Abstract
Objective: Post–stroke shoulder pain (PSSP) is a common complication of stroke, with complex mechanisms involving structural and neurological factors. This study aimed to investigate the role of pain sensitization—specifically peripheral sensitization and dysfunction of the endogenous pain inhibitory system— in patients with PSSP. Methods: Post–stroke patients with and without PSSP were recruited. Pain sensitization was assessed using quantitative sensory testing, including pressure pain threshold (PPT) at the shoulder joint and conditioned pain modulation (CPM). Logistic regression analysis was used to analyze factors associated with PSSP, adjusting for age and sex. Receiver operating characteristic analysis was performed to determine cut–off values for PPT and CPM. The prevalence rate of PSSP was then calculated among patients with lower PPT, diminished CPM, or both. Results: Lower PPT and diminished CPM were independently associated with PSSP. Subgroup analysis revealed that the prevalence of PSSP was 60% among patients with either lower PPT or diminished CPM alone, and 100% among those with both. Conclusion: This study demonstrates that both peripheral and central sensitization are associated with PSSP. These findings suggest that altered pain processing, alongside structural impairments, contributes to its pathophysiology. Incorporating pain sensitization assessment into clinical practice may offer novel insights for the prevention and management of PSSP.
Pain sensitization as a key mechanism in post-stroke shoulder pain: a cross-sectional observational study
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Conclusion: This study demonstrates that both peripheral and central sensitization are closely associated with PSSP. The highest prevalence of PSSP in patients with lower PPT and reduced CPM underscores the clinical relevance of altered pain processing mechanisms.
