Abstract
With recent advances in technology, there has been growing interest in use of eye-tracking and pupillometry to assess the visual pathway in autism spectrum disorder (ASD). Within emerging literature, an atypical pupillary light reflex (PLR) has been documented, holding potential for use as a clinical screening biomarker for ASD. This review outlines dominant theories of neuropathology associated with ASD and integrates underlying neuroscience associated with the atypical PLR through a reciprocal model of brainstem involvement and cortical underconnectivity. This review draws from animal models of ASD demonstrating disruption of cranial motor nuclei and brain imaging studies examining arousal and the influence of the locus coeruleus norepinephrine (LC-NE) system on the pupillary response. Pupillometry methods are explained in relation to existing data examining the PLR in ASD and pupillary parameters of constriction latency and tonic pupil diameter as key parameters for investigation. This focused review provides preliminary data toward future work developing pupillometry metrics and offers direction for studies aimed at rigorous study replication using pupillometry with the ASD population. Experimental conditions and testing protocol for capturing pupil parameters with this clinical population are discussed to promote clinical research and translational application.
Highlights
Since autism spectrum disorder (ASD) was first described by Leo Kanner, maladaptive behaviors impacting socialization and language continue to be the diagnostic indicators of this disorder across the lifespan [1]
As further biometric studies examine the atypical pupillary light reflex (PLR) in ASD, the current body of literature is generally limited by inconsistencies in research design for capturing specific pupillary parameters
Attention should be paid for consistency in use of eye-tracking equipment, pupillometry procedures, and behavioral protocols for study replication
Summary
Since autism spectrum disorder (ASD) was first described by Leo Kanner, maladaptive behaviors impacting socialization and language continue to be the diagnostic indicators of this disorder across the lifespan [1]. This model is paradigm-shifting, taking a concept of ASD as primarily based in behavioral disinhibition associated with neural activity in prefrontal cortex (PFC), to a reciprocal model of atypical PLR and physical symptoms associated with anxiety which are influenced by bottom-up processes and neuromodulation of cranial motor nuclei. Deficient modulation of cranial nerves (CN II and CN III) affects the neural pathway of the visual system which must function efficiently for developing physical behaviors of joint attention and use of eye gaze for identifying dynamic changes in facial expression and nonverbal exchanges between communication partners These eye gaze patterns have been shown to be deficient in ASD, impacting social interaction with caregivers [50,51,52]. Using direct light stimulus presentation, the PRT sensitively detects parasympathetic response in a reflexive manner, whereas eye-gaze measurements using traditional eye-tracking methods are influenced by confounds impacting pupillary response reflective of cognitive processes and visual attention
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