Commonperoneal palsy: clinical electrophysiological review · JournalofNeurology, Neurosurgery, andPsychiatry, 1976, 39, 1162-1171 Commonperoneal nervepalsy: a clinical and electrophysiological

Journal of Neurology, Neurosurgery, and Psychiatry, 1976, 39, 1162-1171

Common peroneal nerve palsy: a clinical andelectrophysiological reviewH. BERRY' AND P. M. RICHARDSON

From the Division of Neurology, St. Michael's Hospital, University of Toronto, Ontario, Canada

SYNOPSIS In a series of 70 patients (75 cases ofcommon peroneal nerve palsy) the common causes

were trauma about the knee or about the hip, compression, and underlying neuropathy. A few palsiesoccurred spontaneously for no apparent reason. The prognosis was uniformly good in the compres-

sion group; recovery was delayed but usually satisfactory in patients who had suffered stretch injuries.In the acute stage, when clinical paralysis appears to be complete, electrophysiological studies are a

useful guide to prognosis. They may also indicate an underlying neuropathy and they detect earlyevidence of recovery. The anatomical peculiarities of the common peroneal nerve are noted andaspects of the clinical picture, management, and prognosis of palsy are discussed.

Drop foot caused by common peroneal (lateralpopliteal) nerve palsy is a common clinical condition.Large studies of the condition in military casualtiesare available (Clawson and Seddon, 1960) and aresummarised by Sunderland (1968). The trauma isoften severe and disruptive with a large number ofmissile wounds and with associated damage to thesciatic nerve. A recent study of a civilian population(Kline, 1972) described a relatively large number ofcases due to gunshot wounds. Other published reportsdeal with small numbers of patients with palsy due tosingle causes. Ferguson and Liversedge (1954) des-cribed nine cases of ischaemic peroneal palsy.Marwah (1964) and Garland and Moorhouse (1952)considered palsies of a spontaneous and compressivetype. White (1968) described traction injuries of thecommon peroneal nerve and reviewed the earlierreports by Platt (1940) and Highet and Holmes (1943).Reports of more unusual cases are also available.Nobel (1966) described two cases of peroneal nervepalsy due to haematoma within the nerve sheath aftersevere inversion injury of the ankle. Others havedescribed ganglia of the common peroneal nerve(Brooks, 1952; Parkes, 1961; Cobb and Moiel, 1974).Most of the patients in these studies were assessedwithout the aid ofelectrophysiological tests.Hodes et al. (1948) demonstrated the technique of

motor nerve conduction velocity measurement in

I Address for correspondence: St Michael's Hospital, 30 Bond Street,Toronto, Ontario, Canada M5B IW8.(Accepted 27 July 1976.)

man, and this was applied to the common peronealnerve by Thomas et al. (1959). Conduction studies ofthe common peroneal nerve have been used chieflyfor detecting peripheral neuropathy. Behse and Buch-thal (1971) described a method of improved localisa-tion of a lesion at the neck of the fibula. Singh et al.(1974) measured sensory and motor conductionvelocity over the upper and lower segments of thecommon peroneal nerve the better to localise thelesion. It seems opportune to describe the clinicalfeatures of a relatively large number of patients withpalsy due to various causes in whom nerve conductionstudies and electromyographical examination havebeen performed.

METHOD

PATIENTS

The series is of 75 cases of palsy in 70 patients whowere referred for assessment as inpatients or out-patients to the electrophysiological laboratory of alarge urban general hospital. Fifty-two were male and18 were female. Their ages ranged from 15 to 84 yearswith a median of45 years. Most patients were assessedwithin one week to six months of the onset of thepalsy and the majority were examined within the firstthree months. Ten patients were first seen six monthsafter the onset ofthe drop foot.

Neurological examination for muscle atrophy,weakness, sensory disturbance, and reflex change wasundertaken in all patients. Muscle weakness wasgraded on the MRC scale and the degree of weakness

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Common peroneal nerve palsy: a clinical and electrophysiological review

of individual muscles innervated by the commonperoneal nerve was noted. Peroneus tertius involve-ment was not specifically assessed.

