REVIEW
Clinical Neurophysiology in the Diagnosis of Peroneal Nerve Palsy
Yoshihisa Masakado, Michiyuki Kawakami, Kanjiro Suzuki, Leon Abe, Tetsuo Ota, and Akio Kimura

Keio University Tsukigase Rehabilitation Center, Shizuoka, Japan(Received for publication on October 23, 2007)(Revised for publication on November 14, 2007)(Accepted for publication on January 17, 2008)

Abstract: Peroneal neuropathy is one of the common focal mononeuropathies in the lower
extremities occurring in both adults and children. Foot drop due to weakness of ankle
dorsiflexion is the most common presentation of a peroneal neuropathy. It may also result from other causes involving the upper or lower motor neurons. Disorders that must
be distinguished from peroneal neuropathy include sciatic mononeuropathy, lumbosacral
plexopathy, motor neuron disease, polyneuropathy, and an L5 radiculopathy. To establish adiagnosis, electrodiagnostic studies have been used to localize the level of the abnormality
and to establish prognosis. The most common site of injury is the fibular head, but focal neuropathies have also been reported at the level of the calf, ankle, and foot. In this article, weoverviewed the peroneal nerve palsy, and its diagnosis by neurophysiologic evaluation, conduction study and needle EMG. The neurophysiologic information gives us the underlying
pathophysiology and its prognosis. Therefore the neurophysiologic evaluation must be performed not only for the differential diagnosis, but also for planning the treatment strategy.
(Keio J Med 57 (2) : 84－ 89, June 2008)
Key words: peroneal neuropathy, neurophysiological evaluation, motor conduction study, sensory
conduction study, needle EMG

Introduction

Anatomy and its Disorders

Peroneal nerve palsy is the most common entrapment
neuropathy in the lower extremity. Most often, peroneal
nerve palsy occurs at the fibular neck, where the nerve issuperficial and vulnerable to injury. Patients usually present with a foot drop and sensory disturbance over the lateral calf and the dorsum of the foot. However patients withsciatic neuropathy, lumbosacral plexopathy, or L5 radiculopathy may reveal similar clinical symptoms. In addition
to establishing a diagnosis, electrodiagnostic (EDX) studies have been used by some authors to localize the level ofthe abnormality and to establish prognosis.1, 2 The mostcommon site of injury is the fibular head as mentioned
above, but focal neuropathies have also been reported at
the level of the calf, ankle, and foot.3 In addition, electrophysiology can localize the level of the nerve palsy, reveal
the underlying pathology, and establish the prognosis. This
review addresses the importance and limitation of EDX
techniques in the evaluation of peroneal neuropathy.4-6

The peroneal nerve is derived from the L4-S1 nerveroots, which travel from the lumbosacral plexus andeventually the sciatic nerve. Within the sciatic nerve, thefibers forming the peroneal nerve run separately fromthose that become the tibial nerve. In the posterior thigh,the peroneal fibers within the sciatic nerve innervate theshort head of the biceps femoris, the only muscle that peroneal fibers innervate above the level of the fibularneck. More distally, the sciatic nerve bifurcates above thepopliteal fossa into the common peroneal and tibial
nerves. The common peroneal nerve first gives rise to thelateral cutaneous nerve of the knee, which supplies sensation to the lateral knee before winding around the neckof the fibula. Then it passes through the attachment of
the superficial head of the peroneus longus muscle, anddivides into the deep and superficial peroneal nerves.
The former innervates the peroneus tertius muscle andthe dorsiflexors of the ankle and toes, including the tibia-

Corresponding Author: Yoshihisa Masakado, MD, Keio University Tsukigase Rehabilitation Center, 3802, Tsukigase, Izu-shi, Shizuoka 410-3293, Japan
Phone: 81-558-85-1701, Fax: 81-558-85-1810, E-mail address: masakado@sc.itc.keio.ac.jp84Keio J Med 2008; 57 (2): 84－ 89
Table 1 Causes of peroneal neuropathy
1. External compression (casts, immobilization)
2. Direct trauma (fracture)
3. Traction injuries (forcible ankle inversion)
4. Masses (ganglion, tumor)
5. Entrapment (fibular tunnel)
6. Vascular conditions
7. Diabetes mellitus
8. Leprosy
9. Idiopathic

