Excursion and Strain of the Superficial Peroneal Nerve During Inversion Ankle Sprain

O'Neill, Patrick J. MD; Parks, Brent G. MSc; Walsh, Russell BSc; Simmons, Lucia M. BSc; Miller, Stuart D. MD

Journal of Bone & Joint Surgery - American Volume:
doi: 10.2106/JBJS.F.00440
Scientific Articles
Abstract

Background: Traction is presumed to be the mechanism of injury to the superficial peroneal nerve in an inversion ankle sprain, but it is not known whether the amount of strain caused by nerve traction is sufficient to cause nerve injury. We hypothesized that the superficial peroneal nerve would experience significant excursion and strain during a simulated inversion sprain, that sectioning of the anterior talofibular ligament would increase excursion and strain, and that an impact force would produce strain in a range that can structurally alter the nerve.

Methods: Differential reluctance transducers were placed in the superficial peroneal nerve in sixteen lower-extremity cadaver specimens to measure excursion and strain in situ. Static weight was applied to the foot in increments starting at 0.454 kg and ending at 4.54 kg. The anterior talofibular ligament was sectioned, and the measurements were repeated. A final impact force of 4.54 kg was applied to each specimen. Two-way repeated-measures analysis of variance was used to evaluate differences in excursion and strain.

Results: The mean excursion and strain of the superficial peroneal nerve increased with increases in the applied weight in both the group with the intact anterior talofibular ligament and the group in which it had been sectioned. Nerve excursion was greater in the sectioned-ligament group than in the intact-ligament group with all applied weights (p < 0.05). The mean nerve strain was greater in the sectioned-ligament group (range, 5.5% to 12.9%) than in the intact-ligament group (range, 3.0% to 11.6%) with application of the 0.454, 0.908, 1.362, and 1.816-kg weights (p < 0.05). With the ligament sectioned, the 4.54-kg impact force produced significantly higher mean nerve excursion and strain than did the 4.54-kg static weight (p < 0.05).

Conclusions: The magnitude of strain with the impact force was in the lower range of values that have been shown to structurally alter peripheral nerves. The superficial peroneal nerve is at risk for traction injury during an ankle inversion sprain and is at additional risk with more severe sprains or with an insufficient anterior talofibular ligament.

Clinical Relevance: Nerve injury may contribute to the high rate of residual morbidity after inversion ankle sprains.

Author Information

1 Union Memorial Orthopaedics, The Johnston Professional Building, #400, 3333 North Calvert Street, Baltimore, MD 21218. E-mail address for S.D. Miller (c/o Lyn Camire, Editor): lyn.camire@medstar.net

Article Outline

Inversion ankle sprains are extremely common, estimated to occur once per 10,000 people every day1-3, and they are the most common injuries in sports4-6. Up to 40% of patients who sustain an inversion ankle sprain have residual symptoms7-11. A potential cause of chronic morbidity is injury to the tibial nerve or to the common peroneal nerve or its branches12-22. Clinical manifestations of nerve injury include gastrocnemius or peroneal weakness, paresthesias, anterolateral ankle pain, instability, and local tenderness with burning13,15,19,20,23-25.

Electrophysiologic studies that have shown nerve abnormalities after inversion ankle sprains have substantiated the clinical findings17,20,22,26. Using electromyographic measurements, Nitz et al. found that 86% of patients with a more severe ankle sprain had a peroneal nerve injury and 83% had a tibial nerve injury20. Other studies have demonstrated marked electromyographic or nerve-conduction abnormalities in the deep peroneal nerve, superficial peroneal nerve, or common peroneal nerve after inversion ankle sprains17,19,22,26.

The mechanism of nerve injury around the ankle may be traction, as has been suggested by previous investigators17,20,21,25. However, we are not aware of any biomechanical studies that have established that nerves around the ankle experience strain during an ankle inversion sprain. Also, it is not known whether the amount of strain produced by an ankle inversion sprain would reach a threshold level sufficient to result in nerve injury. Additionally, there is a lack of evidence regarding the amount of excursion experienced by the nerves around the ankle during inversion sprains. Previous studies of peripheral nerves have shown histological or functional alterations occurring at between 6% and 50% strain27-33. Loading studies have determined that the elastic limit of peripheral nerves is reached with strains of 8% to 21%28,32,34.

