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Sensory- and motor-nerve conduction studies measure compound action potentials from nerve or muscle and are useful for assessing possible axon loss and/or demyelination.. Proximal le-sio

Electrodiagnostic evaluation can

be useful in distinguishing among

a variety of causes for numbness,

weakness, and pain Although

most commonly used in

diagnos-ing entrapment neuropathies, such

as carpal tunnel syndrome and

radiculopathies, electrodiagnostic

evaluation often plays an

impor-tant role in assessing more

com-plex conditions In individuals

with severe traumatic

neuropa-thies, electromyographic (EMG)

and nerve conduction studies can

establish a prognosis for

signifi-cant functional recovery; those

with severe or complete axon loss

will have a less favorable outcome

than those with evidence of

neu-rapraxia Radial and sciatic nerve

lesions are two common examples

of this In patients who present

with diffuse numbness and

weak-ness, it may be difficult to

clinical-ly differentiate central lesions

(such as those of motor neuron dis-ease) from peripheral neuropathy

or spinal stenosis (cervical and/or lumbar) In many cases, electrodi-agnostic evaluation can establish whether central or peripheral pro-cesses (or both) contribute to a pa-tientÕs symptoms

To provide useful information, the electrodiagnostic examination must include a clinical assessment

as well as neurophysiologic testing

The electrodiagnostic medical con-sultation should always start with

a directed history and physical examination and should utilize electrophysiologic testing to help answer the diagnostic questions posed by the differential diagnosis considered by the referring physi-cian and the consultant Diagnoses should not be made solely on the basis of electrophysiologic Òabnor-malities,Ó but rather in the context

of the patientÕs complaints

Neurophysiology of Impulse Transmission and Measurement

The axon membrane is composed of

a lipid bilayer, permeable to water but not to most ions or larger mole-cules This selective permeability, coupled with the presence of the

electro-genic pump, allows for maintenance

of a resting membrane potential of

60 to 90 mV, which is negative inside the axon membrane Sodium ions are accumulated outside the membrane at a concentration about

12 times greater than inside, and potassium ions are concentrated inside the cell, at a concentration about 30 times greater than outside There are also mechanisms pres-ent to allow the generation of an action potential An action poten-tial is a traveling depolarization that allows transmission of infor-mation along the nerve It is gener-ated by a specific set of

mecha-Dr Robinson is Professor of Rehabilitation Medicine, University of Washington School of Medicine, Seattle, and Chief of Rehabilitation Medicine and Director, Electrodiagnostic Medicine Laboratory, Harborview Medical Center, Seattle.

Reprint requests: Dr Robinson, Rehabilitation Medicine, Harborview Medical Center, Box

359740, 325 Ninth Avenue, Seattle, WA 98104.

Copyright 2000 by the American Academy of Orthopaedic Surgeons

Abstract

The electrodiagnostic evaluation assesses the integrity of the

lower-motor-neuron unit (i.e., peripheral nerves, neuromuscular junction, and muscle).

Sensory- and motor-nerve conduction studies measure compound action

potentials from nerve or muscle and are useful for assessing possible axon loss

and/or demyelination Needle electromyography measures electrical activity

directly from muscle and provides information about the integrity of the motor

unit; it can be used to detect loss of axons (denervation) as well as

reinnerva-tion The electrodiagnostic examination is a useful tool for first detecting

abnormalities and then distinguishing problems that affect the peripheral

ner-vous system In evaluating the patient with extremity trauma, it can

differen-tiate neurapraxia from axonal transection and can be helpful in following the

clinical course In patients with complex physical findings, it is a useful

adjunct that can help discriminate motor neuron disease from polyneuropathy

or myeloradiculopathy due to spondylosis.