ELECTROPHYSIOLOGICAL ASSESSMENT

Measurement of common peroneal nerve motor con-duction velocity was attempted in all cases. Bipolarstimulation with a square wave pulse of 0.1 to 0.5 msduration and a voltage up to 500 V was applied to thenerve at the ankle and the neck of the fibula. Theresponse of the extensor digitorum brevis muscle wasdetected with a surface or a concentric needle elec-trode. Appropriate muscles were also sampled withconcentric needle electrodes to detect surviving motorunits, completeness of the interference pattern, andany evidence ofdenervation ofindividual muscles.Conduction measurements of the ipsilateral tibial

(medial popliteal) nerve and the opposite commonperoneal nerve and sensory and motor conductionstudies of the nerves of the upper extremities werealso performed when there was reason to suspect ageneralised neuropathy. Sensory action potentials inlower limbs were not determined. The degree ofelectrical severity was graded as follows. Grade A-motor conduction velocity greater than 40 m/s.Grade B-motor conduction velocity between 30 and40 m/s. Grade C-motor conduction velocity lessthan 30 m/s or unobtainable but with preservedmotor unit potentials on volition or with estimatedsupramaximal stimulation. Grade D-no demon-strable conduction; no action potentials undervoluntary control or with estimated supramaximalstimulation.

This method of grading was used in patientsexamined between one week and six months after theonset of the palsy. In patients seen at a later date itwas occasionally necessary to adjust the electricalgrade to allow for recovery that had occurred.Patients classified in this retrospective manner werenot included in the analysis.

FOLLOW-UP

Assessment was deemed adequate when a patient hadbeen followed up to the point of complete or nearcomplete recovery or when more than one year fromthe onset had elapsed. Follow-up was adequate in 46of the 75 palsies. Seventeen patients were too early inthe course of the condition, eight were lost to follow-up, and four died. The degree ofrecovery was assessedaccording to the following scale: good = full strengthor slight residual weakness, mild numbness; moderate= significant motor and sensory deficit but withuseful function; poor= no useful function.

RESULTS

A summary of the entire series of patients is given inTable 1. The major causes were traumatic or operativeinjury about the knee, injuries or other conditionsaffecting the nerve at the level of the hip joint, forcedankle inversion, spontaneous or compressive formsin patients with or without underlying neuropathy,and a few examples of progressive palsy. In severalpatients in whom more than one possible factorcould be implicated classification to a single causehad to be somewhat arbitrary.

Table 2 relates the electrophysiological grading tooutcome in 34 patients who were assessed earlyenough in the course of the paralysis and for whomadequate follow-up information was available.Patients with progressive palsy were excluded.Electrophysiological grading, as defined, is a goodindicator of prognosis. In those patients with in-complete paralysis electrophysiological examinationis not strictly necessary but it may detect an under-lying neuropathy. When paralysis is completeelectrical studies may indicate an incomplete lesionwith surviving motor units under voluntary controlor responsive to nerve stimulation, and we encoun-tered this finding in 10 out of 26 patients. Electricalgrading does not indicate the prognosis in the pro-gressive cases. It might have been predicted thatcases of peripheral neuropathy and atrophy of theextensor digitorum brevis muscle would be inter-preted as being more severe than they proved to be onfollow-up, but this was not our experience in thislimited series. Similarly, an outcome worse than thatindicated by electrophysiological grading might havebeen predicted in the sciatic nerve cases, but this wasnot our finding in this relatively small number ofpatients.

Table 3 shows the major causes and indicates thedegree of severity in each group. The severity, andhence the prognosis, varied in the knee trauma group.The palsy was usually severe in the hip trauma groupand the prognosis poor. Paralysis in patients withunderlying neuropathy tended to be more severe thanin the spontaneous and compressive groups. Thedegree of involvement in the spontaneous and com-pressive group was relatively mild and the prognosisgood. In those patients with purely blunt traumaabout the knee (14 patients, 15 palsies)-excludinglaceration, Volkmann's ischaemia, penetrating andoperative injuries-the prognosis was favourable.The prognosis was poor in the two patients withVolkmann's ischaemia complicating fracture of thetibia and fibula and was also poor in the two patientswith traumatic section of the nerve associated withknee injury. Follow-up in the group due to operativetrauma was incomplete.

