HOCH, MATTHEW C.1; MCKEON, PATRICK O.2
Lateral ankle sprains are among the most frequently occurring injuries in sports-related activity (23), the military (2), and hospital emergency rooms (29). It is estimated that 23,000 ankle sprains occur daily in the United States with an estimated 4.4 billion dollars spent annually on treatment for these injuries (29,47). In addition to the frequency of acute ankle sprains, approximately 70% of individuals who sustain an acute ankle sprain will experience additional sprains, recurrent joint instability, residual symptoms, and decreases in functional capacity for up to 2 yr after the initial injury (19,21,27). These negative sequelae are associated with a health condition known as chronic ankle instability (CAI) and can lead to the development of posttraumatic ankle osteoarthritis (16,50). Understanding the clinical consequences of ankle sprains is imperative for developing successful rehabilitation strategies that reduce residual symptoms and restore functional capacity.
Several alterations in sensorimotor system function have been investigated after acute ankle sprain as possible contributing factors for recurrent ankle sprains and CAI (19). One such aspect is the ability of the peroneal muscles to create a dynamic defense mechanism to protect the ankle during sudden inversion perturbation. Previous investigators (17,32) have referred to this phenomenon using a variety of terms including peroneal reaction time (PRT), peroneal onset time, or peroneal latency. For the purposes of this systematic review, the temporal reaction of the peroneal muscles to an inversion perturbation will be referred to as PRT and defined as the time between ankle perturbation and the onset of peroneal muscle activity. This aspect of function is typically collected by measuring the timing of peroneal activation in response to a sudden inversion perturbation using electromyography and a trapdoor mechanism.
Measuring PRT after sudden inversion perturbation examines closed-loop neuromuscular control (17). This mechanism may be altered as a result of deleterious changes in the transmission of afferent input or in the ability of the central nervous system to generate an appropriate motor response (17). Delayed PRT has been examined prospectively as a risk factor for ankle sprain; however, no studies have identified any significant association (4,22,53,54). This suggests that delayed PRT may manifest as a consequence of trauma after lateral ankle sprain. PRT has been assessed in individuals with a variety of different ankle sprain histories (ASH), ranging from an initial acute sprain to CAI (17,32). Also, several different inversion tilt platform protocols have been used to create inversion perturbations along with several different methods of determining the activation thresholds for deriving PRT, which have confounded the ability to draw clear interpretations from the literature. These inconsistencies make it difficult to determine whether this aspect of sensorimotor system function should be a clinical consideration during the rehabilitation of patients who have sustained an ankle sprain.
Previous systematic reviews with meta-analysis (38,40) have been performed on this area of research. Munn et al. (40) concluded that PRT was unaffected in those with CAI, whereas Menacho et al. (38) determined that delays in PRT were present in studies which examined a range of ASH. In the case of both systematic reviews, the number of included studies could be substantially increased because additional evidence has become available, which may ultimately change the overall conclusions that can be derived from this body of research. Therefore, providing a comprehensive systematic review with meta-analysis, which critically appraises the research literature, may provide a better indication if PRT alterations are present in those with a history of ankle sprain(s). Therefore, the purpose of this systematic review with meta-analysis was to determine whether PRT impairments are present in individuals with a history of lateral ankle sprain. Specific variables that were evaluated included the type of 1) study comparisons and 2) subject characteristics of the included studies.
In January 2013, we performed a computerized search of EBSCOhost (MEDLINE, Sports Discus, and CINAHL) and PubMed Central entries from January 1, 1965, to January 1, 2013, to identify studies that examined PRT in individuals with a history of ankle sprain (Table 1). Search strategies were limited to studies that were written in English, involved humans, and were reported in peer-reviewed journals. Relevant articles were also identified by cross-referencing the citation lists of the articles identified in the electronic search.
Criteria for Selecting Studies
Only studies assessing PRT in participants using a mechanical tilt (trapdoor) platform to induce a sudden ankle inversion perturbation in individuals with a history of ankle sprain were included. We chose to investigate studies using mechanical tilt platforms, which induced an inversion perturbation during quiet standing or walking because we were most interested in examining the PRT to “sudden” or “unexpected” perturbations, and this form of testing is most commonly described in the literature. To be included, a study had to address the purpose of this systematic review and provide adequate results for calculation of effect size (ES). In cases where median and range were presented, they were converted to estimate means and standard deviations for the purpose of meta-analysis (25).
