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Electrodiagnostic Evaluation Of Peroneal Neuropathy


Electrodiagnostic Evaluation Of Peroneal Neuropathy

Article Author:
Hameer Thatte
Article Editor:
Orlando De Jesus
Updated:
11/14/2020 10:50:14 AM
For CME on this topic:
Electrodiagnostic Evaluation Of Peroneal Neuropathy CME
PubMed Link:
Electrodiagnostic Evaluation Of Peroneal Neuropathy

Introduction

The fibular nerve has been historically referred to as the peroneal nerve because the fibula can also be referred to as the perone. It has recently become more commonplace to refer to the peroneal nerve as the fibular nerve to distinguish it from the similar-sounding perineal nerve. The fibular nerve terminology will be used in all parts of this article. Fibular neuropathy is considered the most common neuropathy in the lower extremities and tends to occur secondary to compression, entrapment, direct trauma, or ischemia.[1][2] In fibular neuropathy, both the deep and superficial nerves tend to be affected. If a single branch is being affected, the deep fibular nerve tends to be more frequently affected than the superficial fibular nerve.[2] This occurs as the deep fibular nerve fascicles are more superficial at the fibular head; thus, they are more exposed to trauma and compression. The fibular nerve's most common compression site is found at the fibular head/neck, where the nerve is most superficial.[2] 

Patients tend to present with either an acute or a gradual foot drop. Patients may give a history of falls and possibly tripping due to the foot drop. They may also complain of paresthesias or numbness in the lower leg's lateral portion and the foot's dorsum. Pain can be absent in many cases presenting with a foot drop.[3] However, pain can be an initial presenting symptom in patients without a foot drop but can show a slight weakness in ankle dorsiflexion only when carefully examined.[4] One-third of these patients can have normal electrodiagnostic tests.[4]

Injuries to the common fibular nerve can be due to compression from the prolonged crossing of legs, poor positioning during surgery (most common in acute settings), weight loss (most common in a subacute or chronic setting), poor application of a cast, prolonged squatting position (carpet layers, carpentry workers, farmworkers), or diabetes mellitus.[2][5] An isolated weakness of the ankle dorsiflexors and evertors can help clinicians differentiate a fibular neuropathy from L5 radiculopathy, which would also involve the ankle invertors.[5] Studies of the tibialis posterior or gluteus medius muscles, which are not supplied by the fibular nerve but have an L5 innervation, can differentiate L5 radiculopathy.[5] Fibular neuropathies can also be mistaken for lumbosacral plexopathy and sciatic neuropathy.[1] Sciatic neuropathy frequently shows a foot drop and can be confused with common fibular neuropathy.[2][6][7] Sciatic neuropathy is the second most common neuropathy in the lower extremity.

Deep fibular neuropathy can occur by patients whose nerves are compressed by trauma (ankle sprains or fractures), footwear (high heeled shoes, tight shoes, or high boots), or intrinsic causes as the nerve passes under the extensor retinaculum (osteophytes, ganglion cysts, or lipomas). Pressure from an anterior compartment syndrome can cause an isolated injury to the deep branch.[5] The superficial fibular nerve can be injured by compression related to trauma, sprained ankles, or lipomas.

Anatomy and Physiology

The common fibular nerve receives innervation from the L4-S1 nerve roots with a minor contribution from the L2 nerve root. The nerve is formed at the lumbosacral plexus and initially travels within the sciatic nerve.[2][5] The sciatic nerve contains fiber bundles that are anatomically separated. Just above the popliteal fossa, these separated fiber bundles form the common fibular nerve and the tibial nerve.

The sciatic nerve’s fibular branch innervates the short head of the biceps femoris muscle. This finding is significant from an electrodiagnostic standpoint because it is the only muscle proximal to the knee that the fibular nerve innervates. If a patient experiences fibular neuropathy at the fibular neck, the short head of the biceps femoris muscle will not be affected. The knee's lateral surface is innervated by the lateral cutaneous nerve, a sensory branch of the common fibular nerve. Following this branch, the common fibular nerve curves around the fibular neck and passes between the fibula and the peroneus longus muscle through the fibular tunnel.

The tibialis longus and brevis muscles are innervated by the superficial fibular nerve, terminating in sensory branches that supply the lateral portion of the two-thirds of the lateral lower leg and the dorsum of the foot and toes except for the first dorsal web space.[2][5] 

The deep fibular nerve, also called the anterior tibial nerve, supplies the tibialis anterior muscle, the extensor digitorum longus muscle, extensor hallucis longus muscle, peroneus tertius muscle, and the extensor digitorum brevis (EDB) muscle. Terminal sensory branches provide innervation of the skin of the first dorsal webspace.[2] Approximately 15 to 25% of people have an accessory fibular nerve that arises from the superficial fibular nerve.[8][9][10] This accessory nerve provides an atypical innervation to the EDB muscle.[8]

Indications

For common fibular nerve neuropathy, the patient may complain of weakness in the dorsiflexors (extensor hallucis longus, extensor digitorum longus, tibialis anterior), which could result in a foot drop or a foot slap with a steppage gait.[5] A sensory loss could also be observed over the deep and superficial fibular nerve distributions. Tinel’s sign could also be positive at the fibular head.[5] Deficits in strength could also be appreciated when the ankle is dorsiflexed and with the great toe extension.

