February 2010

Data suggest proximal links to ankle instability

Research suggests that individuals with chronic ankle instability are also likely to have impaired neuromuscular function at the knee and hip – findings that could change your approach to preventing recurrent ankle sprains.

by Phillip A. Gribble, PhD, ATC

Ankle sprain is one of the most common injuries in the physically active population.1-3 Although ankle sprains often are viewed as mild injuries, with an estimated 23,000 ankle sprains/day in the United States,4 they do represent a significant public health problem. At the high school level, ankle sprain is among the most common of all lower extremity injuries5, and it is the most common injury in collegiate men’s and women’s basketball and women’s volleyball.6

The primary predisposing factor to suffering an ankle sprain is a history of previous sprain.7 It has been estimated that between 30% and 70% of those who suffer a first time ankle sprain will develop chronic ankle instability (CAI).8, 9 Two subcategories of CAI include mechanical ankle instability (MAI), which describes the loss of structural integrity of the ligamentous and other articular structures that provide static stability to the ankle complex, and functional ankle instability (FAI),  which relates to difficulty with activities requiring the use of the ankle as well as feelings of “giving way” at the ankle during these activities.10

Although the problem of CAI is well-recognized, research is ongoing to determine which factors represent the largest contributions to the pathology. While most of the investigation in this area focuses logically on ankle dysfunction, a growing body of work  is identifying alterations in neuromuscular control in the joints proximal to the ankle in patients with CAI.  These studies may provide critical information for understanding the pathology, as well as an avenue for development of effective interventions.

Proximal neuromuscular control deficits

Many sensorimotor alterations and neuromuscular control deficits about the ankle are associated with CAI.11 Intriguingly, alterations in sensorimotor function and neuromuscular control of proximal lower extremity joints are consistently observed in patients with CAI. These proximal changes have manifested themselves as deficits in force production,12-14 kinematic pattern changes,15-20 and deficits in muscle activation patterns21-25 about the knee and hip during a variety of tasks and testing techniques.  Although these alterations are observed consistently, the source of these changes has not been established. However, a consistent theory is that the ankle pathology results in spinal level pathway alterations, potentially resulting in feed-forward patterns that are observed with changes in knee and hip neuromuscular control.15, 16, 20, 21 A neuromuscular feed-forward pattern is different from a feedback response in that it does not require sensory input from peripheral joint receptors to generate a motor output, but instead is more of an anticipatory action. Subsequently, these feed-forward patterns are often considered “learned responses” that are created and maintained at the spinal level of the central nervous system, and therefore occur in a much shorter period of time.

Alterations during static tasks

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Several authors have examined the activation patterns of the muscles controlling the knee and hip in ankle instability populations during isolated joint movements or relatively static tasks. While there is a consistent observable difference in the muscle activation patterns observed in proximal joints between those and without CAI, it is interesting to discover that there is an inconsistency within the literature as to whether the differences present ipsilaterally or contralaterally to the injured ankle, or in some cases, bilaterally.

Bullock-Saxton et al reported a delayed onset of gluteus medius activity during a prone hip extension movement22 and a decreased detection of vibration simultaneously with delayed hip extensor activity26 in subjects with ankle instability.  Similarly, Van Deun et al24 observed a delayed onset time in muscles controlling the ankle and the hip in subjects with CAI during a standing task as the subjects transitioned from a double-limb to a single-limb static stance position. Sedory et al25, using measures of central activation ratio in an open-chain position, reported that subjects with CAI have a bilateral autogenic inhibition of the hamstrings but a facilitation of the quadriceps ipsilateral to the injured ankle.

While the studies above describe a delayed response in hip musculature in CAI subjects during slow, controlled tasks, others have reported a more rapid hip recruitment during a fast task. Beckman and Buchanan21 examined the onset of muscle activation in the peroneus longus and the gluteus medius in subjects with ankle instability in response to a sudden inversion perturbation to the ankle. The peroneal muscle activation times did not differ in patients with CAI compared to a control group. However, the ankle instability group recruited the gluteus medius muscle more rapidly bilaterally than the control group in response to the perturbation, leading to the hypothesis that the pattern of faster hip muscle recruitment during a dynamic activity may be the result of deafferentation of peripheral nerves in the ankle that created a shift from an ankle strategy to a hip strategy in an effort to maintain postural control. 21 However, these responses in hip muscle recruitment likely are too slow to be a central nervous feedback response to an afferent signal and may be indicating that a centrally mediated feed-forward mechanism could recruit proximal muscles to protect against injury at the distal joints.