Assessment of Methodologic Quality
Included studies were evaluated using a quality index for nonrandomized studies (11). This quality index created by Downs and Black (11) encompasses components of the Strengthening the Reporting of Observational Studies in Epidemiology statement and has demonstrated high internal consistency and interrater reliability. An adapted, 16-question version of the original index described by Munn et al. (40) was used to assess methodologic quality in this systematic review. On the basis of the recommendations of Munn et al. (40), studies meeting <60% criteria were considered low quality, 60%–74.9% moderate quality, and >75% high quality. Each author independently performed the quality assessment for each of the included studies. Consensus regarding the quality index score for each study was agreed upon by both authors. In addition, a sensitivity analysis using the one-study-removed method (5) for the effect of study design quality was performed. This analysis was performed to determine whether the results of one particular study substantially influenced the cumulative effect.
Data Extraction and Statistical Analysis
Study comparison refers to the comparison design within each study. The two levels coded for this variable included 1) side-to-side comparison (1,3,10,12,24,26,28,30,33–35,39,41,42,44) and 2) between-group comparison (3,6,13,14,18,24,26,28,31,35,39,46,48,49). Side-to-side comparisons were studies that included the uninvolved limb as the control limb for comparison. Group comparisons used a healthy control group to compare subjects with a history of injury. It was not possible to make between-group and side-to-side comparisons in all included studies.
Subject characteristics refer to the type of subjects included in the study based on the available inclusion and exclusion criteria. The two levels coded for this variable included 1) CAI (1,10,13,18,24,30,31,34,35,39,44,48,49) and 2) ASH (3,6,12,14,26,28,33,41,42,46). Studies which labeled subjects with chronic, mechanical, or functional instability or provided evidence of repeated ankle sprains were classified collectively as CAI. Studies with all other histories of ankle sprain, including acute sprains or studies with nondescript subject information, were classified as ASH.
These variables were also combined to examine possible interactions between study comparison and subject characteristics. The four levels coded for this analysis included 1) CAI between-group comparison (13,18,24,31,35,39,48,49), 2) CAI side-to-side comparison (1,10,24,30,34,35,39,44), 3) ASH between-group comparison (3,6,14,26,28,46), and 4) ASH side-to-side comparison (3,12,26,28,33,41,42). The criteria for coding studies in this analysis were a combination of the previously described criteria for each variable.
Separate meta-analyses were performed on each of the study variables. For each meta-analysis, a random-effects model was used. Individual measures across the multiple variables were pooled from the included studies using a bias-corrected Hedges g ES and 95% confidence interval (CI) to examine the magnitude and precision of the difference from side-to-side or between-group comparisons (5). The calculated Hedges g ES is a unitless measure and represents an effect that exists on a parametric distribution (5). A positive ES indicated delayed PRT in pathologic subjects or limbs as compared with controls or the uninvolved limb. For all studies, pooled standard deviations associated with the involved limb or either the uninvolved limb or the healthy control group was used in the calculation of ES. In studies that assessed multiple different measures associated with the temporal response of the peroneal muscles to inversion perturbation, we included the measure that was most closely associated with our definition of PRT. When applicable, ES was calculated for both peroneus longus and brevis muscles. In studies where multiple comparisons were made, each comparison was treated independently within the statistical analyses. ES were interpreted as weak if they were less than 0.40, moderate if between 0.41 and 0.69, or strong if greater than 0.70 (8,36). ES and CI were interpreted as significant if the P value of the effect was <0.05. All statistical analyses were completed using a comprehensive meta-analysis version 2.2.034 (Biostatic, Inc., Englewood, NJ). In addition to statistical comparisons, a qualitative assessment of subgroup ES and CI was performed for each variable by examining the differences in ES estimates between groups or if CI crossed zero to further describe trends in the pooled data.
Assessment of Publication Bias
To assess the robustness of the observed overall effects of moderators on PRT, we used Orwin’s fail-safe N test. The fail-safe N test determines the number of studies with trivial ES that would be required to counter the pooled ES of the included studies. To assess the likelihood of publication bias, we generated a funnel plot of all included comparisons. In addition, the trim-and-fill method of imputing potentially missing studies was used for an additional assessment of publication bias.
Level of Evidence
The quality, the quantity, and the consistency of the included studies were assessed using the Oxford Centre for Evidence-Based Medicine–Levels of Evidence (CEBM). This taxonomy was used to determine the quality of the included studies and generate the strength of recommendation.
