Abstract
Sixty patients (sixty-two limbs) who had entrapment of the peroneal nerve were managed with operative decompression, and the results were evaluated after an average duration of follow-up of forty-two months (range, twenty-five to 162 months). The entrapment was postural in five patients, dynamic in two (one of whom had bilateral entrapment), and idiopathic in fifty-three (one of whom had bilateral entrapment). Fifty-eight patients (including the two who had bilateral entrapment) had a positive Tinel sign. Twenty-two patients (including the two who had bilateral entrapment) had sensory symptoms only, and thirty-eight had both sensory and motor symptoms. Electrophysiological studies were performed for all patients in order to confirm the diagnosis. Sensory deficits were confirmed on the basis of a marked decrease in the amplitude of sensory potentials, and motor deficits were confirmed on the basis of decreased nerve-conduction velocities.The common peroneal nerve was decompressed by division of both edges of the fibular fibrous arch. The average time from the onset of symptoms to the operation was fourteen months (range, one to 120 months), primarily because of delayed referrals.Twelve of the twenty-two patients who had had only sensory symptoms preoperatively had complete recovery by the time of the latest follow-up. The average delay from the onset of symptoms to the operation was thirty months (range, six to eighty-six months) for the ten patients (eleven limbs) who did not have full recovery compared with nine months (range, four to thirty-six months) for the twelve patients (thirteen limbs) who did. The postoperative recovery of motor function, as determined with use of the grading system of the Medical Research Council, was good for thirty-three (87 per cent) of the thirty-eight patients who had had both sensory and motor symptoms preoperatively. All seven patients who had peroneal nerve entrapment of known etiology had improvement postoperatively. We recommend operative decompression when symptoms persist or recovery remains incomplete for three to four months, provided that the diagnosis has been confirmed with electrophysiological studies.
The common peroneal nerve courses superficial to the lateral border of the fibula and approximately one to two centimeters distal to the head of the fibula before passing through the lateral intermuscular septum and into the fibular tunnel, which is made up deeply by the aponeurosis of the soleus muscle and superficially, laterally, and medially by an extended fibrous arch1,10. This fibrous arch, in turn, consists of two parts: a deep portion, which is formed by the deep aponeurosis of the peroneus longus muscle, and a superficial portion, which stretches from the soleus to the aponeurosis of the peroneus longus (Fig. 1). This arch is wide, thick, and unyielding. In some individuals, it fits tightly around the nerve and induces a state of chronic irritation.
Kopell and Thompson as well as Maudsley described entrapment of the peroneal nerve as a condition in which the nerve is compressed under the fibrous arch in the region of the bifurcation of the nerve into its deep and superficial branches. Subsequently, many authors have reported on entrapment of the peroneal nerve; non-operative therapy generally has been advocated4,11,13, although there have been a few reports of operative treatment3,12,16.
We were unable to identify the cause of the entrapment in most of the patients in the present study, although the patients were questioned thoroughly. When peroneal nerve entrapment occurs in the absence of any discernible etiology, the terms spontaneous or idiopathic peroneal nerve entrapment are appropriate16. Such entrapment might result from chronic irritation, with intraneural or extraneural edema restricting the nerve as it glides in its sheath during flexion and extension of the knee, which in turn could initiate the formation of scars and adherences.
We undertook the present study to evaluate the results of decompression in patients who had had peroneal nerve entrapment that had not responded to non-operative treatment.
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.
†Groupe Hospitalier Pellegrin, Place Amélie Raba Léon, 33076 Bordeaux CEDEX, France.
Sixty patients (sixty-two limbs) were managed with operative decompression for the treatment of peroneal nerve entrapment between 1981 and 1992. The average age of the twenty-two female and thirty-eight male patients was fifty-one years (range, sixteen to eighty-seven years). The etiology was determined to be either postural or dynamic in seven patients. Of the five patients in whom the cause was postural, three had worked in a crouched position and two had fallen asleep with the legs crossed for a prolonged period. Of the two patients in whom the cause was dynamic, one was a triathlete and the other was a soccer player who had bilateral entrapment. In both of these patients, the nerve was pressed against the fibrous arch by the well developed muscles of the leg. It was thought that repeated flexion and extension of the knee during sports activities had caused the nerve to become irritated as it moved within the tight arch. The etiology could not be established with certainty for the remaining fifty-three patients (one of whom had bilateral involvement).
