Chronic Ankle Instability

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Clinically Relevant Anatomy
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Ankle sprain is a common athletic injury. Three-quarters of these injuries involve the lateral ligamentous complex[1] consisting of the anterior talofibular ligament (ATFL), the calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL). Forced plantar flexion and inversion of the ankle while the body’s center of gravity rolls over the ankle are the most common way to injure these lateral ligaments. About 80% percent of acute ankle sprains make a full recovery with conservative management, while 10% to 30%[2] of acute ankle sprains develop mechanical or functional instability due to several reasons like a loss of mechanoreceptors[3], resulting in chronic ankle instability.[2,4,5]

Mechanism of Injury / Pathological Process
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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.

1. 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.[9] Trauma to ligamentous tissues that contains mechanoreceptors may result in partial differentiation, which can lead to proprioceptive deficits and will subsequently contribute to CAI.[10,11] Studies have shown decreased proprioceptive abilities in patients with chronically unstable ankles. [6,12,13]

2. Muscle weakness
Next to the sensorimotor deficits, researchers have suggested weakness of the peroneal muscles to be related to chronic ankle instability.[14] 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[15,16], but eccentric evertor weakness has been demonstrated in patients suffering from chronic ankle instability. [17,18,19] 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 overstretching the peroneal nerve. Another theory they speculated is that the motor neuron pool associated with invertor muscle function has become less excitable by a lateral ankle sprain, whereas the motor neuron pool associated with evertor function is not affected that much.

Clinical Presentation[edit | edit source]

A patient with chronic ankle instability mainly complains about “giving out of the ankle“ and has a past history of at least two or three severe ankle sprains. A patient with CAI often is insecure on uneven surfaces and complains having difficulties with it.

Diagnostic Procedures[edit | edit source]

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.[6] 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.[7] 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 fibers, a lax or wavy ligament, or non-visualization. The ankle should be in neutral or slight plantar flexion to help align ATFL and CFL. Limitations of MRI are cost, time, availability, motion artifact, and being unable to accurately predict chronic sequelae following acute injury.[8]

Outcome Measures[edit | edit source]

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Management / Interventions
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Since research has shown that repetitive ankle joint injuries cause neurosensorial, 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.


1. 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. 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. After 6 weeks of balance training, participants with CAI demonstrated better dynamic balance performance in the anterior medial, medial, and poste¬rior medial directions, ankle inversion joint position sense, and motoneuron pool excitability, compared to a healthy control group that did not com¬plete the training. These results suggest that balance training may lead to a reduc¬tion in the incidence of repeated injury. The level of evidence of this study was 2B. [20]

 

2. Isokinetic exercise
To strengthen the muscles, isokinetic exercise is used. A research[21], with an evidence level of 3A, tried to determine the influence of isokinetic exercise on proprioceptive, functional and strength deficits in athletes with chronic ankle instability. Since these researchers didn’t found any deficits in eccentric invertor and evertor muscle strength, the isokinetic exercise program of the ankle joint was only performed in the concentric mode. Each exercise session was carried out with three settings of 15 repetitions at 120°/s. These sessions were repeated three times a week and lasted for 6 weeks. The isokinetic exercise program had a positive effect on the functional ability, muscle strength and proprioception of the ankle.

Differential Diagnosis
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Key Evidence[edit | edit source]

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