The computerized literature search using all databases yielded 94 articles. After the removal of 48 duplicate results across all databases, the final search resulted in 46 articles to be reviewed. Seven additional articles were identified through a hand search of cross-listed articles. The literature search resulted in 23 relevant studies (1,3,6,10,12–14,18,24,26,28,30,31,33–35,39,41,42,44,46,48,49). Three of the articles (1,6,46) were included after hand measuring means and standard deviations from figures, and one study (44) was included after additional information was provided by the authors. A complete list of search terms, Boolean operators, and results are presented in Table 1. A flow diagram of the study selection process is presented in Figure 1. Reasons for rejection included irrelevant methods, outcome methods, or subjects or inadequate data reporting. With the exception of Hopkins et al. (24), all studies used a bipedal stance trapdoor platform with similar testing procedures to create sudden inversion perturbations. Hopkins et al. (24) used a trapdoor platform that created a sudden inversion perturbation while walking.
The mean quality index score for the included studies was 60.60% (range = 37.50%–81.25%), indicating that the average level of study quality was moderate. Of the 23 included studies, 11 were classified as low quality, 7 were classified as moderate quality, and 5 were classified as high quality. When classifying studies as low, moderate, or high quality based on their respective quality index score, an analysis of the individual influences of methodologic-quality determined that the quality of study design did not influence the overall result (Q2 = 2.20, P = 0.33); however, it should be noted that several low quality CAI studies were associated with large ES. Most studies were retrospective cross-sectional or case–control designs, indicating level 3 evidence based on the Oxford CEBM. A breakdown of each study is presented in Table 2.
Overall summary effect.
Across the multiple studies and the two variables examined, the overall effect was 0.67 (95% CI = 0.37–0.95, P < 0.001), indicating that having a previous ankle sprain, regardless of a side-to-side or between-group comparison, demonstrated a moderate-to-strong deficit in PRT. The individual ES and the cumulative effect are presented in Figure 2 and Table 3.
Summary effects of individual study variables.
No difference was detected between the two levels of study comparisons (Q1 = 3.72, P = 0.07). On the basis of these findings, it can be concluded that either type of comparison may be useful in detecting PRT deficits after ankle sprain. However, from a qualitative perspective, the effect of side-to-side comparisons was strong, with a CI that did not encompass zero (ES = 0.88, 95% CI = 0.49–1.26, P < 0.001), whereas the effect of the between-group comparisons was weak with a CI which narrowly encompassed zero (ES = 0.36, 95% CI = −0.05 to 0.78, P = 0.08). Therefore, side-to-side comparisons may be a stronger design for detecting PRT deficits.
A significant difference was detected between the two levels of subject characteristics (Q1 = 13.78, P < 0.001). Studies labeled as ASH demonstrated a weak effect with a CI which encompassed zero (ES = 0.06, 95% CI = −0.31 to 0.43, P = 0.77), whereas studies labeled as CAI demonstrated a strong effect with a CI which did not encompass zero (ES = 1.04, 95% CI = 0.68–1.41, P < 0.001). Therefore, the magnitude and consistency of PRT deficits are greater in studies with CAI compared with those included with ASH. For subject characteristics, significant differences were detected between the 4 levels of study comparison (Q3 = 13.24, P = 0.004). For those studies with CAI subjects, between-group (ES = 0.72, 95% CI = 0.29–1.14, P = 0.001) and side-to-side comparisons (ES = 1.24, 95% CI = 0.70–1.79, P < 0.001) demonstrated strong effects with CI, which did not encompassed zero. Studies labeled as ASH between-group (ES = −0.21, 95% CI = −1.01 to 0.59, P = 0.61) and side-to-side comparison (ES = 0.21, 95% CI = −0.19 to 0.60, P = 0.31) demonstrated weak effects with CI which encompassed zero. Overall, CAI studies demonstrated large magnitude and consistent PRT deficits in both types of study comparisons, whereas ASH studies demonstrated weak, inconsistent PRT alterations in both types of study comparisons.
Publication bias was assessed with a funnel plot using Duval and Tweedie’s trim-and-fill method (Fig. 3). On the basis of the relative symmetry and distribution of the studies, it is unlikely that publication bias played an important role in the results. This is supported by the trim-and-fill analysis, which exhibited agreement between the observed and the estimated overall summary effect. In addition, the results of the Orwin fail-safe N test indicated that a range of 142–324 additional studies with weak ES (Hedges g ranging from 0.05 to 0.10) would be needed to nullify the overall summary effect.