Because of its anterolateral position, the superficial peroneal nerve appears to be vulnerable to excursion and stretch injury during an inversion ankle sprain. Furthermore, more severe ankle sprains often include injury to the anterior talofibular ligament, an important lateral stabilizing structure. Rupture of the anterior talofibular ligament would be expected to lead to increased ankle motion with an increase in excursion and strain in the superficial peroneal nerve with equal forces applied to the foot.

The purpose of this study was to evaluate excursion and strain of the superficial peroneal nerve during simulated inversion ankle sprains. The hypotheses were that the nerve would experience significant excursion and strain, sectioning of the anterior talofibular ligament would increase excursion and strain, and an impact force would produce strain in a range that has been shown to structurally alter peripheral nerves.

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Materials and Methods

Sixteen lower extremities from fresh-frozen cadavers were used for the study. None of the samples had signs of previous injury or surgery. The average donor age was seventy-three years (range, fifty-eight to ninety-one years). Six donors were male, and ten were female. The specimens were amputated at the midpart of the femur to ensure that any tethering of the nerve proximal to the knee would be retained. The specimens were thawed to room temperature before application of the instrumentation. Two large Steinmann pins were placed into the tibia approximately 20 and 25 cm proximal to the tip of the medial malleolus, perpendicular to the medial cortex. A large bolt was placed from dorsal to plantar through the foot between the fourth and fifth metatarsal heads and then through a rectangular board measuring approximately 20 × 9 × 2 cm (Fig. 1). A hook, on which weights could be applied, was attached at the corner of the board. A pilot specimen, with the board attached, was mounted in an inverted position on a table clamp by the Steinmann pins. It was then placed in various configurations so that, when weight was applied, the foot and ankle would fall into a position simulating an inversion ankle sprain, consequently producing strain in the superficial peroneal nerve. Adjustments were made to optimize the components of inversion, plantar flexion, internal rotation, and supination, which combine to produce an inversion sprain35,36. The board was angled away from the foot, and the tibia was placed at 60° to the floor, which ensured that the board was as horizontal as possible when the weights were applied (Fig. 2).

The superficial peroneal nerve pierces the crural fascia over the lateral compartment approximately 12.5 cm proximal to the distal part of the fibula, crosses the ankle joint near the anterolateral corner of the mortise, and terminates with one medial branch as a dorsal sensory branch to the medial three toes and a lateral branch to the lateral two toes35. Surgical dissection of the superficial peroneal nerve was then carried out. An anterolateral longitudinal incision of approximately 6 cm was made, and the superficial peroneal nerve was identified36 and minimally exposed (Fig. 3).

Two differential variable reluctance transducers (MicroStrain, Williston, Vermont) were placed into the nerve from anterior to posterior with care taken not to pierce the underlying soft tissue (Fig. 4). One gauge was used to measure excursion, and the other was used to measure strain. Each gauge consisted of two stainless-steel barbs on each end of a telescoping barrel that lengthens or shortens as the barbs are either distracted or compressed. The gauge used for measuring excursion was placed 5 cm proximal to the tip of the lateral malleolus. The gauge used for measuring strain was placed 1 cm distal to the excursion gauge so as to not impede the movements of either gauge. The proximal end of the excursion gauge was sutured to a narrow Kirschner wire, which was drilled into the tibia adjacent to the nerve with the use of a tissue protector. Tissues were kept moist with saline solution spray during testing.

After final gauge adjustments, the foot was held by hand in a neutral position and the gauges were set to zero. The foot and the attached bolt and board were gently suspended in a position of simulated ankle sprain. The foot was brought back to neutral by hand, a 0.454-kg (1-lb) weight was applied, and the foot was again suspended in inversion. Additional 0.454-kg weights were applied successively at intervals of approximately five seconds, up to 4.54 kg (10 lb). Gauge lengths were electronically recorded continuously throughout the testing of each specimen with use of LabVIEW software (National Instruments, Austin, Texas). The position of each gauge was also displayed on a computer monitor. After each weight was removed and the foot was brought back to neutral by hand, the computer display was used to ensure that the gauges had returned to the zero starting point. This first set of data for each specimen represented the intact-ligament group. The amounts of weight that were used were based on pilot testing of the construct. Using approximately 15% strain as the elastic limit of peripheral nerves28,32,34, we chose a maximum test weight (4.54 kg) that produced a strain of approximately 10% to 12% to avoid injuring the nerve after repeated measures.

