Pupil changes as a window into autonomic dysregulation after spinal cord injury: A systematic review

Spinal cord injury (SCI) impairs supraspinal control of the spinal cord circuits leading to an array of autonomic dysfunctions. The autonomic neural circuitry of the pupil makes it a unique target for identifying impaired autonomic regulation. This study systematically reviewed the evidence on pupillary dysfunction following SCI.
Methods: MEDLINE, EMBASE, and CINAHL were searched for studies on pupillary dysfunction (e.g., miosis, mydriasis, anisocoria) in individuals with traumatic or non-traumatic SCI. Animal studies, systematic reviews, book chapters, and conference abstracts were excluded. Data on study design, demographics, injury characteristics, and pupillary outcomes were extracted. Study quality was assessed using Joanna Briggs Institute Critical Appraisal checklists.
Results: 37 studies met the inclusion criteria (36 case reports, 1 cross-sectional study) and were of moderate quality overall. Anisocoria was universally reported, with 78% presenting unilateral miosis and 19% unilateral mydriasis. Pupil abnormalities occurred predominantly after cervical (54%-77%) or high thoracic SCI (19%-31%), acutely (0–20 days post-injury) (26/37 studies) or during episodes of autonomic dysreflexia in the subacute-to-chronic phase (>4 months post-injury) (6/37 studies).
Conclusions: Pupil abnormalities were reported across all phases of SCI, indicating damage to the autonomic pathways or autonomic dysregulation. In the acute phase, pupil abnormalities were primarily triggered by trauma as a direct result of SCI or other related injuries, such as traumatic brain injury. In the subacute-to-chronic phase, a common cause of these abnormalities was autonomic dysreflexia. Advanced quantitative pupil detection technologies are needed to validate the utility of pupillary data in SCI research and clinical care.