Biomechanics of Ankle Instability. Part 1: Reaction Time to Simulated Ankle Sprain : Medicine & Science in Sports & Exercise

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Biomechanics of Ankle Instability. Part 1

Reaction Time to Simulated Ankle Sprain


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Medicine & Science in Sports & Exercise 40(8):p 1515-1521, August 2008. | DOI: 10.1249/MSS.0b013e31817356b6
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Several studies have identified the lateral ankle sprain as the most common injury in sports such as netball (19), volleyball (2), football (17), hockey (30), and basketball (9). Patients with ankle sprains account for approximately 5% of all patients visiting accident and emergency departments in the United Kingdom (18), and it is estimated that one lateral ankle sprain occurs daily for every 10000 people (6,29).

Rehabilitation programs enable the majority of patients to return ankle function to preinjury levels. The incidence of reinjuring a previously sprained ankle ranges between 35% and 79% (1,2,19), and previous work suggests that 32-40% of patients will develop symptoms of chronic lateral instability (13,14,26). Karlsson and Lansinger (22) believed that the factors responsible for functional instability are proprioceptive deficit, peroneal weakness, and subtalar joint instability. Safran et al. (33) argued that the loss of normal joint kinematics associated with functional instability contributes to recurrent injury and early degenerative changes within the ankle.

The reaction times of the peroneus longus (PL), peroneus brevis (PB), and tibialis anterior (TA) muscles to an ankle sprain mechanism have been examined together and separately in previous studies, but a variety of methods and the use of different control groups impair comparisons of the research outcomes. Lynch et al. (28) and Benesch et al. (5) looked at the PL, PB, and TA. Brunt et al. (7), Löfvenberg et al. (27), and Ebig et al. (11) examined the PL and the TA. Konradsen and Ravn (23), Karlsson et al. (21), Johnson and Johnson (20), Konradsen et al. (24), and Schmidt et al. (34) examined the reaction times of the PL and the PB. The extensor digitorum longus (EDL), which acts to assist in dorsiflexion and eversion of the foot, has not been included in previous research. The EDL is a muscle important in allowing the ankle to resist the plantarflexion and inversion movements involved in many instances of ankle sprain.

This study hypothesized that ankles with a history of unilateral functional ankle instability (FAI) would demonstrate slower reaction times to a simulated ankle sprain mechanism than the contralateral stable joint, and the stable joints of dominant and nondominant limbs of healthy controls. In addition, it was considered to be of interest to investigate whether muscular activity magnitude played a moderating role in the response of the limb to simulated ankle sprain.



A group of 44 sportsmen volunteered for the study and provided informed written consent to participation as required by the conditions of the university's ethical approval. Subjects completed a preparticipation health questionnaire, allowing identification of subject inclusion and exclusion criteria.

The exclusion criteria were as follows: (a) a self-reported balance or motion disorder, Ménière's disease, diabetes, any moderate or severe foot or muscular pain; (b) any open wounds on the foot; (c) any form of lower-extremity surgery; (d) required use of prescribed foot orthotics; (e) a lower-extremity biomechanical abnormality or any obvious bony or musculoskeletal deformity or asymmetry; and (f) bilateral ankle sprains. Six individuals were excluded; three presented with a history of bilateral ankle instability and three had undergone lower-extremity orthopedic surgery within the previous 2 yr. The remaining subjects all reported involvement in some form of sporting physical activity on a weekly basis.

According to the results of the health questionnaire, 19 subjects were assigned to the FAI group and 19 to the control group. Those in the FAI group were identified as having a history of unilateral chronic FAI, presented a history of at least two ankle sprains within the previous 2 yr, and at least three residual symptoms of ankle instability. The FAI group identified residual symptoms such as episodes of giving way, reduced range of motion, pain, instability, and weakness as a result of an ankle sprain. They had not experienced an ankle sprain in 6 months before taking part in the study. Thirteen reported functional instability in the left and six in the right ankle. Each member of the FAI group had one ankle identified as unstable (UA) and one as stable (SA).