For deep fibular neuropathy, patients may complain of pain, weakness, or atrophy of the foot, especially the EDB muscle. Patients may also experience numbness/paresthesias of the first and second webspace. They may experience pain over the dorsum of the foot, which is relieved with motion.

For superficial fibular neuropathies, patients may complain of pain, numbness, paresthesias, or loss of sensation in the distal anterolateral calf and the foot's dorsum, except for the first webspace. Patients can present with weakness in foot eversion if the injury is proximal to the innervation of the tibialis longus and brevis muscles.[11]

Contraindications

Performing electrodiagnostic studies in patients with fibular neuropathy have few absolute contraindications. Needle electromyography (EMG) should not be performed on patients with severe bleeding disorders. Needles should not be inserted into areas with active soft tissue infections.

Nerve conduction studies are contraindicated in patients with external cardiac defibrillators or implanted cardiac defibrillators. Before conducting electrodiagnostic studies, patients should be screened for pacemakers. It is essential that electrical stimulation not be performed directly or near the device itself.[11]

Equipment

  • EMG/NCS machine
  • Electrodes (needle and surface)
  • Amplifiers and filters

Personnel

  • Technician
  • Physiatrist

Technique

Before performing an electrodiagnostic study, a clinician must conduct a comprehensive review of the patient’s history, including any applicable clinical course and a physical exam. A systematic and empathetic physician will inform the patient, and any relative involved in decision-making, of the indications for the studies and provide an overview of the procedure to be performed.

A comprehensive electrodiagnostic test includes motor conduction to the EDB muscle above and below the knee to assess a conduction block at the fibular head.[5] Should the EDB muscle response be small or unobtainable, it is acceptable to measure the motor response at the anterior tibialis muscle. Superficial fibular sensory nerve action potential (SNAP) is tested, indicating axonal loss distal to the dorsal root ganglion if there is amplitude loss.[5] 

EMG should also sample muscles from the sciatic nerve's branches, including the short head of the biceps femoris, to distinguish it from more proximal fibular nerve lesions.[1][12] It is essential to compare with the opposite side. To evaluate for an accessory fibular nerve, the stimulation is done posterior to the lateral malleolus while recording at the EDB muscle.

Complications

Electrodiagnostic studies have a low risk of complications.

  • Small risk of bleeding
  • Introducing infection at the insertion site
  • Patient discomfort

Clinical Significance

Fibular neuropathy is primarily an axonal sensorimotor peripheral neuropathy, which will be made apparent on electrodiagnostic studies.

Sensory Nerve Conduction Studies

In axonal or mixed axonal/demyelinating lesions, the superficial fibular SNAP amplitude is usually low or absent.[1] Purely demyelinating fibular neck lesions, however, have a normal distal superficial fibular sensory response.[13]  A lesion distal to the dorsal root ganglia will show a decrease in the response with the sensory stimulation of the superficial fibular nerve.[5]

Motor Nerve Conduction Studies

Demyelinating lesions show a conduction block with a focal slowing in fibular motor studies performed across the fibular neck. Focal slowing is observed when there are a greater than 10 meters/sec difference from the distal conduction velocities. Conduction block is observed when there is a greater than 20% drop in amplitude of the proximal compound muscle action potential (CMAP).

