September 2020

Expanding Our Understanding of Chronic Ankle Instability #1259019994

Research is showing that it’s not “just an ankle sprain,” but rather the first step on a perilous journey to physical instability and lower quality of life.

The clinical presentation of chronic ankle instability (CAI) has been defined as the perceived or subjective instability with feelings of giving way, pain, and recurrent sprains.1 When viewed as the long-term sequelae of “an index ankle sprain,” researchers are helping to focus the discussion on the need for improved treatments of the initial sprain and prevention of the well-documented recurrent sprains. The recent findings from the published literature present new insights on this most important topic.

Ankle Sprain Defined

Ankle sprains are quite common both in sporting activities and the general community—data show an estimated 2 million individuals annually seeking emergency department (ED) treatment for ankle sprains, yet it is well known that a majority of individuals who suffer ankle sprains do NOT seek help.2 Indeed, some estimates place the incidence of ankle sprains nearly 5.5 times higher than ED data. Significantly, nearly half of these sprains were not associated with sporting activities, but rather from the general community, meaning their distribution is widespread, not limited to only those who are physically active.

Incidence of ankle sprains is reported to be higher among females compared to males (13.6 vs 6.9/1000 exposures) and appears to decrease with age, with estimated incidence rates as follows:2

  • Children: 2.85/1000 exposures
  • Adolescents: 1.94/1000 exposures
  • Adults: 0.72/1000 exposures

Peak rate also appears at a younger age in females (10- to 14-year-olds) compared with males (15- to 19-year-olds) as noted in the Figure.

Ankle sprains make up nearly 80% of all ED visits and of those, 85% result in injury to the lateral ligamentous complex. This complex includes the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL).  These ligaments play a significant role in maintaining the stability of the ankle joint.3 When the ankle joint is plantarflexed, the ATFL becomes taut and begins to undergo strain. It is this vulnerability of the ATFL that leads to the most common mechanism of injury, an inversion injury where a plantarflexed ankle undergoes supination and adduction. Indeed, MacKenzie et al reported that more than three-quarters of all acute ankle sprains are lateral in nature, with approximately 73% of these being injuries to the ATFL.2 The second most common mechanism of injury is a combination injury that involves both the CFL and the AFTL.3 The PTFL is rarely injured alone. Other structures besides the lateral complex can be injured as well, making a complete physical examination of the ankle and its related structures mandatory.3 Those other injuries can include peroneal tendon tears, chondral and osteochondral fractures of the talus, medial ligamentous injury, ankle syndesmosis injury, and fractures to the hindfoot, midfoot, and forefoot. Most authors also point out the need to assess patients for intrinsic risk factors for lateral ankle instability including hindfoot varus, midfoot cavus, and overall ligamentous laxity.

While multiple classification systems for ligament instability have been described, the most commonly used system sets out 3 grades of injury:3

Grade I: injury to ATFL and/or CFL without rupture.

Grade II: complete rupture of ATFL with CFL intact.

Grade III: complete rupture of both ATFL and CFL; PTFL may or may not be injured.

Functional vs Mechanical Impairments

Distinguishing between mechanical instability and functional instability of the ankle joint is critical. In a study published earlier this year, Wenning et al1 wrote that:

“CAI can be divided into two etiologies: functional ankle instability (FAI) and mechanical ankle instability (MAI). The choice of the appropriate therapeutic approach for CAI patients requires the distinction between these two etiologies as functional deficits may best be addressed by functional, conservative therapy, since deficits in the sensorimotor system and postural control respond well to focused exercise regimes. Conversely, MAI can only be treated mechanically using additional stabilization such as ankle taping, orthoses, or lateral ligament repair.

“Concerning sensorimotor deficits, it has been described that postural control and strength are altered in FAI subjects. Impaired postural control has been one of the few factors which is consistently associated with functional impairment in CAI. Furthermore, a recent systematic review found that impairments of peroneal reaction time and pronation strength strongly contribute to perceived ankle instability in a chronic population. Also, strength deficits resulting from ankle injuries have been described especially in plantarflexion and pronation strength, while dorsiflexion and supination strength seems to remain rather unaffected. It is thought that spinal and cortical pathways may lead to an inhibition of neuromuscular activity and thus contribute to these persisting deficiencies in CAI patients.

Figure 1. Established intrinsic and extrinsic risk factors for lateral ankle sprain. Abbreviations: BMI, body mass index; NCAA, National Collegiate Athletic Association. Reprinted from Delahunt E, Remus A. Risk factors for lateral ankle sprains and chronic ankle instability. J Athletic Train. 2019;54(6):611-616, with permission from the National Athletic Trainers Association. All rights reserved.