The control group was free from any history of ankle sprain and any criteria for exclusion. On the basis of self-reported dominance, the control group had limbs identified as dominant (DA) or nondominant (NDA). In this way, any differences in muscular reaction time associated with limb dominance could be observed and reported, whereas left and right are arbitrary and nonfunctional terms. Means and SD of key physical characteristics are shown in Table 1.

Subjects characteristics (mean ± SD) and right (R) and left (L) limb dominance.

Passive and active motion in inversion, eversion, plantarflexion, and dorsiflexion were painless for each subject. No subject had observable edema in the ankle, lower leg, knee, or thigh. Palpation over the anterior talofibular ligament (ATFL) and the calcaneofibular ligament was painless for each subject. Subjects were asked not to consume alcohol in 24 h before testing.


EMG data from both limbs were recorded using a radiotelemetry system (MIE Medical Research Ltd, Leeds, United Kingdom). The differential preamplifiers had a gain of 4000, with a balance input impedance of 10 mΩ, a common mode rejection ratio of 110 dB, and a signal-to-noise ratio of −50 dB. The differential preamplifiers also had a frequency pass band of 6-330 Hz (3 dB point). Data were collected using Myodat™ 5.0 software (MIE Medical Research Ltd), interfaced with an Amplicon™ 12-bit analog-to-digital converter.

EMG data collection.

After preparatory procedures involving cleaning with medical isopropyl alcohol swabs and mildly abrading the skin surface with a disposable medical abrader, two Medicotest™ N-50-E single-use disposable electrodes were adhered to the skin surface at a 35-mm interelectrode spacing over the belly of each muscle, in line with the underlying muscle fiber alignment (10,35,37). Standard clinical muscle tests and active movements were used to identify muscle position and later to test the EMG activity of each muscle studied and the absence of cross talk interference (37). A common reference electrode was placed on the bony prominence of the lateral malleolus of each leg. Maximum voluntary isometric contraction (MVIC) may be used as a base against which to compare EMG activity in motor tasks, but there are acknowledged problems in this approach. In this study, it was decided not to use MVIC measurements; it was felt that the static MVIC measurement does not reflect muscle activity during forced dynamic movements such as an ankle sprain mechanism. Instead, the relative change in peak linear envelope EMG magnitude recorded by each specific muscle's electrodes was used in the analyses (37).

Purpose-built tilt platform.

A tilt platform was designed and constructed to simulate the lateral ankle sprain mechanism identified as the primary mechanism of injury of forced talocrural joint plantarflexion and subtalar joint inversion (24). The tilt movement consisted of two components from a neutral standing position: 3° of inversion in the frontal plane and 20° of plantarflexion in the sagittal plane (8). The platform was constructed with two movable plates so that either foot could be tilted independently, thus removing any subject anticipatory effect (Fig. 1).

Superior diagram of the tilt platform.

A switch detected the onset of the tilt mechanism, which sent an analog signal to the Amplicon™ 12-bit analog-to-digital converter card of the EMG system. The EMG system software allowed one EMG data channel to be allocated to record and display the tilt onset pulse. The pulse response time was ~2 ms. For safety reasons, the tilt platform was surrounded by a handrail to the front and both sides of the subject.

Experimental protocol.

Subjects carried out the following prescribed movements three times as a warm-up: plantarflexion, dorsiflexion, inversion, eversion, dorsiflexion/eversion, dorsiflexion/inversion, plantarflexion/eversion, and plantarflexion/inversion. The subjects stood barefoot on the platform with feet shoulder width apart in a relaxed stance, and bodyweight spread evenly between both feet. The two foot support bars were adjusted around each foot to provide maximum comfort, support, and safety. One limb at a time was randomly exposed to the unilateral simulated ankle sprain (USAS) and was identified during analyses of each trial as the tilted limb. The limb which was not exposed to the USAS in each trial was identified as the support limb. Each limb was exposed to the USAS six times in a random order. The limbs when acting as support were examined because ankles with FAI are required to function as a support limb in bipedal motion, and it was not known if an ankle with FAI would display deficits while acting as a support limb (Fig. 2).

