Ankle sprains are a common injury and have been reported as a greater health care burden than once believed.1 Following an ankle sprain, development of chronic ankle instability (CAI) is likely.2 As a precursor to post-traumatic osteoarthritis, CAI is the term associated with prolonged symptoms of pain, instability, and impaired function following an initial ankle sprain. When an individual sprains his or her ankle, he or she is more susceptible to re-injury, which can result in a cascade of long-term issues that can lead to post-traumatic osteoarthritis.3 It is reported that 68% to 78% of patients with symptoms of CAI develop post-traumatic ankle osteoarthritis and cartilage damage.4–6 These long-term issues following multiple ankle sprains also include damage to the peripheral neuromuscular system, which can alter the supraspinal aspects of motor control over time.7 Damage to the peripheral nerves can result in poor interaction between the central and peripheral nervous systems. A condition such as CAI can alter the excitability along the axon, which results in a reduced nerve conduction velocity.8 Nerve conduction velocity is an excellent measure of the function of the peripheral nervous system, due to its sensitivity to both the myelin sheath and axonal changes in the motor nerve.9 Dysfunction to the motor nerve can result in skeletal muscle atrophy,9 subsequently leading to deficits in strength.
Following an inversion ankle sprain, tension is exerted on the fibular nerve along with swelling, scarring of the ligament, and adhesion development.10 Reduced nerve conduction velocity may represent a lesion on the nerve that occurs during the initial or recurrent inversion injury11 or follows repetitive bouts of giving way.12 Deficits in motor nerve conduction velocity have been reported in individuals with CAI.12 Slower nerve conduction velocity also explains the prolonged fibular muscle group reaction time that has been identified in individuals with CAI.13–15
Although clinicians have historically relied on balance and strength for neuromuscular control, randomized controlled trials have only been used recently to fully examine the potential success of these interventions.16–18 Recent research17 determined that sensory-targeted ankle rehabilitation strategies (eg, joint mobilization, plantar massage, and triceps surae stretching) improved clinical and patient-oriented outcomes by incorporating both sensory and motor aspects of sensorimotor control. It is unknown whether these strategies improve nerve conduction velocity.
It has often been suggested that the fibular muscles can protect the ankle joint from inversion-induced trauma.19–22 The quick activation of the fibular muscles may be needed to provide protection from repetitive inversion injuries. Improving motor fibular nerve conduction velocity may help prevent recurrent ankle sprains by improving dynamic ankle joint stability to accommodate for reduced static ankle joint stability. Little research has been conducted to determine if therapeutic exercise improves nerve conduction velocity following chronic ankle injuries. Therefore, the purpose of this study was to determine if a balance or strength training protocol improves motor nerve conduction velocity in individuals with CAI.
Fifty participants with CAI from a local university community volunteered for this study.16 Three participants were excluded from testing because they did not meet inclusion criteria. Forty-seven participants were pretested and then randomly assigned to the treatment or control groups. Ten participants were excluded from the analysis due to loss to follow-up, poor compliance, or reported pain during testing, leaving 37 participants for the analysis.
All inclusion and exclusion criteria were in accordance with the International Ankle Consortium recommendations.23 These recommendations include inclusion and exclusion criteria and using a validated self-reported questionnaire to confirm the presence of CAI.23 Participants qualified if they had a history of at least one ankle sprain and the ankle joint “giving way” or feelings of ankle instability. CAI was also determined by the Identification of Functional Ankle Instability Questionnaire (IdFAI) and participants qualified if they reported a score of 11 or more.24 If a participant had a history of ankle injuries in both ankles, only the most severe ankle (higher IdFAI score) was tested. Participants did not qualify if they experienced an acute lower extremity injury within the past 3 months, had participated in formal rehabilitation within the past 3 months, had a history of lower extremity surgery or fracture that required alignment in the involved limb, or had any diagnosed neurological dysfunction, such as multiple sclerosis, Parkinson's disease, or head injuries. All participants completed the National Aeronatics and Space Administration Physical Activity Status Scale (NASAPASS) to determine their physical activity level. Participant demographics are listed in Table 1.
