electrophysiological study ofperoneal palsynaunihalsingh, friedrich behse, andfritz buchthal sensory...

Journal of Neurology, Neurosurgery, and Psychiatry, 1974, 37, 1202-1213

Electrophysiological study of peroneal palsy

NAUNIHAL SINGH1, FRIEDRICH BEHSE, AND FRITZ BUCHTHAL

From the Laboratory of Clinical Neurophysiology, University Hospital (Rigshospital)and the Institute ofNeurophysiology, University of Copenhagen, Copenhagen, Denmark

SYNOPSIS The diagnostic yield of different electrophysiological criteria was examined to establishwhether a peroneal palsy was due to compression of the nerve in the region of the capitulum fibulae.Slowing of sensory conduction along the segment of the nerve across the capitulum fibulae localizedthe lesion in 64% of 47 consecutive patients with a history indicating or suggesting compression ofthe nerve in the vicinity of the capitulum fibulae and there were no false positive findings in 18patients whose peroneal palsy was not due to compression at the capitulum fibulae. In 20% of thepatients with slowing along the segment across the capitulum, conduction velocity was normal whenmeasured from the superior retinaculum to the popliteal fossa. Slowing along motor fibres (m.extensor digitorum brevis) localized the site of the lesion in one-third of the patients. Differences inamplitude and in split-up of the sensory responses recorded in the popliteal fossa as compared withthose recorded distal to the capitulum fibulae were of limited diagnostic value because of manyfalse positive findings among patients whose peroneal palsy was not due to compression of the nerveat the capitulum fibulae.

Though doubt often arises with respect to thesite of the lesion in peroneal palsy, only fewattempts are reported in the literature to localizethe lesion by electrophysiological methods.Gilliatt et al. (1961) found in four patients slow-ing and diminished amplitudes of mixed nerveaction potentials evoked at the ankle and re-corded at the neck of the fibula. Gassel andTrojaborg (1964) interpreted the slower velocityin motor fibres to the extensor digitorum brevisalong the segment of the nerve in the leg as com-pared with that along the nerve in the thigh toindicate a lesion of the peroneal nerve in thevicinity of the capitulum fibulae. Behse andBuchthal (1971) determined sensory and motorconduction along a 10 cm length of the peronealnerve across the capitulum fibulae and comparedthem with the velocity in the segment distal tothe capitulum fibulae along the leg. This proce-dure permits a lesion at the capitulum to belocalized with greater precision, and mild involve-

' On leave from the All-India Institute of Medical Sciences, NewDelhi, India, working with a fellowship from the Danish InternationalDevelopment Agency.

1202

ment can be recognized by excluding the stretchof nerve which usually is less affected or normal.The diagnostic yield can be increased by examin-ing motor and sensory fibres separately. Thesame procedure has previously been applied tolocalize a lesion of the ulnar nerve in the cubitalsulcus (Payan, 1969), ofthe radial nerve proximalto the elbow (Trojaborg, 1970), and ofthe mediannerve at the wrist (Buchthal and Rosenfalck,1971a; Buchthal et al., 1974). To obtain the bestpossible resolution of the small sensory poten-tials and to define the site of recording andstimulation as accurately as possible needleelectrodes were placed near the nerve.The purpose of the study presented in this

report was to evaluate the diagnostic yield ofelectrophysiological procedures and criteriaavailable to localize a lesion of the peronealnerve in the region of the capitulum fibulae. Forthis purpose, findings were compared in consecu-tive patients with peroneal palsy due to or pre-sumably due to compression of the nerve at thecapitulum fibulae with findings in patients inwhom there was evidence that the perone alpalsy was due to other causes.

guest. Protected by copyright.

on April 18, 2021 by

http://jnnp.bmj.com

/J N

eurol Neurosurg P

sychiatry: first published as 10.1136/jnnp.37.11.1202 on 1 Novem

ber 1974. Dow

nloaded from

http://jnnp.bmj.com/

Electrophysiological study ofperoneal palsy

SENSORY

I~~~~~~~g 0

\D -DISTAL TO CAR FIB. ACROSSA

FIG. 1. Placement ofnear-nerve (0) and remote (0)electrodes for measurement of motor and sensory

conduction. Sensory: S, stimulus to medial branch ofsuperficialperoneal nerve at superior extensor retinacu-lum. Recording from sensory fibres of superficialperoneal nerve 2 cm distal to capitulum fibulae (R1)and in the popliteal fossa (R2). Motor: stimulus tocommon peroneal nerve in popliteal fossa (S1), and2 cm distal to the capitulum fibulae (S2); to deepperoneal nerve at ankle (S3). Recording from m.

tibialis anterior, m. peroneus longus, and m. extensordigitorum brevis.

METHOD

SENSORY CONDUCTION The procedure employed tostudy conduction along the superficial peronealnerve has been described (Behse and Buchthal, 1971).In brief:

Stimulation Rectangular current pulses of 8-12 mA,0-2 ms in duration, were applied via needle electrodesto the nerve at the superior extensor retinaculum(Fig. 1). In normal nerve this current strength is 10 to20 times the threshold of the sensory potential.Absence of an action potential of the extensordigitorum brevis muscle ascertained that the stimuluswas confined to the superficial peroneal nerve.