Tilt platform with the near leg undergoing the inversion plantarflexion movement-simulating ankle strain.

Of 10 channels available with the Myodat™ 5.0 software, 4 recorded the EMG activity of four muscles on the limb exposed to the USAS, 4 recorded four muscles on the support limb, and 1 recorded the USAS onset pulse. Raw EMG traces for each movement were displayed on a monitor. The EMG responses and platform tilt (which simulated the ankle sprain mechanism) were recorded at a sampling frequency of 500 Hz for 10 s during which the tilt was initiated. The USAS tilt mechanism was initiated when the subject was relaxed and baseline EMG activity was observed. The end of each test was indicated with an auditory signal from the EMG software.

The EMG trace was displayed allowing calculation of baseline activity from an entire linear enveloped EMG from the beginning of the trial until 100 ms before the onset of activity. On the basis of the methods of Brunt et al. (7) and Ebig et al. (11), the first observable deviation from the baseline was identified as the onset pulse using a purpose-designed reliable computer-generated onset detection method using spreadsheets, formatting and macros from EXCEL™ that accurately identified EMG onset. Peak linear envelope EMG magnitudes were also recorded to allow comparison of muscle activation levels when ankles were exposed to the USAS mechanism.

Statistical analysis.

"Mixed between-within" subjects ANOVA with independent variables limb (tilt and support) and ankle (UA, SA, DA, and NDA) and dependent variable muscle reaction time were carried out. The alpha level was set at P < 0.05. Preplanned independent samples t-tests were used to locate differences in each muscle's reaction time. Due to the multiple comparisons being made between groups, a Bonferroni adjustment was carried out, and the alpha level was set at P < 0.025. Ankles were analyzed as independent variables following the protocol presented by Baumhauer et al. (3).


Reaction times of each muscle of the control group's tilt and support limbs to an ankle sprain mechanism are shown in Table 2. Although reaction times of the DA ankle muscles were consistently faster, there were no differences between the reaction times of the DA ankle and NDA ankle muscles (Table 2). Statistical analysis indicated that there was a significant main effect for the tilted limb exposed to USAS and the support limb (P < 0.05). Preplanned t-tests identified significant differences in reaction times for muscles in different ankle categories in Tables 3-5.

Control group's muscle reaction times (ms) of the tilt and support limbs to a simulated ankle sprain mechanism (mean ± SD).
Longer muscle reaction time (ms, mean ± SD) in UA of FAI group in tilted limb exposed to USAS.
Longer muscle reaction time (ms, mean ± SD) in UA compared to DA.
Longer tibialis anterior reaction time (ms, mean ± SD) in UA compared to NDA ankle in support.

Reaction times of the FAI group's tilt and support limbs to an ankle sprain mechanism indicated that the reaction times to the ankle sprain mechanism (tilt limb) of the UA ankle PL, PB, and TA were significantly slower that those of the stable ankle (Table 3), but EDL reaction time was similar. When comparing the unstable and stable ankles as a support limb, there was a trend for the stable ankle to react more quickly to the USAS mechanism, but further analyses located no significant difference.

Table 4 shows that significant differences were identified in the reaction time between the unstable and dominant ankles, respectively, as a tilt limb for PL, PB, and TA, but not for EDL. As a support limb, the reaction time of the unstable ankle's PL, TA, and EDL was slower than that of the dominant ankle.

There was no difference in the reaction time for any muscle between the unstable ankle and nondominant ankle when tilted (Table 5), but when acting as a support limb, the TA showed a slower reaction time (UA = 121.33 vs NDA = 92.05 ms).