Participant Demographics According to Rehabilitation Group
Participants were excluded if they developed a lower extremity injury during the study period or were non-compliant (attended less than 80% of the 18 rehabilitation sessions). They were also excluded if they reported pain and presented with fear of pain during testing. Before participating in the study, all participants read and signed an informed consent form approved by Indiana University's Institutional Review Board for the Protection of Human Subjects.
Following the informed consent process, nerve conduction velocity testing was completed. Then participants completed additional baseline measures that were part of a larger study.16 Following baseline testing, participants were randomly assigned to one of three groups: balance training protocol (BTP), strength training protocol (STP), and sham control (CON).
The BTP group completed multiple hop to stabilization exercises ranging from static balance to dynamic hopping tasks that were adapted from McKeon et al.25 The exercises consisted of hop to stabilization, hop to stabilization and reach, unanticipated hop to stabilization, and single-limb stances activities with eyes open and eyes closed. For the hop to stabilization exercises, participants completed 10 hops in four different directions (anterior/posterior, medial/lateral, anteromedial/posterolateral, and anterolateral/posteromedial) starting at 18 inches and progressing to 27 and 36 inches. The hop to stabilization and reach exercises were performed similarly to the hop to stabilization exercises, but participants completed 5 repetitions of each direction and were instructed to reach back to the position they hopped to the contralateral limb after each hop. The unanticipated hop to stabilization was a sequence of 9 numbers on a grid. Participants were instructed to hop to the corresponding number, starting at 5 seconds per move and decreasing the time per move to progress. The single-limb stance with eyes open started on a hard floor with arms across chest for 60 seconds, progressed to a foam pad, and concluded with a ball toss with a 6-lb medicine ball. The single-limb stance eyes closed exercise started with arms out on a hard floor for 30 seconds, progressed to arms across chest and with length of time increasing to 60 and 90 seconds, and concluded by incorporating a foam pad to increase the level of difficulty. Participants progressed when they performed the following tasks without errors: touching down with the opposite limb, excessive trunk motion, removing the hands from the hips during hands-on-hips activities, bracing the nonstance limb against the stance limb, or missing the target.25
The STP group performed a progressive strength training program in all four ankle directions. A resistance band was used to provide resistance in the inversion, eversion, and dorsiflexion directions, while standing heel raises were employed for the plantar flexion direction. The STP group also completed progressive proprioceptive neuromuscular facilitation concentric strengthening exercises in diagonal patterns (dorsiflexion/inversion to plantarflexion/eversion and dorsiflexion/eversion to plantarflexion/inversion). Participants progressed by increasing the number sets, repetitions, and resistance each week. For the resistance band progression, participants started with 3 sets of 10 repetitions using a heavy band and progressed to 4 sets of 10 repetitions the following week. The next 2 weeks followed the same sets and repetitions pattern with a super-heavy band, and the final 2 weeks used an ultra-heavy band. The progression for the proprioceptive neuromuscular facilitation and heel raises started with 2 sets of 10 repetitions and then increased each week: 2 × 15, 3 × 10, 3 × 15, 4 × 10, and 4 × 15.
The CON group completed a 20-minute bike exercise at mild to moderate resistance. These protocols are based on previous research.16,25 Participants met with the investigator (EAH) three times per week for 6 weeks and completed their respective protocols. The posttest occurred at the end of the 6 weeks within 24 to 72 hours.
