The common peroneal nerve divides into superficial and deep terminal branches usually near the fibular neck but sometimes more proximally (Figure C8-4). The common peroneal nerve around the fibular neck has a topographical arrangement where the fibers to the superficial branch are placed laterally while those destined to the deep peroneal nerve are located medially in close contact with the fibular bone. This renders the deep peroneal nerve more susceptible to compression at the fibular neck than the superficial nerve.

Figure C8-4 Locations of the division of the common peroneal nerve into its terminal branches, the deep (D) and superficial (S) peroneal nerves. (A) Most common site close to the fibular neck. Less common variations with more proximal divisions close to the knee joint line (C) or in the distal part of the popliteal fossa (B).

The superficial peroneal nerve innervates the peroneus longus and brevis and the skin of the lower two thirds of the lateral aspect of the leg and the dorsum of the foot (see Figure C8-3, top). The deep peroneal nerve is primarily motor; it innervates all ankle and toe extensors (the tibialis anterior, the extensor hallucis, and the extensor digitorum longus and brevis) and the peroneus tertius, in addition to the skin of the web space between the first and second toes (see Figure C8-3, bottom).

The accessory deep peroneal nerve is a common anomaly of the peroneal nerve. It is present in about 20+ of the population and sometimes bilaterally. The nerve arises as a motor branch of the superficial peroneal nerve, usually a continuation of the muscular branch that innervates the peroneus brevis muscle. The accessory deep peroneal nerve traverses along the posterior aspect of the peroneus brevis muscle, and then, accompanied by peroneus brevis tendon, passes behind the lateral malleolus near the sural nerve to reach the foot. There, it sends branches to the lateral part of extensor digitorum brevis, ankle joint, and ligaments (Figure C8-5).

Figure C8-5 The accessory deep peroneal nerve anomaly.

(Adapted with revisions from Preston DC, Shapiro BE. Electromyography and neuromuscular disorders. Boston MA: Elsevier/Butterworth-Heinemann, 2005, with permission.)

Clinical Features

Peroneal mononeuropathy usually presents with a foot drop, defined as severe weakness of ankle dorsiflexion (extension) with intact plantar flexion. Foot drop should be distinguished from flail foot which, in contrast, is characterized by no or minimal ankle and foot movements in all directions, including severe weakness of ankle dorsiflexion, plantar flexion, and intrinsic foot muscles. Voluntary movement at or distal to the ankle occur in foot drop due to intact plantar flexion and intrinsic foot muscles, but are absent in flail foot. Table C8-1 lists the common causes of unilateral and bilateral footdrop, starting caudally and progressing cephalad along the neuraxis.

Table C8-1 Causes of Unilateral and Bilateral Footdrop

Bilateral footdrop

Myopathies

Distal myopathies ^*

Facioscapulohumeral muscular dystrophy

Myotonic dystrophy

Neuropathies

Multifocal motor neuropathy

Chronic inflammatory demyelinating polyneuropathy

Bilateral peroneal neuropathies

Bilateral sciatic neuropathies

Bilateral lumbosacral plexopathies

Radiculopathies

Bilateral L5 radiculopathies

Conus medullaris lesion

Anterior horn cell disorders

Amyotrophic lateral sclerosis

Poliomyelitis and the post-poliomyelitis syndrome

Cerebral lesions

Bilateral cortical or subcortical parasagittal lesions

* Including the Markesburry-Udd, Welander, Nonaka, and Liang types.

Peroneal mononeuropathy is the most common compressive mononeuropathy in the lower extremity. All age groups are equally affected but the disorder is almost three times more common in men. Most peroneal nerve lesions are unilateral, and affect the right and the left side equally. Bilateral lesions constitute about 10+ of cases. In most cases, it results from prolonged compression of the peroneal nerve at the fibular neck between an external object and the rigid bone. Table C8-2 lists the causes of peroneal mononeuropathy at the fibular head.

Table C8-2 Causes of Peroneal Nerve Lesions at the Fibular Neck

* Usually with weight loss.

Adapted with revision from Katirji B. Compressive and entrapment mononeuropathies of the lower extremity. In: Katirji B, Kaminski HJ, Preston DC, Ruff RL, Shapiro BE, eds. Neuromuscular disorders in clinical practice. Boston, MA: Butterworth-Heinemann, 2002.

Most cases of peroneal mononeuropathy present with acute footdrop. However, footdrop develops in some patients subacutely over days or even weeks. The precipitating factors vary according to the mode of onset (acute versus nonacute). Figure C8-6 shows the relative frequency of the precipitating factors in relation to the mode of onset. Perioperative compression and trauma are the two most common causes of acute peroneal mononeuropathy at the fibular head. However, weight loss and prolonged hospitalization are the two major precipitating factors for peroneal nerve lesions with subacute or gradual onset. Extrinsic masses (osteomas, ganglia, lipomas, Baker cysts), or intrinsic nerve sheath tumors usually present with a slowly progressive footdrop.