lis anterior (TA) muscle, extensor digitorum longus andextensor hallucis longus, and extensor digitorum brevis(EDB). It supplies sensation to the web space between
the first and second toes. The superficial peroneal nerve
innervates the ankle evertors (peroneus longus and brevis) and then supplies sensation to the mid and lower lateral calf. It passes over the dorsum of the foot, supplying
sensation to the dorsum of the foot and to the dorsal medial three or four toes. Although the EDB is usually innervated only by the deep peroneal nerve, occasionally(in about one third of the population)4, 6 it derives additional innervation from an accessory peroneal nerve, abranch of the superficial peroneal, which curves aroundthe lateral malleolus and usually supplies the lateral portion of the EDB. When the peroneal nerve is stimulated
at the ankle, the response obtained has a lower amplitude
than that obtained from the knee. This difference is dueto the fact that at the ankle only the deep peroneal nerve
is stimulated but at the knee both deep and superficial
branches (the latter with its accessory peroneal branch)
are stimulated. If the accessory peroneal nerve is stimulated behind the lateral malleolus, a response is obtained
from the EDB, with an amplitude that is equal to the difference between the amplitudes of the responses obtained
from knee and ankle stimulation.5
The common peroneal nerves are vulnerable to external compression in its course around the head and fibula(Table 1). Acute peroneal neuropathy often follows trauma or compression from prolonged immobilization. Thisoccurs often postoperatively in patients who have received anesthesia or sedation. Slow progressive lesions
often suggest a mass, such as a ganglion or nerve sheathtumor.
Several circumstances predispose a subject to peroneal
neuropathy. Habitual leg crossing may repetitively injure
the peroneal nerve at the fibular neck, where it is quite
superficial. Similarly, repetitive stretching from squatting
has also been associated with peroneal neuropathy.
It has been reported that traction injuries are the mostcommon (usually during sport) followed by penetrating
and iatrogenic injuries. On the other hand, traction is presumed to be the mechanism of injury to the superficial
peroneal nerve in an inversion ankle sprain, but it is not85

known whether the amount of strain caused by nerve
traction is sufficient to cause nerve injury. Peripheral
nerves may be injured when they are stretched beyond
their physiologic limits. A previous report has suggested
that the superficial peroneal nerve may be at risk during
actual ankle sprain.7 In 2000, Garozzo et al. reported 5
cases of common peroneal nerve palsy,8 which was associated with inversion sprains of the ankle. Common peroneal nerve palsy associated with inversion sprains of
the ankle has been mentioned in the literature on a casepresentation basis only and is consequently regarded to
be a rare complication. The etiologic mechanisms responsible for the nerve impairment have not been clearly
identified. Some of the cases reported in the literature
eventually required surgical treatment, which was always
followed by complete recovery. In Garozzo’s report theypresented 5 additional cases of this peculiar neuropathy:
all the patients were surgically treated, but the author observed neurological recovery in only 2 cases.
Clinical Evaluation
Peroneal nerve lesions at the region of the knee or distal thigh usually result in patient reports of altered ambulation secondary to paretic or paralyzed ankle dorsiflexors. The loss of sensation in the cutaneous distribution of
the superficial and deep peroneal nerves may be noted,
but the ankle dorsiflexion weakness is most important.
Pain is often related to the specific cause of a compromised common peroneal nerve. For example, a nerve
compromised secondary to traumatic injury from blunttrauma will likely result in pain secondary to soft tissueswelling and inflammation, whereas chronic compression secondary to habitual leg-crossing is often not related with any pain. Tapping of the nerve at the fibular headmay produce pain and tingling (Tinel sign) in the sensory
distribution of the peroneal nerve.
Examination often reveals a variable pattern of weakness, with the EDB muscle being most profoundly affected. Ankle and toe dorsiflexion can be significantly
affected. Dorsiflexion is best tested by having the patient
place the ankle in the neutral position and then dorsiflex
the foot and invert it to optimally test the TA muscle. Often, ankle eversion is normal, as patients can have relative sparing of these muscles. In a pure common peroneal
neuropathy, plantar flexion should be spared. Most importantly, ankle inversion is spared, mediated by the tibialis posterior (L5, sciatic nerve, tibial nerve innervation).
If the ankle is tested in a dropped position, ankle inversion may appear weak. To test ankle inversion in a patient with a footdrop, the ankle should be passively dorsiflexed to avoid the mistaken impression that the tibialis
posterior is weak.4
Observation of the patient’s gait is useful in diagnosing
ankle dorsiflexion weakness. The patient often displays a

