The Effect of Lateral Ankle Sprain on Dorsiflexion ...

The Effect of Lateral Ankle Sprain on Dorsiflexion Range of Motion, Posterior Talar Glide, and Joint Laxity

Journal of Orthopaedic & Sports Physical Therapy® Downloaded from www.jospt.org at on December 31, 2015. For personal use only. No other uses without permission. Copyright © 2002 Journal of Orthopaedic & Sports Physical Therapy®. All rights reserved.

Craig R. Denegar, PT, PhD, ATC1 Jay Hertel, PhD, ATC2 Jose Fonseca, MS, ATC3

Study Design: Retrospective study. Objective: Assess range of motion, posterior talar glide, and residual joint laxity following ankle sprain in a population of athletes who have returned to unrestricted activity. Background: Lateral ankle sprains occur frequently in athletic populations and the reinjury rate may be as high as 80%. In an effort to better understand risk factors for reinjury, the sequelae to injury in a sample of college athletes were assessed. Methods and Measures: Twelve athletes with a history of lateral ankle sprain within the last 6 months and who had returned to sport participation were tested. Only athletes who reported never injuring the contralateral ankle were included. The injured and uninjured ankles of subjects were compared for measures of joint laxity, ankle dorsiflexion range of motion, and posterior talar glide. Friedman’s test of rank order was used to analyze the laxity measures and a MANOVA was used to assess the dorsiflexion and posterior talar glide measures. Results: Laxity was significantly greater at the talocrural and subtalar joints of the injured ankles. There were no significant differences in any of the ankle dorsiflexion measurements between injured and uninjured ankles, but posterior talar glide was significantly reduced in injured ankles as compared to uninjured ankles. Conclusion: In our sample of subjects, residual ligamentous laxity was commonly found following lateral ankle sprain. Dorsiflexion range of motion was restored in the population studied despite evidence of restricted posterior glide of the talocrural joint. Although restoration of physiological range of motion was achieved, residual joint dysfunction persisted. Further research is warranted to elucidate the role of altered arthrokinematics after lateral ankle sprain. J Orthop Sports Phys Ther 2002;32:166–173.

Key Words: arthrokinematic motion, inversion ankle sprain, ligamentous laxity

1

Associate professor, Departments of Kinesiology and Orthopaedics & Rehabilitation, The Pennsylvania State University, University Park, PA. 2 Assistant professor of Kinesiology, Athletic Training Research Laboratory, The Pennsylvania State University, University Park, PA. 3 Assistant athletic trainer, East Tennessee State University, Johnson City, TN. (Master’s student in kinesiology at The Pennsylvania State University, University Park, PA, at the time of this study.) This study was approved by the Institutional Review Board of The Pennsylvania State University at University Park. Send correspondence to Craig Denegar, Penn State University, 269 Recreation Building, University Park, PA 16802. E-mail: [email protected] 166

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ateral ankle sprains are the most common injury suffered during sports participation and are typically due to inversion trauma.1,5,6,11,21,23,26 While not permanently disabling, these injuries are costly25 and can have a considerable effect on the athlete’s ability to train and compete. Moreover, the recurrence rate of ankle injuries has been reported to be as high as 80% among athletes.23 Thus, a lateral ankle sprain often plagues the athlete long after recovery from the initial injury. Sports medicine practitioners strive to return injured athletes to sport participation quickly while minimizing the risk of recurrence. After injury, clinical examination often reveals a loss of the ability to forcefully evert the ankle, compromised proprioception and neuromuscular control, a loss of range of motion, and ligamentous laxity.21 Through rehabilitation, function of the ankle complex is restored and the athlete is typically able to return to unrestricted physical activity. While incomplete rehabilitation after sprain may leave the ankle more susceptible to further injury,10 reinjury is still common after completion of a structured progression of rehabilitative activities.

Journal of Orthopaedic & Sports Physical Therapy


METHODS Subjects A convenience sample of collegiate student-athletes (7 women and 5 men) ages 18 to 22 years (mean age for women 19.3 ± 1.4 years; mean age for men 19.8 ± 1.3 years), volunteered to participate in this study. Potential participants were made aware of the inclusion criteria for this study through advertisements and direct contact with staff athletic trainers. The inclusion criteria for this study were (1) a history of a lateral ankle sprain in the past 6 months for which rehabilitative care was received to expedite a return to sport; (2) no history of lateral ankle sprain contralaterally; (3) no history of fracture or surgery to either ankle; and (4) a return to full activity prior to participation in this study. Because subjects were recruited retrospectively and initially assessed by a variety of medical and allied medical professionals, no attempt was made to classify the severity of each individual’s injury. Subsequent to institutional approval of the study, all subjects provided informed consent in compliance with the university guidelines.

