Atypical eye contact in autism: Models, mechanisms and development

An atypical pattern of eye contact behaviour is one of the most significant symptoms of Autism Spectrum Disorder (ASD). Recent empirical advances have revealed the developmental, cognitive and neural basis of atypical eye contact behaviour in ASD. We review different models and advance a new ‘fast-track modulator model’. Specifically, we propose that atypical eye contact processing in ASD originates in the lack of influence from a subcortical face and eye contact detection route, which is hypothesized to modulate eye contact processing and guide its emergent specialization during development

The eye contact effect: mechanisms and development

The ‘eye contact effect’ is the phenomenon that perceived eye contact with another human face modulates certain aspects of the concurrent and/or immediately following cognitive processing. In addition, functional imaging studies in adults have revealed that eye contact can modulate activity in structures in the social brain network, and developmental studies show evidence for preferential orienting towards, and processing of, faces with direct gaze from early in life. We review different theories of the eye contact effect and advance a ‘fast-track modulator’ model. Specifically, we hypothesize that perceived eye contact is initially detected by a subcortical route, which then modulates the activation of the social brain as it processes the accompanying detailed sensory information

It's all in the eyes: subcortical and cortical activation during grotesqueness perception in autism

Atypical face processing plays a key role in social interaction difficulties encountered by individuals with autism. In the current fMRI study, the Thatcher illusion was used to investigate several aspects of face processing in 20 young adults with high-functioning autism spectrum disorder (ASD) and 20 matched neurotypical controls. “Thatcherized” stimuli were modified at either the eyes or the mouth and participants discriminated between pairs of faces while cued to attend to either of these features in upright and inverted orientation. Behavioral data confirmed sensitivity to the illusion and intact configural processing in ASD. Directing attention towards the eyes vs. the mouth in upright faces in ASD led to (1) improved discrimination accuracy; (2) increased activation in areas involved in social and emotional processing; (3) increased activation in subcortical face-processing areas. Our findings show that when explicitly cued to attend to the eyes, activation of cortical areas involved in face processing, including its social and emotional aspects, can be enhanced in autism. This suggests that impairments in face processing in autism may be caused by a deficit in social attention, and that giving specific cues to attend to the eye-region when performing behavioral therapies aimed at improving social skills may result in a better outcome

Sensory over-responsivity and social cognition in ASD: Effects of aversive sensory stimuli and attentional modulation on neural responses to social cues.

Sensory over-responsivity (SOR) is a common condition in autism spectrum disorders (ASD) that is associated with greater social impairment. However, the mechanisms through which sensory stimuli may affect social functioning are not well understood. This study used fMRI to examine brain activity while interpreting communicative intent in 15 high-functioning youth with ASD and 16 age- and IQ-matched typically-developing (TD) controls. Participants completed the task with and without a tactile sensory distracter, and with and without instructions directing their attention to relevant social cues. When completing the task in the presence of the sensory distracter, TD youth showed increased activity in auditory language and frontal regions whereas ASD youth showed decreased activation in these areas. Instructions mitigated this effect such that ASD youth did not decrease activation during tactile stimulation; instead, the ASD group showed increased medial prefrontal activity. SOR severity modulated the effect of the tactile stimulus on social processing. Results demonstrate for the first time a neural mechanism through which sensory stimuli cause disruption of social cognition, and that attentional modulation can restore neural processing of social cues through prefrontal regulation. Findings have implications for novel, integrative interventions that incorporate attentional directives to target both sensory and social symptoms

Autism spectrum traits in normal individuals : a preliminary VBM analysis

In light of the new DSM-5 autism spectrum disorders diagnosis in which the autism spectrum reflects a group of neurodevelopmental disorders existing on a continuum from mild to severe expression of autistic traits, and recent empirical findings showing a continuous distribution of autistic traits in the general population, our voxel based morphometry study compares normal individuals with high autistic traits to normal individuals with low autistic traits. We hypothesize that normal individuals with high autistic traits in terms of empathizing and systemizing [high systemizing (HS)/low empathizing (LE)] share brain irregularities with individuals that fall within the clinical autism spectrum disorder. We find differences in several social brain network areas between our groups. Specifically, we find increased gray matter (GM) volume in the orbitofrontal cortex, the cuneus, the hippocampus and parahippocampus and reduced GM volume in the inferior temporal cortex, the insula, and the amygdala in our HS/LE individuals relative to our HE/LS (low autistic traits in terms of empathizing and systemizing) individuals

Neural Basis of Self and Other Representation in Autism: An fMRI Study of Self-Face Recognition

Autism is a developmental disorder characterized by decreased interest and engagement in social interactions and by enhanced self-focus. While previous theoretical approaches to understanding autism have emphasized social impairments and altered interpersonal interactions, there is a recent shift towards understanding the nature of the representation of the self in individuals with autism spectrum disorders (ASD). Still, the neural mechanisms subserving self-representations in ASD are relatively unexplored.We used event-related fMRI to investigate brain responsiveness to images of the subjects' own face and to faces of others. Children with ASD and typically developing (TD) children viewed randomly presented digital morphs between their own face and a gender-matched other face, and made "self/other" judgments. Both groups of children activated a right premotor/prefrontal system when identifying images containing a greater percentage of the self face. However, while TD children showed activation of this system during both self- and other-processing, children with ASD only recruited this system while viewing images containing mostly their own face.This functional dissociation between the representation of self versus others points to a potential neural substrate for the characteristic self-focus and decreased social understanding exhibited by these individuals, and suggests that individuals with ASD lack the shared neural representations for self and others that TD children and adults possess and may use to understand others