We separated the patients into two groups: the first group included twenty-two patients who had only sensory symptoms in the cutaneous distribution of the peroneal nerve (Table I), and the second group included thirty-eight patients who had sensory symptoms as well as motor deficits in the muscles innervated by the peroneal nerve (Table II). Sensory symptoms included both subjective findings, such as pain and dysesthesias, and objective findings, such as partial or complete loss of sensation. For the determination of motor deficits, each muscle group supplied by the common peroneal nerve (the tibialis anterior, the extensor hallucis longus, the extensor digitorum longus, and the peroneus longus and brevis) was assessed separately. The motor signs were quantified with use of the system of the Medical Research Council and were graded according to the classification of Seddon as good (M5, normal power and full recovery, or M4, contraction against resistance), fair (M3, contraction against gravity), poor (M2, contraction with gravity eliminated), or bad (M1, perceptible contraction, or M0, no contraction).
Two of the twenty-two patients who had only sensory symptoms had bilateral involvement. Sixteen of the twenty-two (including both of the patients who had bilateral entrapment) had pain and dysesthesias, and six had pain with partial loss of sensation.
Of the thirty-eight patients who had both sensory and motor signs, sixteen had pain and dysesthesias and twenty-two had pain with complete or partial loss of sensation. A preoperative grade7 of M2, M1, or M0 was assigned to the extensor hallucis longus in twenty patients, to the extensor digitorum longus in twenty, to the tibialis anterior in eighteen, and to the peroneus longus and brevis in seventeen (Fig. 2).
Clinical examination revealed a positive Tinel sign at the neck of the fibula in fifty-eight of the sixty patients, including both of the patients who had bilateral involvement.
Ten patients had a history of lumbar disc disease; two of them had had a previous discectomy, with incomplete amelioration of the symptoms. Six patients had diabetes, and two others had a history of alcohol abuse.
Electrophysiological studies were performed for all patients under standard conditions (ambient cutaneous temperature and use of standard skin-surface and coaxial electrodes) in order to confirm the clinical diagnosis; this confirmation was necessary before the operation could be considered. The minimum criterion for the diagnosis of a sensory deficit was a marked decrease in the amplitude of the sensory potentials. The minimum criterion for the diagnosis of a motor deficit was a decrease in nerve-conduction velocity; sometimes, there was an associated conduction block in the motor nerve or evidence of denervation (fibrillation, positive sharp waves, increased insertional activity, or multiphasic potentials), or both. Most of the patients had had electrophysiological testing before they were referred to us. When we saw a patient early in the course of the disorder, an electrophysiological study was requested one month after the onset of symptoms.
The average time between the onset of symptoms and the index operation was fourteen months (range, one to 120 months). Thirty-eight patients, including the two who had bilateral involvement, were referred to us after a delay of at least five months. In this group, the operation was proposed relatively quickly on the basis of clinical and electrophysiological findings. Twenty-two patients were seen by us in the first five months after the onset of the symptoms. In this group, non-operative treatment (massage, physical therapy, or Galvanic stimulation) was attempted for three to eight weeks before the operation was proposed. The absence of recovery, as determined by clinical examination, was the indication for operative treatment in ten of these patients, all of whom were operated on between the third and fourth months. The decision to operate was corroborated by electrophysiological findings that did not change or that worsened in eight of these ten patients. The other twelve patients in this group had early operative intervention (between one and two months after the onset of symptoms) because of severe motor deficits (as indicated by a grade7 of M0 or M1).
All of the patients were managed with an open release of the common peroneal nerve. The nerve was isolated posteromedial to the biceps femoris and was followed distally to its bifurcation. During the operation, the surgeon assessed the compression of the nerve as it coursed under the fibrous arch. The compression was classified as severe if the arch had left its imprint on the nerve (thirty-six patients, including the two who had bilateral entrapment), as moderate if there was no imprint but the compression inhibited easy introduction of 146-millimeter-long Metzenbaum curved dissecting scissors (seventeen patients), and as minor if the Metzenbaum scissors slid under the arch with little opposition (seven patients) (Tables I and II). The lateral septum between the peroneus longus and soleus aponeuroses was then separated, and the peroneus longus muscle was retracted medially to expose the superficial portion of the fibrous arch, which was incised along its entire length. More distally, the deep portion of the fibrous arch was exposed and also was incised completely. It is essential that both parts of this procedure be performed; if only the superficial band of the arch is divided, the nerve may remain compressed under the more distal deep band. The decompression was considered to be sufficient when the nerve was free of all attachments and impingement.
