BackgroundRapid automatized naming (RAN; naming of familiar items presented in an array) is a task that taps fundamental neurocognitive processes that are affected in a number of complex psychiatric conditions. Deficits in RAN have been repeatedly observed in autism spectrum disorder (ASD), and also among first-degree relatives, suggesting that RAN may tap features that index genetic liability to ASD. This study used eye tracking to examine neurocognitive mechanisms related to RAN performance in ASD and first-degree relatives, and investigated links to broader language and clinical-behavioral features.MethodsFifty-one individuals with ASD, biological parents of individuals with ASD (n = 133), and respective control groups (n = 45 ASD controls; 58 parent controls) completed RAN on an eye tracker. Variables included naming time, frequency of errors, and measures of eye movement during RAN (eye-voice span, number of fixations and refixations).ResultsBoth the ASD and parent-ASD groups showed slower naming times, more errors, and atypical eye-movement patterns (e.g., increased fixations and refixations), relative to controls, with differences persisting after accounting for spousal resemblance. RAN ability and associated eye movement patterns were correlated with increased social-communicative impairment and increased repetitive behaviors in ASD. Longer RAN times and greater refixations in the parent-ASD group were driven by the subgroup who showed clinical-behavioral features of the broad autism phenotype (BAP). Finally, parent-child dyad correlations revealed associations between naming time and refixations in parents with the BAP and increased repetitive behaviors in their child with ASD.ConclusionsDifferences in RAN performance and associated eye movement patterns detected in ASD and in parents, and links to broader social-communicative abilities, clinical features, and parent-child associations, suggest that RAN-related abilities might constitute genetically meaningful neurocognitive markers that can help bridge connections between underlying biology and ASD symptomatology.

Currently, the developmental trajectories of neural circuits implicated in autism spectrum disorders (ASD) are largely unknown. Here, we specifically focused on age-related changes in the functional circuitry of the posterior superior temporal sulcus (pSTS), a key hub underlying social-cognitive processes known to be impaired in ASD. Using a cross-sectional approach, we analysed resting-state functional magnetic resonance imaging (fMRI) data collected from children, adolescents and adults available through the autism brain imaging data exchange repository [n = 106 with ASD and n = 109 typical controls (TC), ages 7-30 years]. The observed age-related changes of pSTS intrinsic functional connectivity (iFC) suggest that no single developmental pattern characterizes ASD. Instead, pSTS circuitry displayed a complex developmental picture, with some functional circuits showing patterns consistent with atypical development in ASD relative to TC (pSTS-iFC with fusiform gyrus and angular gyrus) and others showing delayed maturation (pSTS-iFC with regions of the action perception network). Distinct developmental trajectories in different functional circuits in ASD likely reflect differential age-related changes in the socio-cognitive processes they underlie. Increasing insight on these mechanisms is a critical step in the development of age-specific interventions in ASD.

This study examined prosody through characterization of acoustic properties of the speech of individuals with ASD and their parents, during narration. A subset of utterances were low-pass filtered and rated for differences in intonation, speech rate, and rhythm. Listener ratings were minimally related to acoustic measures, underscoring the complexity of atypical prosody in ASD. Acoustic analyses revealed greater utterance-final fundamental frequency excursion size and slower speech rate in the ASD group. Slower speech rate was also evident in the ASD parent group, particularly parents with the broad autism phenotype. Overlapping prosodic differences in ASD and ASD Parent groups suggest that prosodic differences may constitute an important phenotype contributing to ASD features and index genetic liability to ASD among first-degree relatives.

Global visual processing is important for segmenting scenes, extracting form from background, and recognizing objects. Local processing involves attention to the local elements, contrast, and boundaries of an image at the expense of extracting a global percept. Previous work is inconclusive regarding the relative development of local and global processing. Some studies suggest that global perception is already present by 8 months of age, whereas others suggest that the ability arises in childhood and continues to develop in adolescence. We used a novel method to assess the development of global processing in 3-to 10-year-old children and an adult comparison group. We used Kanizsa illusory contours as an assay of global perception and measured responses on a touch screen while monitoring eye position with a head-mounted eye tracker. Participants were tested using a similarity match-to-sample paradigm. Using converging measures, we found a clear developmental progression with age such that the youngest children performed near chance on the illusory contour discrimination whereas 7-to 8-year-olds performed nearly perfectly, as did adults. There was clear evidence of a gradual shift from a local to a global processing strategy: Young children looked predominantly at and touched the pacman inducers of the illusory form, whereas older children and adults looked predominantly at and touched the middle of the form. These data show a prolonged developmental trajectory in appreciation of global form, with a transition from local to global visual processing between 4 and 7 years of age. KeywordsKanizsa illusory contours; perceptual development; global processing; eye tracking; global form perception Visual information about objects is often incomplete. Parts of objects can be occluded, missing, or blend seamlessly into the background, yet adults perceive the objects as complete global forms rather than a collection of disconnected local elements. In the laboratory, adults perceive holistic contours of shapes based on illusory edges that have no Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript physical luminance, color, or texture boundary. How does this global perceptual ability come about? Although some researchers have found evidence for perception of illusory figures in young infants (e.g., Bertenthal, Campos & Haith, 1980;Kavsek, 2002;Otsuka & Yamaguchi, 2003;Bulf et al., 2011), others have reported that global form perception and discrimination of illusory shapes do not reach maturity until late childhood (Abravanel, 1982;Kimchi et al., 2005;Sherf et al., 2009;Hadad, Maurer & Lewis, 2010). Here, we used a novel approach-accuracy on a match-to-sample task paired with several measures of spontaneous manual and visual behaviors-to investigate the development of illusory contour perception as an assay of global form perception in children from 3 to 10 years of age. Our objective methods and converging behavioral evidence show a clear, protracted developmental program for global visual process...

This study examined narrative ability in ASD and parents across two contexts differing in structure and emotional content, and explored gaze patterns that may underlie narrative differences by presenting narrative tasks on an eye tracker. Participants included 37 individuals with ASD and 38 controls, 151 parents of individuals with ASD and 63 parent controls. The ASD and ASD parent groups demonstrated lower narrative quality than controls in the less structured narrative task only. Subtler, context-dependent differences emerged in gaze and showed some associations with narrative quality. Results indicate a narrative ability profile that may reflect genetic liability to ASD, and subtle links between visual attention and complex language skills that may be influenced by ASD genetic risk.