Abstract Introduction Attention deficit hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder with a complex aetiology, involving dysfunctions in serotonergic, noradrenergic and dopaminergic neural pathways, alongside disturbances in the autonomic nervous system. This study evaluated pupillary light responses (PLR) in subjects with ADHD to assess the integrity of the outer retinal photoreceptor‐to‐pathway contributions. Methods This cross‐sectional study assessed 73 eyes from 43 participants, including 22 with ADHD (mean age = 12.62 ± 3.78 years) and 21 controls (mean age = 14.21 ± 4.71 years). All participants underwent a comprehensive optometric examination. Monocular PLR was measured using an eye tracker in a Ganzfeld setup with short‐wavelength (470 nm) and long‐wavelength (640 nm) flashes at intensities of −3, −2, −1 and 1 log cd/m 2 . Pupillometric parameters recorded included baseline peak pupil constriction amplitude (PCA), peak constriction velocity (PCV), peak constriction latency (PCL) and redilation latency at 50% (RL 50%). Results The ADHD group showed reduced PCA for short‐wavelength stimulus at −3 log cd/m 2 ( p < 0.001) and for long‐wavelength stimuli at −2 and −1 log cd/m 2 ( p < 0.04). PCL, PCV and RL 50% also showed significant differences for short‐wavelength stimuli at −3 log cd/m 2 (all p < 0.02). An exploratory sex‐specific analysis revealed that males with ADHD showed reduced contributions from both the rod pathway and the rod–cone transition range to long‐wavelength stimuli, while females exhibited nuanced responses with decreased rod contributions. Conclusions These findings reveal altered PLR in ADHD, providing evidence of disrupted rod‐mediated responses and deficits extending into the rod–cone transition range. The exploratory findings of marked sex‐specific differences highlight the need for further investigation and underscore the importance of considering sex as a critical factor in ADHD research. The results suggest a link between cholinergic and noradrenergic dysregulation and altered retinal signal processing.