| | Deficits in time-to-boundary measures of postural control with chronic ankle instabilityReceived 16 August 2005; received in revised form 2 December 2005; accepted 20 December 2005. published online 01 February 2006. Abstract Our purpose was to examine postural control in single leg stance in subjects with and without unilateral chronic ankle instability (CAI) using traditional center of pressure (COP)-based and time-to-boundary (TTB) measures. Fifteen physically active females with self-reported unilateral chronic ankle instability (CAI) and nine healthy female controls performed three 10-s trials of eyes open single limb quiet standing on a force plate on both their legs. The traditional measures were mean COP velocity, standard deviation of COP, range of COP, and percent of available range utilized. The TTB measures were absolute minimum TTB, mean of the minimum TTB samples, and standard deviation of the minimum TTB samples. All measures were calculated in both the mediolateral (ML) and anteroposterior (AP) directions. A 2 ×2 group (CAI, control) by side (involved, uninvolved) design was utilized. The CAI group had significantly lower scores for five of the six TTB measures compared to the control group, however only one (AP COP velocity) of the eight traditional measures was different between groups. The TTB measures appear to detect postural control deficits related to CAI that traditional measures do not. 1. Introduction  Lateral ankle sprains are among the most common injuries in sports and the most common predisposition to such sprains has consistently been shown to be a history of previous sprain to the same ankle [1]. In their seminal work, Freeman et al. [2] hypothesized that ankle sprains resulted in postural control deficits due to damaged sensory receptors in injured ligaments. This hypothesis, however, has recently been challenged by a pair of studies [3], [4] that failed to find sensorimotor control deficits after anesthetizing the lateral ankle ligaments, thus indicating that in spite of the loss of sensory information from the receptors in these ligaments, adequate sensory information from other receptors (capsular, musculotendinous, cutaneous) was available to allow for unimpaired sensorimotor control. Postural control impairments have consistently been found in patients after acute ankle sprains [5], [6], [7]. While this has been thought to be due to local proprioceptive deficits at the site of injury, a recent report found that postural control in single leg stance was impaired, as demonstrated by increased center of pressure (COP) excursion velocity measures, on not only the limb with an acutely sprained ankle, but also on the contralateral uninjured limb [7]. This suggests that unilateral ankle sprain results in not only local sensorimotor deficits, but also centrally mediated impairments [7]. There are discrepancies in the literature in regards to postural control deficits in those with chronic ankle instability (CAI), defined as having frequent and repetitive bouts of the ankle giving way during functional activities. Impairments in postural control in patients with CAI have been reported [8], [9], but conflicting evidence [10] reporting no postural control deficits in those with CAI also exists. These contradictory findings may be due to discrepancies in methodology and instrumentation employed by different researchers [11]. Postural control has most commonly been assessed by having subjects stand on one limb in the modified Rhomberg position (looking straight ahead with arms held in a fixed position) on an instrumented force plate. The dependent variables have typically been measures of amplitude or variability of the center of pressure or the vertical force vector (Fz). While such measures have been able to detect postural control deficits associated with acute ankle sprains [5], [6], [7], their ability to identify impairments associated with CAI has been questioned [12]. Time-to-boundary (TTB) measures provide a novel method of postural control assessment that may elucidate impairments associated with CAI not clearly identified by traditional COP-based measures. TTB measures estimate the time it would take for the COP to reach the boundary of the base of support if the COP was to continue on its trajectory at its instantaneous velocity. An individual would lose their balance and fall if their COP reached the boundary of the base of support, thus a lower TTB measure indicates greater postural instability as the COP is closer in time to reaching the boundary of the base of support [13]. These measures provide insight to the spatiotemporal characteristics of postural control and have been used to identify postural control impairments during two-legged stance related to aging and Parkinson's disease [13], [14], [15], [16], [17]. TTB measures in single limb stance have been shown to have intrasession reliability at levels consistent with traditional COP-based measures with intraclass correlation coefficients ranging from .34 to .87 for the TTB measures and from .35 to .80 for the traditional measures [18]. TTB measures have also been shown to be weakly correlated to traditional measures thus suggesting that they capture different aspects of postural control than traditional COP-based measures [18]. Specifically, the TTB measures provide information about COP excursions in relation to the boundaries of the base of stability that are not addressed by traditional measures. TTB measures have not been previously assessed in unilateral stance among subjects with CAI and these measures may prove to be more sensitive in detecting postural control deficits associated with CAI than traditional measures because they capture boundary-relevant aspects of postural control. Therefore, our purpose was to assess postural control in single limb stance using traditional COP-based and TTB measures in subjects with and without self-reported unilateral CAI. We hypothesize that postural control impairments will be identified in those with unilateral CAI compared to healthy controls via TTB measures, but not traditional COP-based measures. 