The brain: A new frontier in ankle instability research

Will this help your doctor prevent your ankle from rolling? And where does spasticity fit in?
http://lowerextremityreview.com/article/the-brain-a-new-frontier-in-ankle-instability-research

Among the physically active, no musculoskeletal pathology is more prevalent than lateral ankle sprain. Recent investigations estimate 60% of the general population has experienced an ankle sprain.¹ Several risk factors for ankle sprain have been identified, such as impaired strength or balance, but the single greatest risk factor for a lateral ankle sprain is a history of a previous lateral ankle sprain.² It is estimated that 50% of patients who suffer an ankle sprain subsequently experience frequent sensations of rolling in the ankle, termed functional ankle instability (FAI). This pathology is often compared with similar joint instabilities at the knee³ and shoulder⁴ that have demonstrated a complex etiology, with causes spanning from morphologic changes to neuroplasticity in the cortex.
Although several possible mechanisms for FAI have been proposed, its etiology remains ambiguous. These theories are often complicated by their approach to mechanical laxity in the joint. Original reports of FAI described patients with normal amounts of joint laxity, suggesting the ligaments surrounding the joint may have healed. However, these patients demonstrated deficits in balance, leading the investigators to conclude that “peripheral deafferentation” contributes to this pathology.⁵ This implies that, while normal stiffness may be restored to the ligament as it heals, the mechanoreceptors within the torn ligament remain impaired or are replaced with receptors of a different type (i.e., free nerve endings). It was hypothesized that loss of this afferent (sensory) feedback would affect the joint’s proprioception—its sense of position, movement, and force—which would delay the sensation of ankle rolling and subsequent reflexive responses.⁶

Since these initial paradigms were proposed, extensive research has investigated proprioceptive deficits among populations of patients with unstable ankles, finding an inconsistent relationship between proprioception and joint instability.⁵ Similarly, further measurements of mechanical laxity in this population, originally taken using stress radiography, and more recently through the advent of ankle arthrometry, suggest mechanical laxity does exist in functionally unstable ankles, contributing to the confusion about the etiology of this pathology.⁷

Figure 1. Electromyographic recording from single transcranial magnetic stimulation pulse. MEP = motor evoked potential. (Reprinted with permission from reference 18.)

One important limitation to understanding the cause of this condition is the operational definition of proprioception used in research. Proprioception describes the afferent information that determines joint position sense, kinesthesia, and force sense arising from capsuloligamentous and musculotendinous mechanoreceptors. However, proprioception is often quantified by testing an individual’s ability to recognize a joint angle, identify when the joint is moving, replicate a given amount of force, or maintain balance.⁸ These indirect measures, much like an episode of giving way at the joint, require sensation at the joint, the modulation of a reflex at the spinal cord, integration in the somatosensory cortex, and a motor response initiated in the cortex and superimposed on spinal reflexes. These tests therefore do not account for each level of the nervous system, but rather an isolated motor response incorporating spinal and supraspinal influences.

Much more at link.