Peroneal neuropathy is one of the most common mononeuropathies in the lower extremity. Most often, peroneal neuropathy occurs at the fibular neck, where the nerve is quite superficial and vulnerable to injury. Patients usually present with a foot drop and sensory disturbance over the lateral calf and dorsum of the foot. However, patients with sciatic neuropathy, lumbosacral plexopathy, or L5 radiculopathy may present with a similar pattern of numbness and weakness, due to the preferential susceptibility of the peroneal fibers. It often falls to the electromyographer to differentiate among these lesions. In addition, the electrophysiologic evaluation usually can localize the level of the peroneal neuropathy, identify the underlying pathophysiology, and establish the prognosis.
Anatomy
The peroneal nerve is derived predominantly from the L4–S1 nerve roots, which travel through the lumbosacral plexus and eventually the sciatic nerve. Within the sciatic nerve , the fibers that eventually form the common peroneal nerve run separately from those that distally become the tibial nerve ( Figure 22–1 ). In the posterior thigh, the peroneal fibers within the sciatic nerve innervate the s hort head of the biceps femoris, the only peroneal-derived muscle above the level of the fibular neck ( Figure 22–2 ). More distally, the sciatic nerve bifurcates above the popliteal fossa into the common peroneal and tibial nerves. The common peroneal nerve first gives rise to the lateral cutaneous nerve of the knee , which supplies sensation to the lateral knee before winding around the fibular neck and passing through the fibular tunnel between the peroneus longus muscle and the fibula. At the fibular neck, the internal fascicular anatomy is such that the fibers destined for the deep peroneal nerve lie more medial (adjacent to the fibula) whereas the fibers destined for the superficial peroneal nerve are more lateral ( Figure 22–3 ). The common peroneal nerve then divides into superficial and deep branches. The deep peroneal nerve ( Figure 22–4 ) innervates the peroneus tertius and the dorsiflexors of the ankle and toes, including the tibialis anterior (TA), extensor digitorum longus, extensor hallucis longus (EHL), and extensor digitorum brevis (EDB). It continues on to supply sensation to the web space between the first and second toes. The superficial peroneal nerve ( Figure 22–5 ) innervates the ankle everters (peroneus longus and peroneus brevis) and then supplies sensation to the mid and lower lateral calf. As it passes over the dorsum of the foot, it divides into the medial and intermediate dorsal cutaneous nerves of the foot , supplying sensation to the dorsum of the foot and to the dorsal medial three or four toes up to the level of the interphalangeal joints. In 15 to 20% of patients, an accessory peroneal nerve leaves the main superficial peroneal nerve and runs posterior to the lateral malleolus to ultimately supply the lateral EDB muscle. This is an important normal variant often encountered during routine nerve conduction studies.
Clinical
Peroneal Neuropathy at the Fibular Neck
Patients with peroneal neuropathy at the fibular neck present with a characteristic neurologic picture. Most often, both the deep and superficial peroneal nerves are affected. Involvement of the deep peroneal nerve leads to weakness of toe and ankle dorsiflexion, resulting in a foot and toe drop. Dysfunction of the superficial peroneal nerve results in weakness of foot eversion. Clinically, weakness of these muscles results in a stereotyped set of symptoms. Patients note a slapping quality of their foot as it hits the ground while they are walking. Weakness of eversion leads to a tendency to trip, especially on uneven sidewalks or curbs, and an increased risk of sprained ankles. When observed while walking, patients have a so-called steppage gait whereby they bring their knee up higher than usual so that the dropped foot clears the floor. Sensory disturbance develops over the mid and lower lateral calf and the dorsum of the foot. Local pain and a Tinel’s sign may be present over the lateral fibular neck.
