Common Peroneal Nerve Entrapments


The common peroneal nerve arises from the sciatic nerve at approximately the middle to distal third of the thigh region. At this point, it descends to the popliteal fossa, innervating the short head of the biceps femoris muscle.14 It travels along the lateral aspect of the distal thigh beneath the cover of the long and short heads of the biceps femoris muscle to the region of the fibular head. Proximal to the fibular head, the common peroneal nerve gives off 2 branches: the sural communicating branch, which assists in the formation of the sural nerve with a branch provided by the tibial nerve, and the lateral cutaneous nerve of the calf, which provides cutaneous sensation to the proximal and lateral aspect of the leg. It also supplies the knee joint via its articular branches.

The common peroneal nerve then courses around the fibular neck and passes through the fibro-osseous opening in the superficial head of the peroneus longus muscle. This opening can be quite tough, and can result in the nerve angulating through it at an acute angle. Also, significant fibrous connective tissue secures the nerve to this proximal portion of the fibula, potentially compromising the nerve.

Distal to this fibular tunnel, the common peroneal nerve divides into the superficial and deep peroneal nerves. The superficial peroneal nerve provides innervation to the peroneus longus and brevis muscles, and then travels down the leg to pierce an opening in the deep fascia at about the distal third of the anterior leg. The superficial peroneal nerve splits into the medial and lateral terminal sensory branches to pass anterior to the ankle and innervate most of the dorsum of the foot, except for the region that lies between the first and second toes.

The deep peroneal nerve descends along the leg between the tibialis anterior (TA) and extensor hallucis longus (EHL) muscles, innervating those muscles as well as supplying the extensor digitorum longus (EDL) and peroneus tertius muscles. (Please see Superficial Peroneal Nerve Entrapment and Deep Peroneal Nerve Entrapment for further anatomic detail on these nerve branches.)


Peroneal nerve injuries are the most common peripheral nerve injuries of the lower limb to result from multiple traumatic injuries, such as those suffered in motor vehicle accidents. The common peroneal nerve can be injured at any location along the thigh down to the fibular head region in various forms of trauma, such as lacerations, femoral fractures, bullet wounds, and direct injury. However, most peroneal nerve injuries occur at the region of the fibular head.

As Kaminsky reported, the most common form of neural compromise in the region of the fibular head is due to compression from habitual leg crossing, compression of the nerve against a bed railing or hard mattress in debilitated patients, or prolonged immobility, such as that observed in patients under anesthesia.15 However, in a study of 146 cases, Piton and colleagues noted 55 cases due to idiopathic causes, 16 due to external compression, 59 due to various traumatic causes, and 9 due to intraneural and extraneural tumors.16 Traumatic causes can include wounds and contusions, direct fractures involving the lateral knee, and direct lacerations or postsurgical entrapment in suture hardware.

Common peroneal nerve injuries at the region of the fibular head include ankle sprains with associated proximal fibular fractures, knee dislocations, tibial osteotomies, total knee and hip arthroplasties, and arthroscopies. Compression from intraneural or extraneural tumors has been seen, including compression from neurilemomas, intraneural or extraneural ganglia, schwannomas, desmoid tumors, angiomas, neuromas, fibrolipomatosis hamartomas, exostosis, chondromatosis, Baker cysts, and vascular abnormalities.17

A number of other etiologic factors have been reported in the literature. Compression of the nerve against the fibrous or fascial layers of well-developed muscles of the legs in athletes has also been seen. Patients typically present with exercise-related leg pain with or without associated dermatomal numbness. Coexisting pathologies, such as those in exercise-related compartment syndromes, add to the complexity of this diagnosis. Excessive weight loss can also be a contributing factor in patients (slimmer's paralysis), as rapid weight loss and anorexia can result in loss of the fat pad over the fibular head, predisposing the nerve to external compression at this site. Short casts or braces can result in external compression on the fibular neck region.

Individuals who spend long hours in a squatting position can also present with clinical evidence of peroneal nerve compression (strawberry picker's palsy). This is likely the result of compression of the common peroneal nerve as it penetrates the fibro-osseous opening in the peroneus longus muscle in persons with a fibrous or tight peroneal tunnel. A rare form of common peroneal nerve injury is that associated with natural childbirth, in which the woman compresses both peroneal nerves at the fibular head by pulling back on her knees with wrists resting on the fibular head during birthing. The nerve may also be injured during childbirth in the squatting position.

