Abstract

Adolescent idiopathic scoliosis is a multifactorial disorder including neurological factors. A dysfunction of the sensorimotor networks processing vestibular information could be related to spine deformation. This study investigates whether feed-forward vestibulomotor control or sensory reweighting mechanisms are impaired in adolescent scoliosis patients. Vestibular evoked postural responses were obtained using galvanic vestibular stimulation while participants stood with their eyes closed and head facing forward. Lateral forces under each foot and lateral displacement of the upper body of adolescents with mild (n = 20) or severe (n = 16) spine deformation were compared to those of healthy control adolescents (n = 16). Adolescent idiopathic scoliosis patients demonstrated greater lateral displacement and net lateral forces than controls both during and immediately after vestibular stimulation. Altered sensory reweighting of vestibular and proprioceptive information changed balance control of AIS patients during and after vestibular stimulation. Therefore, scoliosis onset could be related to abnormal sensory reweighting, leading to altered sensorimotor processes.

Highlights

  • Spine deformations, such as adolescent idiopathic scoliosis (AIS), represent 90% of all scoliosis

  • It should be mentioned that vestibular stimulation induced a lateral trunk flexion of less than 4.6%, 15.1% and 41.4% of the maximal trunk angular displacement for the control group (CTR), AIS-M and AIS-S groups, respectively

  • These results confirmed that the amplitude of lateral trunk flexion induced by galvanic vestibular stimulation (GVS) was unconstrained by either scoliosis or the magnitude of spine deformation

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Summary

Introduction

Spine deformations, such as adolescent idiopathic scoliosis (AIS), represent 90% of all scoliosis. AIS affects 1% to 3% of children in the at-risk population of those aged 10 to 16 years [1]. Despite significant efforts to better understand the aetiopathogenesis of AIS, the cause or sequence of events leading to scoliosis onset are unknown. It is clear that AIS is a multifactorial disorder involving genetic factors, neurological dysfunctions, hormonal/metabolic dysfunctions, skeletal growth abnormalities, and biochemical factors [2, 3]. How these factors interact in scoliosis onset and whether a combination of factors is involved in curve progression are still unknown. The central nervous system (CNS) receives feedback about the body sways mainly from proprioceptive, visual and vestibular systems; it integrates the signals from

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