The results of the one-study-removed method indicated that ES remained moderate to strong and ranged from 0.61 to 0.72. The lowest lower bound of the 95% CI was 0.34, and the greatest upper bound of the 95% CI was 1.00. All P values were P < 0.001, indicating that there was no single comparison that substantially influenced the overall summary effect.
The main findings of the meta-analysis revealed that people who have sustained an ankle sprain exhibit delayed PRT to inversion perturbation when compared with an uninvolved limb or a healthy control group. However, secondary analyses determined PRT is significantly delayed in subjects classified with CAI while it was not significantly affected in studies with other ASH regardless of between-group or within-group comparisons. Therefore, the subject characteristics and study design are important considerations for examining PRT in individuals who have sustained a previous ankle sprain.
The results of this study contradict the results of the meta-analysis performed by Munn et al. (40), which concluded that PRT was unaffected in those with CAI when compared with a control group or the uninvolved limb. Although Munn et al. (40) did identify large pooled estimates of mean difference suggesting PRT was delayed in those with CAI, the CI of the pooled estimates crossed zero and the random-effects meta-analyses yielded nonsignificant P values, which ultimately led to the conclusion that this aspect of sensorimotor system function was not affected in those with CAI. However, it should be noted that the P values reported by Munn et al. (40) associated with the between-group (P = 0.10) and side-to-side (P = 0.17) comparisons were trending toward statistical significance and the CI narrowly crossed zero. The meta-analysis in the current study may have generated different results because a greater number of studies examining PRT in those with CAI were included allowing more subjects to be entered into the analysis. As well, Hedges g estimates of ES were used as compared with the unstandardized mean difference. The current meta-analysis also examined these deficits using a different search strategy and inclusion criteria. Lastly, we used a different theoretical perspective by initially including all studies which examined PRT in patients with a history of ankle sprain and then created the CAI and the ASH subcomparisons. The combination of these factors likely led to the differing results between studies.
It was determined that those with CAI had delayed PRT to inversion perturbation; however, this was not detected in the studies included in the ASH group. One potential explanation for the lack of consistency in the findings of the ASH group may have been because these studies potentially examined a broader spectrum of patients with diverse histories of ankle sprain. In addition, several of these studies may have contained subjects that would have been considered to have CAI creating a mixed pool of subjects and possibly overestimating the ES in certain ASH studies. Because subject characteristics, ASH, and stability status were often unclear or not specified, it was difficult to consistently stratify these studies into groups that may have provided clearer recommendations regarding PRT deficits. Conversely, the inclusion criteria for CAI studies were generally more clearly delineated, which may have facilitated more consistent findings across studies. In most studies, subjects had to report a history of more than one ankle sprain, self-reported episodes of ankle “giving way,” and self-reported disability in physical activity or activities of daily living as a result of ankle sprain trauma. These findings suggest that the inclusion criteria used to classify individuals with a history of lateral ankle sprain(s) may create a sensitive dependence on the ability to consistently detect sensorimotor system impairments. This concept is supported by the work of Hiller et al. (20) and Delahunt et al. (9), who stress the importance of reporting subject characteristics for individuals with a history of ankle sprain to draw clearer interpretations of the finding leading to more precise clinical recommendations. Therefore, providing more stringent and detailed information on the inclusion of individuals with other ASH, such as patients with a first-time acute sprain, may elucidate clearer trends in these groups.
This meta-analysis determined that side-to-side comparisons may be more beneficial than between-group comparisons for detecting PRT deficits when CAI and ASH studies were pooled. However, subsequent analyses determined that much of the variability in the between-group comparisons were the result of ASH studies. When examining the combination of study comparison and subject characteristics, it was determined that CAI studies demonstrated strong ES indicative of delayed PRT in both types of study comparison, whereas ASH studies did not demonstrate significant differences in PRT in either type of study comparison. From our results, we cannot determine which study comparison is more effective at identifying PRT deficits in those with CAI because both study designs exhibited strong ES, and the CI were overlapping. Our findings differ from a recent meta-analysis (36), which examined that joint position recognition deficits in those with CAI and determined between-group comparisons were recommended over side-to-side comparisons. Furthermore, another recent meta-analysis (51) determined that postural control deficits were present on the uninvolved limb of individuals with CAI compared with healthy subjects. While it is unclear why PRT side-to-side comparisons yielded large magnitude differences in the CAI group compared with past meta-analyses (36,51), it suggests that PRT may provide a unique neurophysiologic perspective to examine sensorimotor function in those with CAI. Although we do not believe that this aspect of this meta-analysis should support performing side-to-side comparisons over between-group comparisons, we do believe these findings further reinforce the idea that the more clearly defined CAI group elicits deficits more effectively than the ASH group.
