Tricia J Hubbard1. 1. University of North Carolina Charlotte, Department of Kinesiology, Charlotte, NC 28223, USA. thubbar1@uncc.edu
Abstract
BACKGROUND: Not all patients develop chronic ankle instability (CAI) after one or more lateral ankle sprains; some seem to heal or adjust to the ankle laxity after injury. Why do some patients develop CAI and others are able to cope and return to normal function? The purpose of this study was to examine ligament laxity between subjects with and without CAI. MATERIALS AND METHODS: Sixteen subjects with unilateral CAI and 16 subjects without participated in the study. Ligament laxity was measured with an instrumented ankle arthrometer. The arthrometer measured ankle joint motion for anterior/posterior displacement (mm) during loading at 125 N and inversion/eversion rotation (degrees of ROM) during loading at 4000 N/mm. For each dependent variable a 2 x 2 mixed model ANOVA was run with the between factor being group (CAI, No CAI) and the within factor with repeated measures being side (involved, uninvolved). RESULTS: A significant group by side interaction for anterior displacement (F(1,30) = 370.085, p < 0.001), and inversion rotation (F(1,30) = 7.455, p = 0.010) was found. There was significantly more anterior displacement and inversion rotation for the involved ankles of the CAI group than the involved ankles of the stable group and the uninvolved ankles of the CAI group. CONCLUSION: Based on the results of this study it appears that the increased anterior displacement and inversion rotation compared to patients without instability may be why subjects develop CAI. Although the patients without instability have a history of more than one lateral ankle sprain, they did not demonstrate increased laxity, which may be the reason why they do not complain of the functional impairment demonstrated in subjects with CAI.
BACKGROUND: Not all patients develop chronic ankle instability (CAI) after one or more lateral ankle sprains; some seem to heal or adjust to the ankle laxity after injury. Why do some patients develop CAI and others are able to cope and return to normal function? The purpose of this study was to examine ligament laxity between subjects with and without CAI. MATERIALS AND METHODS: Sixteen subjects with unilateral CAI and 16 subjects without participated in the study. Ligament laxity was measured with an instrumented ankle arthrometer. The arthrometer measured ankle joint motion for anterior/posterior displacement (mm) during loading at 125 N and inversion/eversion rotation (degrees of ROM) during loading at 4000 N/mm. For each dependent variable a 2 x 2 mixed model ANOVA was run with the between factor being group (CAI, No CAI) and the within factor with repeated measures being side (involved, uninvolved). RESULTS: A significant group by side interaction for anterior displacement (F(1,30) = 370.085, p < 0.001), and inversion rotation (F(1,30) = 7.455, p = 0.010) was found. There was significantly more anterior displacement and inversion rotation for the involved ankles of the CAI group than the involved ankles of the stable group and the uninvolved ankles of the CAI group. CONCLUSION: Based on the results of this study it appears that the increased anterior displacement and inversion rotation compared to patients without instability may be why subjects develop CAI. Although the patients without instability have a history of more than one lateral ankle sprain, they did not demonstrate increased laxity, which may be the reason why they do not complain of the functional impairment demonstrated in subjects with CAI.
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