Instrumentation We used a fluid-filled bubble inclinometer (Fabrication Enterprises Incorporated, Irvington, NY) to measure range of motion. This inclinometer was custom fitted with Velcro hooks to adhere to a Velcro strap wrapped around the subject’s leg. The reliability of measures of ankle dorsiflexion with a fluid goniometer has been previously classified good by Rome and Cowieson,20 who found the device superior to a standard goniometer.

Procedures Subjects reported to The Pennsylvania State University Athletic Training Research Laboratory for testing. The subject’s ankle joint laxity, range of motion, and arthrokinematic motion were then examined. Measurements were taken in the same order for all subjects. Both examiners were masked to the involved and uninvolved ankles. No warm-up or stretching activities preceded the measurement, though all subjects had walked some distance to enter the laboratory. None had completed an exercise bout within 2 hours prior to participating in this study. Three physical exam techniques were performed on each of the subject’s ankles to assess joint laxity. Laxity estimates were recorded on a 5-point scale 167

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J Orthop Sports Phys Ther • Volume 32 • Number 4 • April 2002

of joint laxity similar to those found in previous reports on the sequelae of lateral ankle sprain.

RESEARCH

The factors responsible for the high risk of reinjury are not fully understood. Several investigators have identified previous injury as a strong predictor of these injuries.2–4,16,23 A loss of ankle dorsiflexion has also been implicated as a risk factor for recurrent ankle sprain, however, investigation of the relationship between heel cord flexibility and ankle sprains has been limited.2–4,13,18,27 Dorsiflexion range of motion can potentially be limited by tightness in the muscles that plantar flex the ankle, particularly the gastrocnemius and soleus, capsular and soft tissue restrictions, loss of normal posterior glide of the talus in the mortise, and loss of other accessory motions at the tibiofibular, subtalar, and midtarsal joints. Leanderson et al13 reported that dorsiflexion range of motion did not differ between injured and uninjured ankles of basketball players, but that basketball players had significantly less dorsiflexion range of motion than a group of physically active subjects without history of ankle sprain. Green et al8 reported that early (less than 72 hours after injury) posterior talocrural joint mobilization in the treatment of lateral ankle sprains resulted in more rapid restoration of dorsiflexion range of motion and normal walking gait than conventional treatment (eg, ice, compression, elevation, and crutch use). These investigators did not, however, assess the amount of posterior talar glide in the patients they treated with or without joint mobilization at the completion of the rehabilitation regimen.8 Nor was the mechanism by which mobilization of the talus improved dorsiflexion range of motion clearly identified in the study by Green et al.8 It is possible that because the talus lacks muscular attachments, it has a propensity towards anterior subluxation following disruption of the ligaments which attach to it. Following injury to the anterior talofibular ligament, the talus may be allowed to subluxate anteriorly and remain malpositioned until it is passively returned to its ‘‘normal’’ position. While the concepts of positional faults and restricted arthrokinematics are accepted in manual therapy circles, there is a clear lack of empirical evidence from clinical investigations to support these hypotheses of joint dysfunction. Given the high rate of reinjury, the limited research on range-of-motion restrictions following lateral ankle sprain, and the implication of restricted posterior talar glide following injury, there is a need for greater understanding of motion restrictions following lateral ankle sprains. The objective of this study was to measure ankle dorsiflexion range of motion and the amount of posterior talar glide of athletes who had suffered a unilateral ankle sprain, completed a rehabilitation program, and returned to competition. We also assessed talocrural and subtalar joint stability to ascertain whether the examined ankles demonstrated patterns