The anterior talofibular ligament was then surgically sectioned, and the weights were again applied in 0.454-kg increments up to 4.54 kg. This group of data represented the sectioned-ligament group. Finally, the foot was again brought back to neutral, the 4.54-kg weight was attached to the hook, and the construct was released in a free fall until it was stopped by the structures of the ankle. This relatively large sudden force was applied to more closely approximate the mechanism of a true ankle sprain. The impact force was not tested with the anterior talofibular ligament intact to avoid irreversible deformation of the nerve before testing with the anterior talofibular ligament sectioned.

Excursion and strain data were analyzed with SPSS statistical software (SPSS, Chicago, Illinois). Two-way repeated-measures analysis of variance was used to compare the mean excursion and strain between all ankles with the anterior talofibular ligament intact and all ankles with the anterior talofibular ligament sectioned in each weight group. In addition, in the sectioned-ligament group, the mean excursion and strain caused by the 4.54-kg impact were compared with the mean excursion and strain caused by the 4.54-kg static weight.

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Results

In the intact-ligament group, the mean excursion (and standard error of the mean) of the superficial peroneal nerve ranged from 0.5 ± 0.1 with the weight of the foot only to 3.0 ± 0.4 mm with the 4.54-kg weight (Fig. 5). In the sectioned-ligament group, the range was from 1.1 ± 0.2 to 3.4 ± 0.5 mm. At every weight increment, the sectioned-ligament group had a higher nerve excursion than the intact-ligament group (p < 0.05). In the sectioned-ligament group, the excursion of the superficial peroneal nerve was higher with the 4.54-kg impact force (4.2 ± 0.5 mm) than it was with the 4.54-kg hanging weight (p < 0.05).

In the intact-ligament group, the strain in the superficial peroneal nerve with weights of up to 4.54 kg ranged from 3.0% ± 0.6% to 11.6% ± 1.9% (Fig. 6). In the sectioned-ligament group, the nerve strain ranged from 5.5% ± 0.9% to 12.9% ± 2.2%. The sectioned-ligament group had a significantly higher nerve strain as compared with the intactligament group with weights of 0.454, 0.908, 1.362, and 1.816 kg (p < 0.05). In the sectioned-ligament group, the strain was 16.1% ± 2.2% with the 4.54-kg impact force, which was significantly higher than the strain with the 4.54-kg hanging weight (p < 0.05).

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Discussion

To our knowledge, this study provides the first biomechanical evidence of nerve excursion or strain about the ankle during extremes of physiologic positioning. We are not aware of any comparable studies involving the lower extremity, but the findings in this study are similar to those in studies that have documented excursion and strain in the median and ulnar nerves during various positions of the hand, wrist, and elbow37-39. Those amounts of excursion and strain have also been found to structurally alter peripheral nerves40-44. Wright et al. speculated that any factor limiting excursion at the sites tested could cause repetitive traction and possibly play a role in pathophysiology39.

Previous authors have suggested traction as the mechanism of nerve injury after inversion ankle sprain17,18,20,25,45. Using cadaver specimens, Nobel speculated that traction caused nerve injury after measuring up to 2.5 cm of excursion of the common peroneal nerve at the sciatic bifurcation when the superficial peroneal nerve was pulled with a clamp25. Johnston and Howell reported on eight patients with superficial peroneal neuralgia who had intraoperative findings of increased tension on the superficial peroneal nerve with inversion and plantar flexion15. Traction has also been implicated as a cause of nerve injury in other areas of the body, including the brachial plexus46, the radial nerve after humeral fracture47, and the peroneal nerve as a result of knee adduction injury48-53 or proximal fibular fracture42.

The superficial peroneal nerve is particularly vulnerable to stretch from an inversion mechanism because of its anterolateral position36,41. When the foot is inverted and plantar flexed, the nerve is stretched and may even be palpable as a tight anterolateral band.

The current data also indicate that the larger the force placed on the foot in the inverted and plantar flexed position, the higher the nerve excursion and strain. The 4.54-kg impact force produced the highest excursion and strain and represents an effort to approximate the type of instantaneous force produced in an actual ankle sprain. The mechanical properties of ligaments and other soft tissues around the ankle are dependent on the rate of loading40,44. With forces sufficient to produce an ankle fracture, the potential for nerve stretch and injury may be increased. Redfern et al. reported that 15% of patients who had an ankle fracture had a symptomatic superficial peroneal nerve injury43.