Figure C8-6 Precipitating factors in peroneal mononeuropathies. Note the difference between lesions of acute versus nonacute onset.

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Katirji MB, Wilbourn AJ. Common peroneal mononeuropathy: a clinical and electrophysiologic study of 116 lesions. Neurology 1988;38:1723–1728, with permission.)

Although the deep peroneal nerve is more frequently affected than the superficial nerve (as in this patient), selective deep peroneal nerve involvement is not uncommon. Peroneal neuropathies in the thigh (i.e., sciatic nerve lesions affecting the common peroneal nerve exclusively) are rare, accounting for less than 5+ of all peroneal mononeuropathies. Table C8-3(A) reveals the most helpful clinical distinctions between peroneal mononeuropathy, lumbar plexopathy, L5 radiculopathy, and sciatic mononeuropathy. In short, weakness of ankle inversion, toe flexion, or plantar flexion, and absent or depressed ankle jerk are findings that are not consistent with a selective peroneal nerve lesion.

Table C8-3 Differential Diagnosis of Common Causes of Footdrop

In the management of acute compressive lesions, patients should be treated in a way that allows for improvement by either remyelination or reinnervation. As can be seen in this patient, conduction block lesions (due to segmental demyelination) recover spontaneously within 2 to 3 months as long as further compression is prevented. Proper padding of beds, prevention of leg crossing, and attempts to arrest or reverse weight loss should be initiated promptly. Ankle bracing is important when the footdrop is profound, to prevent ankle contractures and sprains. Surgical intervention is indicated (1) when the nerve is lacerated; (2) when clinical and/or EMG evidence for reinnervation cannot be established in the anterior compartment muscles (the tibialis anterior and the peroneus longus) 4 to 6 months after injury; and (3) in slowly progressive peroneal mononeuropathies.

Electrodiagnosis

The electrodiagnostic studies in peroneal mononeuropathies help to (1) confirm the site of the lesion (e.g., fibular head, upper thigh, or deep branch); (2) estimate the extent of injury (based on nerve conduction studies data); (3) judge its pathophysiologic nature (demyelinating versus axonal versus mixed); and (4) predict the prognosis and expected course of recovery (weeks or months). Sequential studies are helpful in following the progress of recovery (remyelination, reinnervation, or both).

Electrodiagnostic Strategy

The electrodiagnostic evaluation of patients with foot drop and suspected peroneal mononeuropathy is among the most fulfilling studies in the EMG laboratory. This is due the anatomy of the peroneal nerve and its accessibility to multiple nerve conduction studies and the needle EMG. The following are important electrodiagnostic strategies for use in patients presenting with footdrop, or in those suspected of having a peroneal mononeuropathy:

1. In addition to the common practice of recording the EDB, the peroneal motor study recording tibialis anterior must be included, for two reasons:

• The tibialis anterior is the principal ankle dorsiflexor. Hence, establishing whether the disorder is demyelinating or axonal and prognosticating the outcome of foot drop are more pertinent while recording the tibialis anterior than the EDB.

• The EDB is not uncommonly atrophic (presumably because of the use of tight shoes), resulting in an erroneous conclusion that the lesion is axonal or severe.

2. Peroneal motor (recording tibialis anterior and EDB) and superficial peroneal sensory conduction studies should be obtained bilaterally for comparison. This is particularly helpful in unilateral lesions in order to estimate the extent of axonal loss by comparing the distal peroneal CMAPs and the SNAPs.

3. At least two deep peroneal innervated muscles (such as the tibialis anterior, the extensor hallucis, and the extensor digitorum brevis) and one superficial peroneal innervated muscle (such as the peroneus longus) should be sampled. In “pure” axonal peroneal mononeuropathies, which are unlocalizable by nerve conduction studies, sampling the short head of the biceps femoris is necessary to rule out a high peroneal lesion (sciatic neuropathy affecting the peroneal nerve, predominantly or exclusively).

4. Sampling nonperoneal muscles such as the tibialis posterior, the flexor digitorum longus, or the gluteus medius is also essential. These muscles are normal in peroneal lesions, but abnormal in L5 radiculopathy and lumbosacral plexopathy. Table C8-3(B) lists the distinguishing electrodiagnostic features.