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TABLE 2OUTCOME RELATED TO ELECTROPHYSIOLOGICAL

GRADE IN 34 PATIENTS

Recovery

Electrical Good Moderate Poorgrade 1 2 3 Total

A 10 10

B 3 3

C 1 10 1 12

D 4 5 9

TABLE 3CAUSATION RELATED TO SEVERITY IN 75 PALSIES

Electrical grade

Cause A B C D Total

Traumaabout knee 7 2 9 9 27

Traumaabout hip 1 2 5 6 14

Neuropathy 3 2 6 1 14

Spontaneouscompressive 7 5 2 0 14

Progressive 0 1 4 1 6

Table 4 gives a summary of the five patients whohad complete paralysis secondary to blunt traumaabout the knee, excluding the two patients withVolkmann's ischaemic contracture. The injury seemsto be comparable to what White (1968) has describedas 'severe stretch injuries'. The knee was repaired inall five patients. The nerve was adequately seen in fourpatients and was in continuity. Clinical recovery wasfirst noted after eight to 15 months and it continuedover a further period of more than one year. Four ofthe five patients regained useful function, and, in ourexperience, this type of complete paralysis seems tohave a better prognosis than that due to sciatic nerveinjury or that associated with Volkmann's ischaemia.

Fourteen patients developed drop foot after hiptrauma or after an operation in the region of the hip.Thirteen of them had additional tibial nerve involve-ment, and there was therefore reason to suspectsciatic nerve injury at the level of the hip or proximalthigh. The degree of paralysis of common peronealnerve function was complete in eight of the 14 cases.Tibial nerve function was completely absent in three

and partial or full in the remainder. In this group ofsciatic nerve injury the loss of common peronealfunction was always greater than that of tibial nervefunction. Persisting pain or troublesome dysaes-thesias were a feature in more than half of the patientswith features of sciatic nerve injury, whereas it wasfound in less than one quarter of the patients in thegroups due to other causes.

In 10 patients a generalised peripheral neuropathywas diagnosed from nerve conduction studies, andeight of them had obvious clinical features of neuro-pathy. Alcoholism was present in four, vasculitisassociated with collagen disease in two, and diabetesin one. The neuropathy was idiopathic in threepatients. In four patients the palsy was bilateral. Thepalsy in the neuropathy group tended to be moresevere than in the spontaneous or compressive groupand the outcome was correspondingly poorer. Mulderet al. (1961) demonstrated an increased susceptibilityto pressure palsy in diabetic neuropathy, and this isalso seen in neuropathy due to alcoholism and othercauses.

Fourteen patients (nos. 51 to 64) could be classifiedin the spontaneous or compressive group. In fivepatients there was a history indicative of compression-operative or postoperative, during coma, or duringleg crossing. In six others compression was the likelycause since the palsy was noted on wakening or aftersitting for a long period of time. In three patientscompression could not be invoked and the onset wasspontaneous with further progression over a day ortwo. The prognosis was uniformly excellent in thisgroup of 14 patients, as has also been described byGarland and Moorhouse (1952). There was noclinical evidence of peripheral neuropathy in thesepatients, although sensory and motor conductionstudies in the upper extremities were not performedin all. It is of interest that pain was present at theonset in four patients, in contrast with the experienceof Garland and Moorhouse (1952), who reported anabsence ofpain in a study of20 patients.

Table 5 gives the details in five patients with pro-gressive palsy. Progression occurred over weeks tomonths, often with pain, and the weakness wasusually severe by the time of our examination. Threepatients underwent surgical exploration and adefinite entrapment was encountered in only onepatient. One patient improved and two failed to im-prove after exploration. The severity of the palsy andits duration may have accounted for the lack of im-provement, although no definite abnormality wasseen at exploration. One patient was not exploredalthough there was a palpable thickening of the nerveat the neck ofthe fibula.