J Am Acad Orthop Surg 2000;8:190-199

Lawrence R Robinson, MD

nisms Specifically, voltage-gated

membrane are activated by partial

membrane depolarization; opening

becomes further depolarized and

even briefly hyperpolarized (i.e.,

relatively positive inside the

mem-brane [30 to 40 mV]) Closing of

sodium channels and opening of

efflux, then rapidly brings the

membrane back to the resting state

and ready for another wave of

depolarization after an absolute

refractory period (i.e., time during

which the nerve cannot be

depolar-ized again) of about 1 msec.1

These sequential depolarizations

proceed along the axon membrane

In the absence of myelin (e.g., on

autonomic fibers and slow pain

fibers), this is a slow process, with a

conduction velocity of about 5 to 15

m/sec, depending on axon

diame-ter Myelin, however, allows for

faster conduction, as currents jump

from one node of Ranvier to the

next; saltatory (node-to-node)

con-duction speeds of 40 to 70 m/sec

are achieved Most motor and

sen-sory fibers in human peripheral

nerves are myelinated; the

largest-diameter and most heavily

myelin-ated fibers are spindle afferents and

alpha motor neurons

When a nerve is electrically

stimulated, the propagation of

these action potentials can be

re-corded by using surface electrodes

The voltage at the skin surface for

these action potentials ranges from

a few microvolts to a few hundred

microvolts A recording from

nerve is usually referred to as a

compound nerve action potential

(CNAP) If the action potential is

recorded from a pure sensory

nerve, it is referred to as a sensory

nerve action potential (SNAP)

When motor nerves are stimulated,

potentials can be recorded directly

from muscle Because each axon

synapses with many muscle fibers,

a much larger response is usually produced at the muscle level The amplitude of the resulting com-pound muscle action potential (CMAP) is typically a few millivolts

If mixed axons are involved (e.g., motor and sensory), the response is best referred to as a CNAP

Principles of Nerve Conduction Studies Sensory- and Mixed-Nerve Conduction Studies

Typically, CNAPs and SNAPs are measured by electrically stimu-lating a peripheral nerve and re-cording the response a known dis-tance away Recording that reflects propagation along the nerve in a physiologic direction (e.g., after stimulating a digital sensory nerve and recording from the wrist) is referred to as Òorthodromic record-ing.Ó However, stimulation of a nerve usually activates the nerve in both directions from the point of stimulation If recordings are from

a nonphysiologic direction (e.g., stimulation of the median sensory nerve at the wrist and recording from a digital nerve), this is re-ferred to as Òantidromic recording.Ó The speed of conduction is the same in either direction

For clinical purposes, there are, in broad terms, usually two measures one makes of CNAPs or SNAPs:

(1) speed of conduction (i.e., latency

or velocity) and (2) size of the response (i.e., amplitude) (Fig 1)

Traditionally, the speed of conduc-tion for CNAPs and SNAPs has been measured in terms of latency (i.e., the time between the onset of stimulation and either the onset or the peak of the potential) Peak latency is easier to measure, particu-larly when the potential is small or the baseline is noisy Onset latency, although more difficult to measure, has the physiologic significance of

representing the arrival of the impulse via the fastest-conducting nerve fibers at the recording elec-trode Conduction velocity for CNAPs can be derived by dividing the distance between the stimulation site and the active (G1) electrode by the onset latency, represented by the equation CV = d/t, where CV = con-duction velocity in meters per sec-ond, d = distance between stimula-tion site and recording electrode in millimeters, and t = onset latency in milliseconds

Latency and conduction velocity can be affected by a number of physiologic and pathologic factors

In healthy control subjects, slowed conduction can be a result of fac-tors such as the temperature of the extremity or even normal aging Pathologically, demyelination pro-duces slowing Conditions that result in loss of axons, particularly faster-conducting axons, also pro-duce slowing of nerve conduction

or prolongation of latency

The amplitude of the CNAP can

be measured from baseline to peak

or from peak to peak In general, the size of the CNAP and the SNAP

is roughly proportional to the num-ber of axons depolarizing under the active electrode It can be affected

Figure 1 Measures of the SNAP or CNAP Latency is the time between stimu-lus and the onset or peak of the potential Amplitude is measured from peak to peak Conduction velocity (CV) is calculated as distance divided by onset latency.