Other less common causes include lower-limb lengthening procedures, anorexia nervosa, and paraneoplastic syndromes. Also, peroneal nerve mononeuropathies can occur in hyperthyroidism, diabetes mellitus, vasculitic disorders, and leprosy. Many times, an underlying etiology remains unclear, and the condition is termed idiopathic.


Peroneal nerve lesions at the region of the knee or distal thigh usually result in patient reports of altered ambulation secondary to paretic or paralyzed ankle dorsiflexors. Loss of sensation in the cutaneous distribution of the superficial and deep peroneal nerves may be noted, but ankle dorsiflexion weakness is often of most concern to the patient.18

Pain is not universal with common peroneal nerve injuries, and, if present, is often related to the specific cause of the nerve compromise. For example, a nerve compromise secondary to traumatic injury from blunt trauma will likely be accompanied by pain secondary to soft-tissue swelling and inflammation, while chronic compression secondary to habitual leg-crossing is often nonpainful. Tapping of the nerve at the fibular head may produce pain and tingling (Tinel sign) in the sensory distribution of the peroneal nerve.

Observation of the patient's gait is useful in diagnosing ankle dorsiflexion weakness. The patient often displays a steppage gait pattern in which the affected foot is lifted excessively from the ground during the swing phase of ambulation in order to clear the foot. This results in excessive hip and knee flexion, and the appearance is as if the patient is stepping over an object in his or her path. In addition, a foot slap may be heard on foot strike, as the ankle dorsiflexors cannot provide a controlled descent of the foot toward the floor. The patient might also stumble when walking, secondary to the toes on the affected side dragging or catching on the floor during the swing-through phase of ambulation.

Examination often reveals a variable pattern of weakness, with the extensor digitorum brevis (EDB) muscle being affected most profoundly. Ankle and toe dorsiflexion can be significantly affected. Dorsiflexion is best tested by having the patient place the ankle in the neutral position and then dorsiflex the foot and invert; this tests the TA muscle optimally. Often, ankle eversion is normal, as patients can have relative sparing of these muscles. In a pure common peroneal neuropathy, plantar flexion should be spared. In fibular neck fractures, complete absence of sensation is possible along the anterodistal portion of the leg and the entire dorsum of the foot. Lateral calf sensation may be spared if the lesion is below the nerve branch to this region. When the neural insult occurs at the knee, the short head of the biceps femoris often is spared.

The history and physical examination are the most helpful initial clinical tools in determining a high suspicion for a common peroneal nerve injury.

Plain radiographs may be helpful in excluding underlying traumatic injuries, such as a proximal fibular head fracture, or osseous tumors, or in assessing the severity of angular deformities about the knee. Computed tomography (CT) scans and magnetic resonance imaging (MRI) are helpful in finding a compressive lesion along the course of the nerve in cases in which this is suspected. Metabolic and hematologic studies may be helpful in conditions such as diabetic peripheral polyneuropathy, alcoholic polyneuropathy, polyarteritis nodosa, and hyperthyroidism. Nerve biopsy, although largely unnecessary, may confirm the disorder.

The electrodiagnostic evaluation is arguably the best method for assessing a potential peroneal nerve insult. It is clinically difficult to isolate and test the short head of the biceps muscle, the evaluation of which is critical in determining whether a lesion is proximal to the knee and whether it involves the sciatic nerve, lumbosacral plexus, or nerve roots. In patients with exercise-induced symptoms, electrodiagnostic tests should be performed before and after exercise. Electrodiagnostic studies include the following:

Sensory conduction studies - A superficial peroneal sensory nerve action potential (SNAP) is important, and an abnormality of the sensory evoked response implies that the lesion is distal to the dorsal root ganglion, although this does not completely rule out the possibility of an L5 radiculopathy. A loss in amplitude of this response implies some axonal loss affecting either the common peroneal nerve or its superficial branch. The particular portion of the nerve that is injured cannot be determined if only a superficial peroneal nerve sensory study is performed. Comparison of the latency and amplitude of the superficial peroneal SNAP with the contralateral limb is required to define an approximate degree of axonal loss.

Motor conduction studies - The most commonly performed test in determining peroneal conduction in the leg and across the fibular head is performed with the active electrode placed on the EDB muscle. The peroneal nerve usually is stimulated at the ankle, several centimeters below the fibular head and about 10 cm proximal to the fibular head, just medial to the biceps femoris tendon. This allows for calculation of the nerve conduction velocity (NCV) across the fibular head region, with comparison with the distal leg segment.