The patients were seen one month postoperatively and then every six months until there were clinical signs of recovery. The average duration of follow-up was forty-two months (range, twenty-five to 162 months).
Of the twenty-two patients who had had only sensory symptoms preoperatively, twelve (one of whom had bilateral entrapment) had complete recovery, four (one of whom had bilateral entrapment) had partial recovery, and six had no change. Complete recovery was observed immediately or within a few days after the operation in nine patients (one of whom had bilateral entrapment) and within a few weeks in three. The average delay between the onset of symptoms and the operation was thirty months (range, six to eighty-six months) for the ten patients (eleven limbs) who did not have complete recovery compared with nine months (range, four to thirty-six months) for the twelve patients (thirteen limbs) who did.
Thirty-three (87 per cent) of the thirty-eight patients who had had both sensory and motor symptoms preoperatively had a good result (a grade of M4 or M5) (Fig. 2). The average time to recovery for these thirty-three patients was 2.5 months (range, two weeks to six months). One of these patients had decompression of the superficial peroneal nerve at the site of its emergence through the deep fascia six months postoperatively (after an initial rapid recovery). Both of the patients who had had a previous discectomy had a good result after the index operation. Two patients had a fair result (a grade of M3); one of these patients had diabetes, and the other had a history of sciatica (unilateral pain in the buttock radiating down the posterior side of the thigh and the anterolateral side of the leg without weakness). Two patients had a poor result (a grade of M2); one of these patients had had preexisting sequelae of anterolateral compartment syndrome, and the other patient had a history of alcohol abuse. One patient, who had a history of alcohol abuse, had a bad result (a grade of M1).
Of the thirty-eight patients who had had both motor and sensory deficits preoperatively, twenty-one had complete recovery from the sensory symptoms, twelve had partial recovery, and five had no change. The five patients who had no change in the sensory symptoms were the same five who had a fair, poor, or bad result on motor testing.
Complete or partial recovery of sensory function was observed in forty-two (79 per cent) of the fifty-three patients who had idiopathic entrapment, in both of the patients who had dynamic entrapment, and in all five of the patients who had postural entrapment. Both of the patients who had dynamic entrapment (one of whom was a soccer player who had bilateral involvement and one of whom was a triathlete) had a full recovery and returned to their previous level of physical activity.
Despite the large number of patients in this series, there were no complications such as iatrogenic nerve damage, infection, or wound dehiscence.
Kopell and Thompson, in 1963, reported on the operative treatment of peroneal nerve entrapment. Although some authors have advocated waiting for spontaneous recovery4,11,13, Vastamäki reported that spontaneous recovery takes eighteen to twenty-four months and may be incomplete. Thus, we prefer to operate if symptoms do not begin to resolve within three to four months. In our experience, operative decompression has been safe and the time needed for recovery has been less than that reported in association with non-operative treatment4-11. By virtue of the fact that our center serves a very large demographic area, the fact that the senior one of us (A. D.) has specialized in peripheral nerve repair for more than twenty years, and our conviction that operative treatment should be attempted relatively early after the onset of symptoms, we present here, to the best of our knowledge, the largest series of patients who have had an operation for the treatment of peroneal nerve entrapment.
Peroneal nerve entrapment usually is attributed to an excessively thick fibrous arch and narrowing of the tunnel through which the nerve passes. The fibrous arch can also contribute to dynamic entrapment during activities such as running3,8 and to postural entrapment during activities such as squatting, crouching, or kneeling5,9. However, the fibrous arch is rarely described in current anatomy texts or elsewhere in the literature. This arch is comprised of two bands, one superficial and the other deep. Both of these bands must be incised in order for the decompression to be successful.
Double compression, which is usually associated with nerve entrapment syndromes of the upper extremities15, also may occur in the lower limbs. Nerve-root compression at the level between the fourth and fifth lumbar vertebrae or between the fifth lumbar and first sacral vertebrae can occur concomitantly with peroneal nerve entrapment. Ten of the sixty patients in the present series had a history of compression of the sciatic nerve. Two of these patients had had a previous discectomy for typical sciatica (pain in the buttocks radiating distally to the anterolateral side of the leg). When they were first seen by us, these two patients had residual pain only in the distribution of the common peroneal nerve; the pain was not reproduced by straight-leg lifting. The symptoms resolved completely after the release of the peroneal nerve. In the same manner, entrapment of the superficial peroneal nerve was diagnosed a few months after decompression of the common peroneal nerve in another one of our patients.
