Graduation Year


Date of Submission


Document Type

Campus Only Senior Thesis

Degree Name

Bachelor of Arts



Reader 1

Cathy Reed

Reader 2

Tessa Soloman-Lane

Reader 3

Alan Hartley


Pupillary contagion (PC) is a phenomenon in which pupillary responses in one member of a dyad mimic pupillary changes in the other. It is an autonomic, non-voluntary, innate response that has been observed in social conditions and with circular schematics. The literature lends support to two different hypotheses for why PC occurs: 1) the visual-attention model proposes that PC is driven by early perception-attention processing; 2) the social-cognitive model proposes that PC is driven by later cognitive processing where we recognize another person’s internal state based on our own response. This study investigates what neural processes are associated with PC. Participants viewed human faces (social; eye slits) and scrambled faces (non-social; pixelated faces) with systematically altered pupil sizes (small, medium, large) while pupillometry and EEG data were measured. Pupillometry data showed pupil size differentiation for scrambled faces within 500 ms after stimulus onset and for both faces and scrambled faces after 500 ms. EEG/ERP data showed a clear N170 component for faces but not scrambled faces, indicating selective face processing but it was not related to PC. Differentiated pupil sizes for scrambled faces were observed early, between 100-200 ms. Differentiated pupil sizes for faces were observed later between 200-400 ms. Differential cortical processing was complete by 500 ms when larger PC effects emerged, supporting the visual attention model. Despite pupil effects in each, ERP and PC measures did not correlate. Data suggest that cortical contributions to PC are indirect and subcortical areas may more strongly drive the PC response.

This thesis is restricted to the Claremont Colleges current faculty, students, and staff.