Table 6 gives details of the remaining patients whounderwent operation. Six patients in the injury and

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TABLE 4

TRAUMA ABOUT THE KNEE WITH COMPLETE PARALYSIS IN 5 PATIENTS

Degree of recoveryFirst evidence

Patient Structures Appearance of nerve of recovery Length of Individualno. involved at operation (months) follow-up muscle (MRC) Sensory Overall

1 Knee capsule Damage over 6 cm 15 3i yr Tib. ant. 4 Numbness ModerateCruciate ligament Peronei 4Lateral ligament Others 0

2 Cruciate ligament 'Adhesions' 11 5 yr Tib. ant. 4 No deficit ModerateLateral ligament EHL 4Biceps tendon Evertors 4

3 Cruciate ligament Not seen 13 15 m Tib. ant. 3 No deficit ModerateKnee capsule EDL 3Popliteal Peronei 4

EHL & EDB 04 Cruciate ligament Attenuation over 15 m All 0 No deficit Poor

Lateral ligament long distance (Few motorBiceps tendon units in

Tib. ant.)5 Fractured femur Contusion at head 8 15 m All 4 Slight Moderate

of fibula numbness

TABLE 5

DETAILS OF PROGRESSIVE PALSIES IN 5 PATIENTS

No. of Length of ElectricalCause cases progression Other features grade Management and outcome

Entrapment 1 2 m Pain C Improvement after release ofentrapment

Idiopathic 3 6 w-3 m One with pain. C,C,D Exploration in 2; no definiteAll with absent entrapment; no improvementankle jerks

Palpable cylindrical 1 3 w D Not explored; no improvementthickening of nerveat fibula

TABLE 6DETAILS OF 15 PATIENTS SURGICALLY EXPLORED

No. of ElectricalTime after onset Reason for operation cases grade Findings at operation Recovery

Early or Repair of knee; nerve also 3 D Continuity Slow improvementintermediate examined(4 days to 2 months)

Suspected section of nerve 2 D 1 complete section No improvement1 partial section

Post-meniscectomy palsy 1 A Continuity Not known

Late Suspected entrapment 5 B,C,C,C, 1 entrapment Improvement(after 2 months) D

4 no definite No improvemententrapment

Traumatic palsy with failure 3 B,D,D In continuity with Slow improvement in 2,to improve electrical activity no improvement in 1

Painful post-traumatic neuroma 1 Neuroma Relief of pain, gradualimprovement

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trauma group were explored at the onset or early inthe course of the paralysis. In three the nerve wasinspected during knee repair and was found to be incontinuity in spite of a complete paralysis by clinicaland electrophysiological criteria. Two patients withskin lacerations and complete paralysis requiredexploration to assess continuity and for nerve suturewhen necessary. One patient was explored un-necessarily, one week after the onset of paralysis aftera meniscus removal; electrophysiological testsshowed an incomplete palsy with preserved conduc-tion. Exploration was undertaken late in the course ofthe condition because of failure to improve, progres-sion ofthe paralysis, and, in two instances, continuingpain. These features led to a suspicion of entrapment,although this was verified in only one patient.

Delay in onset of the paralysis was a definite featurein 11 of the 27 patients who had suffered either blunt,penetrating, or operative trauma about the knee. Infour of these patients the apparent delay may havebeen due to the application of plaster, traction, orVolkmann's ischaemia, but in seven there was noidentifiable cause. Furthermore, delayed onset wascommoner in patients who had suffered blunt traumaabout the knee. The mechanism of the delay isobscure but it could be due to compression of thenerve by haemorrhage or oedema.

In most patients individual muscles were involvedto an equal degree. In 21 there was some disparity andthis was notable from the onset; in the remainder itwas noted during recovery. The commonest patternof disparity was that of preservation of peronealmuscle function with little or no function of themuscles of the anterior tibial compartment. Occasion-ally the converse was encountered. Five patients withsevere paralysis of the extensor hallucis muscle wereseen, and in three it was noted in the recovery phase.In the remaining two patients the paralysis developedafter tibial osteotomy and a nerve lesion of the branchto the extensor hallucis longus muscle was suspected.In four of these patients with selective loss ofextensorhallucis function the extensor digitorum brevismuscle was also completely affected. Sunderland(1968) has noted that the fibres which supply theextensor hallucis longus and extensor digitorumbrevis muscles, as well as some of the fibres of theextensor digitorum longus muscle, lie close togetheras the nerve crosses the fibula and may therefore bevulnerable to injury.

