Ankle sprain, although perceived as an innocuous injury, often leads to residual symptoms months to years after the initial injury. Chronic ankle instability (CAI), characterized by perceived ankle joint instability and recurrent ankle injuries, occurs after up to 70% of initial ankle sprains in athletes, and it is a highly prevalent condition (>25%) in collegiate and high school athletes, particularly those playing soccer, basketball, and volleyball (2,5,9,11,48). CAI has been associated with functional limitations, diminished physical activity levels, and lower health-related quality of life. In addition, there is concerning evidence that CAI may trigger the early onset of posttraumatic osteoarthritis (10,11,47). Despite the frequency of CAI in athletes, the underlying mechanisms for this potentially disabling condition have not been clearly established.
CAI has traditionally been thought to be due to either mechanical (i.e., pathological joint laxity) or functional insufficiencies (i.e., proprioceptive deficits) (14). However, the recent consensus statement of the International Ankle Consortium suggests that CAI appears to be largely attributed to sensorimotor impairments, regardless of the presence of mechanical joint instability (11). Of importance is postural control impairment which has been consistently observed in athletes as well as others with CAI (3,38,54,55) and linked to patient-oriented symptoms and a heightened risk of ankle sprain (21,32). The purpose of this article is to provide an update on our understanding of the mechanisms of postural control deficits in patients with CAI and how this may affect its diagnosis and treatment in athletes.
Traditional Mechanism: Peripheral Sensory Impairment
Proprioceptive deficits, characterized by loss of sensory input from the damaged articular mechanoreceptors after ankle sprain, have long been thought to be the origin of impaired postural control associated with CAI in athletes (14,15). However, there is ample evidence that cannot be explained by these peripheral deficits, such as bilateral impaired static balance and deleterious alternations in dynamic postural control before initial contact of the foot with the ground during gait and landing tasks, together which implicate that the central nervous system (CNS) may be involved (15). Additionally, studies disrupting mechanoreceptor function with regional anesthesia did not consistently disrupt postural control (8,17,31). Taken together, these results are suggestive that loss of sensory input from one of the somatosensory structures (i.e., articular, cutaneous, and musculotendinous receptors) may not be sufficient to cause consistent disruption in postural control. These differences in potential etiologies may be secondary to the amount of afferent information available within the somatosensory system requisite for normal postural control (15,31). The presence of redundant sensory information could help explain the findings from a recent meta-analysis that postural control is not impaired after desensitization of the plantar cutaneous receptors with ice or ice water (19). With a great deal of afferent information available within the somatosensory system, the global sensorimotor dysfunction (i.e., bilateral postural deficits) implicates that postural control deficits in patients with CAI may be secondary to central changes in postural control in addition to the peripheral deficits in ankle proprioception arising from the initial injury.
Contemporary Mechanism: Central Sensory Impairment
For effective postural control the CNS requires continuous afferent information from the vestibular, visual, and somatosensory systems (35). Sensory redundancy enables the CNS to select more reliable information for more efficient control, with a selection priority that adapts to the demands of postural tasks and environmental conditions (4,20,24). For example, the CNS relies most heavily on the somatosensory system during postural control on a stable surface. However, the CNS decreases its dependence on the somatosensory system on an unstable surface, and increases the contribution of other systems to maintain joint stability (24). This capability of the CNS to change its relative dependence on each sensory modality, based on various sensory contexts, has been termed “sensory reweighting.” This term refers to the mechanisms by which sensory information for postural control is organized with more reliable afferent input (16,20,22,35). Dynamics in sensory reweighting become more critical to coordination of movements in the athletic environment, involving highly complex and constantly changing sensory demands (i.e., variable surface and playing conditions, and unanticipated perturbations). An enhanced ability of sensory reweighting has been associated with better postural control in gymnastics, whereas alterations in sensory information processing have been suggested as a mechanism of postural instability seen in professional basketball players (41,52). Rehabilitation strategies for athletes with postural control deficits due to the sensory impairment may be different from the conventional rehabilitation that is usually focused on the motor aspect of postural control.
