By Larry Hand
For individuals with chronic ankle instability (CAI), the somatosensory feedback necessary for postural adjustments, walking, and running may be hampered by a decrease in soleus spinal reflex excitability, according to a new study in the Journal of Athletic Training.
The findings of the multicenter study add to the body of evidence suggesting that central nervous system (CNS) issues, as well as mechanical joint laxity, contribute to CAI.
“A successful reorganization of the sensorimotor system after an initial ankle sprain is the critical point when individuals suffer chronic ankle instability or become copers [individuals who do not develop chronic instability after an ankle sprain] who break the cycle of recurrent injuries and disabilities seen in CAI,” corresponding author Masafumi Terada, PhD, ATC, an assistant professor in the College of Sport and Health Sciences at Ritsumeikan University in Kyoto, Japan, told LER by email.
According to this supraspinal modulation theory, the CNS in healthy people and copers modulates neural activity within the motor pathways to prevent the excessive ankle supination that is a mechanism of ankle injury, Terada said. A decrease in soleus spinal reflex excitability in patients with CAI would suggest the initial ankle injury triggers an alteration in that neuromotor process, he said.
Terada and colleagues conducted a case control study to see if spinal reflex excitability differences exist among individuals with CAI, copers, and controls. They measured ankle laxity in 37 individuals with CAI, 30 copers, and 26 healthy controls using an ankle arthrometer. They also assessed the maximum Hoffmann reflex and maximal muscle response for the soleus muscle in response to electrical stimulation; since slow-twitch fibers involved in the Hoffmann reflex make up most of the soleus muscle, a greater Hmax:Mmax ratio indicates greater spinal reflex excitability of the soleus muscle.
They found that individuals with chronic instability had lower Hmax:Mmax ratios than both copers and healthy controls. However, no difference existed between copers and controls. In addition, there were no significant differences among the groups for anterior-posterior or mediolateral ankle laxity.
The slow-twitch fibers in the soleus muscle are mostly innervated by small alpha motoneurons, Terada explained, so the study findings suggest that some people may restore their ability to reflexively recruit alpha motoneurons after ankle injury, and some may not.
“Therapeutic interventions that can increase the H-reflex in the soleus may help to break the cycle of recurrent injuries and disabilities seen in CAI,” he said. “Lower-intensity transcutaneous electrical stimulation, joint manipulations, and reflex conditioning protocols may be effective in increasing the soleus spinal excitability.”
Without a prospective study, however, it is difficult to know the true neurophysiologic mechanism underlying the between-group differences in soleus spinal reflex excitability, he noted.
Patrick McKeon, PhD, ATC, FACSM, an assistant professor of exercise and sports sciences at Ithaca College in New York, told LER in a phone interview that the study’s findings suggest CAI might be more related to the coordination and control of dynamic stabilizers than the function of static stabilizers.
“It really does fit in well with the body of evidence that’s saying chronic ankle instability seems to be related to a functional deficit as opposed to a mechanical one,” said McKeon, who was not involved with the study. “And it lines up well with the idea that we see lots of improvement in people as we have them undergo dynamic interventions.”
McKeon echoed Terada’s comments regarding possible neurophysiologic explanations for the findings.
“One of the mechanisms that might be driving it is a change in the motor neuron excitability,” he speculated. “But this study really can’t establish any cause and effect.”
Bowker S, Terada, M, Thomas AC, et al. Neural excitability and joint laxity in chronic ankle instability, coper, and control groups. J Athl Train 2016 Apr 11. [Epub ahead of print]