In isolated peroneal neuropathy at the fibular neck, function of the sciatic, tibial, and sural nerves remains normal. Most important, ankle inversion is spared, mediated by the tibialis posterior (L5, sciatic–tibial innervated nerve). If the ankle is tested in a dropped position, however, ankle inversion may appear weak (similar to testing finger abduction in a dropped wrist position). Accordingly, to test ankle inversion in a patient with a foot drop, the ankle should be passively dorsiflexed to avoid the mistaken impression that the tibialis posterior is weak. The remainder of the muscles innervated by the tibial and sciatic nerves are normal (ankle and toe plantar flexion, knee flexion). Hip abduction, internal rotation, and extension also are normal, innervated by the superior and inferior gluteal nerves, which come directly off the lumbosacral plexus. Sensation is normal over the lateral foot (sural territory), sole of the foot (medial and lateral plantar territory), and medial calf and foot (saphenous territory). Sensation over the lateral knee is preserved because that area is innervated by the lateral cutaneous nerve of the knee, which arises from the common peroneal nerve above the fibular neck. Finally, all reflexes, including the ankle reflex, remain normal in an isolated peroneal neuropathy.
As already noted, lesions of the sciatic nerve, lesions of the lumbosacral plexus, and L5 radiculopathy may present with a foot drop and numbness over the lateral calf and dorsum of the foot. Indeed, these lesions, especially early on, occasionally mimic a peroneal palsy almost exactly, including abnormalities of sensation ( Table 22–1 ). It is in these cases that electrodiagnostic studies are especially helpful. On the clinical examination, any of the following abnormalities in a patient with a foot drop should suggest a lesion more proximal to the peroneal nerve at the fibular neck:
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Weakness of ankle inversion (tibialis posterior – innervated by the tibial nerve)
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Preferential weakness of the EHL ( L5 –S1) out of proportion to the TA ( L4–L5 ) when the two are compared. In a peroneal neuropathy, these two muscles usually are equally affected; in an L5 radiculopathy, the EHL usually is weaker than the TA because of its predominant L5 innervation
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Sensory loss over the lateral knee (distribution of the lateral cutaneous nerve of the knee)
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Sensory loss over the sole of the foot, lateral foot, or medial calf (distribution of the plantar, sural, or saphenous nerves, respectively)
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Any weakness of hip abduction, extension, or internal rotation (gluteus medius, tensor fascia latae, gluteus maximus – innervated by the superior and inferior gluteal nerves). Because these muscles are quite strong, they must be tested at mechanical disadvantage to demonstrate subtle weakness
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Any asymmetry of the ankle reflex
Deep Peroneal Neuropathy at the Ankle
Compression of the deep peroneal nerve at the ankle is known as “Anterior Tarsal Tunnel Syndrome.” This is a rare entrapment neuropathy that occurs from compression of the deep peroneal nerve under the inferior extensor retinaculum at the ankle. Patients present with foot pain and paresthesias of the dorsum of the foot between the great and second toes. Atrophy and weakness of the extensor digitorum brevis muscle may be present. Sensation may be decreased in the web space between the great and second toes. Plantar flexion may result in increased symptoms, which may be relieved by dorsiflexion. A Tinel’s sign may be elicited by percussing over the anterior ankle.
Etiology
Peroneal neuropathy at the fibular neck can be seen as a result of a variety of conditions ( Box 22–1 ). Acute peroneal neuropathy often follows trauma, forcible stretch injury, or compression from prolonged immobilization. In the hospital, peroneal neuropathy at the fibular neck occurs most often postoperatively in patients who have received anesthesia or heavy sedation. Slowly progressive lesions often suggest a mass lesion, such as a ganglion or nerve sheath tumor. Entrapment of the peroneal nerve at the fibular tunnel, although quite uncommon, also may present in a progressive manner.
