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28 Reweighing of visual information in individuals with chronic ankle instability: systematic review
  1. K Song1,
  2. C Burcal1,
  3. J Hertel2,
  4. EA Wikstrom1
  1. 1Department of Kinesiology, University of North Carolina at Charlotte, USA
  2. 2Department of Kinesiology, University of Virginia, USA


Background While the exact neurophysiological mechanism of chronic ankle instability (CAI) remains unclear, research suggests that CAI associated balance impairments might be due to an inability to appropriately reweight sensory and/or somatosensory information.

Objective To determine if those with CAI place a greater emphasis on visual information relative to uninjured controls.

Design Systematic review.

Setting Not applicable.

Participants Participants with chronic ankle instability.

Assessment of risk factors We searched PubMed, CINAHL, SPORTDiscus, and Scopus databases from origin to May 2015 using the combination of key words including: postural control, postural stability, single limb stance, single leg stance, single leg balance, single limb balance, time-to-boundary, or TTB.

Main outcome measurements Sample sizes, means and SD of TTB outcomes for each group’s EO and EC stance were extracted.

Results Weighted means and SD were calculated and the EC to EO effect size (ES) and 95% confidence interval (CI) for each outcome was generated and compared between groups. The 95% CI of the mediolateral (ML) mean [Control: -1.02 (-1.22 to -0.82), CAI: -1.60 (-1.84 to -1.35)), anteroposterior (AP) mean (Control: -1.31 (-1.51 to -1.10), CAI: -2.16 (-2.42 to  -1.88)), and AP SD (Control: -1.30 (-1.50 to -1.09), CAI: -2.10  (-2.36 to -1.83)] TTB outcomes did not overlap indicating significant differences between two groups. However, the 95% CI for ML TTB SD (Control: -0.77 (-0.97 to -0.58), CAI: -1.11 (-1.33 to -0.88)) did overlap.

Conclusions Those with CAI put more reliance on visual information during single leg stance compared to healthy individuals. This result may indicate that sensory weighting differences may be a potential neurophysiologic mechanism of balance deficits associate with CAI.

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