peak latency

amplitude

onset latency

distance onset latency

CV =

by a number of physiologic and

pathologic factors Cold increases

the amplitude of both the CNAP

and the SNAP Aging produces

smaller-amplitude SNAPs, probably

as a result of gradual loss of large

myelinated axons

Pathologically, loss of axons will

reduce the amplitude of the CNAP

Distal lesions between the sites of

stimulation and recording will

de-crease the amplitude of the CNAP

immediately, as conduction cannot

traverse the lesion Proximal

le-sions (e.g., brachial plexus lele-sions)

that separate sensory axons from

their cell bodies (in the dorsal root

ganglion) will produce distal axon

loss due to axonal (wallerian)

de-generation over time (usually 7 to

reduced-amplitude SNAP can be

due to an axonal lesion anywhere

distal to the dorsal root ganglion

Motor-Nerve Conduction Studies

The principles of stimulation and

recording for motor-nerve

conduc-tion studies are similar to those

used for sensory-nerve conduction

studies with several exceptions

The primary difference is that

motor-nerve conduction studies

involve recording a CMAP over

muscle rather than recording

direct-ly from nerve Therefore, the distal

latency involves not only

conduc-tion along the nerve from the point

of stimulation (proceeding at about

50 m/sec), but also includes

neuro-muscular junction transmission

time (which takes about 1 msec) and

conduction along muscle fibers

(about 3 to 5 m/sec) Although

la-tency from a distal stimulation site

can be measured, it cannot be

con-verted into a nerve conduction

velocity in the same way as a SNAP

can be, because of this additional

time for neuromuscular junction

transmission and muscle fiber

duction Therefore, to evaluate

con-duction velocities, motor nerves are

typically stimulated in two places,

and the distance between the two stimulation sites is divided by the dif-ference in latency; neuromuscular-junction transmission time and muscle-fiber conduction velocity are canceled out in the process (Fig 2)

Many of the same factors affect motor-nerve conduction studies as affect sensory-nerve conduction studies.3 There are, however, two important differences First, be-cause motor-neuron cell bodies reside in the anterior horn of the spinal cord rather than in the dor-sal root ganglion, the amplitude of the response is diminished by axon loss at the anterior horn cell or dis-tally (i.e., not at the dorsal root gan-glion) A root lesion proximal to the dorsal root ganglion, for exam-ple, would diminish the amplitude

of the CMAP but not that of the SNAP Second, because recording

is from muscle, neuromuscular-junction transmission defects or primary myopathies may reduce the amplitude of the CMAP

Late Responses

There are two ÒlateÓ responses (i.e., occurring late after the CMAP

or M wave), which sometimes pro-vide useful information: the F wave

named because it was first recorded

in foot muscles) is a late response usually recorded from distal mus-cles Physiologically, when a motor nerve is stimulated distally, axons are depolarized in both directionsÑ distally (orthodromically) and proxi-mally (antidromically) The ortho-dromic volley activates the muscle distally, and the antidromic volley proceeds proximally to the anterior horn cell It is thought that the F wave occurs when a small percent-age (3% to 5%) of antidromically activated motor cell bodies dis-charge and produce orthodromic activation of their motor axons This

is noted as a small-amplitude (about

100 to 200 µV) late (about 30 msec in the distal upper limb) potential

F-wave measurements usually find their greatest applicability in the assessment of multifocal or dif-fuse processes, especially those af-fecting proximal areas of the periph-eral nervous system Acquired or inherited demyelinating polyneu-ropathies that produce multifocal

or diffuse slowing are clinical set-tings in which F waves can provide additional useful information Although it would seem appealing

to use F waves for the diagnosis of brachial plexopathy or some en-trapment neuropathies, they are usually not of significant help in these applications, nor do they offer unique information not ob-tained by conventional nerve con-duction studies Because the F wave is produced by only a small percentage of the motor axons, the presence of just a few normally conducting fibers will result in nor-mal latencies Moreover, the F-wave volley traverses such a long distance of peripheral nerve that a focal lesion, unless there is severe demyelination, would not be ex-pected to produce marked abnor-malities in F-wave latencies The H wave (named after Hoff-man) involves synaptic

transmis-amplitude

amplitude

latency1

latency2 Wrist

Elbow

∆ distance lat2 − lat1

CV =

Figure 2 Measures of the CMAP Latency

is the time between stimulus and the onset

of the potential Amplitude is measured from baseline to peak Conduction velocity (CV) can be calculated as the distance be-tween two points divided by the latency difference between two points.

