<p>Superior canal dehiscence syndrome (SCDS) is caused by a pathological ‘third window’ in the inner ear that selectively impairs superior semicircular canal function. Here we examined locomotion in individuals with SCDS to explore whether this canal-specific vestibular disruption leads to distinctive changes in movement during natural, overground walking. Participants with unilateral SCDS and healthy controls completed a series of ten walking tasks of varying difficulty (i.e., Functional Gait Assessment), while wearing inertial sensors on the head, trunk, waist, and limbs to capture segment-specific body movements. Participants with SCDS showed significantly lower FGA scores and slower gait cycles, as well as movement changes primarily in the vertical and pitch planes. In particular, quantitative analysis of kinematics revealed reduced vertical head acceleration with increased variability during complex tasks, diminished head pitch velocity, and reduced ipsi-lesional ankle pitch velocity and vertical acceleration. Importantly, these alterations were most pronounced during challenging tasks with limited visual feedback and could not be explained by slower gait speed alone. Overall, our findings suggest that disruption of a single semicircular canal can elicit compensatory movement strategies that reduce stimulation of the affected canal, thereby offering new insight into canal-specific contributions to everyday mobility and informing targeted vestibular rehabilitation.</p>

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Superior canal dehiscence syndrome induces canal-specific kinematic adaptations during locomotion

  • Raabeae Aryan,
  • Jennifer L. Millar,
  • Chenhao Bao,
  • John P. Carey,
  • Michael C. Schubert,
  • Kathleen E. Cullen

摘要

Superior canal dehiscence syndrome (SCDS) is caused by a pathological ‘third window’ in the inner ear that selectively impairs superior semicircular canal function. Here we examined locomotion in individuals with SCDS to explore whether this canal-specific vestibular disruption leads to distinctive changes in movement during natural, overground walking. Participants with unilateral SCDS and healthy controls completed a series of ten walking tasks of varying difficulty (i.e., Functional Gait Assessment), while wearing inertial sensors on the head, trunk, waist, and limbs to capture segment-specific body movements. Participants with SCDS showed significantly lower FGA scores and slower gait cycles, as well as movement changes primarily in the vertical and pitch planes. In particular, quantitative analysis of kinematics revealed reduced vertical head acceleration with increased variability during complex tasks, diminished head pitch velocity, and reduced ipsi-lesional ankle pitch velocity and vertical acceleration. Importantly, these alterations were most pronounced during challenging tasks with limited visual feedback and could not be explained by slower gait speed alone. Overall, our findings suggest that disruption of a single semicircular canal can elicit compensatory movement strategies that reduce stimulation of the affected canal, thereby offering new insight into canal-specific contributions to everyday mobility and informing targeted vestibular rehabilitation.