Comparison with the contralateral limb is often helpful. When significant EDB atrophy is present (eg, with advanced age or with a polyneuropathy), the active electrode should be placed over the TA. Generally, lower extremity motor NCVs of less than 40 m/s are considered abnormal. Generally, proximal segment NCVs should be greater than distal NCVs, given the greater axonal diameter in the proximal segment of the nerve.

If the contralateral limb responses are normal, one can estimate the amount of axonal loss by expressing the compound muscle action potential (CMAP) on the affected side as a percentage of the nonaffected side. This method is independent of the location of the active recording electrode and is valid in both circumstances. A change of 20-50%, depending on the source, is believed to represent a conduction block. In addition, one may assess the degree of conduction slowing and temporal dispersion to determine whether the lesion is predominantly demyelinating versus axonal.

Needle electromyography - Needle electromyography helps in confirming axonal loss and in assessing the degree of involvement of the muscles innervated by the superficial peroneal nerve. This portion of the nerve usually is less severely involved than the deep peroneal nerve. It is possible to localize the lesion to either the deep or superficial peroneal nerves, specifically if appropriate abnormalities are detected in the proper distribution for each nerve. The most valuable aspect of the needle EMG examination is that it can be used to define the proximal extent of the lesion. If an amplitude drop is lacking across the fibular head but the TA CMAP is lower than that of the unaffected side (suggesting axonal loss), it is difficult to localize the lesion to the fibular head, despite the fact that this is the most common site of peroneal nerve injuries.

In any peroneal nerve injury, regardless of the suspected site of nerve compromise, examining the short head of the biceps femoris muscle is important. If this muscle demonstrates membrane instability (positive sharp waves and fibrillations), the lesion is proximal to the fibular head.

Testing muscles innervated by the tibial nerve, particularly the flexor digitorum longus (FDL) and tibialis posterior muscles, is also important, because they contain predominantly L5 neural innervation from the tibial nerve. If a radicular process is present, the muscles innervated by the peroneal and tibial nerves should demonstrate membrane instability.


Initial nonoperative treatment should focus on maximizing mobility and function. In addition, the cause of nerve compromise or compression should be corrected to reduce further nerve damage. NSAIDs or oral corticosteroids may be useful in cases in which an inflammatory process is present. Corticosteroids injected into the affected region may reduce swelling and pressure on the nerve in some cases. Symptomatic pharmacologic treatment may consist of tricyclic antidepressants (amitriptyline) or neuroleptic medications, such as gabapentin and carbamazepine.

A brace (ankle-foot orthosis [AFO]), splints, or orthopedic shoes may control the abnormal dynamics at the ankle and provide dorsiflexion assistance for a more ideal gait pattern during nerve recovery. In-shoe orthotics may be helpful in certain instances, such as in the correction of a biomechanical malalignment in gait (eg, in patients with severe flatfoot or cavus foot).

Many authors have reported spontaneous recovery; therefore, initial nonoperative management for a minimum of 3-4 months is recommended for idiopathic cases and for those suggestive of neuropraxia.

Surgical decompression of the nerve and excision of the offending lesion are indicated in cases of nerve compression due to external causes, such as those associated with intraneural or extraneural tumors or masses. Löwenstein and colleagues recommend early surgical treatment in cases involving intraneural ganglion cysts, in order to minimize neural invasion (which may cause irreversible axonal injury and footdrop).19 In cases in which severe paresis and muscle atrophy are present, surgical exploration may also be warranted, especially if electrodiagnostic evidence of active motor axonal degeneration is present.

In one of the largest studies of patients with idiopathic peroneal nerve entrapment, Fabre and coauthors reported on 62 patients who were treated with operative decompression of the common peroneal nerve.20 The postoperative recovery of motor function was good in 87% of those who had sensory and motor involvement preoperatively. All 7 patients who had peroneal nerve entrapment of known etiology also demonstrated postoperative improvement. On the basis of their results, the authors recommend 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 electrophysiologic studies.

The procedure involves a curved incision about the lateral knee, following the course of the nerve. The nerve is found initially posteromedial to the biceps femoris. It is tracked distally to where it branches to the deep and superficial branches. The nerve is released fully by initially separating the lateral septum between the peroneus longus and soleus aponeurosis, retracting the peroneus longus muscle medially, and fully dividing the superficial and deep portions of the fibrous arch. Any sites of entrapment or compression along this route should be released. Nerve grafting may be warranted in severe cases in which the nerve is structurally damaged or severed.