(0 = hypomobile, 1 = normal, 2 = mild laxity, 3 = moderate laxity, and 4 = gross laxity) defined by the examiner. The 3 laxity tests were an anterior drawer test, a talar tilt test, and a medial subtalar glide test.9 These were selected based on a previous report of good agreement between stress fluoroscopy and test results in a population with a history of lateral ankle sprain.9 The grading scale was modified to include ‘‘hypomobile,’’ based on previous experience in our laboratory, where less laxity has occasionally been observed in a previously injured ankle when compared to an uninjured, contralateral ankle. Joint laxity tests were repeated as needed for the examiner to be confident of the findings, but in no case was a test repeated more than twice. All tests were performed with the subject sitting with legs hanging off the end of an examining table. For the anterior drawer test the examiner stabilized the lower leg, held the subject’s foot at approximately 20° of ankle plantar flexion, and drew the talus forward in the ankle mortise. The talar tilt test was performed with the subject’s foot held in a neutral sagittal plane position while the examiner tilted the rearfoot into inversion. The medial subtalar glide test, as described for joint mobilization by Loudon and Bell14 and advocated and illustrated as an assessment technique by Hertel et al,9 was performed. The foot was held in a neutral position with the talus stabilized while the examiner glided the calcaneus medially in the transverse plane.9,14 The second portion of the study included measurement and recording of ankle dorsiflexion range of motion. Dorsiflexion measurements were taken in 4 different positions and were repeated and recorded 3 times in each position. The 4 positions were sitting straight knee (SSK), prone bent knee (PBK), standing straight knee (STSK), and standing bent knee (STBK). The first 2 measurements were taken with the Velcro strap secured around the subject’s foot and the inclinometer adhered to the strap facing in a lateral direction (Figures 1 and 2). The SSK measurement was taken with the knee joint in terminal extension, with the subject seated on the examining table and the distal half of the lower leg extending past the edge of the table (Figure 1). Following the placement of the inclinometer, the patient was asked to relax as the examiner passively dorsiflexed the talocrural joint until a restriction was met which was indicated by a firm end point. The angle of dorsiflexion was then recorded. The PBK measurement was performed with the subject lying prone, with the knee flexed to 90°. Following the placement of the inclinometer, the patient was again asked to relax as the examiner passively dorsiflexed the talocrural joint until a restriction was met, which was indicated by a firm end point. The angle of dorsiflexion was then recorded. 168

FIGURE 1. Measurement of ankle dorsiflexion with sitting straight knee method.

FIGURE 2. Measurement of ankle dorsiflexion with prone bent knee method.

The two standing measurements were taken with the Velcro strap secured just above the talocrural joint and around the subject’s lower leg, with the inclinometer adhered to the strap and facing in a lateral direction (Figures 3 and 4). To zero the inclinometer, the subject was asked to stand on the examining table with feet shoulder-width apart and relaxed. STSK ankle dorsiflexion was measured with the knee joint in terminal extension while the subject stood on the examining table with one foot held in front of the other (Figure 3). The foot of the limb being tested was aligned so that it was parallel with the long axis of the lower leg in the transverse plane (not internally or externally rotated) and in a neutral position in the frontal plane (not inverted or everted). The subject was instructed to keep the knee of the more posterior leg in extension while slowly leaning forward. The measurement was taken once the subject’s heel began to rise off the examining table. The STBK measurement was also taken with the subject standing on the examining table. The subject was instructed to slowly perform a single leg squat by flexing the hip and knee joints (Figure 4). To maintain balance, the subject was instructed to hold on to a post. Once again, the measurement J Orthop Sports Phys Ther • Volume 32 • Number 4 • April 2002

FIGURE 3. Measurement of ankle dorsiflexion with standing straight knee method.


was taken once the subject’s heel began to rise off the examining table or once the subject could not lower himself or herself any further. For each dorsiflexion range-of-motion measurement, the evaluator verbally reported the measurement to a recorder, instructed the subject to relax, and then repositioned the subject. The subjects were instructed to assume a position as depicted in the figures. Without controlling the orientation of the foot and leg in the frontal and transverse planes, the subjects made an effort to achieve maximal dorsiflexion motion. All three measurements were taken in one position before testing in the next position. The final measurement assessed posterior glide of the talus. This measurement was taken with the Velcro strap secured just above the talocrural joint around the subject’s lower leg, and the inclinometer adhered to the strap facing in a lateral direction (Figure 5). This measurement was performed using an assessment of passive knee flexion during dorsiflexion of the ankle, with the subtalar joint maintained in neutral. The subject was instructed to sit on the end of the examining table and relax. Following the placement of the inclinometer, the subject’s foot was placed into a subtalar neutral position