Strength/force production alterations

Strength loss often accompanies an acute lateral ankle sprain, but there is some controversy in the literature as to whether ankle strength deficits do27-31 or do not32-35 exist in those with CAI. Only a few studies have looked at proximal strength, but the limited evidence suggests that the presence of CAI may also be affecting the force production capabilities in joints proximal to the ankle. Nicholas et al14 and Friel et al12 have reported diminished hip abduction strength in the injured limbs of subjects with CAI. More recently, we have demonstrated that CAI subjects have reduced knee extension and flexion torque capabilities measured isokinetically on the injured and non-injured sides compared to matched control subjects.13 It is interesting to note that McHugh et al reported that weak hip abductors are not a significant predictor of first time ankle sprain in high school athletes.36 This lends support to the theories described above that the ankle injury perhaps creates a sensorimotor change affecting proximal control that is manifesting in the CAI population, but is not present prior to initial ankle injury and instead develops after the injury occurs.

Alterations during dynamic tasks

Important information is gained by examining aspects of sensorimotor function during slower tasks that isolate specific limb segments, as reviewed in the studies above.  However, to understand more completely what impact these proximal alterations may have on patient activity capabilities, it is important to introduce more complex tasks that challenge the functional abilities of the patients. During the tasks, neuromuscular control can be quantified directly, with EMG of muscle activation patterns, or indirectly, using kinematic motion patterns. To examine these contributions, it is critical that tasks are selected that consistently differentiate dynamic stability levels of CAI subjects from non-injured subjects.  Two such tasks, the Star Excursion Balance Test (SEBT) and landing from a jump or hop, have been used to demonstrate dynamic stability deficits in CAI subjects. It appears from a small collection of investigations that the global task deficiencies attributed to the ankle pathology may be influenced by alterations in knee and hip neuromuscular control.

The SEBT is a series of single-limb mini-squats that requires the subject to reach out as far as possible with the non-stance limb into different directions on the testing grid and return the reaching limb back to the starting position under control.37, 38 The task goal is to maintain and optimize dynamic stability of the stance limb during the reaching movements and is quantified by how far the non-stance limb is able to reach. Building on an initial study that demonstrated subjects with ankle instability had diminished dynamic postural control measured with the SEBT39, we have demonstrated that the decline in dynamic stability, as measured by the reduced reaching distances, was associated with reductions in knee and hip flexion in CAI subjects on the injured sided compared to their non-injured side as well as compared to healthy subjects.18, 19 These findings suggest that the reduced recruitment of proximal joint movement is causing dynamic postural control to suffer in CAI subjects.

Another common method for assessing dynamic stability is through the use of jump-landing tasks. Landing and stabilizing on a single leg after a jump or a hop mimics a common mechanism of injury for ankle sprain and provides useful insight into the deficits in dynamic stability in those with ankle pathology. There are several variations on the jump-landing task, as well as a multitude of measures that can be extracted to indicate performance and stability, but it appears that subjects with ankle instability demonstrate deficits during these tasks consistently when landing on the injured limb compared to the non-injured limb, and compared to healthy controls.15-17, 20, 23, 40-48 As with the SEBT, it is important to consider what influence neuromuscular control of joints proximal to the ankle may have on altered dynamic stability in these subjects with ankle pathology.

Caulfield and Garrett16 observed ankle instability subjects to have an altered pattern of ankle and knee sagittal plane motion patterns beginning in the preparatory period for landing compared to matched control subjects. They suggested that the observed kinematic changes in the ankle and the knee of a limb that has suffered ankle instability during a landing task may be indicating the creation of a protective feed-forward mechanism manifesting in a joint proximal to the pathological ankle. In similar tasks, Delahunt et al report that altered ground reaction forces were produced in CAI subjects along with increased rectus femoris activity23 and a more supinated ankle position17 before and after landing. Increased supination is associated with increased tibial rotation,49 which, along with the increased rectus femoris activation, can be linked to a more extended knee position during these hopping tasks.