The relative increase in EMG activity within each muscle in response to the ankle sprain mechanism was assessed (Table 6); however, there was no significant difference in the induced change in EMG magnitude elicited by the ankle sprain mechanism compared to support activity in any ankle category (DA, NDA, UA, and SA) under investigation.

Similar increases in each muscle's peak EMG magnitude (µV, mean ± SD) were evident for all ankle types with change from support to simulated ankle sprain exposure.


The lateral ankle sprain has been found to be one of the most common sports injuries (2,9,17,19,30), with 32-40% of individuals developing FAI (13,14,26). Numerous studies have examined the neuromuscular characteristics of FAI (5,7,11,20,21,24,27,28,34), and although studies have examined forces leading to ligament failure in cadaver ankles (8,32), no data identifying the forces associated with an ankle sprain in living humans exist. In addition, it is difficult to replicate the precise mechanisms of injury in a laboratory setting, such as stepping into a divot on a grass pitch or landing from a jump on another player's foot, and inversion ankle sprains rarely, if ever, occur while an individual stands with their weight evenly distributed between both limbs. However, it is widely accepted that the mechanism of injury for a lateral ankle sprain is talocrural joint plantarflexion and subtalar joint inversion (24).

Several tilt platforms are described within the literature. Some have only one tilting plate, allowing one predetermined limb to be tilted (6,16,22,28). Others have two movable plates so that the subject is unaware which side will tilt (8,20,24,27). Most platforms expose the limb to an inversion mechanism (7,20,22,24,27,34). Ebig et al. (11) carried out the only study within the literature, which used a combined plantarflexion and inversion mechanism to simulate the ankle sprain mechanism; however, the range of motion of the tilting mechanism was not identified. The purpose-built tilt platform used here elicited sudden, forced, and combined 30° inversion in the frontal plane and 20° plantarflexion in the sagittal plane.

The relevance of the current work lies in the fact that a tilt platform was designed to simulate an authentic ankle sprain mechanism of combined plantarflexion and inversion, while remaining within an injury free range of motion. In particular, the anterior talofibular ligament (ATFL) was put on stretch by the plantarflexion and inversion mechanism of the platform. Renström et al. (32) showed that strain increased in the ATFL with increasing plantarflexion, whereas Colville et al. (8) observed increased strain from neutral to 20° of plantarflexion and inversion. Woods et al. (38) observed that 73% of ankle sprains involve some form of disruption of the ATFL. Thus, putting the ATFL under stress with the mechanism induced by the tilt platform was essential.

Lynch et al. (28) encountered problems with the EMG evaluation of TA activity. They suggested that the lack of a large stimulus in the TA as an antagonist muscle after an inversion movement was the cause of reduced reproducibility. This problem did not arise here due to the combined plantarflexion and inversion movement involved. One assumes that the large plantarflexion component was profound enough to elicit a strong reproducible antagonistic response from the TA, which serves to invert and dorsiflex the ankle. As in the study by Löfvenberg et al. (27), the subjects were unaware of the ankle to experience the USAS tilt, thus encouraging equal distribution of body weight between the two platforms. In other studies, tilts were not randomized and equipment only allowed one limb to be tilted (12,31).

In this study, no significant difference in muscular reaction time of the four muscles when exposed to the USAS mechanism (tilt) was observed between the DA and NDA control limbs. This finding is important and is consistent with the findings of Goldie et al. (15) who found controls to be similar. The experimental and control groups were of similar mean age, height, and weight. Both groups participated in a similar level of physical activity per week. Equally, no subject presented with any criteria for exclusion from the study, which included a history of major lower-extremity injury of surgery. It is reasonable to assume that the only quantifiable clinical difference between the two groups was the experimental group's history of ankle sprain and functional instability. It follows that any differences in muscular reaction time between the two groups is associated in some way with the ankle sprain and symptoms of functional instability. If the controls had shown asymmetry, then it would be inappropriate to infer that any asymmetries in the experimental group were due to the residual symptoms of ankle sprain. Simply put, if healthy controls are asymmetric we cannot assume that asymmetry in the experimental group is because of the functional instability.

