The pupil dilates and reconstricts following task events. It is popular to model this task-evoked pupil response as a linear transformation of event-locked impulses, whose amplitudes are used as estimates of arousal. We show that this model is incorrect and propose an alternative model based on the physiological finding that a common neural input drives saccades and pupil size. The estimates of arousal from our model agreed with key predictions: Arousal scaled with task difficulty and behavioral performance but was invariant to small differences in trial duration. Moreover, the model offers a unified explanation for a wide range of phenomena: entrainment of pupil size and saccades to task timing, modulation of pupil response amplitude and noise with task difficulty, reaction time–dependent modulation of pupil response timing and amplitude, a constrictory pupil response time-locked to saccades, and task-dependent distortion of this saccade-locked pupil response.

Autism spectrum disorder (ASD) is characterized partly by atypical attentional engagement, reflected in exaggerated and variable responses to sensory stimuli. Attentional engagement is known to be regulated by the locus ceruleus (LC). Moderate baseline LC activity globally dampens neural responsivity and is associated with adaptive deployment and narrowing of attention to task-relevant stimuli. In contrast, increased baseline LC activity enhances neural responsivity across cortex and widening of attention to environmental stimuli regardless of their task relevance. Given attentional atypicalities in ASD, this study is the first to evaluate whether, under different attentional task demands, individuals with ASD exhibit a different profile of LC activity compared with typically developing controls. Males and females with ASD and age-and gender-matched controls participated in a one-back letter detection test while task-evoked pupillary responses, an established correlate for LC activity, were recorded. Participants completed this task in two conditions, either in the absence or presence of distractor auditory tones. Compared with controls, individuals with ASD evinced atypical pupillary responses in the presence versus absence of distractors. Notably, this atypical pupillary profile was evident despite the fact that both groups exhibited equivalent task performance. Moreover, between-group differences in pupillary responses were observed specifically in response to task-relevant events, providing confirmation that the group differences most likely were specifically associated with distinctions in LC activity. These findings suggest that individuals with ASD show atypical modulation of LC activity with changes in attentional demands, offering a possible mechanistic and neurobiological account for attentional atypicalities in ASD.

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The pupil dilates and re-constricts following task events. It is popular to model this task-evoked pupil response as a linear transformation of event-locked impulses, the amplitudes of which are used as estimates of arousal. We show that this model is incorrect, and we propose an alternative model based on the physiological finding that a common neural input drives saccades and pupil size. The estimates of arousal from our model agreed with key predictions: arousal scaled with task difficulty and behavioral performance but was invariant to trial duration. Moreover, the model offers a unified explanation for a wide range of phenomena: entrainment of pupil size and saccade occurrence to task timing, modulation of pupil response amplitude and noise with task difficulty, reaction-time dependent modulation of pupil response timing and amplitude, a constrictory pupil response time-locked to saccades, and task-dependent distortion of this saccade-locked pupil response.