sion at the spinal cord level and is

in many ways analogous to the

muscle stretch reflex However,

instead of activating stretch

recep-tors within the muscle

mechanical-ly, the large-diameter afferent

nerve fibers are activated

electrical-ly After the afferent volley reaches

the spinal cord, a monosynaptic

reflex excites alpha motor neurons,

and a late response is produced in

the muscle The H reflex can

usual-ly be elicited onusual-ly in the soleus

muscle in adults

The most useful application of

the H wave is in the detection of S1

radiculopathy.5 It has been shown

that the H wave is more sensitive

than needle electromyography in

the assessment of S1 radiculopathy,

probably related to the fact that the

H wave can depict conduction

block and demyelination, whereas

needle electromyography can be

used to detect only motor axon loss

Principles of Needle

Electromyography

Needle electromyography assesses

the function of the motor unitÑthe

combination of an anterior horn

cell, an axon, and all the muscle

fibers supplied by the single axon

It is very sensitive for detection of

axon loss at any level along the

lower motor neuron once sufficient

time has elapsed for fibrillations

and other abnormalities to develop

(usually 2 to 3 weeks).6 There are

usually four distinct steps in the

needle EMG examination for each

muscle: (1) insertional activity, (2)

spontaneous activity, (3)

examina-tion of motor-unit potentials, and

(4) assessment of recruitment

Insertional Activity

Insertional activity is examined

by moving the needle through the

muscle briefly and observing the

amount and duration of the

electri-cal potentials produced Insertional

activity may be decreased or may be prolonged in duration Decreased insertional activity can result if the needle is not positioned in muscle

or is in a muscle that has marginal viability Muscles that have become atrophied and fibrotic will have reduced insertional activity, as will muscles that have become necrotic due to compartment syndrome

Prolonged or increased insertional activity, as an isolated finding, is a very ÒsoftÓ abnormality No diag-nosis should be made on the basis

of this ÒabnormalityÓ when it is an isolated finding, as it may be seen in some asymptomatic individuals In-creased insertional activity can also

be seen in association with fibril-lations or positive sharp waves and thus may be an indicator of either denervation or a primary muscle disorder

Spontaneous Activity

Spontaneous activity consists of electrical discharges that are seen without needle movement or vol-untary contraction Fibrillation potentials represent abnormal spontaneous single muscle-fiber discharges Fibrillation potentials are essentially always abnormal, but they are a nonspecific finding

Fibrillation potentials are often seen

in denervated muscles Myopathies may be associated with fibrillation potentials Disorders characterized

by upper-motor-neuron lesions, such as stroke and spinal cord injury, have been shown to produce fibrillation potentials; these are usu-ally seen early after onset of the lesion and can be confusing when trying to diagnose a peripheral-nerve lesion superimposed on an upper-motor-neuron lesion

Fibrillation potentials are usually graded on a scale from 1+ to 4+, with 1+ representing a repro-ducibly observed fibrillation in an isolated area and 4+ representing sustained fibrillation potentials (which often obscure the baseline)

throughout the muscle The size of fibrillation potentials has been cor-related with the time since onset of denervation Large-amplitude fi-brillation potentials (>100 µV) are seen within the first year after onset

of denervation; smaller amplitudes (<100 µV) are seen later.7 It has been postulated that this relation-ship reflects muscle fiber atrophy over time, with smaller-diameter fibers producing smaller-amplitude fibrillations Consequently, large-amplitude fibrillations in the pres-ence of a neuropathic lesion suggest recent denervation

Positive sharp waves can be thought of in much the same way

as fibrillation potentials They also represent abnormal spontaneous single-muscle-fiber discharges Positive sharp waves can be seen in essentially all the same disorders as fibrillation potentials In some cases of muscle trauma, positive sharp waves may be seen in isola-tion without associated fibrilla-tions Positive sharp waves are thought to have the same patho-physiologic characteristics as fibril-lation potentials and can be graded

by using the same scheme

Complex repetitive discharges, formally known as Òbizarre high-frequency discharges,Ó probably represent groups of muscle fibers firing in near synchrony They are usually seen in chronic neuropathic and myopathic conditions When seen in isolation, they are a nonspe-cific but usually abnormal finding, similar to positive sharp waves and fibrillations

