Case study of a 14 year old female gymnast presents with a 12-month history of repeatedly 'turning her ankle'.

Injuries to the lateral aspect of the ankle are one of the most common injuries in active populations (Fong, Hong, Chan, Yung & Chan, 2007). Although the majority of athletes will return to their previous level of activity without any deficit (Karlsson & Laninger, 1993), it has been reported that up to 20% of these injuries will develop chronic ankle instability (CAI) irrespective of the initial treatment (Valderrabano, Wiewiorski, Frigg, Hintermann & Leumann, 2007). CAI is defined by Brown, Bowser & Orellana, (2010), as ‘repeated, subjective episodes of giving way and spraining at the ankle, coupled with decreased self-reported function’.  Although varying widely, different authors have reported higher incidences of lateral ankle sprains in female athletes when compared to their male counterparts (Hosea, Carey & Harrer, 2000), especially in the school and college going age group. This could be attributed to improperly controlled landing forces and deficits in dynamic postural control (Wikstrom, Tillman, Kline & Borsa, 2006, cited by Brown et al., 2010). Purnell, Shirley, Nicholson & Adams, (2010) report that injury onset is most common between the ages eleven to fourteen in acrobatic gymnastics.  

Ankle stability is attained mainly through static ligament support, dynamic musculotendinous control and congruity of the loaded articular surfaces (Bonnel, Toullec, Mabit & Tourné, 2010). Lateral ankle sprains (LAS) most often occur due to excessive inversion and internal rotation of the rearfoot about an externally rotated lower leg which results in spraining of the lateral ankle ligaments. This normally occurs immediately after rearfoot contact during the gait cycle or landing from a jump (Hertel, 2002). Along with a multitude of extrinsic factors, certain intrinsic factors could predispose individuals to initially spraining their ankle like increased tibial varum and non-pathological talar tilt, while functional predispositions include poor postural control, impaired proprioception, and higher eversion-inversion and plantar flexion dorsiflexion strength ratios (Beynnon, Murphy & Alosa, 2002). A previous ankle injury has been widely reported as the most common predisposing factor in the development of CAI (Ekstrand & Tropp, 1990). Purnell et al., (2010) report an incidence of about 20% of all past injuries in acrobatic gymnastics involving the ankle. The two most common theories postulated are mechanical instability or functional instability, however Hertel (2002) describes the mechanical insufficiency and functional insufficiency as a continuum of pathologic contributions rather than mutually exclusive entities to CAI. This discussion will focus on both theories and how the pathomechanics contribute to CAI in this particular athlete.     

Mechanical Instability

Mechanical ankle instability is defined as either a pathological laxity at the ankle due to structural damage to the ligaments which support the joints or arthrokinematic restrictions resulting in loss of physiological range of movement (Hertel, 2002). A common concept after ankle injuries is joint hypermobility resulting from ligament damage to one or more of the supporting ligament structures which results in an increase in the accessory motion of the joint. This increased accessory motion makes the joint vulnerable during functional activities which can cause recurrent injuries (Hubbard & Hertel, 2006). The anterior talofibular ligament (ATFL), the calcanofibular ligament (CFL), the talocrural and subtalar joints are most often associated with mechanical hypermobility however there are discrepancies in the research as to how each of these structures affects individuals suffering from CAI (Freeman, 1965). It has been reported that mechanoreceptors contained in the ligamentous and musculotendinous structures play a role is proprioception (Hubbard & Hertel, 2006), and injury to these structures affects the afferent input. A study by Konradsen, Ravn, & Sorensen, (1995) showed that intact lateral ankle ligaments are important in correct placement of the foot at heel-strike, but that this input can be replaced by afferent information from active calf muscles when the lateral ligaments are anesthetised. This is in contrary to Feuerbach, Grabiner, Koh & Weiker, (1994) who reports that the cutaneous, joint and muscle mechanoreceptors contributed more to ankle joint proprioception than the ligament mechanoreceptors.

Talocrural joint

Talocrural hypermobility is often reported in individuals with CAI. It has been hypothesised that damage to the ATFL and CFL causes an increase in the accessory movements within the talocrural joint.  Hertel, Denegar, Monroe & Stokes, (1999) performed the anterior draw test, talar tilt test and stress radiographs on individuals with CAI and normal ankles. The results showed that the majority of the CAI individuals demonstrated hypermobility for each test. Hertel et al., (1999) found that 75% of the subjects complaining of recurrent ankle injuries could be associated to a talar tilt greater than 10°. Although the positive value seems high compared to other similar investigations (Freeman, 1965), the involvement of talocrural hypermobility seems to be contributing to CAI. Freeman,  (1965) however showed how after repair or immobilization, where the six week follow up showed no or minimal talar tilt, episodes of ‘giving away’ still occurred after a year. The authors suggest only 20% could be attributed to talocrural hypermobility while the vast majority were caused by some other pathological process, in this case Freeman is referring to functional instability. 

