Chronic Ankle Instability

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Clinically Relevant Anatomy

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

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

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.

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