth is consistent with previous literature and adds new information in suggesting that ASD may be a strong risk factor for PLS even compared to established SCZ risk factors.

Strong evidence for genotype-phenotype correlations in Phelan-McDermid syndrome: results from the developmental synaptopathies consortium.

Individuals with Phelan-McDermid syndrome (PMS) present with a wide range of developmental, medical, cognitive and behavioral abnormalities. Previous literature has begun to elucidate genotype-phenotype associations that may contribute to the wide spectrum of features. Here, we report results of genotype-phenotype associations in a cohort of 170 individuals with PMS. Genotypes were defined as Class I deletions (including SHANK3 only or SHANK3 with ARSA and/or ACR and RABL2B), Class II deletions (all other deletions) or sequence variants. Phenotype data were derived prospectively from direct evaluation, caregiver interview and questionnaires, and medical history. Analyses revealed individuals with Class I deletions or sequence variants had fewer delayed developmental milestones and higher cognitive ability compared to those with Class II deletions but had more skill regressions. Individuals with Class II deletions were more likely to have a variety of medical features, including renal abnormalities, spine abnormalities, and ataxic gait. Those with Class I deletions or sequence variants were more likely to have psychiatric diagnoses including bipolar disorder, depression, and schizophrenia. Autism spectrum disorder diagnoses did not differ between groups. This study represents the largest and most rigorous genotype-phenotype analysis in PMS to date and provides important information for considering clinical functioning, trajectories and comorbidities as a function of specific genetic alteration.

Investigating Motor Preparation in Autism Spectrum Disorder With and Without Attention Deficit/Hyperactivity Disorder.

This study investigated motor preparation and action-consequence prediction using the lateralized readiness potential (LRP). Motor impairments are common in autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), which commonly co-occur. Alterations in predictive processes may impact motor planning. Whether motor planning deficits are characteristic of ASD broadly or magnified in the context of co-morbid ADHD is unclear. ASD children with (ASD + ADHD; n = 12) and without (ASD - ADHD; n = 9) comorbid ADHD and typical controls (n = 29) performed voluntary motor actions that either did or did not result in auditory consequences. ASD - ADHD children demonstrated LRP enhancement when their action produced an effect while ASD + ADHD children had attenuated responses regardless of action-effect pairings. Findings suggest influence of ADHD comorbidity on motor preparation and prediction in ASD.

Social visual attentional engagement and memory in Phelan-McDermid syndrome and autism spectrum disorder: a pilot eye tracking study.

BACKGROUND: The current study used eye tracking to investigate attention and recognition memory in Phelan-McDermid syndrome (PMS), a rare genetic disorder characterized by intellectual disability, motor delays, and a high likelihood of comorbid autism spectrum disorder (ASD). Social deficits represent a core feature of ASD, including decreased propensity to orient to or show preference for social stimuli. METHODS: We used a visual paired-comparison task with both social and non-social images, assessing looking behavior to a novel image versus a previously viewed familiar image to characterize social attention and recognition memory in PMS (n = 22), idiopathic ASD (iASD, n = 38), and typically developing (TD) controls (n = 26). The idiopathic ASD cohort was divided into subgroups with intellectual disabilities (ID; developmental quotient < 70) and without (developmental quotient > 70) and the PMS group into those with and without a co-morbid ASD diagnosis. RESULTS: On measures of attention, the PMS group with a comorbid ASD diagnosis spent less time viewing the social images compared to non-social images; the rate of looking back and forth between images was lowest in the iASD with ID group. Furthermore, while all groups demonstrated intact recognition memory when novel non-social stimuli were initially presented (pre-switch), participants with PMS showed no preference during the post-switch memory presentation. In iASD, the group without ID, but not the group with ID, showed a novelty preference for social stimuli. Across indices, individuals with PMS and ASD performed more similarly to PMS without ASD and less similarly to the iASD group. CONCLUSION: These findings demonstrate further evidence of differences in attention and memory for social stimuli in ASD and provide contrasts between iASD and PMS.

Individuals with FOXP1 syndrome present with a complex neurobehavioral profile with high rates of ADHD, anxiety, repetitive behaviors, and sensory symptoms.

