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Getting to the Bottom of Chronic Ankle Sprains

Posted on: 10/29/2008
One ankle sprain can change the course of your life. When does that happen? When one injury leads to another and another until you have a condition called chronic ankle instability (CAI). Every day in the United States, 23,000 people sprain their ankles. More than two-thirds of those folks will end up with CAI.

What happens with CAI? Why does it happen? And what can be done to prevent this from occurring? Those are the questions scientists are actively seeking to answer. Right now, there are several theories to help explain the mechanism behind chronic sprains.

Mechanical factors, such as the change in tissue tension around the ankle when a ligament is sprained, have always been part of the picture. But this is only one factor. Another is the loss of normal sensorimotor responses.

This refers to the ankle joint's ability to receive and interpret neurologic information about sensation and movement. This is the neurologic side of ankle injury and instability. A decreased awareness of the foot and ankle position (especially with changes in the ground or surface we are walking on) contributes to repeated ankle sprains.

Swelling or edema associated with the injury reduces sensation needed to provide dynamic joint stability. Changes in the joint can also affect communication between the ankle joint and surrounding soft tissues such as muscles. This phenomenon is referred to as arthrogenic muscle inhibition. Arthrogenic means the effect on muscles is generated or starts in the joint first.

In this study, activity-dependent plasticity as it effects ankle stability/instability is the topic. Plasticity refers to the ability of the nervous system to change or modify function. The question is: when the ankle joint is injured, are there changes in the way the nervous system (spinal cord and brain) respond?

The experiment involved two groups of college-aged young adults. One group had a history of more than one ankle sprain in the past 12 months. The second (control) group had no history of ankle sprain and no problems with their feet or ankles.

Using a university research laboratory, they measured motoneuron pool excitability. The motoneuron pool in the spinal cord is the central controller of muscle activation. Excitability of the motoneuron pool comes from descending messages (from the brain) and ascending messages. Ascending messages come from the motor and sensory nerves in the joint and muscles bringing information to the spinal cord and up to the brain.

The Hoffman or H-reflex is used to measure the excitability of the motor neuron pool. In this study, H-reflex was used to look at the effect of CAI on the motoneuron pool excitability of the soleus muscle. The soleus muscle is the smaller of two calf muscles (gastrocnemius and soleus). It has an important role in ankle function. The soleus muscle helps provide postural stability when a person is standing. And postural stability is important in preventing repeated ankle sprains.

Everyone in the study filled out several surveys to assess function, functional limitations, and areas of disability. A special recording device was used to measure the H-reflex of the soleus muscle on the side of the injured ankle.

Electrodes placed over the soleus muscle recorded electric impulses and H-reflex responses when the nerve to the soleus (posterior tibial nerve) was stimulated. Testing was done with the subjects standing on both legs (double-legged stance) and when standing on one leg (single-legged stance).

They found a significant difference in motoneuron excitability between the two groups. The group with chronic ankle instability had more depression (less excitability) of the motoneuron pool. This means less input to the muscle to tell it to contract.

The biggest difference was seen when going from a double- to single-legged stance (standing position). The healthy group was able to modulate (change) nerve signals when changing position or surface stability (going from a stable to unstable surface). The injured group had much slower changes in reflex response and postural control.

This evidence that there may be a neurologic component to CAI will direct us in better understanding how the central nervous system adapts to joint injury. Physical therapists may be able to use this information to develop ways to prevent recurrent or repeated ankle sprains. For example, it may be possible to improve motoneuron excitability with training.

Other studies have already shown it's possible to increase H-reflex responses following a program of dynamic resistance training. Further studies are needed now to find other ways to improve rehab for patients with CAI.

JoEllen M. Sefton, PhD, et al. Segmental Spinal Reflex Adaptations Associated with Chronic Ankle Instability. In Archives of Physical Medicine and Rehabilitation. October 2008. Vol. 89. No. 10. Pp. 1991-1995.

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