Another variation on jump-landing is to have the subject create a steady base of support as quickly as possible after making contact with the ground during unilateral landing. This measure of dynamic stability is referred to commonly as Time-to-Stabilization (TTS).50 Using variations on the TTS variable, several authors have established that those with CAI have a diminished level of dynamic postural stability when landing on the injured limb compared to the non-injured limb and compared to healthy controls.41, 43, 44, 46-48 The majority of these studies, while consistently showing a task deficit, did not quantify what neuromuscular factors may be contributing to the reduced level of dynamic postural control. Brown et al41 did measure EMG of ankle musculature during the landing task in their study, but did not find that the activation of these muscles differed during the task between the CAI and healthy groups, concluding that this measure did not impact the diminished TTS measures. None of the studies included an assessment of proximal joint contributions to the task.

Building on those research questions, in recent investigations we have quantified kinematics of the ankle, knee and hip between those with and without CAI during a single limb landing from a jump while assessing dynamic postural control with TTS variables.15, 20 In both studies, we confirmed the previous literature41, 43, 44, 46-48 that CAI subjects have diminished dynamic postural stability during this functional task.  Additionally, it was discovered that knee flexion angles were significantly reduced at the point of ground impact15 as well as 100 msec prior to ground impact20 in the CAI subjects. Our work, along with that of Caulfield et al16 and Delahunt et al17, 23 demonstrating knee neuromuscular control alterations before landing occurs, suggests that ankle instability may be associated with a feedforward pattern established proximal to the ankle that exists simultaneously with deficits in dynamic stability.

Summary

One possible explanation for these observations is a re-organization in the CNS of the neuromuscular control of the leg. The demonstration of a change in motor responses at the hip and knee in those with ankle instability has been attributed to a change in the CNS, potentially as a protective mechanism for the unstable ankle.21, 50 Related to these theories, several authors have reported bilateral deficits in static postural control following unilateral lateral ankle sprain,52-54 suggesting a modified response by the CNS to altered afferent input from the unilateral ankle injury.

In our recent work, CAI subjects have demonstrated diminished knee extension torque production13 and a reduction in knee and hip flexion observed in conjunction with diminished dynamic postural control during tasks such as the SEBT18, 19 and jump-landing tasks measuring TTS.15, 20 These findings, consistent with the theories presented above, suggest that there is altered neuromuscular control in proximal joints associated with CAI, which may help explain recurrent and lingering ankle pathology. Additionally, although there is limited information, there may be a link between a history of ankle sprain and risk of knee injury.55 Continued work in this area is needed to determine why these patterns exist and why they are linked with deficits in functional assessment. In the future, it will be important to ascertain if interventions targeted at correcting these proximal joint deficits can improve the level of function and subsequently reduce injury incidence related to CAI.

Phillip A. Gribble, PhD, ATC, is an associate professor of kinesiology at the University of Toledo in Toledo, OH.

Disclosure: There are no known financial or otherwise conflict of interests associated with this article.

References

1. Fong D, Hong Y, Chan L, et al. A systematic review on ankle injury and ankle sprain in sports. Sports Med 2007;37(1):73-94.

2. Almeida SA, Williams KM, Shaffer RA, Brodine SK. Epidemiological patterns of musculoskeletal injuries and physical training. Med Sci Sport Exerc 1999;31(8):1176-1182.

3. Anandacoomarasamy A, Barnsley L. Long term outcomes of inversion ankle injuries. Br J Sports Med 2005;39(3):e14.

4. Kannus P, Renstrom P. Treatment for acute tears of the lateral ligaments of the ankle. Operation, cast, or early controlled mobilization. J Bone Joint Surg (Am) 1991;73(2):305-312.

5. Fernandez WG, Yard EE, Comstock RD. Epidemiology of lower extremity injuries among U.S. high school athletes. Acad Emerg Med 2007;14(7):641-645.

6. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train 2007;42(2):311-319.

7. Beynnon BD, Murphy DF, Alosa DM. Predictive factors for lateral ankle sprain: a literature review. J Athl Train 2002;37(4):376-380.

8. Smith RW, Reischl SF. Treatment of ankle sprains in young athletes. Am J Sports Med 1986;14(6):465-471.

9. Peters JW, Trevino SG, Renstrom PA. Chronic lateral ankle instability. Foot Ankle Int 1991;12(3):182-191.

10. Hertel J. Functional anatomy, pathomechanics, and pathophysiology of lateral ankle instability. J Athl Train 2002;37(4):364-375.

