Chronic Ankle Instability

Clinically Relevant Anatomy

Ankle sprain is a common athletic injury and About 20% of acute ankle sprain patients develop chronic ankle instability[1]. Two million lateral ankle sprains occur annually in the United States, [2] affecting the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL) and/or the posterior talofibular ligament (PTFL). The literature reflects a high rate of persistent disability and recurrence.[3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15]

Following an acute ankle sprain, deficits in postural control, proprioception, muscle reaction time and strength typically occur, [16] [17] [7] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32] [33] [3] [34] [4] [5] [35] which can lead to chronic ankle instability (CAI).[35] [6] An inability to complete jumping and landing tasks within 2 weeks of a first-time lateral ankle sprain (LAS) and poorer dynamic postural
control and lower self-reported function 6 months after a first-time LAS were predictive of eventual CAI outcome[36].  CAI includes mechanical instability (motion exceeds normal physiological limits) and functional instability (objectively stable with subjective feelings of instability related to sensorimotor or neuromuscular deficits).[3] [4] [5] [35] [6] [37] [38] [8]

Clinical Presentation

Clinically, the history of patients with chronic ankle instability reveals past recurrent ankle sprains and severe inversion injury. They take special precautions against weight bearing, strenuous activities, and walking on rugged surfaces.

CAI is characterised by a range of deficits that can be evaluated along a continuum of sensorimotor measures. It is apparent that conscious perception of afferent somatosensory information, reflex responses, and efferent motor control deficits are present with ankle instability[39]. The specific origin of these deficits local to the ankle ligaments or at the spinal or supraspinal levels of motor control have yet to be fully elucidated. It is clear, however, that both feedback and feedforward mechanisms of motor control are altered with ankle instability.

The main causes of chronic ankle instability that have been found are: decreased proprioceptive abilities because of a loss of mechanoreceptors and decreased muscle strength of invertor and evertor muscles. When lateral ankle sprain (LAS) occurs, damage not only occurs to the structural integrity of the ligaments but also to various mechanoreceptors in the joint capsules, ligaments, and tendons about the ankle complex. Collectively, these receptors offer feedback regarding joint pressure and tension, ultimately providing a sense of joint movement and position. Via afferent nerve fibres, this information is integrated with the visual and vestibular sensory systems into a complex control system that acts to control posture and coordination. When afferent input is altered after injury, appropriate corrective muscular contractions may be altered. Thus, damage to the mechanoreceptors surrounding the ankle joint with an LAS may contribute to functional impairments and chronic instability subsequent to initial injury

Proprioception

Proprioception has been described as a product of sensory information gathered to the central neural system by mechanoreceptors located in the joint-capsule, ligaments, muscles, tendons, and skin. Trauma to ligamentous tissues that contains mechanoreceptors may result in partial differentiation, which can lead to proprioceptive deficits and will subsequently contribute to CAI.  Postural-control deficits during quiet standing after acute LAS and in those with CAI have been frequently reported[11].

Muscle weakness

Next to the sensorimotor deficits, researchers have suggested weakness of the peroneal muscles to be related to chronic ankle instability.  Deficits in evertor strength would reduce the ability of these muscles to resist inversion and return the foot to a neutral position and thereby prevent inversion sprain. Not concentric, but eccentric evertor weakness has been demonstrated in patients suffering from chronic ankle instability.  Other researchers have shown concentric invertor strength deficits in patients with CAI. They had 2 explanations for the inversion weakness. Firstly it could be the result of selective reflex inhibition of the ankle invertors’ ability to start moving in the direction of initial injury. A second cause could be deep peroneal nerve dysfunction as a result of over-stretching the peroneal nerve. Another theory they speculated is that the motor neurone pool associated with invertor muscle function has become less excitable by a lateral ankle sprain, whereas the motor neurone pool associated with evertor function is not affected that much.

Predictors of Chronic Ankle Instability

Doherty[40] suggests that the combination of the SEBT as a predictor of dynamic balance in combination with the Foot and Ankle Ability measure as a patient self reported outcome can predict the likelihood of CAI.

  • The Star Excursion Balance Test (SEBT) (particularly the posterolateral reach) has very valuable predictive capacity for chronic ankle instability     
  • The Foot and Ankle Ability Measure (specifically the activity of daily living subscale) can be used as an objective measure of recovery following acute LAS. A low score on this questionnaire, in particular in conjunction with the posterolateral reach on the SEBT, is likely to predict CAI.

Read more here - Chronic Ankle Instability Risk Identification

Diagnostic Procedures

Mechanical ankle instability is induced by ligament laxity; while functional ankle instability is caused by postural control deficits, neuromuscular deficits, muscle weakness, and proprioceptive deficits.  The chronic ankle instability selection criteria have recently been updated by the International Ankle Consortium[41] and there may be seven subsets, including mechanical instability interaction, frequency of multiple sprains, and perceived instability[1].