Recording Sensory potentials were recorded via a

needle electrode (3 mm bared tip) placed near thenerve, 1-2 cm distal to the capitulum fibulae andanother at a distance of at least 9 5 and at most11 5 cm proximal to the capitulum fibulae measuredon the fully extended leg. The remote electrode was

placed at a transverse distance of 3-4 cm at the level

of the near-nerve electrode (Fig. 1). At both sites ofrecording the electrode was adjusted near the pero-neal nerve using the threshold of the potentialevoked in the long peroneal muscle as a gauge(stimulus current < 0-8 mA). Five hundred to 1,000sensory responses were averaged electronicallytogether with a calibration signal; 0 03 ,V could beidentified; to obtain the same resolution at differentlatencies (40-60 Hts per point) a delay of 3-10 ms wasused between stimulus and sampling (Buchthal andRosenfalck, 1966, 1971b). The maximum sensoryconduction velocity was calculated from the latencyto the first positive peak of the sensory potential. Thevelocity from the point distal to the capitulum fibulaeto the popliteal fossa was calculated from thedifference in latencies recorded at the two sites. Theamplitude of the potential was measured peak-to-peak.

MOTOR CONDUCTION The near-nerve electrodesplaced in the popliteal fossa and distal to the capitu-lum fibulae were used to stimulate motor nerve fibres(Fig. 1). In addition, electrodes were placed near thedeep peroneal nerve at the ankle. The stimulatingcurrent was 6-10 mA (0 2 m/s in duration), five to 10times the threshold of the muscle action potential.Muscle action potentials were recorded via concen-tric needle electrodes placed in the endplate zone ofthe anterior tibial, long peroneal, and extensordigitorum brevis muscles. Amplitudes were measuredpeak-to-peak, and latencies to the onset of the initialdeflection of the muscle action potential. Latenciesfrom the point distal to the capitulum fibulae to theanterior tibial and long peroneal muscle were com-pared with latencies obtained in normal nerve at thesame distance of conduction. The latency from ankleto the extensor digitorum brevis muscle was cor-rected to a standard distance of 9 cm by means of thevelocity along the nerve from distal to the capitulumfibulae to ankle (Wagner and Buchthal, 1972).

AGE Findings in sensory and motor nerves inpatients were compared with those in normal nervesmatched for age.

ABBREVIATIONS Velocity distal to the capitulumfibulae denotes the sensory velocity from retinacu-lum superior to 2 cm distal to the capitulum fibulaeand the motor velocity from 2 cm distal to thecapitulum fibulae to ankle (Fig. 1). Velocity acrossdenotes the sensory and motor velocity in the seg-ment of the nerve between 2 cm distal to the capitu-lum fibulae and fossa poplitea (Fig. 1).

TEMPERATURE An infra-red heating element (500 W)was placed 20 cm above the extremity. It was con-

1203



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from


Naunihal Singh, Friedrich Behse, and Fritz Buchthal

SENSORY MOTOR

0

40 50 60 70 80

0 13 a0

20 30 40 50 60 70 80YEARS

DISTAL TO CAPIT. FIB.

7D a

- 4~ ,i * ,. l i '8 T-10t*__o1¢l~~ ilIXe

o oo

20 30 40 50 60 70 80 20 30 40 50 60 70 80YEARS

FIG. 2. Conduction velocity along the peroneal nerve as a function of age.Above: across the region of the capitulum fibulae. Below: distal to the capitu-lum fibulae. Left: sensory conduction velocity, stimulus applied to the nierve atthe superior retinaculum (45 patients). Right: motor conduction velocity to theextensor digitorum brevis muscle (31 patients). Patients with a history indi-cating (0) or suggesting (0J) compression of the nerve in the region of thecapitulum fibulae. The full symbols represent patients with local compression inaddition to systemic neuropathy. The full line gives the average of 35 (sensoryconduction) and 32 (motor conduction) normal nerves. The dashed linesrepresent the 95%0 confidence limits.

trolled by a thermocouple on the leg and ensured atemperature of 36-370C, corresponding to 34°-35°Cnear the nerve.

ELECTROMYOGRAPHY M. tibialis anterior, m. exten-sor digitorum brevis, and m. peroneus longus were

examined. When there was suspicion of root com-pression or systemic neuropathy other muscles of thelegs or hands were examined as well.

Findings were characterized by (1) the pattern ofactivity during full effort, (2) the amplitude of itsenvelope curve; (3) the number of sites in whichfibrillation potentials and positive sharp waves were

recorded outside the endplate zone, (4) the mean

potential duration of at least 20 randomly sampledmotor units potentials, and (5) the incidence of poly-

phasic potentials. Findings were evaluated by com-

parison with normal muscles matched for age(Buchthal, 1957).

SUBJECTS AND PATIENTS

Data on normal sensory conduction velocity alongthe superficial peroneal nerve, on motor conductionalong the superficial and deep peroneal nerve, aswell as on amplitude and shape of sensory potentialsand of evoked muscle action potentials were ob-tained in 74 subjects without history, signs, orsymptoms of neuromuscular disease. They were 16to 72 years old. In 33, conduction velocity wasdetermined along the segment distal to and 'across'the capitulum fibulae.