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Masakado Y, et al: Clinical Neurophysiology in Peroneal Nerve Palsy

steppage gait pattern in which the affected foot is lifted
excessively from the ground during the swing phase ofambulation in order to clear the foot. This results in excessive hip and knee flexion, and the appearance is as if
the patient is stepping over an object in his or her path.
In addition, a foot slap may be heard on foot strike, as
the ankle dorsiflexors cannot provide a controlled descent of the foot toward the floor. The patient might also
stumble when walking, secondary to the toes on the affected side dragging or catching on the floor during theswing-through phase of ambulation.
In fibular neck fractures, complete absence of sensation is possible along the anterodistal portion of the leg
and entire dorsum of the foot. Lateral calf sensation may
be spared if the lesion is below the nerve branch to thisregion. When the neural insult occurs at the knee, theshort head of the biceps femoris is often spared.
Patient history and physical examination are the mosthelpful initial clinical tools in arriving at then initial diagnosis of a strongly suspected common peroneal nerve
injury. Plain radiographs may be helpful in excluding
underlying traumatic injuries, such as a proximal fibular
head fracture or osseous tumors, or in assessing the severity of angular deformities about the knee. CT scansand MRI are helpful in finding a compressive lesion
along the course of the nerve in cases in which this issuspected. Metabolic and hematologic studies may be
helpful in conditions such as diabetic peripheral polyneuropathy, alcoholic polyneuropathy, polyarteritis nodosa, and hyperthyroidism. A nerve biopsy, althoughlargely unnecessary, may confirm the disorder. It, however, is better to evaluate the palsy through neurophysiological procedures, which can localize the level of thenerve palsy, reveal the underlying pathology, and establish the prognosis.

side with that of the contralateral non-injured side, always assuming that the contralateral side is normal andnot affected. If the contralateral limb responses are normal, one can estimate the amount of axonal loss by expressing the CMAP on the affected side as a percentageof the nonaffected side. This method is independent of
the location of the active recording electrode and is valid
in both circumstances.
The superficial peroneal sensory nerve action potential(SNAP) is important, and an abnormality of the sensory
evoked response implies that the lesion is distal to thedorsal root ganglion, although this does not completely
rule out the possibility of an L5 radiculopathy. A loss inamplitude of this response implies some axonal loss affecting either the common peroneal nerve or its superficial branch. The particular portion of the nerve that is injured cannot be determined if only a superficial peroneal
nerve sensory study is performed. Comparison of the latency and amplitude of the superficial peroneal nerve
SNAP with the contralateral limb is required to define
the approximate degree of axonal loss. The amplitude of
the SNAP of the superficial peroneal nerve will also be
reduced. Axonal loss is provided by the decrease in the
SNAP and the EMG findings of the peroneally innervated muscles, but it is known that the number of fibrillation potentials or positive sharp waves correlate poorly
with the degree of axonal loss.9 Therefore the best way
to quantify axonal loss is to compare the distal CMAP
amplitude on the symptomatic side with one of the contralateral asymptomatic normal side, or normal control
values. Additionally, CMAP recording from the TA ismore useful than the routine study in patients with a footdrop, because in patients with a foot drop, it is the weakness of the TA that accounts for the clinical deficits. If
the recording the EDB does not localize the lesion bydemonstrating focal slowing or conduction block, theperoneal motor study should be repeated recording theTA (Figure 1). A tibial motor NCS and F wave study, andsural sensory NCS must be performed to exclude a morewidespread lesion and systemic neuropathy. Moreover acomparison with the contralateral side, contralateral peroneal MCS and superficial sensory NCS had better be
performed as mentioned above.

Electrodiagnostic Evaluation
Nerve conduction study
A peroneal motor nerve conduction study (NCS)
should be performed first. The usual method for an NCS
is to record from the EDB muscle while stimulating thenerve first at the ankle and then above and below thehead of the fibula. Superficial peroneal sensory NCSs
should also be performed to localize the site of injury
and to assess the underlying pathology, axonal loss, demyelination, or both; in demyelinating lesions at the fibular neck, focal slowing or a conduction block are demonstrated across the fibular neck with a motor NCS. If
axonal loss predominates, the compound muscle action
potential (CMAP) will be reduced in amplitude at all
stimulation sites along the nerve. The amount of degeneration of the axon can be approximately estimated bycomparing the distal CMAP amplitude of the involved