DISCUSSION

DIFFERENTIAL DIAGNOSIS

The most usual cause of unilateral drop foot is com-mon peroneal nerve palsy of a spontaneous,traumatic, or pressure type. The progressive variety

or that due to vasculitis are much less common. Dropfoot is occasionally caused by lumbar intervertebraldisc disease with herniation and compression of theL5 root; the pattern of muscle involvement within thecommon peroneal nerve territory is identical althoughthe degree ofmuscular paralysis is always incomplete.The sensory disturbance is similar. There is weaknessof the tibialis posterior muscle, and this is a usefulpoint of distinction; in addition there may be weak-ness of the hamstring muscles. Back pain, sciatica,and limitation of straight leg raising are evident andthe two conditions are usually easy to distinguish.Motor conduction velocity remains normal with L5root compression, although evidence of denervationmay be encountered in the appropriate muscles.

Rarely, intervertebral disc disease with multipleroot involvement (L5 and Sl) may produce a similarpicture. We encountered two such cases. There wasevidence of muscle involvement in a wider segmentalterritory and the condition was readily distinguishedfrom that of common peroneal nerve palsy. We havenot seen some of the more unusual causes of singlenerve root disturbance such as schwannomas orspondylolisthesis.Motor neurone disease often begins in the lower

extremities, and when the onset is asymmetrical itmay present as a drop foot. The clinical features oflower motor neurone type weakness-fasciculationand absence of sensory disturbance, with uppermotor neurone manifestations-should allow of aneasy distinction. Motor conduction is normal untillate in the condition and over the next months there isinvolvement of additional muscles and of the op-posite extremity. In general, it can be said that theseconditions are distinguishable and the diagnosis ofcommon peroneal nerve palsy can be establishedclearly on clinical grounds in almost every patient.When the drop foot is bilateral a different order of

causes must be considered. Evidence of involvementof other nerves is almost invariably present as in thegeneralised neuropathy of an idiopathic type, inalcoholism, collagen disease, or Charcot-Marie-Tooth disease. Our eight patients with Charcot-Marie-Tooth disease all showed prolonged motorconduction in the upper limbs. We have seen patientswith cauda equina disturbance due to intervertebraldisc disease and arachnoiditis with bilateral foot dropbut with widespread involvement of the muscles ofthe thighs and pelvic girdle. Distinction from com-mon peroneal nerve palsy has not been a problem.

ANATOMICAL CONSIDERATIONS

Sunderland (1968) states that the fascicles whichmake up the tibial and common peroneal nerve re-main separate throughout the length of the sciatic

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nerve, although they are enveloped in a commonepineurium. Two distinct nerves normally emerge atthe upper border of the popliteal fossa. The commonperoneal nerve passes downward and inferolaterallyunder cover of the biceps tendon and is separatedfrom the lateral femoral condyle by the upper portionof the gastrocnemius and plantaris muscles. It con-tinues posterior to the tendon of the popliteus muscleand to the tendinous attachment of the soleus to thefibular head. The common peroneal nerve now curvesaround the neck of the fibula, and our dissectionstudies show that it is applied to the periosteum of thefibula for a total of about 10 cm. The nerve passesthrough a tunnel, the roof of which is formed by theorigin of the peroneus longus muscle and the inter-muscular septum. The upper portion of the arch ofthetunnel is attached to the head of the fibula and thelower portion of the arch to the lateral aspect of theupper portion of the shaft of the fibula. Kopell andThompson (1963) note that the fibromuscular open-ing of the tunnel may have a J-shaped outline and thatthe curved portion of the J forms the inferior marginof the opening.The common peroneal nerve usually divides into

three branches-the articular branch to the capsule ofthe knee; the deep peroneal nerve (anterior tibialnerve), which passes through a second fibro-osseouscanal formed by the origin of the extensor digitorumlongus muscle about 4 cm below the first tunnel andwhich supplies muscles of the anterior compartmentand the third branch; and the superficial peroneal(musculocutaneous) nerve which runs deep to andbetween the peroneal muscles and supplies theperoneus longus, brevis, and the skin. In one half ofthe cases there is a muscular branch to one of themuscles in either the anterior or lateral compartmentsbefore the regular division of the nerve into its threebranches (Sunderland, 1968). The major branchesalso vary. In 20 patients analysed by Sunderland thedivision into the three branches occurred proximal tothe-tunnel in two, at or within the tunnel in seven, andup to 3.9cm below the tunnel in 1 1.