60m/s

50

40[30

20

1 0

70m/s

60

50~

40[

20 30

30~

HI W-W;77 m-

--a 1 o B

gnL

1204

00

'13 aCP

a a

a a

00 a

0 0 00 a

0 0 0

m Ef co 0lb a

a

0 0



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



The 77 patients were all those referred for investiga-tion of peroneal palsy. They were in a neurologicalor neurosurgical ward. Half were 40 to 60 years old,one-quarter 20 to 40, and one-quarter more than 60years old. Based on history, clinical signs andsymptoms, radiographic and laboratory findings-but not electrophysiological findings-65 patientswere classified in three groups:

GROUP I Twenty-three patients with a definitehistory of local compression of the peroneal nerve atthe capitulum fibulae ('crossed legs' palsy, palsy dueto squatting).

GROUP II Twenty-four patients, whose history sug-

gested or was compatible with local compression ofthe peroneal nerve at the capitulum fibulae; eight ofthese patients had signs and symptoms of systemicneuropathy.

SENSORY

ANKLE

56

DISTAL TOCAR FIB. !I i

'ACROSS' 26

MOTORM.EXT. DIG. BR.

55

" _ 1~10 mV

]1OiV

:0.5 PV

16

POPL IT.

FOSSA 0.sPV

0 5 lOnms 0 10 20 ms

FIG. 3. Sensory and motor conduction along theperoneal nerve. Conduction 'ACROSS' was severelyslowed (sensory: 26 mls; motor: 16 mls) and normalin the segment of the nerve distal to the capitulumfibulae (sensory: 56 mls; motor: 55 mls). Conductionfrom the superior retinaculum to the popliteal fossawas 42 mls. The sensory potential distal to thecapitulum was recorded both at low gain and at thesame high gain as the potential in the popliteal fossa.The sensory potentials were recorded by electronicaveraging of500 responses after a delay ( * * *) of3and 4 ms. Patient 18095, 48 year old male, leftperoneal palsy after sitting with crossed legs for threeto four hours, examined 20 days after the onset of the

palsy. Motor and sensory signs and symptoms were

confined to the left peroneal nerve.

The patients of groups I and II were examinedthree weeks to one year after the onset of the palsy,half within 10 weeks. Two-thirds had a severe palsy(anterior tibial and long peroneal muscles graded as3 or less, Medical Research Council, 1943) and one-third moderate or mild involvement (graded as 4 ormore).Of the patients, 800% had weakness and wasting as

well as diminished sensitivity to touch and pin-prickin the distribution of the peroneal nerve. Four hadpurely motor and four purely sensory signs andsymptoms. Twelve patients complained of pain.

GROUP iII Eighteen patients in whom the clinicalcourse, laboratory, and radiographic studies demon-strated causes of the peroneal palsy other than localcompression at the capitulum fibulae: nine had evi-dence of lumbar root compression or of compressionof the spinal cord; two of a supranuclear affection;two had motor neurone disease; one a mononeuritismultiplex; two a lesion of the sciatic nerve, one hadsequelae after phlebitis, and one after repeated footdistortions.

Half the patients were examined six months orlonger after the onset of signs and symptoms. Halfhad severe involvement (anterior tibial and longperoneal muscles graded as 3 or less) and halfmoderate or mild involvement (graded as 4 or more).Two-thirds of the patients had sensory as well asmotor signs and symptoms in the distribution of theperoneal nerve, one-third had weakness and wastingwithout sensory loss. Three complained of pain.

NOT INCLUDED IN THE STUDY Twelve patients, inwhom the peroneal palsy was due to fracture, whenthe site of the lesion was evident.

RESULTS

CONDUCTION VELOCITY ALONG NORMAL NERVE

In normal subjects motor and sensory conduc-tion velocity and their scatter were the samealong the segment distal to the capitulumfibulae as in the segment across. In 50 year oldnormal subjects the sensory conduction velocityaveraged 54 m/s with a 95%0 confidence limit of47 m/s, the motor conduction velocity (m.extensor digitorum brevis) 51 in/s with a lowerlimit of 44 m/s (Fig. 2). In the individual normalsubject the maximum velocity across the capitu-lum fibulae may be as much as 10 m/s slower orfaster than the velocity distal to it (Fig. 4).Criteria for recognizing slowing along motor and

1205



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



SI SENSORYNORMAL

S2 1 1 .1* GROUP 1+110 00U 00 U

d' dg00 * 00 0d'Us0 0 od o000 000000 000 0

S3 1d GROUP 111

M1 x MOTORx x xxxx xx x NORMAL

xxxx xxxxxx xxxxx x

1M2 °a0 * GROUP 1+11

* 0' d'0oooo o own: 0 o0o0 000000 0 00,

M3 ^ a GROUP III

-20 -10 0 10 20 30 40A VELOCITY, m/s

FIG. 4. Conduction velocity along the segment of the nerve distal to thecapitulum fibulae minus the velocity across in peroneal palsy and in normalnerve (A velocity mls). Each symbol refers to one nerve. A difference of>10 mls was considered abnormal. Si, S2, S3: sensory fibres (superficialperoneal nerve). M1, M2, M3: motor fibres to the extensor digitorum brevismuscle. ( x ) normal nerves, (0) nerves from patients with a history indicating,or (LI) suggesting compression of the nerve in the region of the capitulumfibulae (groups I and II); (A) patients with clinical, laboratory, and radiologicalevidence that the peroneal palsy was due to causes other than local compressionat the capitulum fibulae. The filled symbols indicate evidence of systemicneuropathy. The bars at the symbols denote that the conduction velocity acrosswas normal (within the 95/0 confidence limit).

sensory fibres localized to the segment of thenerve ' across' were then:

1. The velocity across the capitulum fibulaewas slowed to below the normal range and thevelocity along the segment distal to the capitulumfibulae was within the normal range (95°4 confi-dence limit).