2. Methods 2.2. Procedures Subjects performed three, 10-s trials of quiet single leg standing barefoot on a force plate with eyes open. Subjects were instructed to stand as still as possible while focusing on a visual target placed 1m in front of them. If subjects lost their balance and were unable to complete a trial, which only happened on a handful of occasions, that data were discarded and the trial was repeated. The stance foot was meticulously placed in the same position on the force plate for all three trials. The force plate has a detailed grid on its surface to allow for exact placement so that the foot was precisely bisected by the anteroposterior (AP) and mediolateral (ML) midlines of the force plate. Postural control was assessed using an Accusway® force platform (AMTI Corp., Watertown, MA) interfaced with a computer. Triaxial forces (Fx, Fy, Fz) and moments (Mx, My, Mz) were recorded at 50Hz and a time series of 500 COP data points for each trial were calculated by the Swaywin® software program (AMTI Corp., Watertown, MA). COP data were then filtered with a fourth order zero lag, low pass filter with a cutoff frequency of 5Hz [6]. To calculate TTB measures, the foot was modeled as a rectangle to allow for separation of the AP and ML components of COP as suggested by van Wegen et al. [16], [17]. COP data files were processed using a custom software program using Matlab (Mathworks Inc. Natik, MA) [18]. For each COP ML data point, the COP ML position and velocity were used to calculate TTBML. If the COP MLi was moving medially, the distance between COP MLi and the medial border of the foot was calculated. This distance was then divided by the corresponding velocity of COP MLi to calculate the time it would take the COP MLi to reach the medial border of the foot if it were to continue moving in the same direction with no acceleration or deceleration. If the COP MLi was moving laterally, the distance between COP MLi and the lateral border of the foot was calculated and divided by the corresponding velocity of COP MLi Fig. 1. Thus, a time series of TTBML measures was generated. A time series of corresponding TTBAP measures was similarly generated by determining the time it would take COP APi to reach either the anterior or posterior boundary of the foot [18]. A typical TTB series shows a sequence of peaks and valleys with each valley representing a change in direction of COP. We identified TTB measures at the valleys, or minima, in each trial Fig. 2. These valleys represent transition points where the COP is closest, in the time domain, to a boundary of the base of the support immediately before it changes directions to move towards the opposite, and farther away, boundary of the base of support. The valleys in the data may be viewed as points of potential postural instability, whereas the peaks represent points of postural stability. To identify these minima, derivatives of the TTB measures were computed using first order finite difference equations. The first derivative values were used to identify minima and maxima, and the second derivative values to compute the minima. Due to problems in accurately calculating derivatives, the software performed a local search around the derivative-identified minima to precisely locate the minima [18]. It should be noted that the TTB measures in the ML direction most likely underestimate the actual time it would take the COP to reach the medial or lateral border of the foot. This is because the ML boundaries of the foot were operationally defined at their widest point near the metatarsal heads, whereas the AP location of the COP is almost always posterior to these and in a narrower ML portion of the foot. TTB measures serving as dependent variables were the absolute minimum (smallest of the minima), mean of minimum samples, and standard deviation of minimum samples in the ML and AP direction [19]. The traditional COP-based dependent variables included the mean velocity (total COP excursion length in cm divided by time of the trial, 10s), standard deviation of COP excursions, range of COP excursions (distance between the minimum and maximum COP positions), and percent of available range used (range divided by width or length of the foot, respectively) in the ML and AP directions [6], [13]. 