Post-traumatic benign paroxysmal positional vertigo: mechanisms, clinical phenotypes, and a structured clinical pathway for management

Post-traumatic benign paroxysmal positional vertigo (BPPV) is a common but frequently underrecognized cause of dizziness following trauma. Unlike idiopathic BPPV, trauma-related BPPV arises from diverse injury mechanisms and is often characterized by heterogeneous canal involvement, greater need for repeated treatment, and frequent coexistence with broader vestibular dysfunction. These features contribute to diagnostic delays and variable clinical outcomes, particularly in the trauma and emergency care settings. We conducted a structured literature search and synthesized clinical, epidemiological, mechanistic, and implementation-focused evidence across diverse trauma contexts. This review aimed to synthesize current evidence on the mechanisms, epidemiology, and clinical characteristics of post-traumatic BPPV, contrast it with idiopathic BPPV, and propose a pragmatic clinical pathway to improve early recognition and management. We reviewed the clinical, epidemiological, mechanistic, and implementation-focused literature on post-traumatic BPPV across trauma contexts, including head injury, concussion, whiplash, sports-related injury, and traumatic brain injury. Evidence from cohort studies, comparative analyses, meta-analyses, and qualitative and feasibility studies was integrated to inform a clinically oriented framework. Accumulating evidence suggests that post-traumatic BPPV should not be regarded solely as a mechanical disorder of displaced otoconia. Trauma may disrupt the otolithic membrane, promote otoconial detachment, and induce utricular dysfunction, leading to canalithiasis or cupulolithiasis and potential interaction with central vestibular injury. Compared with idiopathic BPPV, post-traumatic cases more frequently involve horizontal or multiple canals, often require repeated canalith repositioning maneuvers, and demonstrate variable recurrence patterns. System-level barriers, including limited screening, insufficient training, and fragmented care pathways, further contribute to underdiagnosis and suboptimal management. Post-traumatic BPPV represents a distinct clinical phenotype within the spectrum of trauma-related vestibular disorders. Early identification through systematic screening, comprehensive positional testing, and timely canal-specific interventions provides practical opportunities to improve outcomes. We propose a structured clinical pathway emphasizing early recognition, planned reassessment, and escalation to integrated vestibular care when symptoms persist. Future research should clarify the relationships between trauma biomechanics and BPPV phenotypes, identify predictors of recurrence, and evaluate the real-world effectiveness of pathway-based care models across diverse trauma populations.