11. Hertel J. Sensorimotor deficits with ankle sprains and chronic ankle instability. Clin Sports Med 2008;27(3):353-370.

12. Friel K, McLean N, Myers C, Caceres M. Ipsilateral hip abductor weakness after inversion ankle sprain. J Athl Train 2006;41(1):74-78.

13. Gribble PA, Robinson RH. An examination of ankle, knee, and hip torque production in individuals with chronic ankle instability. J Strength Cond Res 2009;23(2):395-400.

14. Nicholas JA, Strizak AM, Veras G. A study of thigh muscle weakness in different pathological states of the lower extremity. Am J Sports Med 1976;4(6):241-248.

15. Gribble PA, Robinson RH. Alterations in knee kinematics and dynamic stability associated with chronic ankle instability. J Athl Train 2009;44(4):350-355.

16. Caulfield BM, Garrett M. Functional instability of the ankle: differences in patterns of ankle and knee movement prior to and post landing in a single leg jump. Int J Sports Med 2002;23(1):64-68.

17. Delahunt E, Monaghan K, Caulfield B. Changes in lower limb kinematics, kinetics, and muscle activity in subjects with functional instability of the ankle joint during a single leg drop jump. J Orthop Res 2006;24(10):1991-2000.

18. Gribble PA, Hertel J, Denegar CR, Buckley WE. The effects of fatigue and chronic ankle instability on dynamic postural control. J Athl Train 2004;39(4):321-329.

19. Gribble PA, Hertel J, Denegar CR. Chronic ankle instability and fatigue create proximal joint alterations during performance of the Star Excursion Balance Test. Int J Sports Med 2007;28(3):236-242.

20. Gribble P, Robinson R. Differences in spatiotemporal landing variables during a dynamic stability task in subjects with CAI. Scand J Med Sci Sports 2009 Jun 9 [Epub ahead of print].

21. Beckman S, Buchanan T. Ankle inversion injury and hypermobility: effects on hip and ankle muscle electromyography onset latency. Arch Phys Med Rehabil 1995;76(12):1138-1143.

22. Bullock-Saxton JE, Janda V, Bullock MI. The influence of ankle sprain injury on muscle activation during hip extension. Int J Sports Med 1994;15(6):330-334.

23. Delahunt E, Monaghan K, Caulfield B. Ankle function during hopping in subjects with functional instability of the ankle joint. Scand J Med Sci Sports 2007;17(6):641-648.

24. Van Deun S, Staes FF, Stappaerts KH, et al. Relationship of chronic ankle instability to muscle activation patterns during the transition from double-leg to single-leg stance. Am J Sports Med 2007;35(2):274-281.

25. Sedory EJ, McVey ED, Cross KM, et al. Arthrogenic muscle response of the quadriceps and hamstrings with chronic ankle instability. J Athl Train 2007;42(3):355-360.

26. Bullock-Saxton JE. Local sensation changes and altered hip muscle function following severe ankle sprain. PhysTher 1994;74(1):17-28.

27. Hartsell HD, Spaulding SJ. Eccentric/concentric ratios at selected velocities for the invertor and evertor muscles of the chronically unstable ankle. Br J Sports Med 1999;33(4):255-258.

28. Munn J, Beard D, Refshauge KM, Lee RY. Eccentric muscle strength in functional ankle instability. Med Sci Sport Exerc 2003;35(2):245-250.

29. Wilkerson GB, Pinerola JJ, Caturano RW. Invertor vs. evertor peak torque and power deficiencies associated with lateral ankle ligament injury. J Orthop Sports Phys Ther 1997;26(2):78-86.

30. Willems T, Witvrouw E, Verstuyft J, et al. Proprioception and muscle strength in subjects with a history of ankle sprains and chronic instability. J Athl Train 2002;37(4):487-493.

31. Yildiz Y, Aydin T, Sekir U, et al. Peak and end range eccentric evertor/concentric invertor muscle strength ratios in chronically unstable ankles: comparison with healthy individuals. J Sports Sci Med 2003;2(3):70-76.