The reaction time for the EDL as a support limb was similar for the dominant and nondominant control ankles. Statistically, the controls were similar, which was a new finding as no previous research has examined muscular reaction time of contralateral support limbs to an ankle sprain mechanism. The mean reaction times of PL of 54.8 ms (DA) and 57.6 ms (NDA) were similar to the reaction times of 57 ms reported by Konradsen et al. (25) and of 49 ms by Löfvenberg et al. (27) for healthy controls. The times were faster than 65 ms described by Konradsen and Ravn (23), 65.3 ms described by Ebig et al. (11) 67.6 ms described by Johnson and Johnson (19), and 68.8 ms described by Karlsson et al. (21) respectively.

The mean reaction times of PB for healthy controls of 56.9 ms (DA) and 61 ms (NDA) were faster than reaction times presented by Konradsen and Ravn (23) of 69 ms and Karlsson et al. (22) of 81.6 ms. Differences in reaction times presented in different studies may be due to the differing methods of EMG onset detection sensitivity or similar methodological inconsistencies. The mean reaction times of TA found in this study for healthy controls of 55.8 ms (DA) and 60.2 ms (NDA) were slower than 49.2 ms found by Löfvenberg et al. (27) but faster than the 71.6 ms found by Ebig et al. (11). Previous data for EDL were not found within the literature.

In this study, significant differences were found between the stable and unstable ankles functioning as the tilt limb in the PL, PB, and TA. The unstable ankle PL reaction time was significantly slower and this finding is consistent with those from Konradsen and Ravn (23), Karlsson et al. (22), Löfvenberg et al. (27), and Vaes et al. (36) who also observed slower reaction times in functionally unstable ankles. It contrasts, however, with findings from Brunt et al. (7), Johnson and Johnson (20), Beckman and Buchanan (4), Ebig et al. (11), and Konradsen et al. (25) who all found no significant difference in PL reaction time between ankles with a history of chronic ankle sprain and healthy controls. It must be accepted that these studies each had different definitions of SA and functionally UA, contrasting subject recruitment methods, and diverse EMG activity onset detection methods, such as setting a very high EMG activity onset threshold.

The unstable ankle mean TA reaction time was significantly slower than the stable ankle, in agreement with results presented by Löfvenberg et al. (27) but contrasted with the findings of Ebig et al. (11) who found no significant difference in TA reaction time between ankles with a history of lateral ankle instability and healthy controls. Our finding and methodology are supported by the fact that the unstable ankle TA reaction time is similar to that reported in three other studies (11,12,27).

As a support limb, there was no significant difference between the unstable and stable ankles in the PL, PB, TA, or EDL. Very few studies have examined the effect of the contralateral support limb to an ankle sprain mechanism. Beckman and Buchanan (4) observed the reaction times of the gluteus medius and peroneals of both the tilt and support limbs to a lateral perturbation, although they did not compare them in the same way to the current study. Löfvenberg et al. (27) examined support limb reaction times of the PL and TA muscles and observed no significant difference between unstable and healthy control ankles.

It could be argued that support limb reaction times may have other as yet unknown influencing factors, which only further investigations may uncover. Support limbs are exposed to a different mechanism at ankle sprain than the tilt limb, but possibly any delayed reaction time would be apparent in an ankle whether it was functioning as a support or a tilt limb. The reactions of the muscles are associated with the functional roles and mechanical demands placed on them, and if the unstable ankle has deficits in exerting eversion and dorsiflexion mechanisms, this deficit may not transpose onto an inversion and plantarflexion mechanism. If both the unstable and stable ankles have pathologically delayed reaction times as support limbs, no significant differences may be apparent until the unstable ankle is compared with the dominant and nondominant control ankles. These results suggest that there is no change in muscular reaction time to an unloaded and everted movement (support), but there is when the ankle is loaded in a plantarflexed and inversion position (tilt).

