This position is often used in gynecologic as well as abdominal surgery. In addition to positioning during surgery, patients who require prolonged bed rest after surgery may be at risk for peroneal neuropathy. Gravity, the shape of the lower extremity, and muscular imbalance contribute to the tendency of the lower limb to rest in external rotation of the hip and knee flexion while lying supine.
This position, together with the bony prominence of the fibular head, may jeopardize the peroneal nerve unless a preventative program is instituted. This involves the use of bilateral padded ankle foot orthoses which maintain the feet in dorsiflexion and the lower limbs in neutral without external rotation while the patient is resting in bed.
Frequent repositioning of the supine patient can also minimize pressure on the lateral knee. In addition to peroneal neuropathy, prolonged bed rest is a risk factor for deep venous thrombosis.
Currently, the medical community has an increased awareness of the post-operative risk of thromboembolic disease. Pneumatic compression devices may be used in the prevention of this life-threatening disorder. Bilateral peroneal nerve palsies following intermittent pneumatic compression have been reported [ 12 ]. Unfortunately, malnutrition is a common comorbid condition with bed rest or prolonged surgery. Since malnutrition leads to weight loss, this may be a complicating factor when considering positioning as the cause of peroneal neuropathy.
Since both weight loss and bed rest may result in a neuropathy of subacute onset, chronology does not help to identify the causative factor. Patients who have weight loss, independent of bed rest or compressive lesion, have developed peroneal neuropathy [ 13 ]. Bilateral peroneal neuropathy has been reported after bariatric surgery [ 14 ].
As more patients undergo this weight loss surgery, we may come to a better understanding of the role of weight loss in peroneal mononeuropathy. Currently, there is no agreement as to the quantity of weight loss that will result in peroneal nerve damage. The proposed mechanism is loss of fat previously protecting the peroneal nerve. In a series of patients with common peroneal neuropathy, Katirji and Wilbourn describe twenty-five patients with gradual or indeterminate onset of the disorder who had weight loss of more than twenty pounds over 2—3 months [ 15 ].
Of interest, peroneal neuropathy has also been reported with prolonged squatting [ 16 ]. Biomechanical comparisons of compression of the peroneal nerve in squatting have not been evaluated in terms of body mass index. Less commonly, peroneal nerve injury occurs as a result of laceration. These were due to injury from broken glass, knives, boat propellers, chain saws, or lawn mower blades. Three of the 39 patients had continuity of the nerve despite this mechanism of injury and subsequently had better recovery.
In this same series, 12 patients had peroneal nerve injuries due to gunshot wound. The majority of these patients still had lesions in continuity [ 17 ]. The case series of Kline and colleagues also addressed mass lesions. The most common of these was intraneural ganglion cyst.
Other tumors, in order of decreasing frequency, included schwannoma, neurofibroma, osteochondroma, neurogenic sarcoma, focal hypertrophic neuropathy, desmoid tumor, and glomus tumor [ 17 ]. In a much smaller study of nine patients presenting with peroneal nerve palsy who underwent MRI, six patients had ganglion cyst, one had a synovial cyst, one had osteochondroma, and one had an aneurysm [ 18 ].
Intraneural ganglion cyst appears to be a frequently occurring mass lesion in peroneal neuropathy. Of note, the most common site of intraneural ganglia within the peripheral nervous system is the common peroneal nerve [ 19 ].
Osteoarthritis of the knee may contribute to peroneal neuropathy via mechanisms involving nerve stretch or compression. A case of varus knee deformity due to arthritis resulting in peroneal neuropathy at the level of the knee has been reported. There was no evidence of compressive lesion at the time of operative exploration. Consequently, the lesion was thought to be due to repetitive traction injury from varus malalignment.
The patient responded to treatment with total knee arthroplasty with attention to prevention of post-operative varus knee laxity [ 20 ]. There was no noted lateral knee osteophyte in this patient. However, an osteophyte causing peroneal nerve palsy has been reported in a younger patient [ 21 ].
Initially, patients with peroneal neuropathy complain of lateral lower limb and dorsal foot pain. Concurrent low back pain or posterolateral thigh pain suggests L5 radiculopathy. Pain usually precedes sensory changes in a similar distribution. The patient may complain of foot drop as the first manifestation of this disorder. Table 1 presents the various possible lesions resulting in ankle weakness of peripheral neurogenic origin.
Evidence of trauma or vascular comprise may help to determine the cause of the lesion. The peroneal nerve may be palpated as it winds around the head of the fibula. Tapping over this area may reproduce dysesthesia in the lateral calf or foot. Careful sensory examination can assist with localizing the lesion. The deep peroneal nerve supplies the area between the first and second toes. The remaining dorsum of the foot is innervated by the superficial peroneal nerve, except for a small area laterally.
Sensation of the plantar foot is spared in lesions of the peroneal nerve. All muscles of the lower limb should be examined for weakness and compared to the contralateral side.