Although this study identified delayed PRT in those with CAI, the causal-link between alterations in PRT and CAI have yet to be established because of retrospective study designs and limited evidence regarding concurrent changes in other aspects of sensory or motor function. The current methods of estimating PRT examine the ability of the sensorimotor system to utilize feed-back loops to manage a perturbation. Deficits in this aspect of function permit speculation that PRT alterations could be associated with the ability to detect the perturbation and/or generate the appropriate motor response once the perturbation is detected. This suggests that delayed PRT may be related to decreases in somatosensory system acuity after repetitive damage to structures surrounding the ankle, previously referred to as partial articular deafferentation (7,15,17,32). This is supported by a meta-analysis (36), which determined that those with CAI have impaired ankle joint position recognition. Also, supraspinal adaptations in peroneal motoneuron excitability have been observed in those with CAI, which may inhibit various aspects of muscle function (37,43,45). Collectively, this evidence points toward sensorimotor system impairments, which may impact several aspects of lower extremity function. Ultimately, these sensorimotor alterations may dictate who develops into an ankle sprain coper with relatively no residual impairments versus individuals with CAI after an ankle sprain. Further examining how underlying sensorimotor impairments influence PRT and the development of CAI requires additional investigation.
With the exception of Hopkins et al. (24), all studies used a bipedal stance trapdoor platform with similar testing procedures to create sudden inversion perturbations. Hopkins et al. (24) assessed PRT through unexpected inversion perturbations created during (52) walking gait. This investigation exhibited large ES for both side-to-side and between-group comparisons with CI, which did not encompass zero. Although this is the only investigation that has used a dynamic technique, examining PRT during activity warrants further investigation. Inducing inversion perturbations during dynamic activity may provide a greater challenge to the sensorimotor system because of increased task complexity and more unpredictable environments. In addition, subjects do not have consistent somatosensory information because the plantar cutaneous receptors are not in constant contact with the ground and articular and musculotendinous receptors are moving through a large range of motion during the gait cycle. Therefore, subjects are required to adapt to the rapidly changing spatiotemporal aspects of movement at the time of perturbation which may be more challenging then static stance. Further examining PRT using similar methods may identify even more consistent and larger magnitude deficits in those with CAI and other ASH.
Although this meta-analysis did identify delayed PRT in those with CAI, several aspects of this impairment in this patient population require further study. It remains unclear how delayed PRT may relate to deleterious changes in levels of activity and participation that may be meaningful to patients with CAI. This suggests that the mere presence of a PRT impairment may have no bearing on the magnitude or progression of CAI as perceived by the individual. Furthermore, the lack of a causal link between CAI and PRT indicates that improving PRT may not prevent future ankle sprains or influence disability. In addition to examining underlying changes in sensory and motor function, examining the response of the peroneal muscles along with more proximal muscles, such as the gluteus medius, would begin to provide a better depiction if this phenomenon is local or global in nature. Gaining a greater understanding of the extent of PRT deficits in patients with CAI from both a patient-centered and disease-oriented perspective may lead to clinical intervention strategies that can address this particular impairment as well as larger-scale issues such as decreased functional capacity and degenerative joint conditions. Finally, future studies that investigate sensorimotor function in individuals with a history of ankle sprain should provide detailed descriptions of the included subjects based on the sensitive dependence of this information for detecting sensorimotor alterations in this study.
Electronic searches were conducted in the databases that we considered to be the most relevant to impairments associated with ankle sprain, which was followed by a hand search of the identified studies. However, it is possible that other evidence is available, which was not indexed in the selected search databases or identified through hand searching. We also limited our search to studies published in English, but we do not believe any relevant articles were excluded with this search parameter.
For the purposes of meta-analysis we decided to group studies based on subject characteristics, study design, and study quality. Several other variables such as velocity of the trapdoor perturbation, the end range angle of the trapdoor, if subjects were blindfolded or wore headphones, the methods of EMG normalization, and the parameters and methods used to determine muscle onset may influence the PRT observed in each study. We selected not to use these variables to further group studies because they varied considerably across studies and certain elements were often not reported. Although this meta-analysis was able to determine the influence of subject characteristics, study design, and study quality on PRT, several of the aforementioned variables require careful consideration when designing future studies.