32. Bernier JN, Perrin DH, Rijke A. Effect of unilateral functional instability of the ankle on postural sway and inversion and eversion strength. J Athl Train 1997;32(3):226-231.

33. Docherty CL, Moore JH, Arnold BL. Effects of strength training on strength development and joint position sense in functionally unstable ankles. J Athl Train 1998;33(4):310-314.

34. Lentell G, Baas B, Lopez D, et al. The contributions of proprioceptive deficits, muscle function, and anatomic laxity to functional instability of the ankle. J Orthop Sports Phys Ther 1995;21(4):206-215.

35. McKnight CM, Armstrong CW. The role of ankle strength in functional ankle instability. J Sport Rehabil 1997;6(1):21-29.

36. McHugh MP, Tyler TF, Tetro DT, et al. Risk factors for noncontact ankle sprains in high school athletes: the role of hip strength and balance ability. Am J Sports Med 2006;34(3):464-470.

37. Gribble P. Utilization of the Star Excursion Balance Test in assessing dynamic postural control. Athl Ther Today. 2003;8(2):46-47.

38. Hertel J, Miller SJ, Denegar CR. Intratester and intertester reliability during the Star Excursion Balance Test. J Sport Rehabil 2000;9(2):104-116.

39. Olmsted LC, Carcia CR, Hertel J, Shultz SJ. Efficacy of the star excursion balance tests in detecting reach deficits in subjects with chronic ankle instability. J Athl Train 2002;37(4):501-506.

40. Brown CN, Mynark R. Balance deficits in recreational athletes with chronic ankle instability. J Athl Train 2007;42(3):367-373.

41. Brown C, Ross S, Mynark R, Guskiewickz KM. Assessing functional ankle instability with joint position sense, time to stabilization, and electromyography. J Sport Rehabil 2004;13(2):122-134.

42. Caulfield B, Garrett M. Changes in ground reaction force during jump landing in subjects with functional instability of the ankle joint. Clin Biomech 2004;19(6):617-621.

43. Ross SE, Guskiewicz KM. Examination of static and dynamic postural stability in individuals with functionally stable and unstable ankles. Clin J Sports Med 2004;14(6):332-338.

44. Ross SE, Guskiewicz KM, Gross MT, Yu B. Assessment tools for identifying functional limitations associated with functional ankle instability. J Athl Train. 2008;43(1):44-50.

45. Ross SE, Guskiewicz KM, Gross MT, Yu B. Balance measures for discriminating between functionally unstable and stable ankles. Med Sci Sport Exerc 2009;41(2):399-407.

46. Ross SE, Guskiewicz KM, Yu B. Single-leg jump-landing stabilization times in subjects with functionally unstable ankles. J Athl Train 2005;40(4):298-304.

47. Wikstrom EA, Tillman MD, Chmielewski TL, et al. Dynamic postural stability deficits in subjects with self-reported ankle instability. Med Sci Sport Exerc 2007;39(3):397-402.

48. Wikstrom EA, Tillman MD, Borsa PA. Detection of dynamic stability deficits in subjects with functional ankle instability. Med Sci Sport Exerc 2005;37(2):169-175.

49. Riegger-Krugh C, Keysor J. Skeletal malalignments of the lower quarter: correlated and compensatory motions and postures. J Orthop Sports Phys Ther 1996;23(2):164-170.

50. Ross S, Guskiewicz K. Time to stabilization: a method for analyzing dynamic postural stability. Athl Ther Today. 2003;8(3):37-39.

51. Konradsen L, Voigt M, Hojsgaard C. Ankle inversion injuries: the role of the dynamic defense mechanism. Am J Sports Med. 1997;25(1):54-8.

52. Hertel J, Buckley W, Denegar C. Serial testing of postural control after acute lateral ankle sprain. J Athl Train. 2001;36:363-8.

53. Evans T, Hertel J, Sebastianelli W. Bilateral deficits in postural control following lateral ankle sprain. Foot Ankle Int. 2004;25(11):833-9.

54. Tropp H, Ekstrand J, Gillquist J. Factors affecting stabilometry recordings of single limb stance. Am J Sports Med. 1984;12(3):185-8.

55. Kramer L, Denegar C, Buckley W, Hertel J. Factors associated with anterior cruciate ligament injury: history in female athletes. J Sports Med Phys Fitness 2007;47(4):446-454.

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