The ATFL courses from the lateral malleolus anteriorly and medially toward the talus at an angle of approximately 45 degrees from the frontal plane(8). The ATFL is an average of 7.2mm wide and 24.8mm long. Studies have shown that the ATFL prevents anterior displacement of the talus from the mortise, and excessive inversion and internal rotation of the talus on the tibia(7,9). The strain in the ATFL increases as the ankle moves from dorsiflexion into plantar flexion. Furthermore, compared with the PTFL, CFL, anterior inferior tibiofibular ligament, and deltoid ligament, the ATFL demonstrates lower maximal load and energy to failure values under tensile stress. This is the reason why it is the most commonly injured ligament in the classic inversion with or without plantar flexion mechanism.

The CFL courses from the lateral malleolus posteriorly and inferiorly to the lateral aspect of the calcaneus at a mean angle of 133 degrees from the long axis of the fibula(8). The CFL restricts excessive supination of both the talocrural and subtalar joints. Studies have demonstrated that the CFL restricts excessive inversion and internal rotation of the rearfoot, and is most taut when the ankle is dorsiflexed(7). Considering that the CFL is under less strain in plantarflexion, injury to this ligament is not as common. It is more commonly injured if the inversion mechanism occurs in neutral to dorsiflexion positions – hence the CFL runs a distant second as the most-often injured of the lateral ankle ligaments.

The PTFL runs from the lateral malleolus posteriorly to the posterolateral aspect of the talus. The PTFL has broad insertions on both the talus and fibula and provides restraint to both inversion and internal rotation of the loaded talocrural joint(7,8).It is the least commonly sprained of the lateral ankle ligaments as it is only under a strain load when the ankle is in full dorsiflexion; the congruency position where the talus and ankle mortise are closely locked together and hence relatively stable.

Other ligaments such as the syndesmosis ligament, subtalar joint ligaments, bifurcate ligaments and also the supporting tendons may also be injured in the inversion ankle sprains however they will not be discussed in the context of chronic ankle instability.

What Is CAI?

The term chronic ankle instability (CAI) has been interchanged with other names and definitions in the literature such as ‘recurrent ankle instability’ and ‘residual ankle instability’. For the purposes of this article, the term CAI will be used. It has often been assumed that all cases of CAI follow the same sequalae from the original lateral ligament injury, which then progresses to episodes of recurrent giving way and CAI. This leads to the assumption that a consistent relationship between impairments and activity limitations exists. However, it is clear that sufferers of CAI are not a homogenous group but can consist of heterogenous groups of patients all with varying deficiencies and what leads to CAI may be multifactorial(10).

It has been reported that 32-74% of individuals with a previous history of ankle sprain suffer from some type of residual and chronic symptoms, recurrent ankle sprains, and/or perceived instability(11,12). Historically, CAI has been divided into two subgroups; mechanical and functional instability. Mechanical instability relates to the anatomical changes that follow an acute ankle sprain(13, 14). These include factors such as:

• Pathological laxity in the lateral ankle ligaments
  Altered joint mechanics of the talocrural joint and distal tibiofibular joint
• Synovial inflammation
• Soft tissue of bony impingement
• Degenerative changes

Functional instability is an ambiguous term that defines instability based on functional performance tests such as balance and proprioception, and a patient’s perception that the ankle feels ‘weak’ and ‘unstable’(14-17). This definition attempts to highlight and categorise the proprioceptive changes that follow lateral ligament injury. However, confusion and disagreement exists in the literature as to how mechanical and functional instability relate to each other – and if indeed they do interact(10).

Hertel (2002) proposed arguably the best model, which describes CAI as ‘having components of mechanical and functional instability that are not mutually exclusive and co-exist on a continuum, and when combined lead to recurrent sprain’(13). The changes with mechanical instability (anatomical) are proposed to lead to insufficiencies that predispose the person to further episodes of instability. Functional instability results from impairments such as impaired proprioceptive and neuromuscular control. When mechanical and functional insufficiencies are both present, recurrent sprain results and Hertel defined ‘recurrent sprain’ as his third subgroup (see Figure 2).

Anecdotally however, participants have reported residual feelings of instability and ankle laxity after ankle sprain but have not reinjured their ankles. Furthermore, studies on patients with both mechanical and functional instability performed differently to patients with only functional instability in areas such as postural sway(18) and peroneal reaction times(19). This suggests that the Hertel model may not be completely inclusive of all types of CAI.