It could be argued that it is the mechanism which is pathological and not the functional movement. As a result of a lateral ankle sprain and subsequent damage to the lateral ligaments, possibly mechanical instability exists in inversion of the subtalar joint but not in eversion because the medial deltoid ligaments were not compromised. Konradsen et al. (24) have already shown that a 10° eversion significantly delays reaction time. This links with the argument that if mechanoreceptor stretching occurs at a set fraction of subtalar joint motion then mechanical instability would increase postural sway and decrease muscular reaction time.

No significant differences were found in the unstable or stable ankles' EDL reaction times to the tilt mechanism. This suggests that although PL, PB, and TA may be affected by ankle sprain and functional instability, the EDL remains unaffected. This is a significant finding because the EDL functions to dorsiflex and evert the foot, which is the precise mechanism required to resist the lateral ankle sprain mechanism. In the experimental group, the unstable ankles had significantly slower reaction times in three of the four lateral muscles examined. If it is accepted that these muscles contribute in some way to the dynamic defense mechanism, then it suggests that the unstable ankles are at an increased risk of reinjury compared to the healthy controls.

Comparison between the unstable and dominant ankles as a tilt limb identified significant differences in three muscles. The unstable ankles were significantly slower in the PL, PB, and TA, whereas no significant difference was observed in the EDL. This finding was consistent with that of Löfvenberg et al. (27) who found the PL and TA of ankles with a history of ankle sprain to be significantly slower than healthy controls. Several studies have shown that ankles with a history of functional instability have significantly slower reaction times than healthy contralateral controls. However, the current finding shows that the unstable ankles had reaction time deficits compared to healthy control subjects with no history of ankle sprain or lower extremity injury. One can argue that it is the history of ankle injury that influences the reaction times of the injured ankles. Konradsen and Ravn (23) suggested that a shorter peroneal reaction time would protect the ankle from injury in a greater number of situations. That is a logical assumption, and it could be assumed that the subjects in the FAI group are at a greater risk of reinjuring their ankles as a result of their inherent reaction time deficits. Once again, the EDL remained unaffected by the history of ankle sprain and functional instability, because unstable and dominant ankles reaction times were similar.

Comparison of the unstable and dominant ankles as support limbs provided some interesting results. The unstable ankles were significantly slower in the PL, TA, and EDL, although there was no significant difference found in the PB. These are the first results of their kind and provide evidence that ankles with a history of functional instability as a result of lateral ankle sprain have deficits while acting as support limbs to a contralateral ankle sprain mechanism. This finding supports the argument that proprioceptive deficits are centered more locally in the mechanoreceptor-efferent loop and not a deficit in the higher control centers. Once again, it seems that the mechanoreceptors sense the changes in tension later in the unstable ankle. The reaction of the support limb to a contralateral ankle sprain mechanism is to accelerate toward the center of the base of support to dampen the ankle sprain mechanism. If it is accepted that this dampening mechanism of the support limb is part of the dynamic defense mechanism, then it is reasonable to assume that the ankle sprain subjects are at an increased risk of injuring their contralateral stable ankle. This is a new finding and may be the root cause of the occurrence of individuals who have bilateral ankle sprains, where previously a central deficit had been blamed.

Comparing the EMG magnitudes of the four muscles may identify their contribution to the dynamic defense mechanism. The dynamic defense mechanism is predominantly an eversion movement, which is indicated by the relative change in peak linear EMG magnitude of the PL, PB, and EDL. The dorsiflexion component of the dynamic defense mechanism is a smaller but critical component. The role of the TA as a dorsiflexor in the dynamic defense mechanism is less than that of EDL. There was a trend for the TA of both the unstable and stable ankles to present a larger relative change in peak linear envelope EMG magnitude than both control ankles, but these differences were not statistically significant. It may be speculated that because of the existing deficits in the evertors, the experimental ankles rely more heavily on a dorsiflexion contribution from the TA to the dynamic defense mechanism. Further research is required in this area to examine if these differences are related to single-limb postural sway.

