Background: Spinal cord injury (SCI), typically resulting from trauma or cranial surgery, often causes motor and sensory deficits and may also impair brain function, leading to cerebral edema, elevated intracranial pressure, and cognitive decline. Growing evidence implicates systemic inflammation as a key mediator of SCI-related cognitive impairment, yet clinical validation remains limited. This study explores the association between SCI and cognitive dysfunction, with a focus on the mediating role of inflammation.
Methods: A retrospective cohort of 157 participants (SCI patients and controls) at the Affiliated Hospital of Qingdao University (January 2023-October 2024) was analyzed. Neurological impairment (ASIA) and acute-phase inflammatory markers (NLR, PLR, LMR, and SII) were assessed. MoCA evaluated cognitive function at 3 months. Logistic regression and mediation analysis quantified associations.
Results: SCI patients had a 151% higher risk of cognitive impairment than controls (adjusted OR=2.51, 95% CI: 1.82-3.64), especially among older adults, those with lower education, and hypertensive individuals. NLR and SII mediated 12% and 16% of the association, respectively; PLR showed a weaker effect (6%). LMR mediated 11% (P=0.02) but had a protective direct effect (β=0.79), indicating possible compensatory mechanisms. Smoking and alcohol use further increased risk, while higher education was protective (OR=0.38).
Conclusion: Systemic inflammation partially mediates SCI-related cognitive decline, with NLR and SII as key contributors. Blood-based inflammatory markers may aid in risk stratification and guide anti-inflammatory, lifestyle-based interventions to improve cognitive outcomes in SCI patients.
Keywords: Cognitive impairment; inflammation; mediation; spinal cord injury.
Copyright © 2025 by Mutaz B. Habal, MD.