Weakness of the ankle dorsiflexors, toe extensors, and ankle evertors, commonly referred to as foot drop, is suggestive of peroneal neuropathy. Another Less frequently, lumbosacral plexopathy can result in weakness in a similar distribution. Often, patients with L5 radiculopathy or sciatic neuropathy will have similar deficits as those with common peroneal neuropathy.
The tibialis posterior, innervated by the tibial nerve, receives its main segmental innervation from L5. This muscle provides the majority of ankle inversion.
If ankle inversion is weak, the lesion involves more than the common peroneal nerve. Examination of normal and pathologic reflexes can further narrow the differential. The patellar tendon reflex is innervated by the L2 through L4 nerve roots. The Achilles reflex is primarily from S1. Absent or diminished reflexes suggest a peripheral origin of foot drop. The presence of pathologic reflexes, such as a Babinski reflex, suggest foot drop of central origin.
Table 1 below presents the most common peripheral causes of foot drop. Since peroneal neuropathy appears clinically most similar to L5 radiculopathy, L4 and S1 were excluded from this table. As previously mentioned, the L4, L5, and S1 roots contribute to the common peroneal nerve.
Plain radiographs of the knee and ankle should be obtained to evaluate for concurrent fracture, mass lesion, or arthritis if the history suggests one of these etiologies. Lumbar MRI can provide evidence of L5 radiculopathy if radiographs are negative. Knee and ankle MRI can further elucidate a bony lesion or demonstrate intraneural ganglia. In order to view the anatomy of the actual nerve, 3-tesla MRI is necessary [ 23 ].
These machines are now becoming available at large centers. Kim and his group [ 18 ] suggest that knee MRI should be performed in all cases of non-traumatic peroneal nerve palsy since intraneural ganglia may be the most common etiology.
Another newer technique to assess the area around the fibular head is high-resolution sonography. Visser suggests that ultrasonography is an accessible and easy way to evaluate the common peroneal nerve in its superficial location [ 24 ]. Electrodiagnostic studies assist with confirming the diagnosis of peroneal neuropathy, excluding alternative diagnoses, and determining prognosis.
Recommended examination includes motor nerve conduction studies of the peroneal nerve and tibial nerve and sensory nerve conduction studies of the sural and superficial peroneal nerves. In general, if the lesion involves demyelination, focal slowing or conduction block amplitude loss at more proximal stimulation sites can be seen. If the lesion is due to axon loss, compound muscle action potential amplitudes will be decreased at all stimulation sites.
Needle electromyographic exam can further localize the lesion. Routine muscles examined for this study include two muscles innervated by the deep peroneal nerve, one muscle innervated by the superficial peroneal nerve, the tibialis posterior, another muscle innervated by the tibial nerve i. If any of the muscles supplied by the peroneal nerve are abnormal, further muscles supplied by the L5 nerve root but not the peroneal nerve i.
Pain is the earliest symptom in peroneal neuropathy and may be the most difficult to treat. As these provide symptomatic relief only, the choice of medication depends on comorbidities and possible adverse effects. A review of these choices is beyond the scope of this article, but treatment should be individualized to the patient. Modalities such as heat and ice can also provide effective pain relief. However, patients with sensory loss should be carefully observed during the use of modalities to prevent skin damage.
Also, superficial ice treatment may injure the peroneal nerve at the fibular head when applied incorrectly. This was reported in the case of a football player who applied ice to a hamstring muscle strain [ 25 ].
Skin damage from superficial cold application does not usually occur with the use of a protective barrier for the skin and limited duration of therapy. Superficial heat may result in burn injury. This can occur with lying on a heating pad or prolonged therapy. Iontophoresis has been suggested for the relief of pain in peroneal neuropathy [ 26 ]. This involves the transcutaneous delivery of ionic medications i.
Although there has been little evidence to suggest the actual absorption of steroids into human soft tissue, this may provide symptomatic relief for the patient and is generally well tolerated. Weakness in peroneal neuropathy may lead to functional gait impairment.
Muscle atrophy can become clinically apparent at 2 weeks after injury. If there is transection of a nerve or a complete axon loss lesion, it will be of no use to attempt to strengthen the denervated muscles.
If there is compression, it is best to relieve the offending agent prior to a trial of strengthening. If the patient has subtle peroneal nerve injury, strengthening may help with functional recovery.
If the patient has complete loss of strength, passive range of motion may be all that is possible. It is imperative to maintain proper ankle range of motion so that residual heel cord contracture will not preclude the ability to walk. Recently, peroneal nerve stimulators have been gaining in popularity for the treatment of foot drop of central etiology [ 27 , 28 ].
These devices require an intact functioning peroneal nerve and are not useful in patients with peripheral nerve injury. Patients with sensory loss should check their feet daily to prevent progression of ulcers. A simple lace-up ankle sleeve with medial and lateral support may assist a patient with proprioceptive loss.
In peripheral neuropathy, it is rare to have proprioceptive loss until the late stages of disease. If sciatic or peroneal palsy is severe enough to demonstrate proprioceptive loss, the patient is more likely to have gait impairment and require intervention [ 29 ].