As a tilt limb, there was no significant difference in the reaction times of the unstable and dominant ankles in the EDL. It seems that the EDL makes a significant contribution to the dynamic defense mechanism but experiences none of the deficit in reaction time as a result of ankle sprain observed in the peroneal muscles. This finding has substantial implications in the rehabilitation of the ankle after lateral ankle sprain. Rehabilitation of a lateral ankle sprain should include strengthening the evertors (peroneals and EDL) at the subtalar joint and the dorsiflexors (TA and EDL) at the talocrural joint.


This investigation identified deficits in neuromuscular control in ankles with FAI, exhibited as slower reaction times when exposed to USAS and when acting as a support limb compared to healthy stable controls. The slower reaction times when acting as a support limb seen in the unstable ankle may put the contralateral stable ankle at an increased risk of ankle sprain. Our findings suggest that EDL plays a significant role in the dynamic defense mechanism but seems to experience none of the deficits in reaction time observed in the peroneals of individuals with FAI. It would seem that focusing solely on peroneal rehabilitation is inappropriate. Instead, evertor and dorsiflexor rehabilitation exercises should be undertaken, which acknowledge the functional roles of both the peroneals and EDL in the dynamic defense mechanism.

This study was conducted at the University of Chichester, Chichester, West Sussex. No author or related institution has received financial benefit from research in this study.