“Furthermore, it has been shown that CAI patients display alterations during gait as for instance a laterally deviated pressure distribution, an increased inversion angle, and a decreased foot clearance. Whether or not these alterations during gait are caused by deficits in sensorimotor control, strength imbalance or other factors remains unclear. However, CAI patients seem to benefit from locomotor training by improving mediolateral pressure shift during gait. Furthermore, strengthening and increasing preactivation of the peroneus longus muscle have been shown to reduce ankle inversion during gait. On the other hand, also mechanical stabilization like ankle orthoses, taping, or operative stabilization improve gait performance by reducing maximal ankle inversion, which can be attributed to the mechanical insufficiency which is destabilizing the joint during the ankle sprain mechanism itself. Furthermore, the finding that functional performance also improves after mechanical stabilization like lateral ligament reconstruction or wearing an orthosis underlines the fact that the two etiologies are intertwined, which of the observed alterations can be attributed to mechanical and/or functional insufficiencies is the focus of ongoing research.

“Current literature suggests that a certain degree of mechanical instability cannot be compensated by functional training but may instead require mechanical stabilization. Whether an undetermined severity of mechanical insufficiency inevitably leads to an additional perception of instability, according to the model of Hiller et al,4 remains unclear in current literature.

“Especially in the clinical approach to CAI patients, it is important to distinguish between those suffering from predominantly functional deficits and those patients suffering due to an insufficient mechanical stability. Ultimately, it may be suggested that only the latter will benefit from operative stabilization, while the others should be treated conservatively. As mentioned above, the exact definitions of CAI, FAI, and MAI have been subject to increasing debate in the last decade. It is of note that many earlier studies did not differentiate the patients’ mechanical and functional insufficiencies possibly because quantifying mechanical ankle instability remains a diagnostic challenge. At present, the extent to which FAI and MAI interact remains unclear.”

Methods, Results, Discussion

In their study, Wenning et al retrospectively looked at 43 patients (22 female; mean age 26 ± years) who suffered chronic, unilateral MAI and in which long-term conservative treatment had failed and surgery was scheduled. Functional testing prior to surgery was used to assess the extent of persisting unilateral, functional deficits and included maximal isokinetic strength measurements, posture, and gait control.

As for results, they found: “Plantarflexion, supination, and pronation strength was significantly reduced in MAI ankles. A sub-analysis of the strength measurement revealed that in non-MAI ankles, the peak pronation torque was reached earlier during pronation (maximum peak torque angle at 20° vs. 14° of supination, p < 0.001). Furthermore, active range of motion was reduced in dorsiflexion and supination. In balance testing, patients exhibited a significant increased perimeter for the injured ankle (p < 0.02). During gait analysis, we observed an increased external rotation in MAI (8.7 vs. 6.8°, p<0.02).”

In their discussion, they noted:

“A significant reduction in strength, an impaired postural control, and subtle changes of kinematics during locomoting were observed unilaterally on the affected side. Applying our findings to patients with persisting subjective instability despite functional treatment may help to identify those patients that will benefit from mechanical stabilization, e.g., bracing or surgery.

Strength: “Comparable to our data, several studies have provided evidence that concentric pronation and supination strength are impaired in CAI. The novel finding in this study was that the joint angle in which the maximum pronation strength can be produced is significantly different between the two ankles (MAI 14° vs. non-MAI 20° of supination). The detailed analysis according to the joint position showed that it is especially in the early phase of pronation where a significant strength deficit exists (Fig. 1). This pattern is of high clinical relevance regarding joint stabilization during gait because it will limit the ability to actively prevent excessive supination once the joint comes close to a prone-to-injury position. The etiology behind this observation may either be related to fear of pain approaching the end-range supination, which unfortunately was not systematically recorded; it may also be a shift in torque curve due to the general decrease in ROM. The strength deficits have further been attributed to neuromuscular impairment as well as muscle atrophy. Also, earlier studies revealed that delayed peroneal reaction time is a characteristic of CAI patients, which can be improved by functional training. However, since long-term functional treatment had not lead to a sufficient alleviation of symptoms in this study’s population, it may be suggested that the combination of pronounced end-range strength deficits in pronation with clinically apparent, unilateral mechanical instability results in the inability to actively prevent an ankle sprain on the previously injured side. Whether or not these unilateral impairments of end-range pronation strength are caused by the mechanical instability itself, fear of pain, or posttraumatic neuromuscular dysfunction cannot be concluded. However, in our view, these patients may not be able to develop a sufficient functional performance in order to cope with their mechanical deficits. In summary, the clinical application of this finding could be that patients presenting with deficits in the end-range pronation strength and clinically apparent mechanical ankle instability will benefit from mechanical treatment, e.g., operative ligament reconstruction.