A technical pitfall may arise during peroneal motor NCS recording EDB if there is an associated accessory deep peroneal nerve anomaly. The peroneal CMAP amplitude is larger stimulating proximally than distally since the anomalous fibers are not present at the ankle. This anomaly can be confirmed by stimulating behind the lateral malleolus (Figure C8-7). This yields a CMAP (not present in normal situations) that, when added to the distal CMAP, is approximately equal or higher than the CMAP obtained with proximal peroneal nerve stimulations.

Figure C8-7 Stimulation sites in a situation associated with the accessory deep peroneal nerve anomaly while performing a peroneal motor conduction study recording extensor digitorum brevis. (I) Peroneal nerve anatomy revealing the course of the accessory deep peroneal nerve anomaly and the stimulation sites. (II) Electrodiagnostic findings in accessory deep peroneal nerve anomaly is shown. The distal stimulation of the deep peroneal nerve at the ankle (A) results in a CMAP that is lower in amplitude that the proximal response following knee stimulation (B). Stimulation behind the lateral malleolus over the accessory deep peroneal nerve yielded a CMAP (C).

(I is adapted with revisions from Preston DC, Shapiro BE. Electromyography and neuromuscular disorders. Philadelphia, PA: Elsevier Butterworth-Heinemann, 2005, with permission.)

Electrodiagnostic Findings in Peroneal Mononeuropathies

The findings on nerve conduction studies in peroneal mononeuropathies are extremely helpful in establishing a correct diagnosis and excluding other causes of foot drop, particularly L5 radiculopathy or sciatic mononeuropathy (see Table C8-3(B)). The EDX findings in peroneal mononeuropathies can be divided into several patterns (Figure C8-8 and Table C8-4):

1. “Pure” conduction block across the fibular neck (partial or complete) (see Figure C8-8B and B¹). These cases represent 20–30+ of all peroneal nerve lesions. In this situation, the distal peroneal CMAPs (recording EDB and tibialis anterior) and the superficial peroneal SNAP are normal and symmetrical to the asymptomatic limb in unilateral lesions. However, there is complete or partial conduction block (i.e., >20–50+ decrease in amplitude and/or area) across the fibular head. Sometimes, the pathology is fascicular and the conduction block affects only fibers destined to either the EDB, or more commonly TA (Figure C8-9).

Figure C8-8 Diagrams of the nerve conduction studies in peroneal mononeuropathy. (RTA = peroneal CMAP, recording tibialis anterior; RSP = recording site of the superficial peroneal SNAP.) (A) Normal. (B) and (B¹) “Pure” conduction block, partial and complete. (D) and (D¹) “Pure” axonal loss, partial and complete. (C) Mixed. (E) Deep peroneal. (Proximal latencies are not shown to scale.)

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Katirji MB, Wilbourn AJ. Common peroneal mononeuropathy: a clinical and electrophysiologic study of 116 lesions. Neurology 1988;38:1723–1728, with permission.)

Table C8-4 Electrophysiological Patterns of Peroneal Mononeuropathies

Figure C8-9 Fascicular demyelinating peroneal nerve lesion at the fibular neck. This case shows a nerve conduction pattern that is not uncommon in peroneal mononeuropathy and emphasizes the importance of peroneal motor nerve conduction study recording tibialis anterior. Note that the motor conduction study recording extensor digitorum brevis is normal with no conduction block. In contrast, a significant conduction block (>50+ drop in CMAP amplitude and area) is detected across the fibular neck recording tibialis anterior.

(From Preston DC, Shapiro BE. Electromyography and neuromuscular disorders. Philadelphia, PA: Elsevier Butterworth-Heinemann, 2005, with permission.)

Conduction block lesions are due to segmental demyelination and carry excellent prognosis with expected recovery in two to three months provided the cause of compression is eliminated. In contrast to carpal tunnel syndrome and ulnar neuropathy across the elbow, peroneal motor conduction velocities are usually normal and focal slowing across the fibular head is not a common feature of peroneal mononeuropathy. When present, it is always associated with a localizing conduction block, and it may be seen during the recovery phase of these lesions.

Before establishing the diagnosis of conduction block due to segmental demyelination, the time required for wallerian degeneration should be considered. Axon loss lesions will manifest as conduction block on NCS when performed soon after the onset of symptoms. In these axon loss lesions, the distal peroneal CMAP amplitudes decline to reach nadir in 5–6 days while the distal superficial peroneal SNAP takes 10–11 days to plateau.