2. The conduction velocity across the capitu-lum fibulae was slower than that distal to it bymore than 10 m/s, though both values werewithin the normal range or the velocity wasslightly slowed distal to the capitulum fibulae.

SENSORY CONDUCTION IN PERONEAL PALSYPatients ofgroups I and II In 38 of 47 patients(81%), with a history that indicated or suggestedcompression of the nerve in the region of thecapitulum fibulae, localized slowing manifesteditself in three ways: (1) slowing across and

normal conduction velocity distal to the capitu-lum fibulae (30 patients, Figs 2, 3); (2) conduc-tion velocity across more than 10 m/s slowerthan distal but within the normal range (fourpatients, Fig. 4); (3) slowing along both seg-ments but more severe across than distal(difference > 10 m/s, four patients, Fig. 2).

Slowing localized to the segment across mayremain hidden, when conduction velocity isdetermined only from the superior retinaculumto the popliteal fossa, since this portion of thenerve contains a large stretch with normal con-duction. In 10 patients conduction velocity fromretinaculum to the popliteal fossa was normal,although it was slowed across (six patients) orthe velocity across was more than 10 m/s slowerthan distal to the capitulum fibulae.

Slowing along the segment distal to thecapitulum fibulae was due to loss of fast con-ducting nerve fibres, as indicated by the linear

1206

xx x

x x x x x xx x x x x x x x

x x x x x x x x x x

xx xx x



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



10 3 1

decrease in conduction velocity with thelogarithm of amplitude (Fig. 5).

In nine patients the lesion could not be local-ized: in five slowing was as pronounced distal tothe capitulum fibulae as across, in one patientsensory conduction was normal; in three theaction potential in the popliteal fossa could notbe distinguished from noise.

Sensory slowing was as pronounced threeweeks as 40 weeks after the onset of signs andsymptoms. It tended to be less in patients studiedafter one year or later. The incidence of slowingin sensory conduction was the same whether theperoneal palsy was mild or severe, but severeslowing occurred more frequently when the

L I force of the anterior tibial or long peroneal0.3 0.1 eV 03 muscles was graded as 3 or less.

FIG. 5. Sensory conduction velocity (v) along thesuperficial peroneal nerve from retinaculum superiorto distal to the capitulum fibulae as a function ofdecreasing amplitude (a, log scale) of the sensory

potential. Forty-four patients with a history indicating(0) or suggesting (O) compression of the nerve in theregion of the capitulum fibulae. The regression line(full line) is given by v (mls)= 53-8+ 6-9 x log a (, V),the 95%0 confidence limits by the dashed lines (SD4.7 mls). The relation indicates that the decrease inconduction velocity is due to loss of fast-conductingfibres.

DISTAL TO.CAP. FIB.

"ACROSS"

POPLIT.FOSSA

45yr

I

5 10 15ms

Patients ofgroup III In 17 of the 18 patients inwhom compression at the capitulum fibulae wasunlikely as the cause of the peroneal palsy, con-

duction was normal or borderline across anddistal to the capitulum fibulae. However, in twothe velocity across was more than 10 m/s slowerthan along the distal segment (Fig. 4). In one

patient conduction was slowed in both segmentsof the nerve.

47yr

A 562PV

10 15ms

FIG. 6. Sensory potentials of the superficial peroneal nerve recorded2 cm distal to the capitulum fibulae and in the popliteal fossa in twonormal subjects, 45-47 years old. The numbers above the traces giveconduction velocities (mls) from superior extensor retinaculum todistal to the capitulumfibulae (upper traces) and to the poplitealfossa(lower traces). 'ACROSS': conduction velocity (m/s) calculatedfromdistal to the capitulum fibulae to the popliteal fossa. * * *: delay of3-5 ms introduced after the stimulus before electronic averaging of500 respQnses.

70

60

501-

30_

20L_30 20

1207



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



10.00

pv

1.00k

0.50 _

0.10

_

FIG. 7. Amplitude (log scale) of thesensory potential of the superficial

KX/X X -, - 0 : -V- -f--X---X- peroneal nerve recorded in the fossa0:fXX; poplitea as a function of age. Stimulus___-0 _ *applied to the nerve at the superior

0 retinaculum. Forty-four patients with a° 0o history indicative (O) or suggestive (E)0 0 00 of compression in the region of the

O O ° OoO ° O capitulumfibulae. Thefull symbolsrepresent eight patients with local com-

° ° * ° ° ° pression in addition to systemic neuro-* pathy. The full line gives the average of

0° ° 36 normal nerves, the dashed lines thel Oo0 95%0 confidence limits.