Nerve Conduction Velocity
Nerve conduction velocity is a reliable26 measure of the integrity of the fibular nerve by measuring the abnormalities in the length of nerves.27 Procedures and parameters for obtaining nerve conduction velocity replicated those used by Simon and Docherty.12 Briefly, participants were in a side-lying position on the uninvolved limb with hips and knees flexed to 90° and a small pillow between the legs (Figure 1). The temperature of the room was consistent throughout testing sessions. The surface temperature of the participant's skin was monitored and recorded using a temperature probe that was placed on the mid-shaft of the fibula. Participants rested for 10 minutes prior to testing to acclimate to the temperature of the room. A SierraWave II electroneuromyography system (Cadwell Laboratories, Kennewick, WA) equipped with an oscilloscope, amplifier, and stimulator was used to quantify nerve conduction velocity. The amplifier settings were 2,000 uV/Div gain, 10,000 Hz hicut, 10 Hz locut, and 10 ms/Div sweep speed. The stimulation site was located just posterior to the fibular head, which varied between participants. Surface electrodes were used to determine the compound action potential and the computer produced the latency, which is the amount of time from the stimulus to the onset of the compound action potential. The stimulus intensity with direct current square wave was increased until a compound action potential was identified consistently three times. The location from the cathode was marked to calculate the distance from the active electrode located on the dorsum of the foot 6 cm distal and anterior to the ground electrode placed on the lateral malleolus. Nerve conduction velocity (m/s) was calculated as the distance of the cathode to the active electrode in meters by the latency in seconds. This value was used for statistical analysis.
Configuration of the nerve conduction velocity to stimulate the peroneal nerve.
A repeated measures analysis of covariance was conducted with nerve conduction velocity as the dependent variable. The independent variables were time (pretest and posttest) and group (BTP, STP, and CON). Adjustments were made for three covariates: skin temperature of the leg, body mass index, and age based on a previous study.28 Adjusting for these covariates ensured that any difference between the independent variables was due to the intervention. Finally, a Bonferroni post-hoc test identified the specific location of group and group × time differences. A priori alpha level was set at a P value of less than .05. Additionally, bias-corrected Hedge's g effect sizes and corresponding 95% confidence intervals were calculated29 and interpreted as weak (≤ 0.39), moderate (0.40 to 0.69), or strong (≥ 0.70).30 Finally, minimal detectable change (MDC95) score and the mean differences were calculated. The MDC95 equation is 1.96 × the standard error of the mean (SEM) × √2,31,32 where the SEM was calculated by multiplying the pooled standard deviation from the control group by √(1–ICC.32 The intraclass correlation coefficient (ICC) used was from reliability testing (ICC3,k = 0.90).
At baseline, the mean and standard deviation for each group were the following: 37.08 ± 4.19 m/s for BTP, 37.08 ± 4.03 m/s for STP, and 38.09 ± 4.66 m/s for CON. At posttest, the values were: 37.85 ± 2.54 m/s for BTP, 37.00 ± 3.85 m/s for STP, and 38.00 ± 5.04 m/s for CON. The repeated measures analysis of covariance did not result in a significant time by group interaction (F2,30 = .43, P = .66, power = 0.11) (Figure 2). There was also no main effect for time (F1,30 = .54, P = .47, power = 0.11). The covariates of skin temperature did have a significant interaction on time, indicating that skin temperature is correlated to the dependent variable (skin temperature: F1,30 = 16.0, P = .01, power = 0.97). Age and body mass index did not have a significant interaction with time (age: F1,30 = 0.05, P = .83, power = 0.06 and body mass index: F1,30 = 2.5, P = .125, power = 0.33). Hedge's g effect size for each group from pretest to posttest was weak: BTP: 0.20 (95% confidence interval [CI]: −0.57 to 0.97), STP: 0.02 (95% CI: −0.75 to 0.79), and CON: 0.02 (95% CI: −0.82 to 0.85). The MDC calculated was 4.25 m/s compared to the mean differences for BTP (0.77 m/s), STP (0.08 m/s), and CON (0.09 m/s).