4. Discussion Our primary finding was the identification of significant impairments in all but one of the TTB measures of postural control in subjects with CAI. In contrast, only one of the eight traditional COP-based measures of postural control identified differences between the CAI and control groups. There are conflicting reports in the literature in regards to postural control deficits as assessed by traditional measures in those with CAI [10], [11], thus our finding of a CAI-related deficit with COP AP velocity, but no other traditional variables, is not surprising. The lack of side by group interactions for any of our dependent measures indicates that the relationship between postural control performance on the involved and uninvolved limbs of CAI subjects was not significantly different than side-to-side differences of the controls. The presence of significant group differences for five of the six TTB measures and COP AP velocity indicates that the group with unilateral CAI had significantly different measures of postural control than the control group when performance of both limbs were pooled together. The most plausible explanation for this is that the CAI group had centrally-mediated alterations in postural control that caused impairments when subjects balanced on both their involved and uninvolved limbs. Based on the tests of statistical significance and the interpretations of the group effect sizes, it appears that TTB measures were able to identify postural control deficits associated with CAI that all but one of the traditional COP-based measures could not. Slobounov et al. [14] surmised that TTB might serve as a control parameter in the maintenance of postural equilibrium in double leg stance. If this is also true in single limb balance, our results appear to demonstrate an alteration in this postural control parameter occurs in both the involved and uninvolved limbs of subjects with unilateral CAI. We believe that this is the first study to demonstrate differences in boundary-relevant measures of postural control in subjects with ankle instability. The measures of the absolute minimum TTB samples and the mean of the minimum TTB samples provide estimates of the proximity in time an individual is to losing their balance during single limb stance. The CAI group had significantly lower values for these measures in both the ML and AP directions compared to the control group. This indicates that while CAI subjects were controlling their balance (i.e., they did not fall during testing), they were doing so in a manner that placed the COP closer to the limits of stability, in the time domain, compared to the healthy controls. In other words, their postural control system operated in a manner that placed them nearer in time, to episodes of potential postural instability than controls. These measures of the magnitude of TTB provide more insight into the spatiotemporal aspects of postural control than do traditional COP-based measures such as mean velocity of COP excursions because they take into account not only the rate of displacement of COP but also the direction and position of COP excursions in relation to the boundaries of the foot. It must be noted that TTB measures are inherently linked to COP velocity measures because COP velocity is included in the equation to calculate TTB. The most important distinction between these categories of measurement is that the traditional COP velocity measure represents the mean of all COP excursions from an entire trial, while TTB variables are based only on those select data points that yield minima in the TTB data stream. The reason for CAI subjects to operate closer to their limits of stability is not clear. The increased postural unsteadiness is most likely due to altered muscular recruitment strategies in the muscles acting on the ankle to maintain upright stance, however further research involving simultaneous measurement of postural control and electromyography is needed to identify specific mechanisms for the postural alterations. Traditionally, increased variability in postural control measures has been associated with neuromuscular dysfunction, however this notion has been recently challenged [13]. We found lower standard deviations of the TTB minimum samples on both limbs of our CAI group compared to the controls. A reduced standard deviation of the TTB minima suggests diminished variability in the TTB profiles of subjects with self-reported CAI. Previous authors have hypothesized that lower standard deviations of the TTB minima in bipedal balancing tasks are representative of decreased complexity in the postural control systems in the elderly [15], [17] and patients with Parkinson's disease [16]. This decreased variability is thought to be due to a reduction in the use of available degrees of freedom to accomplish postural tasks and to lead to an increased risk of loss of balance because large perturbations cannot be dealt with as effectively as in those who have TTB profiles with greater variability [13]. It is unclear if this reduction in variability related to ankle instability is due to central or peripheral mechanisms. The etiology of chronic instability after an initial ankle sprain is not clearly understood [20]. The role of proprioceptive and neuromuscular control impairments in those with CAI has been extensively investigated, however most of this work has focused on dysfunction local to the involved ankle. Our current results combined with those of others [21], [22] who have demonstrated neuromuscular control changes at joints proximal to involved ankles provide evidence that the etiology of CAI involves alteration in the central nervous system control of lower extremity neuromuscular function. There is mounting evidence of central neuromuscular alterations in response to unilateral joint injuries with reports in the literature describing the phenomenon in patients with acute ankle sprain [7], anterior cruciate ligament injury [23], [24], and shoulder impingement syndrome [25]. Impaired motor control contralateral to the side of injury may be mediated via gamma motoneuron loops [23]. Gamma motoneurons innervate muscle