20 30 40 50 60 70 YEARS 80

AMPLITUDE AND SHAPE OF SENSORY POTENTIALS

Normal nerves In subjects 50 years of age, theamplitude ofthe sensory potential recorded distalto the capitulum fibulae and in the poplitealfossa averaged 3 p±V (Fig. 7). The lower 9500confidence limit was 0 5-1 p1V. Considering indi-vidual nerves, in half the amplitude recordeddistal to the capitulum fibulae was 30-100%greater than when recorded in the poplitealfossa; in one-third amplitudes were equal, and in2000 the amplitude distal to was smaller than inthe popliteal fossa.With one exception, the main phase of the

sensory potential recorded distal to and in thepopliteal fossa was split up into at most sixcomponents (Figs 6 and 8). The duration of thepotential was 30-50%o longer in the poplitealfossa than distal to it.

In patients with indication or suggestion ofcompression of the peroneal nerve in the regionof the capitulum fibulae (groups I and II), 7000of the potentials recorded distal to and 80% ofthe potentials recorded in the popliteal fossa hadamplitudes below the 9500 confidence limit ofnormal; half the potentials were diminished to0 3 ,uV or less (Fig. 7). The amplitude was how-ever a poor indicator of the site of the lesion:only 15% of the potentials recorded distallywere at least 2-5 times greater than potentialsrecorded in the popliteal fossa.

In patients of group III, in whom compression

in the region of the capitulum fibulae was un-

likely, amplitudes of the sensory potentials were

usually normal. In four patients the amplitude

was diminished proximal as well as distal to thecapitulum fibulae.

In three patients the amplitude of the sensorypotential was diminished in the popliteal fossabut not distal to the capitulum fibulae. However,in one patient the difference in amplitude wasprobably due to inaccurate placement of therecording electrode, because the long peronealmuscle, ordinarily used to position the electrode,was completely denervated. In the two otherpatients the diminished amplitude might, infact, indicate block of conduction of sensoryfibres at the level of the capitulum fibulae. Thisis, however, unlikely because there was no otherelectrophysiological evidence of a lesion of thenerve at the level of the capitulum fibulae, andbecause there was evidence of root compression(L4, surgically verified) in one and of mono-neuritis multiplex in the other patient.

Shape of sensory potentials An increase intemporal dispersion of the potential recorded inthe popliteal fossa as compared with thatrecorded distally was evaluated only whenamplitudes were 0 1 ,±V or greater. Whenamplitudes were lower, so many fibres hadceased to conduct that an increase in temporaldispersion may remain hidden in noise.

In 80% of the nerves of patients from groupsI and lI the potentials recorded in the poplitealfossa were dispersed to more than six compo-nents, as compared with 10% in normal nerves(Fig. 8). The dispersion of the potential re-corded distal to the capitulum fibulae was as in

1208



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



DISTAL TOCAP. FIB.

POPLI T.FOSSA

PERCENT40

2 0

0

40-

2 0-

71

cjiI200j'ej

2 4 6 8 1>10 2 4 6 8 10 >10NUMBER

FIG. 8. Number of components of sensory potentials(abscissa) in peroneal palsy and in normal peronealnerve. Ordinate: per cent of nerves. Left: recordeddistal to the capitulum fibulae; right: in the poplitealfossa. Top: 16 normal nerves. Middle: 39 nervesfrompatients of groups I and I. Bottom: 16 nerves frompatients of group III. Split-up of the sensory poten-tials into more than six components was consideredabnormal.

normal nerve. In three of the five patients inwhom the lesion could not be localized becauseof uniform slowing and of equally low ampli-tudes at both sites of recording, a potential with10 to 12 components recorded in the poplitealfossa and a normal shape of the potentialrecorded distal to the capitulum fibulae pointedto a localized lesion.

In patients of group III, one-third of sensorypotentials were dispersed to more componentsthan normal both proximal and distal to thecapitulum fibulae.

MOTOR CONDUCTION ACROSS AND DISTAL TO

CAPITULUM FIBULAE Patients of groups I and IIIn one-quarter of the patients of group I andhalf of the patients of group II a potential could

not be evoked in the extensor digitorum brevismuscle. In nine of the remaining 18 patients ofgroup I and in five of 12 patients of group IIslowing across and normal velocity along thesegment of nerve distal to the capitulum fibulaelocalized the affection to the region of thecapitulum (Figs 2, 4). Four patients of eachgroupshowed uniform slowing along the nerve. Inthree patients conduction along both segmentswas slowed but was more than 10 m/s sloweracross the capitulum fibulae. Thus, motor con-duction across the capitulum fibulae localizedthe lesion in one-third of 47 patients. In twopatients with slowing of conduction across thecapitulum fibulae, conduction velocity from thepopliteal fossa to ankle was normal. Localizedslowing along motor fibres occurred irrespectiveof whether the palsy was mild or severe butsevere slowing was more frequent when theforce of the anterior tibial and long peroneal

SENSORY

ANKLE

60

DI STALTOCAR FIB. %41)'ACROSS' 24 10.5vV

MOTORM. EXT. DIG.BR.

]~~~~53

32

POPLIT. 4 2

FOSSA 1.0FJ~~jOmVLLJ +

0 5 lOms 0 10 20 ms

FIG. 9. Sensory and motor conduction along theperoneal nerve. Slowing in conduction 'ACROSS'was most severe along sensory fibres (24 mls); normalconduction along the segment of the nerve distal to thecapitulum fibulae (sensory: 60 mls; motor: 53 mls).Conduction from the superior retinaculum to thepopliteal fossa was 42 mls. The sensory potentialswere recordedby electronic averaging of500 responses,in the popliteal fossa after a delay of 6 ms ( * * *).Patient 17622, 54 year old female, examined fiveweeks after the onset ofperoneal palsy. The palsy wasnoticed after waking up in the morning. Clinical signsand symptoms were purely motor and confined to theright peroneal nerve (classified as group II).

