Proprioception Deficits and Neurophysiological Mechanisms in Adolescent Idiopathic Scoliosis: A Systematic Review

Background: Adolescent idiopathic scoliosis (AIS) is a three-dimensional spinal structural change affecting 0.5%–5.2% of adolescents worldwide. Proprioceptive dysfunction is implicated in the pathogenesis or maintenance of AIS, although the underlying neurophysiological mechanisms are not well understood. A clear synthesis of these mechanisms is warranted to guide future research and targeted interventions.
Objective: To systematically synthesize evidence on central and peripheral neurophysiological abnormalities associated with proprioceptive deficits in individuals with AIS.
Study Design: A systematic review
Methods: The protocol was registered with PROSPERO. Eight databases were searched from inception to April 21, 2025. Articles were eligible for inclusion if they investigated neurophysiological mechanisms of proprioception in patients with AIS using objective assessments. Two independent reviewers screened all identified abstracts and full-text articles for eligibility. They also independently extracted data and assessed study quality using the Crowe Critical Appraisal Tool (CCAT) and risk of bias using the Risk Of Bias In Non - Randomized Studies - of Exposures (ROBINS-E) tool. Findings were synthesized narratively according to a structural and functional framework. This review followed PRISMA reporting guidelines.
Results: Of 606 records identified, 36 underwent full-text screening. Fifteen studies met the inclusion criteria. Individuals with AIS demonstrated multidimensional neurophysiological abnormalities. Structural brain magnetic resonance imaging (MRI) revealed reduced cerebellar volume, impaired white matter integrity in the corpus callosum and corticospinal tract, and brainstem asymmetry. Functional assessments showed abnormal cortical inhibition, compensatory overactivation in the supplementary motor area (SMA) on functional MRI, and dysfunctional neural oscillation patterns on electroencephalography. Evidence also pointed to asymmetry in peripheral somatosensory pathways, disrupting sensorimotor integration. Methodological heterogeneity, and the cross-sectional nature of most studies precluded the establishment of casualty between neurophysiological changes and AIS progression.
Conclusion: This systematic review finds that proprioceptive dysfunction in AIS is associated with complex, bidirectional abnormalities across both the central and peripheral nervous systems, These findings suggest a disrupted sensorimotor feedback loop that may contribute to postural instability and curve progression. Future longitudinal studies should adopt standardized multimodal assessments to evaluate the temporal association between neurophysiological changes, proprioception deficits, and curve progression in these patients. Future clinical trials should investigate the effects of proprioception training on neuroplastic changes and proprioception of these patients.
Clinical implications: Monitoring neurophysiological changes in patients with AIS could help identify patients who may benefit most from proprioception-focused therapies, highlighting a critical direction for future clinical trials and personalized care in AIS.