Needle EMG
The role of needle EMG is to confirm the localization
revealed by NCS, to assess the severity of the lesion, andto exclude other causes. The muscles to be sampled first
are those innervated by the deep and superficial peroneal
nerves (TA, extensor hallucis longus, peroneus longus orbrevis). If any of these muscles are shown to be abnormal, non-peroneal-innervated muscles supplied by theL5 root (for example, tibialis posterior, flexor hallucis
longus) must be sampled. Muscle sampling of the shortKeio J Med 2008; 57 (2): 84－ 89

Fig. 1 Usefulness of recording the tibialis anterior in peroneal
neuropathy. When performing peroneal conduction studies,recording the tibialis anterior is more informative than routine
studies. In these traces, the tibialis anterior and extensor
digitorum brevis are co-recorded while the peroneal nerve isstimulated below the fibular neck (upper trace) and at the lateralpopliteal fossa (lower trace). The conduction block is only
detected in the recording from the tibialis anterior, but not evident
in the extensor digitorum brevis recording.

head of the biceps femoris may be important, because itis the only muscle supplied by the peroneal division of
the sciatic nerve that originates above the deep peroneal
nerve. Abnormalities in this muscle, therefore, imply thatthe lesion is proximal to the deep peroneal nerve, that is
to say, injury at the level of the sciatic nerve or higher.
If any abnormalities are found in the hamstrings or distal tibial-innervated muscles, more extensive needle
EMG must be performed, including sampling the paraspinal and gluteal muscles (Table 2).
Information gained by needle EMG is derived fromspontaneous and voluntary activity.1 0 The presence ofabnormal spontaneous activity represents neurogenic
disorders and is most important in needle EMG. The
evaluation of voluntary activity includes an assessmentof the shape of individual MUPs and MU recruitment(interference pattern: IP). Each of these assessments canbe performed by both quantitative and qualitative analyses. However, quantitative analyses of MUP recruitment
and interference pattern are not widely used in clinicalsettings, because of their low sensitivity.11, 1 2 Therefore
the quantitative analysis of individual MUP parameters
has been the main aim of quantitative EMG. However,there are fundamental limitations to quantitative MUP
analyses that rely on MUP parameter measurements. In
MUP parameters, the duration has been considered a cardinal feature that can specifically differentiate between
normal and neurogenic changes,13 as confirmed by simulation studies.1 4 Those studies revealed that MUP duration was determined mainly by the number of muscle fi-

87bers belonging to a MU that lay within a rather wide (2.5mm in radius) uptake area and was expected to differentiate between normal and neurogenic grouping.
The most important characteristics of neurogenic
changes manifest themselves as a recruitment pattern in
the IP, rather than as a change in the MUP waveforms.
Neurogenic disease typically produces a reduced numberof functioning MUs. At a given level of force, the remaining MUs fire at a higher rate. To differentiate between normal and neurogenic changes, the relationshipbetween the recruitment of MU and how the patient produces a force must thus be examined. In contrast, MUP
shapes in neurogenic disease reflect the stage of reinnervation, acute or chronic, ongoing denervation or reinnervation, and inactive denervation. This can range fromnormal MUPs, when there has been a loss of MUPs frompartial denervation in an acute phase, to “so called” giant
MUPs in a chronic process, in which collateral sprouting
is occurring at the time of assessment, has almost finished or has already completely occurred. That is the significance of MUP waveform analysis, which helps determine the time course.
The current form of individual MUP analysis usually
fails to resolve two important factors that can affect
MUP sampling: focusing and level of contraction.10 Focusing, adjusting the electrode position to acquire sharp
MUPs with the highest possible amplitude, is attempted
differently among different examiners. The different degree of focusing affects the MUP amplitude values. For
example, the upper limit of 1.6 mV in the tibialis anterior
described by Bischoff et al.15 is quite different from thatused in our laboratory. Fortunately, simulation studies
suggest that the MUP duration is theoretically uninfluenced by focusing.1 3 However, in actual observations,the duration of MUPs from one MU varies considerably.
The level of contraction is also expected to influence the
MUP parameter according to the size principle. However
Ertas et al.1 6 did not find evidence of the size principle
for the few earliest recruited MUPs. Our investigation
over a wider range of contraction did clearly reveal thesize principle in needle EMG.17 That is, MUPs recruitedwith stronger contractions had higher amplitudes andlonger durations. The measurement of the MUP duration
also has several serious problems.18 The terminal portionof the MUP waveform returns very gradually to the baseline. Visual assessment of the MUP duration, therefore,
is difficult. The MUP duration measured visually is affected by the amplifier gain, and duration values so measured are comparable only with those recorded with thesame gain. Inter- and intraoperator reproducibility of duration measurements is quite low,19 even with automatedmeasurements, and the cursor positions for duration
made by automated techniques often require operator
correction. A quiet baseline is required for accurate duration measurements, so very weak contractions are suit-Masakado Y, et al: Clinical Neurophysiology in Peroneal Nerve Palsy