1209

I I -H



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



TABLEELECTROMYOGRAPHIC ABNORMALITIES IN PER CENT OF

MUSCLES EXAMINED

M. tibialis M. extensor M. peroneusant. dig. br. long.

Group

I+1H III I+1H III +II+ III

Number of muscles (pts)

47 18 42 17 24 8

No response 9 0 26 7 13 0Discrete activity* 70 78 67 94 71 90Diminished amplitude(>50%) 32 11 - - - -

Increased duration(> 20%/) 17 18 - - - -

Polyphasia (> 12%.) 54 67 - - - -Fibrillation a/o pos.

sharp waves 79 72 77 41 71 50

* During full effort.

muscles was graded as 3 or less. The localizingvalue of slowing across the capitulum fibulaewith the response of the long peroneal andanterior tibial muscles as gauge is limited becauseit requires comparison with the distal conductiontime. In normal subjects, the latency from distalto the capitulum fibulae to the long peroneal andanterior tibial muscle has a greater scatter thanthe conduction velocity (25% as compared with17%). Motor conduction velocity across thecapitulum fibulae in the fibres to the longperoneal and anterior tibial muscles wasdetermined in 80% of the patients. In 29 of 38conduction was slowed along this segment of thenerve, equally often along the nerve fibres toboth muscles. Distal latency was normal in 12of 29 patients with slowing across the capitulumfibulae, compatible with but not diagnostic oflocal slowing. Distal latency was prolonged in 17patients, indicating either local slowing com-bined with loss of fast conducting nerve fibres orgeneralized slowing, as is, for example, seen insystemic neuropathy.Of four patients with purely motor signs (Fig.

9) and symptoms and slowing along motorfibres across the capitulum fibulae, three hadslowing of conduction along sensory fibres aswell; in one patient sensory conduction velocitywas borderline but 11 m/s slower across thandistal to the capitulum fibulae.

Patients of group III In 14 of 18 patients, inwhom compression of the nerve in the region ofthe capitulum fibulae was unlikely, motor con-duction velocity could be determined with theaction potential of the extensor digitorum brevismuscle as gauge. In nine, conduction was nor-mal and in five it was as slow across as distal tothe capitulum fibulae. Conduction across thecapitulum fibulae to the anterior tibial and longperoneal muscles was normal in 16 and slowed intwo patients. The slowing was associated withprolonged distal latency. Thus, in none of thepatients was there evidence of localized slowingin motor fibres.

AMPLITUDE OF RESPONSE EVOKED IN EXTENSORDIGITORUM BREVIS MUSCLE A four times loweramplitude of the potential evoked by stimulationin the popliteal fossa than by stimulation distalto the capitulum fibulae indicated a localizedlesion in six of 32 nerves from patients of groupsI and II. A difference of this order was neverfound in the 14 patients of group III or in 31normal subjects.

LATENCY FROM ANKLE TO EXTENSOR DIGITORUMBREVIS MUSCLE A prolonged latency was foundin 10 of 36 nerves of the patients of groups I andII and in five of 14 nerves of patients of groupIII. The increase in latency was moderate(usually less than 50%. above the average ofnormal) and compatible with loss of fast con-ducting fibres.

ELECTROMYOGRAPHIC FINDINGS Abnormalitieswere similar in the patients of the three groups,except that voluntary activity was more apt to beabsent in muscles of the patients of groups I andII than of group III (Table). Thus, the electro-myographic findings gave no clue as to whetheror not the peroneal palsy was due to local com-pression in the region of the capitulum fibulae.Clinically and electromyographically the extensordigitorum muscle was the most severely involved.It was completely denervated in one-quarter ofthe muscles of groups I and II. A pattern of dis-crete activity as evidence of loss of many motorunits was seen in 70 to 90%. of the muscles andfibrillation potentials and positive sharp wavesin 40 to 80%/. The parameters of single motorunit potentials were analysed in the anterior

1210



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



GROUP III NORMAL

23456

~ I -II I I*~0 20 40 60 80 100 0 20 40 60 0 20

PER CENT NERVESFIG. 10. Cumulative diagnostic yield of sensory and motor conduction in peroneal palsy. Left: 47 patients(groups I and 1I) with a history indicating or suggesting compression of the nerve at the capitulum fibulae.Middle: 18 patients (group III) without such history. Right: 33 normal subjects. (1) Column 1 (criterion 1)shows the percentage ofpatients in whom the lesion was localized by slowing in sensory conduction across thecapitulum fibulae with normal conduction distal to it. Each subsequent column gives the diagnostic yield by eachcriterion over and above that obtained by the preceding criterion or criteria. The hatched areas indicate thepercentage ofpatients whose lesion would have been localized by that criterion alone. The diagnostic criteria2-6 are listed in the order of their incidence in group III (middle). (2) Motor conduction velocity across to theextensor digitorum brevis muscle slowed, conduction distal to the capitulum fibulae normal or slightly slowed butmore than 10 mlsfaster than across. (3) Amplitude ofmotor response in the extensor digitorum brevis muscle atleast four times greater when the stimulus was applied distal to the capitulum fibulae than in the poplitealfossa.(4) Sensory conduction velocity along both segments normal or slowed but slower across than distal to thecapitulum fibulae by more than 10 mls. (5) Motor conduction velocity across slowed to the anterior tibial andlong peroneal muscle; distal latency normal. (6) Amplitude of the sensory potential recorded distal to thecapitulum fibulae at least 2 5 times greater than when recorded in the popliteal fossa.

tibial muscle. Most prominent was an increase inthe incidence of polyphasic potentials, probablyindicating reinnervation. It was found in half totwo-thirds of the muscles examined. The poten-tial duration was increased in 2000 and de-creased in none.

