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.
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).
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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