The diagnosis of peroneal nerve entrapment is made on the basis of a combination of clinical and electrophysiological findings. Patients typically complain of dysesthesias, hypoesthesias, or anesthesia. Clinical examination may reveal a partial or total loss of sensation in the distribution of the peroneal nerve; often, the sensory symptoms are accompanied by motor deficits. A positive Tinel sign, elicited by percussion of the lateral side of the knee near the head of the fibula, was found in fifty-eight of the sixty patients in the present study (including the two patients who had bilateral involvement). When clinical findings are suggestive of entrapment, the diagnosis must be confirmed with electrophysiological studies before an operation is performed. Sensory deficits are confirmed on the basis of a marked decrease in the amplitude of sensory potentials, and motor deficits are confirmed on the basis of decreased nerve-conduction velocities.
Compression by the fibular fibrous arch should be considered separately from other etiological factors, such as edema, inflammation, ligamentous injury of the knee, fracture, or tumor. During the period of the present study, eighty-four patients sought treatment for peroneal nerve lesions that were due to a factor other than entrapment, such as fracture, an operation around the knee, compression by a cast, or tumor. These patients were managed operatively at our university hospital, which serves a population of approximately eight to ten million. These eighty-four patients were not included in the present study.
If the patient is seen sufficiently early, we propose open decompression of the peroneal nerve between the third and fourth months if symptoms persist or recovery is incomplete, even if the patient has only sensory symptoms that have been substantiated by electrophysiological studies. In the present study, twelve patients who had severe motor deficits (a grade of M1 or M0) had the operation one or two months after the onset of symptoms. In light of our subsequent experience with a number of severely affected patients who recovered relatively quickly without operative treatment, our position has evolved, and, regardless of the severity of symptoms, we now wait three to four months after the onset of symptoms before operative treatment is proposed. We believe that this delay should be observed so as not to interfere with a rapid spontaneous recovery, which is always a possibility.
Both of our patients who had dynamic entrapment responded well to the operation. This finding is in agreement with those of other authors3,7,16. Dynamic entrapment must be distinguished from chronic anterolateral or anterior compartment syndrome. Clinical and electrophysiological evaluation should rule out these possibilities; however, dynamic studies of compartment pressure should be performed if any doubt remains.
Sitting cross-legged5 and crossing the legs9 are two classic positions that can contribute to entrapment of the common peroneal nerve. The five patients in the present study who had postural entrapment had complete or partial recovery postoperatively; this finding is consistent with the experience of other authors5,12,16.
Vastamäki reported four cases of unknown etiology in a group of ten patients who had peroneal nerve entrapment that was not due to trauma or to a previous operation. In the present study, clinical examination rarely led to the identification of a specific causative factor. This was of little consequence from a practical standpoint, as the results of the operation were good regardless of whether the entrapment was considered to be secondary or idiopathic; specifically, a good result or improvement was documented for all seven patients who had dynamic or postural entrapment and for forty-two (79 per cent) of fifty-three patients in whom no specific etiological factor could be identified. Most of the failures were in patients who had been referred to us several months after the onset of symptoms. Previous authors have reported that a chronic state of irritation can lead to compression of peripheral nerves1,16; this may have been the case in the present investigation as well.
Most of the poor results in the present study were seen in the group of patients who had had only sensory symptoms, and an unsatisfactory result appeared to be more likely when the delay before referral had been long. In the group of patients who had both sensory and motor symptoms, the result was unsatisfactory for both of the patients who had a history of alcohol abuse, probably because a polyneuropathy was involved. In light of these findings, we now consider polyneuropathy to be a contraindication to this procedure and we are very cautious about recommending the procedure for patients who have had sensory symptoms for more than twenty-four months.
In conclusion, we found operative decompression to be effective for the treatment of peroneal nerve entrapment in patients who had not responded to non-operative measures. We recommend operative decompression when symptoms persist or recovery remains incomplete for three to four months, provided that the diagnosis has been confirmed with electrophysiological studies.
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