2. “Pure” axonal loss (partial or complete) (see Figure C8-8D and D¹). These lesions constitute about 45–50+ of all peroneal neuropathies. On NCS, the distal and proximal peroneal CMAPs, recording EDB and tibialis anterior, are low in amplitude or absent. The superficial peroneal SNAP is usually absent. The conduction velocities are normal in mild or moderate lesions but can be slightly decreased diffusely in severe lesions. Focal slowing does not accompany these types of lesions. These axon loss injuries are slow to improve because recovery is dependent on reinnervation. In general, the weakness in partial lesions improves faster as a result of local sprouting. Based on the needle EMG, these cases are localized to one of two sites:

• At or above the fibular neck, i.e., at or above the peroneal nerve bifuraction. The lesion cannot be localized accurately due the absence of both conduction block and focal slowing. When the short head of the biceps femoris is normal, this axon loss lesion is likely at the fibular head, but may be between the gluteal fold (the take off of the branch to short head of the biceps femoris) and the fibular neck, or even more proximally in fascicular lesions that may spare the fibers to the short head of the biceps femoris.

• Proximal to the gluteal fold. These are technically sciatic nerve lesions affecting the peroneal nerves exclusively. They are relatively rare lesions, accounting for less than 5+ of all peroneal mononeuropathies. More often, the tibial component of the sciatic nerve is affected slightly, as evidenced by an abnormal H reflex, a low-amplitude or absent sural SNAP on NCS, or mild denervation in the tibial-innervated muscles (such as the medial gastrocnemius, the flexor digitorum longus, the tibialis posterior, or the abductor hallucis) on needle EMG.

3. Mixed lesions (conduction block across the fibular neck with axonal loss) (see Figure C8-8C). These lesions constitute 25–30+ of peroneal nerve lesions. In these lesions, the distal peroneal CMAPs, recording EDB and tibialis anterior, are low in amplitude and/or area, but there also is additional partial or complete conduction block across the fibular head. The superficial peroneal SNAP is low in amplitude or absent. Conduction velocities usually are normal, although occasionally there is an accompanying focal slowing. Recovery usually is biphasic; the first phase is relatively rapid, occurring over 2 to 3 months and is due to remyelination; the second phase is slower because it depends on reinnervation and sprouting.

In mixed common peroneal nerve lesions at the fibular head, it is not uncommon to find low-amplitude peroneal CMAP, recording EDB, without conduction block, along with a definite conduction block across the fibular head, while recording tibialis anterior. This is extremely helpful prognostically, since conduction block due to segmental demyelination carries an excellent prognosis for recovery, while axonal lesions require much longer time for reinnervation.

4. Deep peroneal axonal loss lesions (see Figure C8-8E). The deep peroneal branch is often more severely affected than the superficial branch in most cases of common peroneal mononeuropathy at the fibular head. This is related to the topographic arrangement of the common peroneal nerve around the fibular head, where the exiting fascicles that form the superficial branch are placed laterally, and do not directly contact the fibular bone. However, selective deep peroneal mononeuropathies are less common and constitute about 5+ of all peroneal nerve lesions. In these cases, the distal peroneal CMAPs, recording EDB and tibialis anterior, are low in amplitude and/or area, with normal superficial peroneal SNAP. The peroneus longus and brevis are normal. Motor conduction velocities are normal or borderline without focal slowing. The pattern on NCSs is identical to that seen in patients with moderate or severe L5 radiculopathy. Thus, sampling other L5-innervated muscles such as the flexor digitorum longus, the tibialis posterior, or the gluteus medius, as well as the lumbar paraspinal muscles, is important for distinguishing a deep peroneal lesion from an L5 radiculopathy.

In general, axon-loss peripheral nerve lesions are common encounters in the EMG laboratory. The peroneal nerve takes no exception for the following reasons:

• Fibrillation potentials are seen in all weak muscles, when examined by needle EMG at least 3 weeks after the onset of footdrop. These are found in “pure” axonal as well as demyelinating lesions (conduction block). In “purely” demyelinating lesions, the occurrence of fibrillation potentials is best explained by the loss of a few clinically irrelevant axons in the midst of significant demyelination.

• Significant axonal loss is common in most peroneal nerve lesions. This is based on low distal peroneal CMAPs with or without low superficial peroneal SNAPs, and is present in about 80+ of peroneal nerve lesions (alone or mixed with conduction block due to segmental demyelination).

• Significant axonal loss is common in all types of peroneal nerve lesions. Axonal loss is evident (based on low distal peroneal CMAPs) independent of the mode of onset of foot drop (acute, subacute, or undetermined) or the cause of peroneal nerve lesion (perioperative compression, trauma, etc.). This applies to all compressive peroneal lesions including the perioperative cases, such as following anesthesia for coronary bypass surgery or craniotomy. This finding is in contrast to the common belief that patients with acute perioperative compressive peroneal lesions are due to neurapraxia (i.e., segmental demyelination) and should recover rapidly. This is incorrect since 80+ of patients have evidence of significant axonal loss. It is only after a detailed EMG that the primary pathophysiologic process is determined and the prognosis is predicted.