DISCUSSION

In many patients in this study clinical signs andsymptoms left doubt as to whether the peronealpalsy was due to involvement of a lumbar root or

of the peripheral nerve. Electromyography mayfail to distinguish between these two possi-bilities. Weakness and wasting due to root com-

pression may be confined to muscles innervatedby the peroneal nerve. Although root compres-sion may be associated with paresis of othermuscles than those innervated by the peronealnerve, which muscles to investigate varies, sincesegmental innervation varies (Thage, 1965); andone-third of affected muscles do not show evi-dence of partial denervation-that is, fibrillation

potentials and positive sharp waves (Buchthal,1957).In some patients the peroneal palsy was

associated with mild clinical signs and symptomsof systemic neuropathy. Although electromyo-graphic investigation allows recognition of wide-spread involvement, it does not establishwhether in addition there is local impairment ofconduction after pressure.

RECOGNITION OF DAMAGE OF NERVE LOCALIZED TOREGION OF CAPITULUM FIBULAE To demonstrateslowing in conduction along the segment of theperoneal nerve across the capitulum fibulae, it isnecessary to confine measurements to this very

segment. If a larger stretch of normal nerve isincluded, localized slowing may remain hidden,as demonstrated in lesions of the ulnar nerve atthe cubital sulcus (Payan, 1969) and in thecarpal tunnel syndrome (Buchthal and Rosen-falck, 1971a). In fact, in 10 of our patients withperoneal palsy and slowing along the segment ofthe nerve across the capitulum fibulae, sensory

GROUP 1+11

1211

L



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



conduction was within the range of normal whendetermined from the superior retinaculum to thepopliteal fossa. Conversely, if conduction isslowed from the superior retinaculum to thepopliteal fossa or distal to it, this may or may notoriginate from a lesion localized to the region ofthe capitulum fibulae. It may be due to loss offast conducting fibres, as in axonal neuropathy,or to more widespread demyelination. Not un-less conduction across is significantly slowed ascompared with conduction along the segment ofthe nerve distal to the capitulum fibulae does itindicate damage to the nerve which is primarilylocalized to the region of the capitulum.

DIAGNOSTIC YIELD OF CONDUCTION STUDIESAmong 65 consecutive patients with peronealpalsy, sensory potentials were large enough todetermine a conduction velocity proximal anddistal to the capitulum fibulae in 9500. Motorconduction velocity to the extensor digitorumbrevis muscle could be determined in 7000 of thepatients.The localizing value of slowing of conduction

and of changes in sensory and motor responsesis shown in Fig. 10 (hatched areas). Slowingof sensory conduction velocity across the capi-tulum fibulae with normal conduction velocitydistal to capitulum fibulae gave the best diag-nostic yield. Two-thirds of the patients with ahistory indicating or suggesting local compres-sion at the capitulum fibulae exhibited thischange, a criterion with no 'false positive' find-ings, since none of the patients of group III,without history or evidence of local compression,showed it (Fig. 10, middle). In one of the 33normal subjects sensory conduction velocity wasjust outside the 9500 confidence limit (Fig. 10,right).

Slowing across combined with normal con-duction velocity distal to the capitulum fibulaewas probably due to demyelination or incompleteremyelination in the region of the capitulumfibulae causing retardation in conduction orlocalized block of the fastest fibres or both. Thatthe potential recorded distal to the capitulumfibulae was markedly diminished in two-thirds ofthe nerves examined indicates that there was, inaddition, degeneration of many nerve fibres.Among these were the fastest conducting fibresas seen from the slight decrease in conduction

velocity associated with a marked decrease inamplitude (Fig. 5).The diagnostic yield of slowing across the

capitulum fibulae along motor fibres (m. extensordigitorum brevis) was only half that of slowingalong sensory fibres. With the long peroneal oranterior tibial muscle as a gauge the diagnosticyield was apparently as good as slowing ofsensory conduction. In fact, this criterion wasless valuable than it seemed for reasons statedon p. 1210.An increase in temporal dispersion proximal

as compared with distal to the site of compres-sion was observed in half the patients of groupsI and II. It was of little diagnostic help becauseof similar findings in patients of group III.

Increased temporal dispersion and block ofnerve fibres in the region of the capitulumfibulae should render the amplitude recorded inthe fossa poplitea lower than that recorded distalto the capitulum fibulae. In fact, this criterionwas of little diagnostic value because it wasabsent in many patients of group I and II,probably because the recording electrode was atsome distance from sensory fibres. They areoften located in a separate branch of the nerve atvarying distance from motor fibres whosethreshold was used to place the electrode nearthe nerve. This may also explain why the ampli-tude of the sensory potential was diminished inthe popliteal fossa and normal distal to thecapitulum fibulae in three patients of group III,although there was no other clinical or electro-physiological indication of a lesion of theperoneal nerve at the level of the capitulumfibulae.