The intratester reliability for each of the 5 rangeof-motion measurements was estimated by calculating intraclass correlation coefficients (ICC3,1)22 and standard error of measurements. Reliability was estimated separately for measures on the injured and uninjured limbs. The joint laxity measurements between injured and uninjured ankles were compared using Friedman’s test of rank order. The following separate analyses were conducted on each physical exam test: anterior drawer, talar tilt, and medial subtalar glide. Data were then analyzed to identify differences in posterior talar glide and ankle dorsiflexion measurements between the injured and uninjured ankles. Means of the three trials of each range-of-motion measurement were calculated for the injured and uninjured ankles. A 1-factor repeated-measures MANOVA was performed on the dorsiflexion angle and posterior talar glide measurements with the limb


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Data Analysis

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FIGURE 4. Measurement of ankle dorsiflexion with standing bent knee method.

while the examiner gently pushed the talus posteriorly, and the ankle into dorsiflexion, until a firm capsular end-feel was encountered.7,19 Once the examiner felt a restriction in movement, indicated by a firm end point, the movement was halted and the angle of knee flexion recorded. In this position, posterior displacement of the talus is accompanied by passive knee flexion. When the talus can no longer be displaced posteriorly, the ankle cannot be further dorsiflexed and further passive knee flexion is limited. Thus, the angle of passive knee flexion provides an estimate of posterior talar glide.7,19 Measurements were repeated and recorded 3 times.

RESEARCH

FIGURE 5. Measurement of posterior talar glide. The angle of knee flexion is measured when restriction of posterior glide of the talus is felt by the examiner.7,19

DISCUSSION

as the independent variable. Post hoc analyses were performed using paired t-tests with Rom’s method of the Bonferroni adjustment. The level of significance was preset at 0.05 for all analyses. All statistical analyses were performed using SPSS 8.0 statistical software (SPSS Incorporated, Chicago, IL).

The joint laxity observed in our sample suggests that most of our subjects had sustained some degree of ligamentous injury, and that the subjects we assessed were typical of young adults following an ankle sprain.9,15 Unilateral laxity was present at both the subtalar and talocrural joint in the majority of the subjects’ injured ankles, suggesting that after ankle sprain there is a pattern of biarticular laxity.9,15,21

RESULTS Reliability Measures


Intratester reliability estimates for the range-ofmotion measures, including assessment of posterior gliding of the talus, ranged from 0.88 to 0.99 with standard errors of measurement between 0.34° and 2.00° (Table 1).

TABLE 1. Intratester reliability estimates on range of motion measurements on injured and uninjured ankles. Test

ICC*

SEM**

Laxity Measurements

Dorsiflexion, sitting, straight knee, injured

.96

1.34°

Significant differences in joint laxity between injured and uninjured ankles were found for the anterior drawer test (␹2 = 5.33, df = 1, P = 0.02), the talar tilt test (␹2 = 4.46, df = 1, P = 0.04), and the medial subtalar glide test (␹2 = 5.44, df = 1, P = 0.02). Results of the physical exam tests can be seen in Table 2.

Dorsiflexion, sitting, straight knee, uninjured

.97

.99°

Dorsiflexion, prone, bent knee, injured

.97

.96°

Dorsiflexion, prone, bent knee, uninjured

.97

1.10°

Dorsiflexion, standing, straight knee, injured

.98

.86°

Dorsiflexion, standing, straight knee, uninjured

.99

.58°

Dorsiflexion, standing, bent knee, injured

.99

.54°

Dorsiflexion, standing, bent knee, uninjured

.98

.96°

Knee flexion with posterior talar glide, injured

.88

2.00°

Knee flexion with posterior talar glide, uninjured

.99

.34°

Range of Motion Measurements The repeated measures MANOVA revealed a significant main effect for injury history (Wilks ␭ = .215; df = 5, 7; P = 0.03). Post hoc analysis revealed a significant difference in measurement of passive knee flexion obtained during the posterior talar glide test between injured and uninjured ankles (P ⬍ 0.01). No significant differences were found between groups for the SSK (P = 0.22, 1 ⫺ ␤ = 0.78), PBK (P = 0.58, 1 ⫺ ␤ = 0.92), STSK (P = 0.94, 1 ⫺ ␤ = 0.95), or STBK (P = 0.18, 1 ⫺ ␤ = 0.74) dorsiflexion measurements. Means and standard deviations of the range-of-motion measurements are listed in Table 3.