Several peculiarities of the common peroneal nervemake it vulnerable to injury. It is exposed over a bonyprominence for about 4 cm covered only by skin andsuperficial fascia and is susceptible to direct blows andlacerations. It is readily compressed at that site whenthe patient sits with legs crossed or when conscious-ness is diminished and it is endangered in fractures.Nobel (1966) has noted limited longitudinal mobilityof the nerve and our dissection studies show that thepassage of the common and deep peroneal nervesthrough the two tunnels limits mobility in a longi-tudinal direction to about 0.5 cm. The large numberof branches which arise immediately below the kneecontribute to this fixation. The epineurium is not

usually adherent to the superficial fascia or perios-teum but adhesions may occur as a result of injury,and we saw this at the time ofexploration in several ofour patients. It can thus be seen that longitudinalstretch forces applied to the nerve in injuries such asforced ankle inversion or in proximal injuries such asposterior hip dislocation can result in a stretch injuryof the common peroneal nerve. Several examples areincluded in this series. The relative thickness of theepineurium-that is, the ratio of epineurium tofascicular area on cross section-influences the sus-ceptibility to stretch injuries (Haftek, 1970). The ratiois greatest with respect to the sciatic nerve in thegluteal region and is least with respect to the commonperoneal nerve (Sunderland, 1968). The presence ofthe fibro-osseous tunnel creates an opportunity forentrapment analogous to that seen in carpal tunnelsyndrome, but this appears to be a relatively rarefactor in causation with respect to the commonperoneal nerve.

Passage through the fibro-osseous tunnel can leadto interference if any of the structures should beinvolved in swelling or haemorrhage; this may be thebasis of the delayed type of palsy seen in our patientswho suffered blunt trauma about the knee. Nobel(1966) operated on two patients who developed pain-ful common peroneal nerve palsy after torsionalinjuries about the knee and found haematoma withinthe nerve sheath at the level of the popliteal fossa.Swelling and haemorrhage within the anterior tibialcompartment due to local trauma may result in apainful partial peroneal nerve palsy (Rorabeck et al.,1972). It might be argued that some of our delayedcases were due to this type of haematoma within thenerve sheath, except that pain was not a feature.

ELECTROPHYSIOLOGICAL ASSESSMENT

Electrical studies are usually superfluous to thediagnosis of drop foot but they are of value inassessing prognosis and in detecting early signs ofrecovery. Prolonged motor conduction of othernerves may indicate an underlying neuropathy. It isadequate to sample muscles within the anterior andlateral compartments and to obtain conductionvalues from the neck of the fibula to the extensordigitorum brevis muscle. When this muscle is totallyatrophic or inaccessible conduction velocity cannotbe measured but latency values to individual musclescan be determined (Redford, 1964). Our experiencewith this has been too limited to allow of any usefulcomment. The technique of nerve stimulation atconsecutive points, as described by Carpendale(1966), could be applied to the common peronealnerve in order to define the site of the lesion, and thetechnique of sciatic nerve conduction (Gassel and

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Trojaborg, 1964) could be used to detect lesions with-in the thigh. We have not had any experience withthese techniques nor with that ofBehse and Buchthal(1971). In the patients with complete paralysis wefound the earliest evidence of recovery to occurwithin the upper portion of the tibialis anteriormuscle or the peronei; nascent motor unit potentialsshould be looked for, and these were first detectedtwo to eight months after the onset of the palsy.The lateral half of the extensor digitorum brevis

muscle may be innervated by a branch of the super-ficial peroneal nerve (musculocutaneous nerve) andLambert (1969), by means of nerve stimulation,found this in 22% of limbs. Gutmann (1970) des-cribed two patients with lesions of the deep peronealnerve (anterior tibial nerve) due to fibular chondromaand a ganglion cyst, in which a portion of the extensordigitorum brevis muscle was preserved, with normalmotor conduction velocity of the common peronealnerve. The practical importance of this 'accessorydeep peroneal nerve' is not great since the site ofmostlesions is situated at or proximal to the neck of thefibula and is above the origin of the accessory branch.We did not experience any misleading observationsdue to this anatomical variant.