In only 2000 of the patients of groups I and IIwas the muscle action potential evoked in theextensor digitorum brevis muscle by a stimulusdistal to the capitulum fibulae significantlylarger than the response evoked by stimulationin the popliteal fossa.

In 23 of 24 patients of group II, in whom thehistory suggested compression of the peronealnerve at the capitulum fibulae as the cause of thepalsy, studies of sensory and motor conductionconfirmed this suspicion. One patient had analcoholic neuropathy with uniform slowingalong all segments of the peroneal nerve.The cumulative diagnostic yield of the differ-

ent electrophysiological criteria to localize com-

1212



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from



pression of capitulum fibulae is shown in Fig. 10.The sequence in which the criteria were listedwas chosen from their incidence in patients ofgroup lII. Thus, motor conduction velocityacross the capitulum fibulae (criterion 2) wasslowed in 4%0 of the patients whose lesion was notlocalized by local slowing of sensory conduction(criterion 1) bringing the diagnostic yield from64% to 68% of the patients. Criterion 3 (Fig. 10,motor response at least four times greater whenthe stimulus was applied distal to the capitulumfibulae than proximal to it) localized the lesion inan additional 2% of the patients whose lesionwas not localized by slowing in conductionacross the capitulum fibulae along sensory andmotor fibres; and so forth. The last threecriteria in Fig. 10 are of doubtful diagnosticvalue because they gave many false positivefindings in patients of group III.

In four of the 47 patients the site of compres-sion could not be localized: one patient hadnormal motor and sensory conduction through-out. He was examined five weeks after the onsetof signs and symptoms when the paresis hadrecovered markedly. In three patients damagewas so severe that a sensory potential could notbe distinguished from noise and motor conduc-tion could not localize the lesion.

Recently, Lovelace et al. (1973) reportedrecording of sensory potentials from the super-ficial peroneal nerve via surface electrodes usingelectronic averaging of 400 responses. In theserecordings the amplitude of the potentials innormal nerve was one half of that which wehave found by using a near-nerve electrode.Thus, if we had used surface electrodes we wouldhave failed to detect a response in 30%0 of ourpatients with peroneal palsy localized to theregion of the capitulum fibulae.

We wish to thank Dr A. Rosenfalck for helpfuldiscussions and for the calculation of findings in

normal nerves. The work was supported by grantsfrom the Muscular Dystrophy Associations ofAmerica and from the Michaelsen Foundation,Copenhagen.

REFERENCES

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

Buchthal, F. (1957). An Introduction to Electromyography.Gyldendal: Copenhagen.

Buchthal, F., and Rosenfaick, A. (1966). Evoked actionpotentials and conduction velocity in human sensorynerves. Brain Research, 3, 1-122.

Buchthal, F., and Rosenfalck, A. (1971a). Sensory conduc-tion from digit to palm and from palm to wrist in thecarpal tunnel syndrome. Journal of Neurology, Neuro-surgery, and Psychiatry, 34, 243-252.

Buchthal, F., and Rosenfalck, A. (1971b). Sensory potentialsin polyneuropathy. Brain, 94, 241-262.

Buchthal, F., Rosenfaick, A., and Trojaborg, W. (1974).Electrophysiological findings in entrapment of the mediannerve at wrist and elbow. Journal of Neurology, Neuro-surgery, and Psychiatry, 37, 340-360.

Gassel, M. M., and Trojaborg, W. (1964). Clinical andelectrophysiological study of the pattern of conductiontimes in the distribution of the sciatic nerve. Journal ofNeurology, Neurosurgery, and Psychiatry, 27, 351-357.

Gilliatt, R. W., Goodman, H. V., and Willison, R. G. (1961)The recording of lateral popliteal nerve action potentialsin man. Journal ofNeurology, Neurosurgery, andPsychiatry,24, 305-318.

Lovelace, R. E., Myers, S. J., and Zablow, L. (1973). Sensoryconduction in peroneal and posterior tibial nerves usingaveraging techniques. Journal of Neurology, Neurosurgery,and Psychiatry, 36, 942-950.

Medical Research Council (1943). Aids to the Investigation ofPeripheral Nerve Injuries. War Memorandum No. 7H.M.S.O.: London.

Payan, J. (1969). Electrophysiological localization of ulnarnerve lesions. Journal of Neurology, Neurosurgery, andPsychiatry, 32, 208-220.

Thage, 0. (1965). The myotomes L2-S2 in man. ActaNeurologica Scandinavica, 41, Suppl. 13, 241-243.

Trojaborg, W. (1970). Rate of recovery in motor andsensory fibres of the radial nerve: clinical and electro-physiological aspects. Journal of Neurology, Neurosurgery,and Psychiatry, 33, 625-638.

Wagner, A. L., and Buchthal, F. (1972). Motor and sensoryconduction in infancy and childhood: reappraisal.Developmental Medicine and Chlild Neurology, 14, 189-216.

1213



http://jnnp.bmj.com

/J N

eurol Neurosurg P


ber 1974. Dow

nloaded from


electrophysiological study ofperoneal palsynaunihalsingh, friedrich behse, andfritz buchthal sensory...

Documents