Similar studies have been conducted (Tropp, Odenrick, & Gillquist, 1985, cited by Hubbard & Hertel, 2006) suggesting that subjects presenting with CAI did not always have an associated laxity, however this study used manual examination techniques which question the reliability of the results. The anterior draw test has been shown to have a sensitivity from 32%-80% while the talar tilt test has been reported to be about 56% sensitive (Vela, Tourville & Hertel, 2003) and there are questions regarding the validity of stress radiographs for the assessment of talocrural instability (Frost & Amendola, 1999).The current literature seems to suggest that talocrural instability is present after ankle injuries involving the lateral ligament. What is unclear is whether talocrural hypermobility is a cause of CAI or simply a product of the dysfunction.

Hypomobility following an ankle sprain is typically seen as a decrease in dorsiflexion (Denegar & Miller, 2002) which has been reported in individuals with CAI and has been suggested as a possible cause of recurrent injury during walking (Barker, Beynnon & Renstrom, 1997) and jogging (Drewes, McKeon, Kerrigan, & Hertel, 2009). Although the shortening of gastrocnemius-soleus muscle complex could contribute to this loss of range, it is more likely due to restrictions within the talus limiting posterior glide (Denegar & Miller, 2002). This not only stresses the surrounding tissue but also affect the proprioceptive input (Hubbard & Hertel, 2006). There is research which states that dorsiflexion in CAI is comparable to the uninjured side (Denegar, Hertel & Fonseca, 2002). They reported no difference in dorsiflexion but found a decrease posterior talar glide attributed to anterior displacement of the talus. For normal arthrokinematics to occur posterior talar glide is required to achieve full dorsiflexion. To achieve full dorsiflexion without this element requires hypermobility at other joints and also forces the talocrural joint to move through an abnormal anterior axis, which prevents the ankle from achieving the closed pack position which allows for decreased stability (Spaulding, Livingston & Hartsell, 2003). Although the sample size was relatively small So, Sui, Chan, Chin & Li, (1994) demonstrated using an isokinetic dynamometer that gymnasts had a greater dorsiflexion range and strength compared to other athletes and normal controls. This may indicate that gymnasts with CAI may have preserved a greater degree of their dorsiflexion compared to normal CAI individuals.

Subtalar Joint

Traditionally, laxity at the talocrural joint has been the focus of most research however more studies are focusing on the subtalar involvement in CAI (Hubbard & Hertel, 2006). Injuries involving the CFL have been shown to affect the subtalar joint capsule and the other lateral ligaments (Meyer, Garcia & Hoffmeyer, 1986). The Broden stress radiographic technique has often been used to assess the degree of subtalar tilt (Hertel et al., 1999), finding in this study that 56% of the subjects with talocrural hypermobility also have subtalar hypermobility. Similarly Meyer et al., (1986) reports an incidence of 80% subtalar injury in individual with LAS. Ishii, Miyagawa, Fukubayashi & Hayashi, (1996) also found an increase in subtalar joint injury following LAS using a stress view for the lateral subtalar joint that uses a supination stress with the foot held in dorsiflexion. The Broden view has also been criticised (Harper, 1992) as it exhibits similar gapping in healthy individuals compared to individuals with CAI. The author concluded that the stress Broden view was not sensitive in the assessment of lateral subtalar instability. Hertel et al., (1999) suggests that subtalar involvement may be more common in LAS and in CAI than previously reported and repairs need to take this into account and investigate all the ligaments not just the ones commonly injured. Conversely Wright, Neptune & Van Den Bogert, (2000) investigated the effect of subtalar mechanical laxity on landing during side stepping and found that the laxity did not contribute to sprain occurrence during side stepping. There is no information on whether the subjects had stable or unstable ankles and the population group was quite small. 