On physical examination the hindfoot motion should be recorded and peroneal muscle strength should be tested. Signs of ligamentous laxity need to be checked. Stability tests like the anterior drawer and talar tilt test should be performed. In patients with chronic ankle instability, proprioception is often abnormal; 86% of patients with grade III ankle sprains has peroneal nerve and 83% has tibial nerve stretch injury.  To test proprioception the modified Romberg test can be used: the patient stands on the non-affected ankle with open eyes and then with closed eyes and this is repeated with the injured ankle.

MRI is most useful for chronic ankle instability. Ligament injury can be seen on MRI as swelling, discontinuity of fibre, a lax or wavy ligament, or non-visualisation. The ankle should be in neutral or slight plantar flexion to help align ATFL and CFL. Limitations of MRI are cost, time, availability, motion artefact, and being unable to accurately predict chronic sequelae following acute injury.

Outcome Measures

Patient Report

Objective Tests

Management / Interventions

Differentiation between functional and anatomical ankle instability is very essential to guide the proper treatment. Unlike acute ankle sprain, chronic ankle instability might require surgical intervention. Before conducting any surgical procedure, nonsurgical management is highly recommended for patients with chronic ankle instability. During the rehabilitation stage, neuromuscular and proprioceptive training should be provided as well as orthotics if indicated.

Since research has shown that repetitive ankle joint injuries cause neuro-sensorial, proprioceptive and mechanical impairments, exercises that increase proprioception, balance and functional capacity are routinely performed after an ankle joint injury in addition to strengthening the muscles.

Conservative Management

Balance training

Problems found in patients with CAI are the decreased postural control and joint position awareness and the increased instability. Changes in sensorimotor system function are thought to be on the origin of these problems. Balance training is an important part of the current rehabilitation protocols for CAI[8][9][7]. The effects of  balance training on the sensorimotor deficits typical for CAI, including postural control, dynamic balance, joint position sense and segmental spinal reflexes, have been determined.  The Star Excursion Balance Test has been suggested as an excellent rehabilitation exercise for balance in CAI[40].     

Progressive loading

Isokinetic muscle strengthening has been shown to have a positive effect on the functional ability, muscle strength and proprioception of the ankle.

Braces

Docherty[40] recommends brace use in individuals with CAI for high risk activity such as return to sport for 6 months following ankel sprain.  Individual needs should be considered such as risk of dependency, likelihood of appropriate use, cost etc.    

Surgical Intervention

When bracing and taping methods fail to provide support for chronically unstable ankles persistently fail to recover, surgery is to be considered[1].  Surgically, the injured ligaments are repaired by applying tendon grafts or local tissues. Among the surgical methods is the Broström procedure that primarily repairs the damaged ligaments. Augmenting the primary repair by tendon transfer protects the repair and adds to the stability. Arthroscopy is ready to lend a hand to diagnose and treat the ankle instability.

Associated lesions

Chronic ankle instability is often associated with lesions that evolve from contributory factors. They do not necessarily occur with chronic ankle instability, and if any, not all these lesions occur together. Associated lesions that may accompany chronic ankle instability are chronic regional pain syndrome, neuropraxia, sinus tarsi syndrome, tendon disorders such as peroneal tendinopathy, dislocation or subluxation, impingement syndromes, fractures such as anterior calcaneal process, fibula and lateral talar process, loose bodies, and osteochondral lesion of talar dome or distal tibia[1].

Al-Mohrej[1] describes the following lesions as frequently present with chronic ankle instability:

Sinus Tarsi Syndrome

Sinus tarsi syndrome is common among basketball and volleyball players, dancers, and overweight people. It is also common among patients with flatfoot and hyper-pronation deformities. It consists of pain and tenderness of the sinus tarsi; that is, the lateral side of the hindfoot. It may occur following a single or series of ankle sprains. It is diagnosed by exclusion although magnetic resonance imaging could show evidence of the inflammation. Sinus tarsi syndrome is treated by primary repair of the sinus tarsi ligaments, augmentation by tendon, or both

Osteochondral Defects

Osteochondral defects (OCD) are injuries to the talus. They may include cartilage layers blistering and in-the-bone cyst-like lesions or even bone layers and cartilage fracture. OCD may occur as a result of one traumatic injury or recurrent trauma. OCD display swelling, ankle joint instability, and long pain. The exact mechanism of both pain and instability is not fully understood. Treatment is ideally operative depending on the nature, size, and location of the lesions.

Peroneal Tendinopathy

Peroneal tendinopathy is chronic inflammation of the peroneal tendon resulting in weakness of the active ankle stabilisers. This happens when a person performs a repetitive activity that annoys the tendon over a long period. In addition, poor and rapid training and poor shoe-wear may cause peroneal tendinopathy. People who have a hindfoot varus posture are more likely to experience peroneal tendinopathy. Most cases of peroneal tendinopathy are treated conservatively although surgical debridement and stimulation of healing either open or tendoscopically are gaining popularity.

Subtalar Instability

Subtalar instability is an incidence whose aetiology is still not known. It seems to be under diagnosed. It can have the symptoms of the chronic ankle instability. Clinically, the patients with subtalar instability have increased inward rotation. It is treated by a tendon transfer or tenodesis procedure such as Chrisman–Snook or alternatively by an anatomic ligament reconstruction.

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