Spinal Reflex Excitability of Lower Leg Muscles Following Acute Lateral Ankle Sprain: Bilateral Inhibition of Soleus Spinal Reflex Excitability

Abstract

Neural changes in the ankle stabilizing muscles following ankle sprains are thought to be one contributing factor to persistent ankle dysfunction. However, empirical evidence is limited. Therefore, we aimed to examine spinal reflex excitability of lower leg muscles following acute ankle sprains (AAS). We performed a case-control study with 2 groups consisting of 30 young adults with AAS and 30 aged-matched uninjured controls. Hoffmann reflex (H-reflex) testing was performed to estimate spinal reflex excitability of lower leg muscles: soleus, fibularis longus (FL), tibialis anterior (TA). Maximal H-reflex (Hmax) and motor responses (Mmax) were determined by delivering a series of electrical stimuli at the sciatic nerve. Hmax/Mmax ratios were calculated to represent normalized spinal reflex excitability. Separate group-by-limb analyses of variance (ANOVA) with repeated measures found there were no significant interactions for any of the muscles (SL: F1,56 = 0.95, p = 0.33, FL: F1,51 = 0.65, p = 0.42, TA: F1,51 = 1.87, p = 0.18), but there was a significant main effect of group in the soleus (F1,56 = 6.56, p = 0.013), indicating the Hmax/Mmax ratio of soleus in the AAS group was significantly lower bilaterally (AAS = 0.56 ± 0.19, control = 0.68 ± 0.17, p = 0.013), with no significant group differences in the other muscles (FL: F1,51 = 0.26, p = 0.61, TA: F1,51 = 0.93, p = 0.34). The bilateral inhibition of the soleus spinal reflex excitability following AAS may be significant in that it may explain bilateral sensorimotor deficits (postural control deficits) following unilateral injury, and provide insights into additional therapies aimed at the neural change.

Conduction Velocity of Spinal Reflex in Patients with Acute Lateral Ankle Sprain

“…The present study was a secondary analysis of data from a previously published cross-sectional study that examined the effects of ALAS on the magnitude of spinal reflex excitability of lower leg muscles [ 11 ]. For this study, there were two independent variables: group (ALAS, healthy control) and limb (involved, uninvolved).…”

“…All participants were recruited from the university community through advertisements using flyers, phone calls, and emails. As described in the previous study [ 11 ], inclusion criteria for ALAS patients were (1) acute ankle sprain that occurred within the past three days (72 h) prior to reporting for testing; (2) ALAS that affects at least one of three lateral ankle ligaments including anterior talofibular ligament (ATFL), calcaneofibular ligament (CFL), and/or posterior talofibular ligament (PTFL); and (3) the presence of acute injury symptoms such as swelling, pain/tenderness, and loss of ankle and foot functions [ 11 ]. We excluded ALAS patients who had (1) other ankle sprains such as medial or high ankle sprains or (2) a history of lower extremity injuries (e.g., knee and hip) within the past six months prior to the study.…”

“…A similar proportion of right and left limbs in the ALAS group were classified as involved and uninvolved and as sham involved and sham uninvolved in the control group [ 20 ]. The detailed H-reflex testing protocol was described in the previous study [ 11 ]. Briefly, a unipolar stimulating electrode (cathode) was placed in the popliteal fossa over the sciatic nerve, and the dispersive electrode (anode) was placed over the suprapatellar region.…”

“…The H-reflex is conducted using 1 ms electrical pulses over a peripheral nerve, observing a direct muscle response (M-wave) from descending transmission from the stimulus to the muscle, and the reflexive muscle response (H-wave) from the ascending sensory stimulus over a reflexive arc. Only three studies have described reflexive excitability characteristics among patients with ALAS, with Hall et al [ 9 ] failing to find differences between involved and uninvolved limbs, Klykken et al [ 10 ] observing muscle-specific facilitation and inhibition between involved and uninvolved limbs, and Kim et al [ 11 ] reporting bilateral soleus inhibition between injured and uninjured groups. It has been hypothesized that arthrogenic muscle inhibition resulting from pain and swelling effectively diminishes the excitability of the alpha motor neuron pool and makes it more difficult to activate muscles, a factor that can potentially predispose these individuals to subsequent injury [ 12 ].…”

“…It has been hypothesized that arthrogenic muscle inhibition resulting from pain and swelling effectively diminishes the excitability of the alpha motor neuron pool and makes it more difficult to activate muscles, a factor that can potentially predispose these individuals to subsequent injury [ 12 ]. Interestingly, many of these changes have been observed independent of symptom severity (e.g., swelling, pain), suggesting that any degree of pain and swelling may yield inhibitory changes [ 9 , 11 ]. However, while this collective evidence suggests that reflexive excitability may contribute to activation deficits among patients with ALAS, this reflects only one property of nervous system function that can be assessed with this technique.…”