Face blindness

Facial recognition is a complex task, often done immediately and readily, involving discrimination of subtle differences in facial structures with differences in facial expressions, ageing, perspectives and lighting. Facial recognition requires fast identification of stimuli which are then correlated against reservoirs of faces which are accumulated throughout life (Barton and Corrow, 2016). The facial recognition system is extremely complex, and if impaired, cannot be fully remedied by other areas of the brain. When such injury occurs early on in life, juvenile brain plasticity has been shown to be potentially inadequate to restore facial recognition functions, thereby suggesting that such an impairment can have severe, permanent implications, even at an early age (Barton et al., 2003) Damage to any part of the facial recognition mechanism may result in the development of face blindness. Such dysfunction results in the development of selective face-recognition and visual learning deficits, a condition called prosopagnosia. Prosopagnosia can be either acquired or congenital. The acquired form of prosopagnosia is considered to be a rare consequence of occipital or temporal lobe damage, possibly due to stroke or lesions occurring in adulthood. Congenital prosopagnosia, on the other hand, is usually not found associated with any gross abnormalities, and no clear underlying causative agent is found to be associated with the development of the disease (Grüter et al., 2008). Nevertheless, face blindness in children may also be associated with inherited or acquired brain lesions, and may not be exclusively of a congenital/hereditary aetiology. Moreover, prosopagnosia can also occur in association with other disorders, which may be psychiatric, developmental or associated with multiple types of visual impairment (Watson et al., 2016).peer-reviewe

Brain Activity in College Students with the Broad Autism Phenotype

Abstract This study examined brain activity in college students with the broad autism phenotype (BAP) while viewing facial expressions. Quantitative Electroencephalogram assessments were conducted in the temporal lobe area in the brains of 38 college students declared as Science, Technology, Engineering, and Math (STEM) majors. Participants were divided into BAP+ versus BAP- groups based on their scores on the Broad Autism Phenotype Questionnaire (BAPQ). Findings revealed that individuals categorized as BAP+ demonstrated a higher alpha relative power score and a higher T4 relative to T3 coherence Z score when looking at expressive faces than when looking at neutral faces when compared to the BAP- individuals. Also, participants classified as BAP+ had significantly lower social adjustment than those classified as BAP-. Findings discuss the possibility of using QEEG BAP+ brain markers as an objective measure of social impairments in at-risk college students. Keywords: Broad Autism Phenotype (BAP), Autism Spectrum Disorder (ASD), Electroencephalography (EEG), alpha activity, face processin

Atypical disengagement from faces and its modulation by the control of eye fixation in children with Autism Spectrum Disorder

By using the gap overlap task, we investigated disengagement from faces and objects in children (9–17 years old) with and without autism spectrum disorder (ASD) and its neurophysiological correlates. In typically developing (TD) children, faces elicited larger gap effect, an index of attentional engagement, and larger saccade-related event-related potentials (ERPs), compared to objects. In children with ASD, by contrast, neither gap effect nor ERPs differ between faces and objects. Follow-up experiments demonstrated that instructed fixation on the eyes induces larger gap effect for faces in children with ASD, whereas instructed fixation on the mouth can disrupt larger gap effect in TD children. These results suggest a critical role of eye fixation on attentional engagement to faces in both groups

Conceptual and methodological challenges for neuroimaging studies of autistic spectrum disorders

Autistic Spectrum Disorders (ASDs) are a set of complex developmental disabilities defined by impairment in social interaction and communication, as well as by restricted interests or repetitive behaviors. Neuroimaging studies have substantially advanced our understanding of the neural mechanisms that underlie the core symptoms of ASDs. Nevertheless, a number of challenges still remain in the application of neuroimaging techniques to the study of ASDs. We review three major conceptual and methodological challenges that complicate the interpretation of findings from neuroimaging studies in ASDs, and that future imaging studies should address through improved designs. These include: (1) identification and implementation of tasks that more specifically target the neural processes of interest, while avoiding the confusion that the symptoms of ASD may impose on both the performance of the task and the detection of brain activations; (2) the inconsistency that disease heterogeneity in persons with ASD can generate on research findings, particularly heterogeneity of symptoms, symptom severity, differences in IQ, total brain volume, and psychiatric comorbidity; and (3) the problems with interpretation of findings from cross-sectional studies of persons with ASD across differing age groups. Failure to address these challenges will continue to hinder our ability to distinguish findings that outline the causes of ASDs from brain processes that represent downstream or compensatory responses to the presence of the disease. Here we propose strategies to address these issues: 1) the use of simple and elementary tasks, that are easier to understand for autistic subjects; 2) the scanning of a more homogenous group of persons with ASDs, preferably at younger age; 3) the performance of longitudinal studies, that may provide more straight forward and reliable results. We believe that this would allow for a better understanding of both the central pathogenic processes and the compensatory responses in the brain of persons suffering from ASDs