*Intraclass correlation coefficients. **Standard error of measurement.

TABLE 2. Number of cases by laxity classification, limb and stress test. Joint Mobility Tests Anterior Drawer*

Talar Tilt*

Medial Subtalar Glide*

Degree of Laxity

Injured

Uninjured

Injured

Uninjured

Injured

Uninjured

4 3 2 1 0

0 3 5 3 1

0 0 1 11 0

0 6 3 1 2

0 0 1 11 0

0 3 5 3 1

0 0 1 11 0

*Significant difference between injured and uninjured limbs (P ⬍ 0.05) 0 1 2 3 4

= = = = =

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hypomobile normal mild laxity moderate laxity gross laxity J Orthop Sports Phys Ther • Volume 32 • Number 4 • April 2002

TABLE 3. Means and standard deviations of dorsiflexion range of motion measurements (in degrees). Limb Movement SSK PBK STSK STBK GLIDE*

Injured

Uninjured

17.4 ⫾ 6.7 16.4 ⫾ 5.5 22.8 ⫾ 6.1 24.5 ⫾ 5.6 8.0 ⫾ 5.8

15.2 ⫾ 5.7 17.2 ⫾ 6.4 22.8 ⫾ 5.6 27.4 ⫾ 6.8 16.6 ⫾ 3.4


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REPORT

Green et al8 reported a more rapid restoration of dorsiflexion range of motion and normalization of gait in patients treated with posterior talar mobilization following lateral ankle sprain. Their findings suggest that an anterior displacement of the talus or a loss of posterior talar glide, or both, may occur following a lateral ankle sprain. To our knowledge, residual restriction of posterior talar glide following ankle sprain has not been previously reported. Loss of dorsiflexion range of motion is a common observation following lateral ankle sprain and has been suggested to be a risk factor for reinjury.2–4,13,18,27 Limitations in dorsiflexion range of motion can be caused by a lack of gastrocnemius and soleus flexibility or accessory motion restrictions.7,19 It has been hypothesized that restricted posterior glide of the talus on the mortise as well as restricted accessory motions at the tibiofibular, subtalar, or midtarsal joints, or any combination thereof, may limit ankle dorsiflexion.7,19 We observed bilaterally comparable dorsiflexion range of motion in our subject population, despite findings of restricted posterior talar glide on the injured side. We believe that muscle flexibility limitations would have been detected in the dorsiflexion range-of-motion assessments. By constraining subtalar motion, and gliding the talus posteriorly until a firm end-feel was engaged, a restriction in dorsiflexion was detected that cannot be attributed to a lack of flexibility of the gastrocnemius and soleus. Therefore, subjects appear to have achieved normal physiological dorsiflexion range of motion, despite restricted posterior glide of the talus on the mortise. The mechanisms of this apparent arthrokinematic compensation are unclear. Potential explanations for normal ankle dorsiflexion despite restricted posterior glide of the talus include hypermobility at other joints or rotation about an abnormal instantaneous axis of rotation at the talocrural joint. While hypermobility of joints other than the talocrural joint is a plausible explana-

RESEARCH


*Significant difference between injured and uninjured limbs (P ⬍ 0.05). SSK = sitting straight knee PBK = prone bent knee STSK = standing straight knee STBK = standing bent knee GLIDE = assessment of posterior talar glide through passive knee flexion during dorsiflexion with subtalar joint maintained in neutral