Trauma (including fracture)
Stretch (forcible ankle inversion)
Compression
Casts
Stockings
Immobilization after anesthesia, sedation, or intoxication
Occupational
Gardening
Farm work (squatting, kneeling)
Entrapment (fibular tunnel)
Mass lesions (ganglia, tumors, Baker’s cyst)
Miscellaneous (weight loss, habitual leg crossing)
Several other circumstances predispose one to peroneal neuropathy at the fibular neck. Habitual leg crossing may repetitively injure the peroneal nerve at the fibular neck, where it is quite superficial. Similarly, repetitive stretch from squatting, for example, by gardeners has been associated with peroneal neuropathy at the fibular neck. In addition, patients who are thin or who have recently lost a substantial amount of weight may be prone to peroneal palsy, probably because of the lack of protective supporting adipose tissue at the fibular neck.
Isolated neuropathy of the superficial peroneal sensory nerve is rarely reported. However, this nerve can be compressed externally, especially by tight-fitting boots. Most often, this is seen from ski boots ( Figure 22–6 ).
Compression of the deep peroneal nerve at the anterior tarsal tunnel has been reported with trauma, tight shoes (especially in dancers), bony abnormalities of the ankle, ganglion cysts, and pes cavus.
Electrophysiologic Evaluation
Nerve Conduction Studies
In a patient with a foot drop and suspected peroneal neuropathy, peroneal motor, F response, and superficial peroneal sensory studies should be performed first ( Box 22–2 ). The findings will depend on the location and severity of the lesion and on whether the underlying pathophysiology is demyelination, axonal loss, or a combination of both ( Figure 22–7 ). In demyelinating lesions, if focal slowing or conduction block is seen across the fibular neck in the peroneal motor study, this can be used to localize the lesion. Usually, any slowing of more than 10 m/s is considered significant. Any drop in amplitude or area of more than 20%, especially over a very short segment, suggests focal conduction block ( Figure 22–8 ). The amount of conduction block can be approximated by comparing the compound muscle action potential (CMAP) amplitude at the lateral popliteal fossa with that below the fibular head. In purely demyelinating lesions at the fibular neck, the distal superficial peroneal sensory response remains normal.
Routine studies:
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Peroneal motor study, recording extensor digitorum brevis, stimulating ankle, below fibular head and lateral popliteal fossa. If there is no focal slowing or conduction block at the fibular neck, perform a peroneal motor study, recording tibialis anterior and stimulating below the fibular head and lateral popliteal fossa.
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Tibial motor study, recording abductor hallucis brevis, stimulating medial ankle and popliteal fossa
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Superficial peroneal sensory study, stimulating lateral calf, recording lateral ankle
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Sural sensory study, stimulating calf, recording posterior ankle
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Tibial and peroneal F responses
Special consideration: If any study is abnormal or borderline, especially the motor or sensory amplitudes, comparison to the contralateral asymptomatic side is often useful.
If axonal loss predominates, peroneal CMAP amplitudes will be reduced at all stimulation sites (ankle, below the fibular head, lateral popliteal fossa). As in other axonal loss lesions, conduction velocities and the distal motor latency may be normal or slightly slowed if the fastest-conducting axons have been lost. Likewise, the superficial peroneal sensory nerve action potential (SNAP) amplitude will be reduced or absent. If the pathophysiology is entirely axonal loss, the nerve conduction studies, although they demonstrate a peroneal neuropathy, cannot localize the level of the lesion. The amount of axonal loss can be approximated by comparing the distal CMAP amplitude on the involved side with that on the contralateral asymptomatic side. Often, there may be evidence of both axonal loss and demyelination in the same patient.
The EDB muscle usually is chosen as the recording site for peroneal motor studies. However, in patients with a foot drop, it is weakness of the TA that accounts for the clinical deficit. Hence, recording the TA when performing the peroneal motor study often is more useful than the routine motor study recording the EDB . Indeed, in some cases of peroneal neuropathy at the fibular neck, conduction block may be seen when recording the TA but not the EDB ( Figure 22–9 ). If recording the EDB does not localize the lesion by demonstrating focal slowing or conduction block, the peroneal motor study should be repeated recording the TA, stimulating below the fibular head and at the lateral popliteal fossa.