MANAGEMENT

When the palsy is incomplete, with slight to moderateweakness, the prognosis is uniformly good and thepatient may be reassured of this. If the drop footdevelops after diminished consciousness due to headinjury, anaesthesia, or other cause there is no clearindication for any further medical or electro-physiological investigation and such patients usuallyrecover in a few weeks. When the condition developsspontaneously in an otherwise healthy patient aninquiry into general health, alcoholism, or diabetesis relevant. Here nerve conduction studies may showreduced velocity in other nerves and indicate ageneralised neuropathy. This should lead to appro-priate medical investigation.

Progressive cases do require investigation. Under-lying neuropathy should be looked for, although wedid not find any examples of it. Electrical tests serveto confirm the progression, and if the cause is notapparent it is reasonable to recommend surgicalexploration.

Total paralysis, apart from the occasional patientwith underlying generalised neuropathy or a pro-gressive palsy, is, in our experience, always on thebasis of trauma. In blunt injuries about the kneeseverance of the nerve is unlikely and is also unlikelyin most patients with dislocations of the hip or kneeor fractures of the femur, tibia, fibula, or ankleinjuries. If the lesion is incomplete clinically there is

no definite need for electrical testing and recovery canbe followed by clinical observation alone. In thosepatients where the lesion appears to be completeelectrical testing and a more careful follow-up isrequired. Electromyographic evidence of recoveryshould be looked for. In our experience this occurredwithin two to 15 months. When the continuity of thenerve is in doubt it is probably unreasonable to waitfor evidence of recovery beyond six months. Explora-tion was thus performed in three of our patients threemonths, six months, and one year after injury andcontinuity was found in all. As in our study a numberof patients will already have undergone explorationat the time of surgical repair to the knee. Observationsmade at that time as to the appearance of the nerve-bruising, attenuation, and length of the injured seg-ment-indicate the severity of the injury and help toindicate whether the recovery will be delayed or in-complete. It should be noted that all patients in ourseries in the group who suffered blunt trauma aboutthe knee had a nerve in continuity at the time ofsurgical repair of the knee.

Reports have given a poor prognosis for stretchinjuries, and the role of surgical intervention in thesepatients deserves some comment. Platt (1940) des-cribed nine cases, four of which had complete ruptureof the nerves at operation. In the remaining caseswhere the nerve was in continuity exploration hadbeen undertaken within the first seven weeks, and theauthor concluded that the injured nerve should beexplored within the first few weeks of the accident.We would say that this is too early to allow of thedetection of recovery. Highet and Holmes (1943)operated on eight patients with traction injury fromfour to 11 months after the accident. In six of thesepatients resection and suture were carried out. Onlyone patient made any recovery. White (1968) des-cribed a better outlook. Six traction injuries of thecommon peroneal nerve were documented in associa-tion with severe adduction forces to the knee. In twothere was disruption of the nerve and suture wasperformed with good results. In the other four thenerve was in continuity and all made a good recovery.This author recommended exploration at threemonths if there was no evidence of recovery. Ourexperience justifies a more optimistic note; four out offive patients experienced a return of useful function.We would defer surgical exploration for about sixmonths and wait for evidence of recovery unless therewas an additional reason to suspect discontinuity ofthe nerve.

In cases of a penetrating or lacerating injury or ofextensive bony injury, severance of the nerve shouldbe suspected. If nerve conduction is absent with nosurviving motor units surgical exploration is needed.There were two such patients in our study, and the

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operative findings were complete transection of thenerve in one and partial in the other. In such patientssurgical repair should be undertaken and end-to-endsuture is usually possible (Kline, 1972). In theexperience of Seddon (1972) one-third ofsuch patientshad a useful recovery.Of all the patients with complete paralysis (group

D) about half experienced a useful degree of recoveryand the outcome was slightly better in the blunt kneetrauma group. A permanent drop foot brace may berequired in patients who do not recover and the usualremedial surgical treatment is that of tendon transfer.

REFERENCES

Behse, F., and Buchthal, F. (1971). Normal sensory con-duction in the nerves of the leg in man. Journal ofNeurology, Neurosurgery, and Psychiatry, 34, 404-414.

Brooks, D. M. (1952). Nerve compression by simpleganglia. JournalofBone andJoint Surgery, 34B, 391-400.

Carpendale, M. T. (1966). The localization of ulnar nervecompression in the hand and arm: an improved methodof electroneuromyography. Archives of Physical Medi-cine and Rehabilitation, 47, 325-330.