tion for our findings, the purpose of our study was to solely examine talocrural joint function. We did not assess accessory motion at joints other than the talocrural joint, and are thus unable to comment on the adaptations that may have occurred at other joints. An abnormal restrictive barrier to accessory motion changes the normal pattern of movement of a joint’s instantaneous axis of rotation.24 Under normal conditions, as two articulating bones glide on one another, the instantaneous axis of rotation of the joint changes accordingly. For example, as the talus glides posteriorly on the mortise, the instantaneous axis of rotation of the talocrural joint also translates posteriorly. If a restrictive barrier is encountered which limits accessory motion, the instantaneous axis of rotation becomes fixed by this restriction. Further motion thus occurs around an abnormal axis leading to subsequent joint dysfunction. At the talocrural joint, restricted posterior glide of the talus results in an abnormally anterior instantaneous axis of rotation. While full dorsiflexion range of motion may still occur, it is not necessarily reflective of normal arthrokinematic function. The impact of this joint dysfunction on performance and risk of reinjury has not been explored and is beyond the scope of this paper. The residual loss of posterior talar glide may represent a positional fault. The concept of a positional fault following lateral ankle sprain is not new. Mulligan17 has proposed that some individuals diagnosed with lateral ankle sprains experience an anterior subluxation of the distal fibula on the tibia. Kavanagh12 has provided evidence that this may occur in some cases of lateral ankle sprain. While the distal fibula may subluxate, there is currently a lack of empirical evidence that this phenomenon occurs in all episodes of lateral ankle sprain.12 Another possibility may be that a positional fault of the talus occurs in some individuals after lateral ankle sprain. Our methods did not allow us to establish the resting position of the talus. We did, however, identify a pattern of restricted posterior and excessive anterior glide of the talus. If the talus were subluxated anteriorly, posterior glide could be restricted because the talus is ‘‘stuck’’ anteriorly, while anterior translation of the talus beyond normal end range could be present due to damage to the anterior talofibular ligament. This hypothesis is speculative and must be further studied. Our findings, and those of Green et al,8 have implications for rehabilitation following lateral ankle sprains, as well as the risk of reinjury. All of the athletes we studied had completed a rehabilitation program as directed by their physician under the supervision of a certified athletic trainer, and had returned to sport participation. Furthermore, all had performed some form of heel-cord stretching. None,


however, had received joint mobilization of the talocrural complex. Despite the return to sports and evidence of restoration in dorsiflexion range of motion, there was restriction of posterior talar mobility in most of the injured ankles. Posterior talar mobilization shortens the time required to restore dorsiflexion range and a normal gait.8 Without posterior talar mobilization, dorsiflexion range of motion may be restored through excessive stretching of the plantar flexors, excessive motion at surrounding joints, or forced to occur through an abnormal axis of rotation at the talocrural joint. We acknowledge that the reliability and validity of the assessment of posterior talar glide has not been previously established. Our data suggest high reliability with small standard error of measurement. This method of assessing posterior glide of the talus was chosen because we could generate interval data through the use of fluid goniometry. We could have attempted to categorize posterior talar mobility in the same manner that talocrural and subtalar joint laxity were assessed. In those cases, however, good agreement between physical exam and fluoroscopic images has been previously reported.9 Thus, we elected to quantify posterior talar glide using a previously described mobilization technique, rather than attempting to subjectively grade the posterior mobility of the talus. It must be noted that the validity of our assessment of posterior talar glide has not been confirmed with imaging studies, and that the results of our study must be interpreted accordingly.

Clinical Applications Physical therapists, athletic trainers, and others involved in the athlete’s care often recommend weightbearing and non–weight-bearing stretching exercises for the gastrocnemius-soleus complex to restore dorsiflexion after lateral ankle sprain. Our results suggest that these therapeutic exercises and the passage of time restore dorsiflexion range of motion but not normal talocrural joint arthrokinematics. While more study of talocrural joint restrictions and the risk of reinjury following lateral ankle sprain is clearly needed, our results and those of Green et al8 suggest that (1) a restriction of talocrural arthrokinematics may be common following lateral ankle sprain; (2) the restriction may persist despite restoration of dorsiflexion range of motion; and (3) treatment of such restrictions may need to be considered in the rehabilitation following lateral ankle sprain.

CONCLUSION The optimal treatment of lateral ankle sprains in athletes remains an enigma. Recent studies have in172

vestigated the presence of altered arthrokinematics after ankle sprain.8,12 We attempted to assess ligament laxity, dorsiflexion range of motion, and posterior talar glide in a population of athletes who had returned to participation following ankle sprain and found evidence of increased joint laxity and restored dorsiflexion, but restricted posterior talar glide in the injured ankles. Our measure of quantifying posterior talar glide has not been previously reported for experimental purposes and the validity of this measure may be open to criticism. These results should be interpreted accordingly. Further research is clearly warranted to investigate the role of arthrokinematic changes following lateral ankle sprain.

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