We chose to use standardized ES versus the unstandardized mean differences in the time domain (ms) to answer the questions posed in this systematic review. We believe the use of standardized ES was more appropriate than unstandardized mean differences because although these studies were homogenous in several ways, they were also methodologically different in several ways, which were identified in the previous paragraph. Also, the time domain values varied considerably across studies (range = 51–106 ms), and some studies exhibited high levels of dispersion around the measures of central tendency. Cumulatively, we believe that ES was a more prudent method to answer the question posed in this systematic review. The limitation to our meta-analysis technique is that we cannot specify the mean latency differences between groups or limbs. We believe calculating this information may not be directly useful for future studies on this topic because it may not be consistent with the values obtained in individual studies. However, the ES estimates provided in this study indicate large magnitude PRT deficits are present in individuals with CAI, which suggests these deficits are clinically relevant and supports further investigating this aspect of function in these patients.
The overall results of this meta-analysis determined that individuals with a previous ankle sprain exhibit impaired PRT. Further analyses determined that those with CAI have a delayed PRT when compared with the contralateral uninvolved limb or a healthy control group. However, individuals with all other ASH did not demonstrate significant deficits in PRT. On the basis of the CEBM guidelines, the strength of recommendation associated with PRT deficits in patients with CAI is grade B based on the consistency of the findings from primarily level 3 evidence. However, the strength of recommendation associated with PRT deficits in people with ASH is grade C based on the inconsistency of the findings and extrapolations from level 3 and level 4 evidence. Gaining deeper insights into underlying sensory or motor alterations responsible for delayed PRT, the role of delayed PRT in activity limitation and participation restriction, and the extent to which delayed PRT contributes to CAI progression will elucidate the clinical relevance of this impairment and clinical intervention strategies to address these deficits.
This study did not receive any funding.
The authors have no conflicts of interest to declare that are related to the content of this study
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
1. Akhbari B, Takamjani IE, Salavati M, Sanjari MA. A 4-week biodex stability exercise program improved ankle musculature onset, peak latency and balance measures in functionally unstable ankles. Phys Ther Sport
. 2007; 8 (3): 117–29.
2. Almeida SA, Williams KM, Shaffer RA, Brodine SK. Epidemiological patterns of musculoskeletal injuries and physical training. Med Sci Sport Exer
. 1999; 31 (8): 1176–82.
3. Beckman SM, Buchanan TS. Ankle inversion injury and hypermobility: effect on hip and ankle muscle electromyography onset latency. Arch Phys Med Rehabil
. 1995; 76 (12): 1138–43.
4. Beynnon BD, Renström PA, Alosa DM, Baumhauer JF, Vacek PM. Ankle ligament injury risk factors: a prospective study of college athletes. J Orthop Res
. 2001; 19 (2): 213–20.
5. Borenstein M, Hedges LV, Higgins JPT, Rothstein HR. Introduction to Meta-analysis
. West Sussex (UK): John Wiley & Sons, Ltd; 2009. p. 21–291.
6. Brunt D, Andersen JC, Huntsman B, Reinhert LB, Thorell AC, Sterling JC. Postural responses to lateral perturbation in healthy subjects and ankle sprain patients. Med Sci Sport Exer
. 1992; 24 (2): 171–6.
7. Bullock-Saxton JE. Local sensation changes and altered hip muscle function following severe ankle sprain. Phys Ther
. 1994; 74 (1): 17–31.
8. Cohen J. Statistical Power Analysis for the Behavioral Sciences
. 2nd ed. Hillsdale (NJ): Lawrence Erlbuam Assoc.; 1988. p. 20–26.
9. Delahunt E, Coughlan GF, Caulfield B, Nightingale EJ, Lin CW, Hiller CE. Inclusion criteria when investigating insufficiencies in chronic ankle instability. Med Sci Sport Exer
. 2010; 42 (10): 2106–21.
10. Donahue M. The effect of tape and semi-rigid brace on peroneus longus latency. I J Fitness
. 2010; 6 (1): 9–15.
11. Downs SH, Black N. The feasibility of creating a checklist for the assessment of the methodological quality both of randomised and non-randomised studies of health care interventions. J Epidemiol Community Health
. 1998; 52 (6): 377–84.