88
Table 2 EDX localizing the lesion site

Peroneal nerve
NCS
Peroneal nerve
conduction block or temporal dispersion at fibular head
CMAP low amplituteSuperficial peroneal SNAP abnormal
Sural SNAP abnormal
Tibial nerve
CMAP low amplitute
Needle EMG sampling
Tibialis anterior
Extensor halluics longus
Peroneus longus
Tibialis posterior
Short head of the biceps femoris
Tensor fascia latae
Paraspinal muscles

×
×
×

×
×
×

Sciatic nerve

Lumbosacral plexus

L5 root lesion

×
×
×

×
×
×

×

×

×

×
×
×
×
×

×
×
×
×
×
×

×
×
×
×
×
×
×

x means abnormality might be detected.

able for analysis. The sensitivity of duration measurements in discriminating between normal and neurogenic
is not very high, probably because of the aforementioned
factors.20
When performing needle EMG, detection of the abnormal spontaneous potential at rest is therefore most important for diagnosing neurogenic diseases. The recruitment pattern and interference pattern are also importantwhen understanding how the patient produced the force.
However the value of the quantitative analysis of MUP
is quite limited for diagnosis. If the abnormal spontaneous activity was not detected at rest and no obvious abnormal recruitment pattern was seen in needle EMG,
care must be taken when evaluating the lesion only by
quantitative MUP analysis.
Pathophysiology and Prognosis
Determining the underlying pathophysiology is very
important in assessing the prognosis. In general, theprognosis for a demyelinating lesion is much more favorable than for an axonal loss lesion. By nerve conduction studies, we can explore whether demyelination oraxonal loss is the responsible pathophysiology.
In demyelination, there is evidence of conduction
block and slowing across the lesion. The number ofblocked fibers can be approximated by comparing the
CMAP amplitude above and below the lesion. To approximate the number of fibers that have undergone axonal degeneration, the distal CMAP amplitude on the involved side is compared with that on the contralateralside, again always provided that the contralateral side isnormal.9 In demyelination, the underlying axon remains
intact, and the repair process consists only of remyelination. Remyelination usually occurs over several weeks.
In contrast, recovery from axonal loss lesions requires
the regrowth of the terminal axon or collateral sprouting
from unaffected axons. These processes are usually quite
slow and may be incomplete. It will take many months
to a year or more to recover function in a patient with severe axonal loss, which may not even then recover sufficiently. In contrast, a patient with a pure demyelinatingneuropathy may recover completely over a month or
two.6
Summary and Future Research
The American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM)2 1 reported that fromthe point of an evidence-based review, in patients withsuspected peroneal neuropathy, the following EDX studies are possibly useful, to make or confirm the diagnosis:
1. NCSa. Motor NCSs of the peroneal nerve recording fromthe TA and EDB muscles, including an assessmentof peroneal conduction through the leg and acrossthe FH (Fibula Head) (Level C recommendation,
Class III evidence);b. Orthodromic and antidromic superficial peroneal
sensory NCS (Level C recommendation, Class III
evidence);c. At least one additional normal motor and sensory
NCS in the same limb, to assure that the peroneal
neuropathy is isolated, and not part of a more wide-Keio J Med 2008; 57 (2): 84－ 89

spread local or systemic neuropathy (Expert opinion).
2. Data are insufficient to determine the role of needle
EMG in making the diagnosis of peroneal neuropathy(Data inadequate or conflicting, Class IV evidence).
However, abnormalities on needle examination outsideof the distribution of the peroneal nerve should suggest
alternative or additional diagnoses (Expert opinion).
3. In patients with confirmed peroneal neuropathy, EDX
studies are possibly useful in providing prognostic information, with regards to recovery of function (Level C
recommendation, Class III and IV evidence).
This report reviewed the utility of electrodiagnostic
techniques in evaluating patients with suspected peroneal
nerve palsy. Due to the widespread utilization of EDX
testing in the evaluation of patients with suspected peroneal neuropathy (suggesting that clinicians have found
EDX testing to be useful in this setting) most studies
were published prior to the development of more rigorous standards for study design and assessment of the literature. Consequently, available studies only provided
Class III and IV evidence, resulting in a conservative assessment of their utility. In particular, classifying of needle EMG data as Class IV evidence because the examiner is not masked to clinical data, results in understatement of its utility. It is important that future studies toevaluate the usefulness of EDX examine not only suspected peroneal neuropathy, but also other entrapment
neuropathies.
References
1.
2.
3.