spindles which are sensory organs within skeletal muscles that are perceptive to changes in muscle length. Muscle spindles also contain contractile units that allow the sensitivity of the spindles to be adjusted and are thought to be under both supraspinal and spinal level control. Johansson et al. [26] speculated that muscle spindles may be influenced not only by changes in muscle length, but also by signals from descending pathways and joint receptors in contralateral peripheral nerves. Such signals from the central nervous system could be present in subjects with CAI and be responsible for the altered postural control, as assessed by TTB measures, on both involved and uninvolved limbs in our study. Dysfunction of the gamma motoneuron loop has been previously implicated in neuromuscular impairments associated with ankle instability [11], [27]. Studies aiming to eliminate ligamentous mechanoreceptor input at the ankle through local anesthesia have not shown substantial proprioceptive or postural control deficits after elimination of mechanoreceptor input [3], [4]. Despite these findings, Freeman et al.'s [2] hypothesis of ligament mechanoreceptor damage after ankle sprain leading to impaired proprioception, and hence inadequate neuromuscular responses to protect the ankle from injurious situations, should not be completely negated. Instead, a more comprehensive paradigm of joint injury, proprioception, and neuromuscular control should be considered (Fig. 3) [20]. The multiple inputs of afferent information from articular, musculotendinous, and cutaneous receptors (and the potential redundancy of the information these receptors convey) to the central nervous system must be acknowledged. Additionally, the existence of both feedforward and feedback mechanisms on muscle spindles must be appreciated. It is possible that in the presence of chronic joint instability that altered mechanoreceptor activity from an injured ligament is sensed in the central nervous system, and this leads to descending signals causing adjustments in muscle spindle sensitivity bilaterally. These changes may lead to broader alterations in neuromuscular control. Further research is needed to study this hypothesis and identify if these processes are due to changes at the spinal or supraspinal levels of motor control.Another possible explanation of our findings is that those subjects with CAI had poor postural control before they suffered initial ankle sprains. Diminshed postural control during single leg stance has previously been linked to increased risk of ankle sprains using traditional measures [28], [29], however conflicting findings [30] also exist. We are aware of only one study that has reported pre- and post-injury postural control measures in subjects who suffered acute ankle sprains. Evans et al. [7] demonstrated that while COP velocity measures increased substantially after acute ankle sprain, they returned to near pre-injury levels within 4 weeks of injury. They did not make comparisons of baseline measures to a control group in their study [7]. It is possible that our CAI group had lower TTB measures of postural control than controls prior to them ever suffering an initial ankle sprain, however, it is unclear why they would go onto to have multiple sprains on one ankle but none on the contralateral side. The potential of intrinsically poor sensorimotor performance as a potential risk factor of ankle sprain warrants further study. Our study did have a few limitations. We had a relatively small, and quite homogenous, sample. Our sample consisted of physically active female young adults and the generalizability of our findings to other populations cannot be made without further investigation. Additionally, we examined 14 dependent variables so the possibility of making a type I error exists, however, all of our statistically significant differences were associated with moderate to strong effect sizes. Likewise the possibility of type II error also exists, but we did not identify any strong effect sizes in the absence of statistical significance. Lastly, we must acknowledge that TTB analysis does not evaluate the entire time series of the COP data set, but does so only at the valleys, or minima, in the TTB data set. Other nonlinear tools such as approximate entropy, Lyapunov exponent, or Hurst exponent assessments may allow for assessment of continuous COP and TTB changes throughout an entire data set and may provide further insight into the variability of postural control strategies associated with CAI. In conclusion, females with self-reported unilateral chronic ankle instability demonstrated postural control deficits as assessed by time-to-boundary measures on both their involved and uninvolved limbs in relation to the control group. This suggests that an alteration in centrally mediated spatiotemporal postural control strategies may be associated with chronic ankle instability. The time-to-boundary measures appear to detect postural control deficits related to chronic ankle instability that most of the traditional COP-based measures fail to. 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a Kinesiology Program, University of Virginia, 210 Emmet Street South, Charlottesville, VA 22904, USA b Department of Kinesiology, University Park, PA 16802, USA  Corresponding author. Tel.: +1 434 243 8673; fax: +1 434 924 1389.
PII: S0966-6362(05)00281-X doi:10.1016/j.gaitpost.2005.12.009 © 2006 Elsevier B.V. All rights reserved. | |
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