12. Ebig M, Lephart SM, Burdett RG, Miller MC, Pincivero DM. The effect of sudden inversion stress on EMG activity of the peroneal and tibialis anterior muscles in the chronically unstable ankle. J Orthop Sport Phys Ther
. 1997; 26 (2): 73–7.
13. Eechaute C, Vaes P, Duquet W, Van Gheluwe B. Reliability and discriminative validity of sudden ankle inversion measurements in patients with chronic ankle instability. Gait Posture
. 2009; 30 (1): 82–6.
14. Fernandes N, Allison GT, Hopper D. Peroneal latency in normal and injured ankles at varying angles of perturbation. Clin Orthop Relat Res
. 2000; 375: 193–201.
15. Freeman MA, Dean MR, Hanham IW. The etiology and prevention of functional instability of the foot. J Bone Joint Surg Br
. 1965; 47 (4): 678–85.
16. Gross P, Marti B. Risk of degenerative ankle joint disease in volleyball players: study of former elite athletes. Int J Sport Med
. 1999; 20 (1): 58–63.
17. Gutierrez GM, Kaminski TW, Douex AT. Neuromuscular control and ankle instability. PMR
. 2009; 1 (4): 359–65.
18. Han K, Ricard MD. Effects of 4 weeks of elastic-resistance training on ankle-evertor strength and latency. J Sport Rehabil
. 2011; 20 (2): 157–73.
19. Hertel J. Sensorimotor deficits with ankle sprains and chronic ankle instability. Clin Sports Med
. 2008; 27 (3): 353–70.
20. Hiller CE, Nightingale EJ, Lin CW, Coughlan GF, Caulfield B, Delahunt E. Characteristics of people with recurrent ankle sprains: a systematic review with meta-analysis. Br J Sports Med
. 2011; 45 (8): 660–72.
21. Hoch MC, McKeon PO. Integrating contemporary models of motor control and health in chronic ankle instability. Athl Train Sports Health Care
. 2010; 2 (2): 82–8.
22. Hoch MC, McKeon PO. Peroneal reaction time is not a risk factor for ankle sprain in healthy adults. J Sport Rehabil
. 2011; 20 (4), 505–11.
23. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train
. 2007; 42 (2): 311–9.
24. Hopkins JT, Brown TN, Christensen L, Palmieri-Smith RM. Deficits in peroneal latency and electromechanical delay in patients with functional ankle instability. J Orthop Res
. 2009; 27 (12): 1541–6.
25. Hozo SP, Djulbegovic B, Hozo I. Estimating the mean and variance from the median, range, and the size of a sample. BMC Med Res Methodol
. 2005; 5 (1): 13.
26. Isakov E, Mizrahi J, Solzi P, Susak Z, Lotem M. Response of the peroneal muscles to sudden inversion of the ankle during standing. Int Jf Sport Biomech
. 1986; 2 (2): 100–9.
27. Itay SA, Ganel H, Horoszowski H, Farine I. Clinical and functional status following lateral ankle sprains—follow-up of 90 young adults treated conservatively. Orthop Rev
. 1982; 11 (5): 73–6.
28. Johnson MB, Johnson CL. Electromyographic response of peroneal muscles in surgical and nonsurgical injured ankles during sudden inversion. J Orthop Sport Phys Ther
. 1993; 18 (3): 497–501.
29. Kannus P, Renstram P. Treatment for acute tears of the lateral ligaments of the ankle. Operation, cast, or early controlled mobilization. J Bone Joint Surg Am
. 1991; 73 (2): 305–12.
30. Karlsson J, Andreasson GO. The effect of external ankle support in chronic lateral ankle joint instability: an electromyographic study. Am J Sports Med
. 1992; 20 (3): 257–61.
31. Khin Myo H, Ishii T, Sakane M, Hayashi K. Effect of anesthesia of the sinus tarsi on peroneal reaction time in patients with functional instability of the ankle. Foot Ankle Int
. 1999; 20 (9): 554–9.
32. Konradsen L. Sensori-motor control of the uninjured and injured human ankle. J Electmyography Kinesiology
. 2002; 12 (3): 199–203.
33. Konradsen L, Olesen S, Hansen HM. Ankle sensorimotor control and eversion strength after acute ankle inversion injuries. Am J Sports Med
. 1998; 26 (1): 72–7.
34. Konradsen L, Ravn JB. Ankle instability caused by prolonged peroneal reaction time. Acta Orthop Scand
. 1990; 61 (5): 388–90.