Tibiofibular joint

During forced inversion where the foot is supinated past its normal range, it has been hypothesised that the tension on the ATLF subluxes the inferior head of the fibula forward and due to effusion and soft tissue damage it remains in this anterior position (Hubbard, Hertel & Sherbondy, 2006). Mavi, Yildirim & Gunes, (2002) found a significantly greater anterior displacement for the fibula on subjects having two or more LAS on magnetic resonance imaging (MRI) while Kavanagh, (1999) cited (Hubbard & Hertel, 2006), found greater anterior/posterior movement in 33% of subjects following an LAS. Other research has suggested that CAI individuals may conversely have a posterior displaced distal fibula head (Berkowitz & Kim, 2004), which opens up the mortise allowing for less congruency.  These measurements were using the talus as a reference point. It has been suggested that CAI sufferers may also have an anterior displaced talus (Denegar et al., 2002). This may create a perception of a posterior displaced talofibular head. There are questions on whether this anterior displacement is caused by the initial and subsequent injuries or whether it is a predisposing factor (Hubbard et al., 2006). They hypothesize that after a LAS the anterior position is maintained due to changes in the afferent input from musculotendinous and ligamentous mechanoreceptors which in turn affect the tone of the peroneal muscles. This altered afferent input causes the peroneal muscles to contribute to maintaining the anterior fibula position. This anterior positioning of the fibula head creates slack in the ATLF allowing a greater degree of movement before tension is reached. It may also cause anterior displacement of the axis of rotation.

Functional instability

Questions arise on biomechanical differences between mechanically unstable individuals and functionally unstable individuals and how this relates to CAI. Mechanical ankle instability (MAI) has been described as having a difference of 5° in talar tilt and 4mm difference in the anterior draw (Peri, 1992, cited Nystra & Mann, 2002) compared to the uninjured opposite side. While functional ankle instability (FAI) is described as ‘a subjective feeling of ‘’giving away’’ with negative talar tilt and anterior draw tests’ (Nystra & Mann, 2002). Hubbard, Kaminski, Vander Griend & Kovaleski, (2003) tried to determine whether if any mechanical laxity occurred in individuals who report FAI using ankle arthrometer and stress radiographs. The results showed some laxity in the saggital plane but nothing significant in the eversion/inversion plane. This suggests that there is some overlap between FAI and MAI individuals. Individuals with CAI tend to be more plantar flexed (Spaulding, Livingston & Hartsell, 2003) and more inverted (Monaghan, Delahunt & Caulfield, 2006) at initial contact. Brown, Padua, Marshall & Guskiewicz, (2008), however compared motion patterns of individuals with MAI, individuals with FAI and controls over different tasks and found that individual’s with MAI exhibit altered motion patterns. They showed greater dorsiflexion during a number of tasks which may indicate greater reliance on bony stability rather than ligament support and greater maximum eversion indicating less reliance on the CFL and more on the musculotendinous support from a concentrically activated peroneal group suggesting a coping mechanism to improve dynamic stability. Interestingly the group with FAI and controls showed no difference in motion patterns. This study alludes to the fact that the two entities may have separate mechanisms suggesting joint kinematics having a greater effect on the mechanically unstable ankles than the functionally unstable ankles. Gymnasts exhibit a difference between the injured and uninjured ankles (Mulloy Forkin, Koczur, Battle & Newton, 1996), but are still able to compete at high levels despite these deficits, indicating that coping mechanisms may contribute to maintaining stability. 

Proprioception

Proprioception deficits are considered one of the major contributors to FAI (Hertel, 2002) and ultimately CAI. Proprioception is defined collectively as: force sense, the ability to accurately reproduce a given force; joint reposition sense, the ability to accurately reproduce a given angle and kinaesthesia, the ability to detect movement (Riemann & Lephart, 2002). The detection measures for force sense, joint positioning and kinaesthesia have been hypothesised to involve the mechanoreceptors which if damaged may fail to provide accurate afferent information. It is thought that muscle spindles mediate joint reposition while the golgi tendon organ (GTO) mediate force sense (Grigg, 1994). Most studies show some kinaesthesia deficits in individuals with CAI compared to a healthy population. Lentell, Baas & Lopez, (1995) showed defects in passive inversion and plantar flexion while Refshauge, Kilbreath & Raymond, (2003) found impairment in passive inversion and eversion in individuals with CAI at different velocities. If you can properly regulate the amount of tension in the muscle you can move with a stable joint. Improper regulation of tension could predispose individuals to joint instability and potential injury. Docherty, Arnold & Hurwitz, (2006) found a significant correlation with FAI and force sense using a load cell. The result showed greater variance compared to uninjured side. Although the tests were done at 10-30% of the participant’s maximal eversion strength the authors agree that the results would be consistent for any force and by using smaller forces they could exclude factors such as fatigue and muscle assistance.