BACKGROUND: FOXP1 syndrome is an autosomal dominant neurodevelopmental disorder characterized by intellectual disability, developmental delay, speech and language delays, and externalizing behaviors. We previously evaluated nine children and adolescents with FOXP1 syndrome to better characterize its phenotype. We identified specific areas of interest to be further explored, namely autism spectrum disorder (ASD) and internalizing and externalizing behaviors. METHODS: Here, we assess a prospective cohort of additional 17 individuals to expand our initial analyses and focus on these areas of interest. An interdisciplinary group of clinicians evaluated neurodevelopmental, behavioral, and medical features in participants. We report results from this cohort both alone, and in combination with the previous cohort, where possible. RESULTS: Previous observations of intellectual disability, motor delays, and language deficits were confirmed. In addition, 24% of the cohort met criteria for ASD. Seventy-five percent of individuals met DSM-5 criteria for attention-deficit/hyperactivity disorder and 38% for an anxiety disorder. Repetitive behaviors were almost universally present (95%) even without a diagnosis of ASD. Sensory symptoms, in particular sensory seeking, were common. LIMITATIONS: As FOXP1 syndrome is a rare disorder, sample size is limited. CONCLUSIONS: These findings have important implications for the treatment and care of individuals with FOXP1 syndrome. Notably, standardized testing for ASD showed high sensitivity, but low specificity, when compared to expert consensus diagnosis. Furthermore, many individuals in our cohort who received diagnoses of attention-deficit/hyperactivity disorder or anxiety disorder were not being treated for these symptoms; therefore, our findings suggest that there may be immediate areas for improvements in treatment for some individuals.

Hippocampal contributions to social and cognitive deficits in autism spectrum disorder.

Autism spectrum disorder (ASD) is characterized by hallmark impairments in social functioning. Nevertheless, nonsocial cognition, including hippocampus-dependent spatial reasoning and episodic memory, is also commonly impaired in ASD. ASD symptoms typically emerge between 12 and 24 months of age, a time window associated with critical developmental events in the hippocampus. Despite this temporal overlap and evidence of hippocampal structural abnormalities in ASD individuals, relatively few human studies have focused on hippocampal function in ASD. Herein, we review the existing evidence for the involvement of the hippocampus in ASD and highlight the hippocampus as a promising area of interest for future research in ASD.

Oculomotor corollary discharge signaling is related to repetitive behavior in children with autism spectrum disorder.

Corollary discharge (CD) signals are "copies" of motor signals sent to sensory regions that allow animals to adjust sensory consequences of self-generated actions. Autism spectrum disorder (ASD) is characterized by sensory and motor deficits, which may be underpinned by altered CD signaling. We evaluated oculomotor CD using the blanking task, which measures the influence of saccades on visual perception, in 30 children with ASD and 35 typically developing (TD) children. Participants were instructed to make a saccade to a visual target. Upon saccade initiation, the presaccadic target disappeared and reappeared to the left or right of the original position. Participants indicated the direction of the jump. With intact CD, participants can make accurate perceptual judgements. Otherwise, participants may use saccade landing site as a proxy of the presaccadic target and use it to inform perception. We used multilevel modeling to examine the influence of saccade landing site on trans-saccadic perceptual judgements. We found that, compared with TD participants, children with ASD were more sensitive to target displacement and less reliant on saccade landing site when spatial uncertainty of the post-saccadic target was high. This pattern was driven by ASD participants with less severe restricted and repetitive behaviors. These results suggest a relationship between altered CD signaling and core ASD symptoms.

Face perception predicts affective theory of mind in autism spectrum disorder but not schizophrenia or typical development.

Autism spectrum disorder (ASD) and schizophrenia spectrum disorder (SCZ) have overlapping symptomatology related to difficulties with social cognition. Yet, few studies have directly compared social cognition in ASD, SCZ, and typical development (TD). The current study examined individual differences in face recognition and its relation to affective theory of mind (ToM) in each diagnostic group. Adults with ASD (n = 31), SCZ (n = 43), and TD (n = 47) between the ages of 18 and 48 years-old with full scale IQ above 80 participated in this study. The Reading the Mind in the Eyes Test (RMET) measured affective ToM, and the Benton Facial Recognition Test (BFRT) measured face perception. Adults with ASD and SCZ did not differ in their affective ToM abilities, and both groups showed affective ToM difficulties compared with TD. However, better face recognition ability uniquely predicted better affective ToM ability in ASD. Results suggest that affective ToM difficulties may relate to face processing in ASD but not SCZ. By clarifying the complex nature of individual differences in affective ToM and face recognition difficulties in these disorders, the present study suggests there may be divergent mechanisms underlying pathways to social dysfunction in ASD compared with SCZ. (PsycInfo Database Record (c) 2021 APA, all rights reserved).