4.

5.

Kanakamedala RV, Hong CZ: Peroneal nerve entrapment at theknee localized by short segment stimulation. Am J Phys Med Rehabil 1989;68:116－122
Smith T, Trojaborg W: Clinical and electrophysiological recovery
from peroneal palsy. Acta Neurol Scand 1986;74:328－335
Oh SJ, Demirci M, Dajani B, Melo AC, Claussen GC: Distal sensory nerve conduction of the superficial peroneal nerve: newmethod and its clinical application. Muscle Nerve 2001; 24:689－
694
Preston DC, Shapiro BE: Peroneal Nerve Palsy. In: Preston DC,
Shapiro BE eds, Electromyography and Neuromuscular disorders:Clinical -Electrophysiologic Correlations 2nd ed, Philadelphia,
Elsevier 2005;343－354
Dimitru D: Lumbosacral plexopathies and proximal mononeuropathies. In : Dimitru D, ed, Electrodiagnostic Medicine, Philadel-

89

6.

7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.

19.

20.
21.

phia, Hanley & Belfus 1995;643－688
Kimura J: Mononeuropathies and entrapment syndromes. In: Kijura J, ed, Electrodiagnosis in Diseases of Nerve and Muscle.
3rd ed, Principles and Practice, 3rd ed, New York, Oxford Universoty Press 2001:711－750
O’Neill PJ, Parks BG, Walsh R, Simmons LM, Miller SD: Ankle
sprain excursion and strain of the superficial peroneal nerve during inversion. J Bone Joint Surg Am 2007;89:979－986
Garosso D, Ferraresi S, Buffatti P: Common peroneal nerve palsy
complicating ankle sprain: report of 5 cases and review of the literature. J Orthopaed Traumatol 2003; 4:142－145
Gilchrist JM, Sachs GM:Electrodiagnostic studies in the management and prognosis of neuromuscular disorders. Muscle Nerve
2004;29:165－90
Sonoo M:New attempts to quantify concentric needle electromyography. Muscle Nerve 2002;S11:S98－S102
Fuglsang-Frederiksen A, Ronager J: EMG power spectrum, turnsamplitude analysis and motor unit potential duration in neuromuscular disorders. J Neurol Sci 1990;97:81－91
Fuglsang-Frederiksen A, Smith T, Hogenhaven H: Motor unit firing intervals and other parameters of electrical activity in normal
and pathological muscle. J Neurol Sci 1987;78:51－62
Buchthal F, Pinelli P: Analysis of muscle action potentials as a diagnostic aid in neuro-muscular disorders. Acta Med Scand
1952;266:315－327
Nandedkar SD, Sanders DB, Stålberg EV, Andreassen S: Simulation of concentric needle EMG motor unit action potentials. Muscle Nerve 1988;11:151－159
Bischoff C, Stålberg E, Falck B, Eeg-Olofsson KE: Reference
values of motor unit action potentials observed with multi-MUAP
analysis. Muscle Nerve 1994;17:842－851
Ertas M, Stålberg E, Falck B: Can the size principle be detectedin conventional EMG recordings? Muscle Nerve 1995;18:435－
439
Akaboshi K, Masakado Y, Chino N: Quantitative EMG and motor
unit recruitment threshold using a concentric needle with quadrifilar electrode. Muscle Nerve 2000;23:361－367
Sonoo M, Stålberg E: The ability of MUP parameters to discriminate between normal and neurogenic MUPs in concentric EMG:
analysis of the MUP “thickness” and the proposal of “size index”.
Electroencephalogr Clin Neurophysiol 1993;89:291－303
Nandedkar SD, Barkhaus PE, Sanders DB, Stålberg E: Analysisof amplitude and area of concentric needle EMG motor unit action potentials. Electroencephalogr Clin Neurophysiol
1988;69:561－567
Daube JR: Quantitative EMG in nerve-muscle disorders. In:Stålberg E, Young RR, eds, Clinical neurophysiology, London,
Butterworths 1981;33－65
Marciniak C, Armon C, Wilson J, Miller R: Practice parameter:
utility of electrodiagnostic techniques in evaluating patients withsuspected peroneal neuropathy: an evidence-based review. Muscle Nerve 2005;31:520－7