If the patient has weakness of the toe extensors only, as would occur in distal deep peroneal neuropathy, sturdy footwear may be all that is needed to optimize gait. A rocker-bottom shoe may decrease the energy required for ambulation. If the patient has isolated superficial peroneal nerve palsy, he may benefit from a shoe insert with a lateral wedge to prevent supination of the foot from weakness of the evertors.
If the patient has a proximal deep peroneal neuropathy, he may be unable to dorsiflex the ankle. Ankle dorsiflexion is necessary to clear the toes while ambulating. An ankle foot orthosis maintains the foot in neutral so that the patient can achieve a normal gait pattern.
If the lesion is at the level of the common peroneal nerve, the foot may tend toward plantarflexion and inversion. This patient would also require an ankle foot orthosis for toe clearance during gait.
Patients with common peroneal neuropathy require a more solid, less flexible AFO than those with only deep peroneal neuropathy. All patients with weakness should stretch daily to prevent contracture.
Equinovarus foot deformity is a common complication of ankle dorsiflexion weakness. It is essential that the patient maintain his range of motion to have the ability to ambulate. After contracture has developed, the patient may be unable to tolerate bracing. If bracing is not effective, the tibialis posterior tendon can be transferred to the dorsum of the foot to restore active dorsiflexion. This is often performed in conjunction with fusion of the subtalar joint and after one year post-injury [ 7 ].
Removal of the offending agent, lesion, or activity is the best treatment of peroneal neuropathy. Consequently, prompt recognition and diagnosis is imperative in order to preserve maximum function. Initially, treatment may be conservative in most peroneal nerve lesions. Open wounds associated with peroneal nerve palsy should undergo immediate surgical exploration [ 30 ]. Other lesions are followed clinically and may be investigated electromyographically. If there is no evidence of functional recovery, surgery may be performed at 3—7 months from injury.
Operative technique and time to intervention vary according to the nature of the injury. Neurolysis yields the best outcome. End-to-end suture repair is preferable to graft repair, and shorter grafts yield better outcomes. National Center for Biotechnology Information , U. Curr Rev Musculoskelet Med. Published online Mar Jennifer Baima 1, 2 and Lisa Krivickas 1, 2. Author information Copyright and License information Disclaimer.
Jennifer Baima, Email: gro. Corresponding author. This article has been cited by other articles in PMC. Abstract Peroneal nerve compromise results in the clinical complaint of weakness of the ankle dorsiflexors and evertors. Keywords: Peroneal nerve, Ankle dorsiflexors, Foot drop, Sciatic nerve injury. Anatomy The sacral plexus is formed from the L4—S4 ventral rami.
Open in a separate window. Etiology Peroneal nerve compromise has been reported due to numerous traumatic and insidious causes. Patient evaluation Initially, patients with peroneal neuropathy complain of lateral lower limb and dorsal foot pain. Table 1 Foot drop of peripheral origin. Imaging and electrodiagnostic testing Plain radiographs of the knee and ankle should be obtained to evaluate for concurrent fracture, mass lesion, or arthritis if the history suggests one of these etiologies.
Treatment Pain is the earliest symptom in peroneal neuropathy and may be the most difficult to treat. References 1. Jenkins DB. The Leg. Philadelphia: WB Saunders; Peroneal neuropathy. In: Electromyography and neuromuscular disorders. Consequences of foot drop the affected foot catches on the floor when walking high stepping gait - the affected leg is lifted high to clear the floor swinging of the affected leg to clear the floor Key message Common peroneal nerve palsy is only one of the many possible causes of foot drop.
Presentation Foot drop often is the most striking feature Weakness in foot eversion may occur if the superficial peroneal component is involved The pattern of sensory loss would suggest either superficial or deep peroneal nerves or both are involved Tinel's sign is a reliable clinical sign to localise area of nerve irritation or entrapment - Tapping along the course of the nerve particularly around the fibular neck causing shooting pain and tingling into the foot Investigations Neurophysiology is used to confirm the diagnosis Radiographs of the knee MRI to look for lesions compressing the nerve Treatment Nonoperative Ankle-foot orthoses Physiotherapy Operative In atraumatic situations, if there is strong indication of a focal nerve lesion positive Tinel's spot that is not advancing with time , exploration and neurolysis are recommended.
In open injury, the nerve needs to be explored and repaired if necessary. In closed injury, judgement is required regarding the potential severity of the nerve lesion in order to decideupon the period of observation waiting for spontaneous recovery.
If in doubt, exploration is recommended. Reported outcomes of neurolysis or nerve grafting have been poor. This is probably related to the length of nerve graft and the level of energy involved in the initial injury.
Other reconstructive options include tendon transfer or nerve transfer. Common peroneal nerve palsy Superficial peroneal nerve lesion Tarsal tunnel syndrome Print Page. Contact Information. Book your consultation today.
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