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.
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.
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Keywords:©2008The American College of Sports Medicine
DOMINANCE; LIGAMENT; PLATFORM; TILT; TIME