  • A reduction in fibular CMAP amplitudes (ankle, below the lateral popliteal fossa or fibular head) indicates an axonal loss. This is because the pickup is measured at a distal muscle (EDB muscle) whose nerve has experienced Wallerian degeneration. The motor nerve's conduction velocity and the distal latency can either be normal or slightly slowed, depending on whether there is a loss of the fastest conducting axons. The patient usually experiences a combination of axonal loss and demyelination in the injured area.
  • Motor studies are usually recorded at the EDB muscle. However, the EDB muscle can be atrophied due to the patient's prior actions rather than a pathology. For example, a patient wearing tight shoes can lead to EDB muscle atrophy. If atrophy is present, the tibialis anterior muscle is a viable alternative to perform motor studies. This is especially important if a motor study at the EDB muscle does not show focal slowing or conduction block, while the tibialis anterior may display the deficit. Should there be any question of abnormal studies, it is acceptable to compare the result to the contralateral side. Additionally, sampling non-fibular muscles such as the tibialis posterior, flexor digitorum longus, or gluteus medius is also essential. These muscles are normal in fibular lesions but may be abnormal with L5 radiculopathy and lumbosacral plexopathy.
  • When comparing proximal versus distal EDB muscle amplitudes, if the proximal amplitude is greater, one should consider the presence of an accessory fibular nerve.[12] In this case, stimulating the area posterior to the lateral malleolus will create a CMAP at the EDB muscle.
  • Late responses: When fibular neuropathy is present, F-wave responses at the affected side of the fibular neck may be prolonged or absent, while those on the unaffected side may be normal. The slowing of the fibular F-waves may be more apparent if performed with ankle stimulation. This is because the F-response crosses the area of slowing twice with ankle stimulation but only once with either fibular or popliteal stimulation. However, one must remember that these responses tend to be non-specific, and it is not recommended to use them to diagnose fibular neuropathy. Alternate diagnoses can be ruled out using H-reflexes, which would be normal in fibular neuropathy, given that they exclude fibular nerve involvement.

Needle Electromyography

This test tends to be abnormal in fibular axonal lesions if axonotmesis is present. Clinicians will find abnormalities in lesions distal to the fibular nerve innervated muscles. Axonal lesions will show fibrillation potentials, positive sharp waves, and spontaneous activity, with decreased motor unit action potential recruitment depending on the timing of an injury. The results can be used to determine the chronicity of an injury.[1]

  • Chronic axonal lesions may show evidence of decreased motor unit action potential recruitment. The morphology of motor unit action potentials in these lesions may be polyphasic, with high amplitudes and long durations. The study will show fibrillation potentials and positive sharp waves.
  • In principally demyelinating lesions, clinicians will find normal firing frequency with only decreased motor unit action potentials. These lesions will have normal motor unit action potential morphology.
  • EMGs are critical to rule out other nerve lesions. For this reason, paraspinal and proximal leg muscles are tested concurrently to rule out radiculopathy. Additionally, muscles innervated by the tibial nerve are sampled distal to the knee. The tibial nerve supplies the hamstrings except for the short head of the biceps femoris muscle, which is innervated by the fibular nerve.[5]
  • Analyzing the results of the short head of the biceps femoris muscle can distinguish an injury of the fibular nerve at the fibular head versus an injury of the sciatic nerve. The fibular fibers are more susceptible to injury than the tibial fibers, especially in the gluteal regions and the sciatic notch. This is due to the unique anatomy of the sciatic nerve. If a patient experiences concurrent traumatic injuries to the buttock and the fibular head areas, the EMG result of the short head of the biceps femoris muscle is critical in distinguishing these lesions.[14]

Enhancing Healthcare Team Outcomes

Fibular neuropathy is the most common lower extremity neuropathy. Physiatrists, neurologists, neurosurgeons, and orthopedists must recognize that further evaluation with electrodiagnostic testing is warranted when patients present with foot drop/slaps, steppage gait, weakness, or sensory deficits in areas of the lower extremity innervated by the fibular nerve. Doing so will help expedite a patient’s recovery process and improve their quality of life in the long term.

Electrodiagnostic studies can prove to be an integral component for determining etiology and guiding management.[1] Once a fibular neuropathy diagnosis is made, an interprofessional team involved in the management should include physiatrists and therapists for physical/occupational rehabilitation. Nutritionists, social workers, and case managers from the inpatient standpoint must coordinate and ensure early mobilization with bedside therapy and aggressive multifaceted rehabilitation. Only through a well-coordinated effort between these multidisciplinary components will a patient achieve their best outcome.


References

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[3] Campbell WW, Diagnosis and management of common compression and entrapment neuropathies. Neurologic clinics. 1997 Aug;     [PubMed PMID: 9227952]
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[10] Tzika M,Paraskevas GK,Kitsoulis P, The accessory deep peroneal nerve: a review of the literature. Foot (Edinburgh, Scotland). 2012 Sep;     [PubMed PMID: 22795551]
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[12] Roy PC, Electrodiagnostic evaluation of lower extremity neurogenic problems. Foot and ankle clinics. 2011 Jun;     [PubMed PMID: 21600444]
[13] Izzo KL,Sridhara CR,Rosenholtz H,Lemont H, Sensory conduction studies of the branches of the superficial peroneal nerve. Archives of physical medicine and rehabilitation. 1981 Jan;     [PubMed PMID: 7458628]
[14] Nandedkar SD,Barkhaus PE,Sanders DB,Stålberg EV, Analysis of amplitude and area of concentric needle EMG motor unit action potentials. Electroencephalography and clinical neurophysiology. 1988 Jun;     [PubMed PMID: 2453333]