The GTO is the most likely structure to modulate force sense (Grigg, 1994). If damaged, inconsistencies may occur in the feedback system which in turn affects the ankles ability to stabilize. The sensation of giving way tends to occur sporadically within most population groups which may indicate a deficiency in the force sense at that moment which could account for the inconsistencies in the research. Joint position sense could be linked to improper foot positioning at initial contact and thus more likely to suffer injury. Mulloy Forkin et al., (1996) showed that gymnasts with unilateral CAI; joint reposition sense and single leg stance ability, was significantly less on the injured limb. Conversely Docherty, Arnold, & Hurwitz, (2006) investigated the joint reposition sense in individuals with FAI and found no difference. This may suggest that afferent information is received from other structures like the cutaneous receptors. Incidentally warming up seemed to improve joint reposition sense in an active population (Konradsen & Magnusson, 2000) which could indicate how gymnasts can still perform with CAI.

Postural defects

After a significant injury to the ankle joint postural defects can affect the joint and thus single stance balance (Freeman, Dean & Hanham, 1965). Common tests to assess balance include the modified Rhomberg tests however it’s very subjective (Freeman et al., 1965). Docherty, Arnold & Hurwitz, (2006) assessed individuals with FAI on progressively more difficult tasks and evaluated how they coped with the balance error score system (BESS). As expected, the FAI group had more errors as the tasks got harder which is consistent with other studies using different balance measures. Olmstead identified reach deficits in a CAI population using the star excursion balance test (SEBT). They found that individuals with CAI had significantly less reach in all directions when compared to healthy controls. Poor proprioception and neuromuscular control are likely the cause of postural defects. The ankle supinates and pronates to keep the centre of mass over its base of support. Individuals with CAI tend to use more hip movement to maintain their balance (Pintsaar, Brynhildsen & Tropp, 1996). This hip strategy is less efficient than using the ankle strategy and could potentially lead to recurrent injury. Postural sway is the phenomenon of constant displacement and correction of the position of the centre of gravity within the base of support.  Mitchell, Dyson, Hale & Abrahams (2008) showed that individuals with FAI had greater side to side and front to back postural sway compared to healthy controls, indicating less precise correction at the ankle which requires greater correction higher up the kinetic chain to maintain balance. Furthermore this may indicate centrally controlled adaptation which causes a postural shift similarly likened to the changes seen in aging and disability (Hass, Bishop, Doidge & Wikstrom, 2010). Even with these supraspinal alterations, recurrent injuries still occur which suggests that these changes may be maladaptive or ineffective in preventing injuries but may also contribute to the development of degenerative joint changes.

Strength defects

Although strength retraining is a common part of the ankle rehabilitation process different authors question the presence of strength defects in chronic ankle instability. Hartsell & Spaulding (1999) report weakness in both concentric and eccentric muscle actions during eversion, which correlates with earlier findings and in inversion which was reported as a new finding. The authors report that eccentric muscle function was reduced during eversion at higher velocities contrary to the force-velocity relation. As most injuries occur during high velocity movements, these results suggest that the ankle is impaired to function eccentrically under high velocity conditions. Coupled with the weakness associated with instability, recurrent injuries appear more likely. Conversely Kaminski, Perrin & Gansneder, (1999) found no eversion defects when compared to matched controls. This puts in to question strength training as part of rehabilitation, suggesting clear evaluation before prescribing time consuming exercises. So et al., (1994) reported a significantly greater strength and endurance capacity in gymnasts when compared to a non-athletic population.  

Peroneal reaction time

Inversion injuries in most cases are spontaneous events, forcing the ankle past its normal physiological range. Along with the bony congruency and ligament support, the musculotendois unit should act as a dynamic control to prevent this inversion maneuver. The peroneal muscles would normally respond through a feedback loop, initiated by the mechanoreceptors in the joint, capsule and ligaments to concentrically return the ankle back to neutral range. Konradsen & Bohsen Ravn, (1990) however has reported that individuals with CAI have a delayed response to inversion pertubirations (84msec compared to 69msec), which ultimately prevents the ankle from correcting its self before it has to rely on the already stressed non-contractile structures.

Conclusion

CAI is a difficult condition to manage as the pathomechanics are complex and varied. Two clear ideas emerge as the most likely to cause this condition but is it a case of one condition which possesses multiple facets or is it a multitude of different conditions all lumped under a combined heading. Mechanical instability may be due to hypermobility or hypomobility changes to the joints of the ankle complex. While functional instability is driven by insufficiencies in proprioception, neuromuscular control, postural control, and strength. It seems however that mechanical instability and functional instability both seem to contribute to the pathology rather than present as mutually exclusive entities to CAI.

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