Central Sensitisation After Orthopaedic Trauma: An Overlooked Contributor to Chronic Pain and Functional Disability—A Scoping Review

Background: Persistent pain following orthopaedic trauma is common, often disproportionate to structural healing, and increasingly attributed to central sensitisation (CS). However, the mechanisms, clinical features, diagnostic approaches, prognostic indicators, and management strategies relevant to trauma-related CS remain poorly understood. Objective: To map and synthesise existing evidence on CS following orthopaedic trauma, addressing mechanistic pathways, clinical manifestations, epidemiology, assessment methods, management approaches, and health system implications. Methods: A scoping review was conducted in accordance with PRISMA-ScR. Twenty-one studies met the eligibility criteria, comprising nine primary trauma cohorts and 12 contextual mechanistic or review studies relevant to trauma-associated CS. Data were charted across six prespecified domains of mechanistic processes, clinical presentation and diagnostic features, epidemiology and prognosis, assessment tools and outcome measures, interventions, and health system and care delivery considerations. Results: Mechanistic studies demonstrated trauma-induced neuroimmune activation, altered cortical and spinal excitability, and molecular pathways consistent with sensitisation. Clinical studies have identified neuropathic features, widespread pain, and heightened sensory responsiveness following fractures and other injuries. Neurophysiological evidence has indicated early cortical disinhibition following upper limb trauma, whereas epidemiological cohorts have reported persistent pain and disability years after major trauma. Measurement studies have highlighted the limited reliability and specificity of current tools in trauma populations, including quantitative sensory testing and self-report instruments. Early predictors of adverse trajectories include severe acute pain, neuropathic descriptors, psychological distress, and opioid-dominant analgesia. Evidence regarding early intervention, rehabilitation strategies, and system-level screening pathways remains limited. Conclusions: CS after orthopaedic trauma is supported by convergent mechanistic, neurophysiological, and clinical findings. However, trauma-specific diagnostic criteria, prognostic models, and management frameworks remain underdeveloped. High-quality longitudinal research is needed to clarify early trajectories, refine assessment methods, and establish targeted interventions to reduce long-term pain and disability.