35. Löfvenberg R, Kärrholm J, Sundelin G, Ahlgren O. Prolonged reaction time in patients with chronic lateral instability of the ankle. Am J Sports Med
. 1995; 23 (4): 414–7.
36. McKeon JMM, McKeon PO. Evaluation of joint position recognition measurement variables associated with chronic ankle instability: a meta-analysis. J Athl Train
. 2012; 47 (4): 444–56.
37. McVey ED, Palmieri RM, Docherty CL, Zinder SM, Ingersoll CD. Arthrogenic muscle inhibition in the leg muscles of subjects exhibiting functional ankle instability. Foot Ankle Int
. 2005; 26 (12): 1055–61.
38. Menacho MdO, Pereira HM, Oliveira BIRd, Chagas LMPM, Toyohara MT, Cardoso JR. The peroneus reaction time during sudden inversion test: systematic review. J Electromyogr Kinesiol
. 2010; 20 (4): 559–65.
39. Mitchell A, Dyson R, Hale T, Abraham C. Biomechanics of ankle instability. Part 1: reaction time to simulated ankle sprain. Med Sci Sport Exer
. 2008; 40 (8): 1515–21.
40. Munn J, Sullivan SJ, Schneiders AG. Evidence of sensorimotor deficits in functional ankle instability: a systematic review with meta-analysis. J Sci Med Sport
. 2010; 13 (1): 2–12.
41. Nawoczenski DA, Owen MG, Ecker ML, Altman B, Epler M. Objective evaluation of peroneal response to sudden inversion stress. J Orthop Sport Phys Ther
. 1985; 7 (3): 107–9.
42. Osborne MD, Chou L, Laskowski ER, Smith J, Kaufman KR. The effect of ankle disk training on muscle reaction time in subjects with a history of ankle sprain. Amer J Sports Med
. 2001; 29 (5): 627–32.
43. Palmieri-Smith RM, Hopkins JT, Brown TN. Peroneal activation deficits in persons with functional ankle instability. Amer J Sports Med
. 2009; 37 (5): 982–8.
44. Rosenbaum D, Becker HP, Gerngroß H, Claes L. Peroneal reaction times for diagnosis of functional ankle instability. Foot Ankle Surg
. 2000; 6 (1): 31–8.
45. Sefton JM, Hicks-Little CA, Hubbard TJ, et al. Segmental spinal reflex adaptations associated with chronic ankle instability. Arch Phys Med Rehabil
. 2008; 89 (10): 1991–5.
46. Shima N, Maeda A, Hirohashi K. Delayed latency of peroneal reflex to sudden inversion with ankle taping or bracing. Int J Sport Med
. 2005; 26 (6): 476–80.
47. Soboroff SH, Pappius EM, Komaroff AL. Benefits, risks, and costs of alternative approaches to the evaluation and treatment of severe ankle sprain. Clin Orthop Relat Res
. 1984; (183): 160–8.
48. Vaes P, Duquet W, Van Gheluwe B. Peroneal reaction times and eversion motor response in healthy and unstable ankles. J Athl Train
. 2002; 37 (4): 475.
49. Vaes P, Van Gheluwe B, Duquet W. Control of acceleration during sudden ankle supination in people with unstable ankles. J Orthop Sport Phys Ther
. 2001; 31 (12): 741–52.
50. Valderrabano V, Hintermann B, Horisberger M, Fung TS. Ligamentous posttraumatic ankle osteoarthritis. Am J Sports Med
. 2006; 34 (4): 612–20.
51. Wikstrom EA, Naik S, Lodha N, Cauraugh JH. Balance capabilities after lateral ankle trauma and intervention: a meta-analysis. Med Sci Sports Exerc
. 2009; 41 (6): 1287–95.
52. Wikstrom EA, Tillman MD, Chmielewski TL, Cauraugh JH, Naugle KE, Borsa PA. Discriminating between copers and people with chronic ankle instability. J Athl Train
. 2012; 47 (2): 136–42.
53. Willems TM, Witvrouw E, Delbaere K, Mahieu N, Bourdeaudhuij I, De Clercq D. Intrinsic risk factors for inversion ankle sprains in male subjects: a prospective study. Am J Sports Med
. 2005; 33 (3): 415–23.
54. Willems TM, Witvrouw E, Delbaere K, Philippaerts R, De Bourdeaudhuij I, De Clercq D. Intrinsic risk factors for inversion ankle sprains in females–a prospective study. Scand J Med Sci Sports
. 2005; 15 (5): 336–45.