Bar graph of nerve conduction velocity between groups and between pretest (pre) and posttest (post). BTP = balance training protocol; STP = strength training protocol; CON = sham control
This was the first study to evaluate the effect of a 6-week ankle rehabilitation program on nerve conduction velocity. As previously reported, both the BTP and STP resulted in improved strength, balance, and functional performance.16 Yet, despite controlling for important covariates, there was no significant improvement in fibular nerve conduction velocity following any intervention. Both experimental conditions had small effect sizes with 95% CIs that crossed zero.
The lack of significant findings may be attributed to multiple factors, including an insufficient time period for rehabilitation. A previous study33 used biofeedback to treat foot drop in stroke patients and was unable to find significant improvements in fibular nerve conduction velocity, despite having enhanced function. Participants in this study only met three times per week for 5 weeks. Their lack of significant findings agrees with our study, indicating that 5 to 6 weeks is not enough time to improve nerve conduction velocity despite improving physical function. Previous research indicates that strength gains occur in the first 3 to 5 weeks of training due to neural factors, whereas hypertrophic gains occur within 4 to 6 weeks.34 However, it remains unknown if motor fibular nerve conduction velocity is one of the neural factors involved in the reported strength gains. Rather, proprioceptors have been shown to improve following 6 weeks of strength training.18,35 However, a 12-week plyometric training protocol improved motor tibial and fibular nerve conduction velocity while improving isokinetic strength at the ankle in untrained college women36 and boys soccer players with no history of ankle sprains.37 The plyometric training protocol used in these studies met for 1 hour per day, twice weekly for 12 weeks. These studies infer that motor nerve conduction velocity may manifest improvements well beyond 6 weeks for 30 minutes per session three times per week. Intensity of the treatment protocols may also play a factor. The current study only employed balance training and strength training protocols, whereas the previous research36,37 that sought improvements in fibular nerve conduction velocity followed a plyometric training protocol.
A second factor when comparing to previous research is the diverse variables that have been studied. A similar neuromuscular variable to nerve conduction velocity is muscle reaction time. A previous study38 examined muscle reaction time following a 6-week multi-station proprioceptive rehabilitation protocol in individuals with CAI. Eils and Rosenbaum38 determined a significant improvement in fibularis brevis and longus muscle reaction time in the exercise group, whereas the control group did not change. Another study39 found that a 4-week Biodex Stability program was effective in improving fibularis longus muscle reaction time following an inversion perturbation. The improvements from the previous studies38,39 in fibularis longus muscle reaction time, following a stretch-reflex mechanism, may suggest that rehabilitation protocols are effective at improving the sensory deficits of the nerve compared to the motor speed deficits of the nerve in 4 to 6 weeks.
Although it has been previously reported that individuals with CAI have decreased nerve conduction velocity compared to healthy participants,12 it is unknown if the decrease in nerve conduction velocity was present prior to injury. Our cohort of participants with CAI had a nerve conduction velocity of approximately 2 m/s slower compared to previous research using the same procedures (37.4 vs 39.3 m/s).12 Many believe the slower nerve conduction velocity is explained by a traction lesion following injury;11,12 however, the decreased velocity could have caused the inversion trauma due to the nerve's inability to control the ankle back into a stable position. Previous research determined that immediately following an ankle sprain, there was a significant decrease in nerve conduction velocity compared to the contralateral healthy ankle.11 Researchers found that these values improved 5 weeks after trauma.11 In comparison to our study and previous research,12 individuals with CAI continue to experience a deficit in nerve conduction velocity well after the acute injury. This suggests that the healing of the motor nerve may take much longer for a chronic injury than an acute trauma. Future research should examine prospective studies to determine if slower nerve conduction velocity is a risk factor for CAI, or if nerve conduction velocity is different depending on the chronicity of the most recent ankle sprain or giving way episode.
Our study had a low sample size, which contributed to low statistical power. Another limitation is that only surface electrodes were used to assess the activation pattern of the fibular muscles. Thus, future research should determine if in-dwelling electromyography is a more sensitive measure of nerve conduction velocity following rehabilitation in those with CAI.