1. Aagaard H, Scavenius M, Jørgensen U. An epidemiological analysis of the injury pattern in indoor and in beach volleyball. Int J Sports Med. 1997;18:217-21.
2. Bahr R, Bahr IA. Incidence of acute volleyball injuries. A prospective cohort study of injury mechanisms and risk factors. Scand J Med Sci Sports. 1997;7:166-71.
3. Baumhauer JF, Alosa DM, Renström Per AFH, Trevino S, Beynnon BA. A prospective study of ankle injury risk factors. Am J Sports Med. 1995;23:564-70.
4. Beckman SM, Buchanan TS. Ankle inversion injury and hypermobility. Effect on hip and ankle muscle electromyography onset latency. Arch Phys Med Rehabil. 1995;76:1138-43.
5. Benesch S, Pütz W, Rosenbaum D, Becker H. Reliability of peroneal reaction time measurements. Clin Biomech. 2000;15:21-8.
6. Brooks SC, Potter BT, Rainey JB. Treatment for partial tears of the lateral ligament of the ankle. A prospective trial. BMJ. 1981;282:606-7.
7. Brunt D, Andersen JC, Huntsman B, Reinhert LB, Thorell AC, Sterling JC. Postural responses to lateral perturbations in healthy subjects and ankle sprain patients. Med Sci Sports Exerc. 1992;24(2):171-6.
8. Colville MR, Marder RA, Boyle JJ, Zarins B. Strain measurements in the lateral ankle ligaments. Am J Sports Med. 1990;18:196-200.
9. Deitch JR, Starkey C, Walters SL, Moseley JB. A comparison of Women's National Basketball Association and National Basketball Association athletes. Am J Sports Med. 2006;34:1077-83.
10. Dyson RJ, Buchanan M, Farrington TA, Hurrion P. Electromyographic activity during windsurfing on water. J Sports Sci. 1996;14:125-30.
11. 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 Sports Phys Ther. 1997;26:73-7.
12. Eils E, Rosenbaum D. A multi-station proprioceptive exercise program in patients with ankle instability. Med Sci Sports Exerc. 2001;33(12):1991-8.
13. Freeman MA, Dean MR, Hanham IW. The etiology and prevention of functional instability in the foot. J Bone Joint Surg Br. 1965;47-B:678-85.
14. Gerber JP, Williams GN, Scoville CR, Arcierio RA, Taylor DC. Persistent disability associated with ankle sprains. A prospective examination of an athletic population. Foot Ankle Int. 1998;19:653-60.
15. Goldie PA, Evans OM, Bach TM. Steadiness in one-legged stance: development of a reliable force platform testing procedure. Arch Phys Med Rehabil. 1992;73:348-54.
16. Grüneberg C, Nieuwenhuijzen PH, Duysens JA. Reflex responses in the lower leg following landing impact on an inverting and non-inverting platform. J Physiol. 2003;550:985-93.
17. Hawkins RD, Fuller CW. A prospective epidemiological study of injuries in four English professional football clubs. Br J Sports Med. 1999;33:196-203.
18. Heyworth J. Ottawa ankle rules for the injured ankle. Br J Sports Med. 2003;37:194.
19. Hopper D, Elliott B, Lalor JA. A descriptive epidemiology of netball injuries during competition. A five-year study. Br J Sports Med. 1995;29:223-8.
20. Johnson MB, Johnson CL. Electromyographic response of peroneal muscles in surgical and nonsurgical injured ankles during sudden inversion. J Orthop Sports Phys Ther. 1993;18:497-501.
21. Karlsson J, Peterson L, Andreasson G, Högfors C. The unstable ankle. A combined EMG and biomechanical modelling study. Int J Sports Biomech. 1992;8:129-44.
22. Karlsson J, Lansinger O. Chronic lateral instability of the ankle in athletes. Sports Med. 1993;16:355-65.
23. Konradsen L, Ravn JB. Prolonged reaction time in ankle instability. Int J Sports Med. 1991;12:290-2.
24. Konradsen L, Voight M, Højsgaard C. Ankle inversion injuries. The role of the dynamic defence mechanism. Am J Sports Med. 1997;25:54-8.
25. Konradsen L, Olesen S, Hansen HM. Ankle sensorimotor control and eversion strength after acute ankle inversion injuries. Am J Sports Med. 1998;26:72-7.
26. Konradsen L, Bech L, Ehrenberg M, Nickelsen T. Seven years follow-up after ankle inversion trauma. Scand J Med Sci Sports. 2002;12:129-35.
27. 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;23:414-7.
28. Lynch SA, Eklund V, Gottlieb D, Renström Per AFH, Beynnon B. Electromyographic latency changes in the ankle musculature during inversion moments. Am J Sports Med. 1996;24:362-9.
29. McCulloch PG, Holden P, Robson DJ, Rowley DI, Norris SH. The value of mobilization and non-steroidal anti-inflammatory analgesia in the management of inversion injuries of the ankle. Br J Clin Pract. 1985;39:69-72.
30. Murtaugh K. Injury patterns among female field hockey players. Med Sci Sports Exerc. 2001;33(2):201-7.
31. 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. Am J Sports Med. 2001;29:627-32.
32. Renström P, Wertz W, Incavo S, et al. Strain in the lateral ligaments of the ankle. Foot Ankle. 1988;9:59-63.
33. Safran MR, Benedetti RS, Bartolozzi AR, Mandelbaum BR. Ankle sprains: a comprehensive review. Part 1. Med Sci Sports Exerc. 1999;31(7 suppl):S429-37.
34. Schmidt R, Gergrou H, Friemert B, Herbst A, Claes I. The peroneal reaction time-reference data in a healthy sample population. Foot Ankle Int. 2005;26:382-6.
35. Smith NAS, Dyson RJ, Hale T. Lower extremity muscular adaptations to curvilinear motion in soccer. J Hum Movement Stud. 1997;33:139-53.
36. Vaes P, van Gheluwe B, Duquet W. Control of acceleration during sudden ankle supination in people with unstable ankles. J Orthop Sports Phys Ther. 2001;31:741-52.
37. Winter DA. Biomechanics and Motor Control of Human Movement. Hoboken (NJ): John Wiley; 2005. p. 243-52.
38. Woods C, Hawkins R, Hulse M, Hodson A. The Football Association Medical Research Program: an audit of injuries in professional football: an analysis of ankle sprains. Br J Sports Med. 2003;37:233-8.


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