Clawson, D. K., and Seddon, H. J. (1960). The late con-sequences of sciatic nerve injury. Journal of Bone andJoint Surgery, 42B, 213-225.

Cobb, C. A., and Moiel, R. H. (1974). Ganglion of theperoneal nerve. Journal ofNeurosurgery, 41, 255-259.

Ferguson, F. R., and Liversedge, L. A. (1954). Ischaemiclateral popliteal nerve palsy. British Medical Journal, 2,333-335.

Garland, H., and Moorhouse, D. (1952). Compressivelesions of the external popliteal (common peroneal)nerve. British AedicalJournal, 2, 1373-1378.

Gassel, M. M., and Trojaborg, W. (1964). Clinical andelectrophysiological study of conduction times in thedistribution of the sciatic nerve. Journal of Neurology,Neurosurgery, andPsychiatry, 27, 351-456.

Gutmann, L. (1970). Atypical deep peroneal neuropathy.Journal ofNeurology, Neurosurgery, and Psychiatry, 33,453-456.

Haftek, J. (1970). Stretch injury of peripheral nerve.Journal ofBone andJoint Surgery, 52B. 354-365.

Highet, W. B., and Holmes, W. (1943). Traction injuries tothe lateral popliteal nerve and traction injuries toperipheral nerves after suture. British Journal ofSurgery, 30,212-233.

Hodes, R., Larrabee, M. G., and German, W. (1948). Thehuman electromyogram in response to nerve stimula-

tion and thc conduction velocity of motor axons.Archives of Neurology and Psychiatry (Chic.), 60,340-365.

Kline, D. G. (1972). Operative management of majornerve lesions of the lower extremity. Surgical Clinics ofNorth America, 52, 1247-1265.

Kopell, H. P., and Thompson, W. A. L. (1963). PeripheralEntrapment Neuropathies. Williams and Wilkins:Baltimore.

Lambert, E. H. (1969). The accessory deep peroneal nerve.Neurology (Minneap.), 19, 1169-1176.

Marwah, V. (1964). Compression of the lateral popliteal(common peroneal) nerve. Lancet, 2, 1367-1369.

Mulder, D. W., Lambert, E. H., Bastron, J., and Sprague,R. G. (1961). The neuropathies associated with dia-betes mellitus. A clinical and electromyographic studyof 103 unselected diabetic patients. Neurology,(Minneap.), 11,275-284.

Nobel, W. (1966). Peroneal palsy due to hematoma in thecommon peroneal nerve sheath after distal torsionalfractures and inversion ankle sprains. Journal of BoneandJoint Surgery, 48A, 1484-1495.

Parkes, A. (1961). Intraneural ganglion of the lateralpopliteal nerve. Journal ofBone andJoint Surgery, 43B,784-790.

Platt, H. (1940). Traction lesions of the external poplitealnerve. Lancet, 2,612-614.

Redford, J. B. (1964). Nerve conduction in motor fibers tothe anterior tibial muscle in peroneal palsy. Archives ofPhysical Medicine and Rehabilitation, 45,500-504.

Rorabeck, C. H., Macnab, I., and Waddell, J. P. (1972).Anterior tibial compartment syndrome: a clinical andexperimental review. Canadian Journal of Surgery, 15,249-256.

Seddon, H. J. (1972). Surgical Disorders of the PeripheralNerves. Churchill Livingstone: Edinburgh.

Singh, N., Behse, F., and Buchthal, F. (1974). Electro-physiological study of peroneal palsy. Journal ofNeurology, Neurosurgery, andPsychiatry, 37, 1202-1213.

Sunderland, S. (1968). Nerve and Nerve Injuries. Williamsand Williams: Baltimore.

Thomas, P. K., Sears, T. A., and Gilliatt, R. W. (1959).The range of conduction velocity in normal motornerve fibres to the small muscles of the hand and foot.Journal ofNeurology, Neurosurgery, and Psychiatry, 22,175-181.

White, J. (1968). The results of traction injuries to thecommon peroneal nerve. Journal of Bone and JointSurgery, 50B, 346-350.

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Commonperoneal palsy: clinical electrophysiological review · JournalofNeurology, Neurosurgery, andPsychiatry, 1976, 39, 1162-1171 Commonperoneal nervepalsy: a clinical and electrophysiological