The data also indicate that the excursion and strain are higher with compromise of the anterior talofibular ligament. Eighty-five percent of ankle sprains involve ligament injury6, most commonly a sprain of the anterior talofibular ligament54. In the current study, there was an increase in both the excursion and the strain of the nerve after the anterior talofibular ligament was sectioned. Previous studies have documented the importance of the anterior talofibular ligament as a stabilizer against inversion injury41,55. Thus, injury to this important stabilizing structure may lead to higher nerve strain and increased morbidity.

Peripheral nerves may be injured when they are stretched beyond their physiologic limits. Previous studies have shown functional impairment, arrest of blood flow, and structural damage with as little as 15% strain27,28,30,31,49,56,57. A study of human peripheral nerves by Sunderland and Bradley showed the elastic limit to be at 8% to 21% strain with mechanical failure occurring at 10% to 32% strain34. Other studies have documented nerve damage with strains of 12% to 50%29,32,33. The mean strain of 16% produced by the relatively small 4.54-kg impact force in the current study is in the lower range of values that have been shown to structurally alter peripheral nerves40-44. The weights placed in this study were small compared with those experienced in a traumatic inversion ankle sprain with full body weight. This suggests that the superficial peroneal nerve may be at risk during actual ankle sprains.

Given the substantial strain measured in this study and the fact that 90% of ankle sprains are caused by an inversion mechanism54,58, it is interesting that nerve injury is not more commonly reported. This may be due to anatomic variations or to the lack of active muscular protection in cadaver specimens. Alternatively, as previous authors have suggested19,20,50,59, nerve injury may actually be relatively common. The true incidence of nerve injuries may be underestimated if they are masked by the acute pain of an ankle sprain or the longer-term morbidity of a ligament injury19,50,59. Nitz et al. observed electrophysiologic changes in the peroneal nerve in >80% of patients with a severe ankle sprain20. Kleinrensink et al. found that the mean conduction velocity of the superficial peroneal nerve was acutely decreased after an inversion ankle sprain but returned to normal in five weeks17. Slowed conduction velocity may contribute to functional instability, a common cause of morbidity after an inversion ankle sprain17,20,22,60 that is found in up to 40% of patients13,61. Functional instability may be caused by a loss of proprioceptive reflexes or decreased sensation, which may result from nerve injury20,22,60-62. Chronic disability may also be caused by weakness resulting from injury to the superficial or deep peroneal nerve13,14,19.

Normal peripheral nerve function may be compromised if excursion is not adequate during normal motion. Decreased excursion due to tethering may result in higher strains. Several previous studies have demonstrated improved excursion and clinical findings following surgical release of nerve fibrosis or soft-tissue tethers in patients with superficial peroneal neuralgia due to an inversion ankle sprain12,15,16,21,63,64. In the upper extremity, it was found that ulnar nerve strain at the elbow with flexion ranged from 0% to 14% and that increased ulnar nerve strain at the elbow was caused by various amounts of tethering65. In the current study, some nerves appeared qualitatively to be much more naturally tethered than others, and additional study of this phenomenon may be warranted.

Weaknesses of this study include the use of fresh-frozen cadaver limbs, in which the properties of the nerves and soft tissues may differ from those of in vivo specimens. In addition, although dissection of the nerves was held to a minimum, the exposure could have altered their behavior. Also, the specimens were created by midfemoral amputation, which may alter the amount of excursion or strain. The specimens used were from elderly donors, whose anatomy or soft-tissue mechanical properties may differ from those of younger individuals. The biomechanical model of the current study also may not precisely recreate the biomechanics of a true injury with regard to either the magnitude or the direction of forces applied. Finally, sectioning of only the anterior talofibular ligament may not simulate the actual injury pattern of a severe inversion ankle sprain.

This study provided biomechanical evidence of excursion and strain produced in a nerve around the ankle in an extreme physiologic position. The observation of strain supports the possibility that superficial peroneal nerve injury could be caused by an inversion ankle sprain. ▪

Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the authors, or a member of their immediate families, are affiliated or associated.

Investigation performed at the Department of Orthopaedic Surgery, Union Memorial Hospital, Baltimore, Maryland

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