Balance: “The impairments of postural sway have been widely described in the literature. However, in our population, the differences in balance testing of approximal 10% were not as pronounced as in other studies. Furthermore, it has been shown that functional adaptations like preparatory neuromuscular activation capacitate patients to cope with mechanical insufficiencies. Since all patients in our population had received long-term conservative treatment, it may be assumed that in these patients, the potential benefit resulting from functional training had been exhausted. Since the modalities of conservative training were not controlled for in this observational study, we are unable to conclude the reasons why conservative treatment was not successful in individual cases. From a clinical point of view, it is important to reflect upon persisting unilateral functional deficits in unilateral mechanical instability. Potentially, the observed deficit in postural control may therefore be attributed to a mechanical instability that lays beyond functional compensation. This supports the finding that the mechanical deficit itself impairs functional performance. Again, in a clinical setting this could mean that a certain degree of mechanical instability can never be compensated and in patients with persisting perceived instability (non-copers) may require operative stabilization. Future studies need to clarify whether different degrees of severity of MAI also show different degrees of the functional deficits reported in this study. Potentially, this will also allow to estimate the risk for associated injuries following lateral ankle instability and therefore increase the therapeutic value. To achieve this, however, a reproducible manner of quantitively assessing MAI is indispensable.

Gait: “Several studies have also analyzed gait in patients suffering from chronic ankle instability. In our analysis, we aimed to monitor whether mechanical insufficiency leads to subtle gait imbalances. While walking at a preferred speed, the distribution of weight during the stance phase showed no difference between rear- and forefoot on either leg resulting in a harmonic gait pattern. However, the foot in which mechanical instability is present was set with a slightly increased external rotation of 1.9°. This is comparable to the findings in earlier publications, where CAI had not yet been further divided into MAI vs. FAI. This phenomenon of a more pronounced exo-rotated foot may be interpreted as a subconscious preventive adaptation leading to a broader mediolateral distribution of weight due to increased support surface which will help stabilizing the ankle joint during gait. As a limitation, it needs to be respected that kinematic adaptations take place during treadmill walking as opposed to overground. However, since we compared intra-subject differences, we consider our results valid in regard to gait adaptation as a component of unilateral MAI, since the observable differences, that take place due to the treadmill condition were assumed to affect both ankles in the same way.” (See “Gait Biofeedback,” page 45.)

“Finally, to underscore these novel findings, it is promising to continue developing means for quantifying mechanical ankle instability like 3D stress-MRI. Future research may then be able to establish cutoff values of severe, chronic mechanical ankle instability in which functional treatment is likely to fail and early operative stabilization should be recommended.

“In addition to quantifying the individual’s mechanical insufficiency, these findings will require future confirmation and a prospective study design including FAI patients and postoperative analysis in a clinical setting.

“As a limitation, in the present retrospective analysis, we were not able to quantify the amount of perceived instability via questionnaires. However, all patients agreed to undergo operative lateral ligament repair, which makes it evident that perceived instability and subjective malfunction must have been high. Unfortunately, we were unable to retrospectively distinguish those with predominantly pathological talar tilt vs. anterior drawer in order to correlate our findings to ATFL vs. CFL rupture, which should be a focus of additional research.


“This retrospective analysis shows certain functional characteristics that persist in patients suffering from MAI despite functional treatment. Especially the maldistribution of peroneal strength could impede functional coping of mechanical deficits. This may support the observation that severe mechanical instability cannot be compensated and causes functional impairment itself. Thus, a certain degree of mechanical instability will eventually require operative stabilization. Future research should focus on quantifying mechanical ankle instability to verify this hypothesis.”

See Gait Biofeedback and Impairment-based Rehabilitation article

  1. Wenning M, Gehrin D, Mauch M, Schmal H, Ritzmann R, Paul J. Functional deficits in chronic mechanical ankle instability. J Orthop Surg Res. 2020;15:304. Use is per the Creative Commons License 4.0 BY.
  2. Mackenzie M. Herzog, Zachary Y. Kerr, Stephen W. Marshall, Erik A. Wikstrom; Epidemiology of Ankle Sprains and Chronic Ankle Instability. J Athletic Train 1 June 2019; 54 (6): 603–610.
  3. Hur ES, Bohl DD, Lee S. Lateral ligament instability: review of pathology and diagnosis. Curr Rev Musculoskel Med. 2020;13:494-500.
  4. Hiller CE, Kilbreath SL, Refshauge KM. Chronic ankle instability: evolution of the model. J Athletic Train. 2011;46:133–41.

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