CAI appears to be associated with alternations in sensory reweighting. Meta-analyses (3,38,54,55) have consistently concluded that postural control deficits are present in patients with CAI. These impairments were consistently found during single-leg stance with eyes closed, but not with eyes open (16,25,30,36,53). These results suggest that the CNS constrained by CAI relies more heavily on the visual system to maintain single-limb stance. This may be the result of CNS adaptation to proprioceptive deficits by the injured joint. A recent meta-analysis (46) has confirmed the importance of visual input in patients with CAI because it demonstrated greater disruption in postural control during a transition from eyes-open to eyes-closed single-limb stances relative to healthy individuals without a history of ankle sprain. Thus, sensory reweighting to the visual system provides a compensatory mechanism for altered somatosensory input to successfully accomplish a goal of maintaining single-limb stance. However, athletes with CAI may be in danger during sport activities where attention and visual focus may be diverted from postural control, which may subsequently cause loss of balance and risk of injuries.
Contemporary Mechanism: Central Motor Impairment
In addition to sensory control of posture in the feedback manner, feedforward control of the CNS plays an important role (15). It is well documented that both spinal and corticospinal excitability mediate postural control. As postural demands increase, the CNS tends to suppress the spinal reflex, but increases the supraspinal input to accommodate greater postural demand (49). For example, during the postural transition from a simple to more complex motor task, neural drive from the spinal cord to the motor neuron pool innervating ankle stabilizing muscles decreases, whereas the supraspinal control increases (6). This has been interpreted as a shift in postural control from the low-level to high-level control centers and serves as a feedforward mechanism of postural control (23,49). This task-related modulation of both spinal and supraspinal control appears to be essential for developing highly skilled athletic performance (40). Badminton players exhibited reduced spinal excitability during receive stance while football juggling experts displayed enhanced supraspinal excitability, both of which represent better postural control (18,34). These similar neural adaptations were not surprisingly observed in dancers (39,42).
There is emerging evidence suggesting that athletes in CAI may be linked to decreased neural control at both the spinal and supraspinal levels (7,13,26–28,33,37,44,45,50). Earlier studies (28,44,45) found altered modulation of spinal excitability in patients with CAI, and this finding was further demonstrated by a recent study that found the strong relationship between the spinal reflex modulation and postural control, both of which differed between those with and without CAI (26). The heightened spinal response has been attributed to a decrease in presynaptic inhibition (44,45), which may be reflective of diminished supraspinal postural control. However, no studies have evaluated this hypothesis, making it difficult to determine the supraspinal contribution to postural control deficits associated with CAI. Nonetheless, given a growing body of evidence that a decreased level of corticospinal excitability at rest was consistently observed in the physically active with CAI (13,33,37,50), it is conceivable that the supraspinal postural control might be altered in athletes as well as others with CAI.
Clinical Implications for Rehabilitation
Impaired postural control is a key risk factor for CAI. An enhanced understanding of neurophysiologic mechanisms responsible for postural control deficits is needed to provide insights into more targeted intervention strategies for athletes with CAI. Briefly, proprioceptive deficits can be relieved by active and passive joint repositioning exercises. This appears to be effective not only in improving motor function (1) but also preventing recurrent ankle injuries (43). Additionally, visual reliance in sensory reweighting can be addressed through a visually challenging rehabilitation environment (12), whereby patients perform postural tasks with limited visual input. This in turn could enhance sensory reweighting of the CNS to the somatosensory system by forcing it to develop adaptive strategies to select more reliable proprioceptive input from the injured ankle. A potential adjunct to this could be the use of stroboscopic vision in therapeutic exercise. This intermittent vision obstruction has the potential to be incorporated into rehabilitation to create progressive visual perturbations (29). Finally, a heightened spinal response in postural control could be reduced by modulatory training of the spinal excitability. The training involves biofeedback on the spinal reflex response during a postural task that is given to patients in an attempt to decrease the magnitude of the response (51). Depending on the specific mechanism involved, one or more of these approaches would be indicated to further improve balance control.
The authors declare no conflict of interest and do not have any financial disclosures.
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