Implications for Clinical Practice
The purpose of this study was to determine if nerve conduction velocity improved following strength or balance training in individuals with CAI. Because nerve conduction velocity deficits are present in individuals with CAI and neural impairments are thought to contribute to the development of post-traumatic ankle osteoarthritis, understanding which functional rehabilitation protocols can improve neural impairments in individuals with CAI is important. Our 6-week interventions improved balance, strength, and self-reported function but not nerve conduction velocity, which may need more than 6 weeks to have a clinically meaningful improvement.
- Gribble PA, Bleakley CM, Caulfield BM, et al. Evidence review for the 2016 International Ankle Consortium consensus statement on the prevalence, impact and long-term consequences of lateral ankle sprains. Br J Sports Med. 2016;50:1496–1505. doi:10.1136/bjsports-2016-096189 [CrossRef]27259753
- Beynnon BD, Vacek PM, Murphy D, Alosa D, Paller D. First-time inversion ankle ligament trauma the effects of sex, level of competition, and sport on the incidence of injury. Am J Sports Med. 2005;33:1485–1491. doi:10.1177/0363546505275490 [CrossRef]16009979
- McKeon PO, Hubbard-Turner T, Wikstrom EA. Consequences of ankle inversion trauma: a novel recognition and treatment paradigm. In: Zaslav KR, ed. An International Perspective on Topics in Sports Medicine and Sports Injury. London, England: IntechOpen Limited; 2012. https://www.intechopen.com/books/an-international-perspective-on-topics-in-sports-medicine-and-sports-injury/consequences-of-ankle-inversion-trauma-a-novel-recognition-and-treatment-paradigm.
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- Hintermann B, Boss A, Schäfer D. Arthroscopic findings in patients with chronic ankle instability. Am J Sports Med. 2002;30:402–409. doi:10.1177/03635465020300031601 [CrossRef]12016082
- Hirose K, Murakami G, Minowa T, Kura H, Yamashita T. Lateral ligament injury of the ankle and associated articular cartilage degeneration in the talocrural joint: anatomic study using elderly cadavers. J Orthop Sci. 2004;9:37–43. doi:10.1007/s00776-003-0732-9 [CrossRef]14767703
- Hass CJ, Bishop MD, Doidge D, Wikstrom EA. Chronic ankle instability alters central organization of movement. Am J Sports Med. 2010;38:829–834. doi:10.1177/0363546509351562 [CrossRef]20139327
- Johnson EW, Olsen KJ. Clinical value of motor nerve conduction velocity determination. J Am Med Assoc. 1960;172:2030–2035. doi:10.1001/jama.1960.03020180040007 [CrossRef]14407441
- Walsh ME, Sloane LB, Fischer KE, Austad SN, Richardson A, Van Remmen H. Use of nerve conduction velocity to assess peripheral nerve health in aging mice. J Gerontol A Biol Sci Med Sci. 2015;70:1312–1319. doi:10.1093/gerona/glu208 [CrossRef]
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Participant Demographics According to Rehabilitation Groupa
|Group||N||IdFAI||Previous Ankle Sprains||Age (y)||Height (cm)||Weight (Kg)||Sex||NASAPASSb|
|BTP||13||21.5 ± 3.8||4.23 ± 2.80||23.5 ± 6.5||175.0 ± 8.5||72.8 ± 10.9||7 M, 6 F||6.2, 6.1|
|STP||13||21.3 ± 3.1||5.23 ± 3.11||24.6 ± 7.7||173.2 ± 9.0||76.0 ± 16.2||8 M, 5 F||5.6, 6.1|
|CON||11||20.6 ± 4.5||4.63 ± 2.11||24.1 ± 9.1||173.5 ± 7.1||73.3 ± 10.0||4 M, 7 F||6.6, 6.7|