Fasciculation potentials repre-sent spontaneous discharges of a single motor unit As opposed to a fibrillation potential (in which only

a single muscle fiber fires), a fascic-ulation potential involves the entire motor unit (the axon and all the muscle fibers that it supplies) Unlike fibrillation potentials, fasci-culations produce enough force that they can be seen on the skin

clinically Fasciculation potentials

are often generated at the anterior

horn cell, as in motor neuron

dis-eases, but they may also be

ectopi-cally generated distally along the

axon, possibly even in

intramuscu-lar axons

Fasciculation potentials can be

seen in a variety of neuromuscular

disorders In addition to motor

neuron disease and the syndrome of

benign fasciculations, fasciculation

potentials can be seen in chronic

radiculopathies, peripheral

polyneu-ropathies, thyrotoxicosis, and

over-dosage of anticholinesterase

med-ications

Motor-Unit Analysis

A great deal of information can be

obtained from analysis of voluntarily

activated motor-unit action

poten-tials (MUAPs) (Fig 3) The MUAP

represents the electrical potential

cre-ated by the synchronous discharge

of all the muscle fibers supplied by a

single motor axon

Theoretically, in neuropathic

conditions in which there has been

partial denervation and

reinnerva-tion, one will see changes

represen-tative of the underlying process of

axonal sprouting (Fig 4) Within

days after partial denervation,

intra-muscular axons that remain

unaf-fected will send sprouts, usually

emanating from distal nodes of Ranvier, to reinnervate nearby denervated muscle fibers These sprouts, particularly early on, are not yet well myelinated and, there-fore, conduct slowly Consequently,

in the early phases of reinnervation, one will note increased

polyphasici-ty and increased duration of the MUAP as a result of temporal dis-persion in newly formed sprouts and poor synchronization of muscle-fiber discharges As these sprouts mature, synchronization of muscle-fiber discharges improves; the polyphasicity tends to be reduced, and one is left with large-amplitude, long-duration MUAPs The in-crease in amplitude is a result of the increased number of muscle fibers belonging to the same motor unit within the recording area of the tip

of the EMG needle

Myopathic changes in the MUAP result from loss of individual mus-cle fibers In myopathic conditions, the MUAPs are typically small in amplitude and short in duration Furthermore, fewer muscle fibers from the same motor unit fire

with-in the recordwith-ing area of the needle electrode

Recruitment

Evaluation of motor unit recruit-ment can assess whether reduced strength is due to a reduction in the lower-motor-neuron pool or to poor central effort In distinguish-ing between these two possibilities, the primary feature that is mea-sured is the motor-unit firing rate Central recruitment implies that there are reduced numbers of mo-tor units firing but that they are fir-ing at normal or slow speed This

1

2

3 duration

amplitude

Figure 3 Measures of the MUAP include

duration (from onset to termination),

amplitude (from peak to peak), and

num-ber of phases (numnum-bered, as shown).

Figure 4 Top,Normal MUAP, recorded by a needle electrode from muscle fibers within

its recording area Middle, After denervation, single muscle fibers spontaneously dis-charge, producing fibrillations and positive sharp waves Bottom, When reinnervation by

axon sprouting has occurred, the newly formed sprouts will conduct slowly, producing temporal dispersion (i.e., prolonged MUAP duration) and MUAP polyphasicity The

high-er density of muscle fibhigh-ers within the recording area of the needle belonging to the enlarg-ing second motor unit results in an increased-amplitude MUAP.

Normal

Denervation

Reinnervation

is by far the most common

Òabnor-malityÓ in recruitment, but in

isola-tion it is completely nondiagnostic

Central recruitment can be

reflec-tive of upper-motor-neuron

le-sions, pain, or poor voluntary

ef-fort Reduced recruitment (noted

in less severe conditions) and

dis-crete recruitment (noted in more

severe conditions) are pathologically

significant and imply that there are

reduced numbers of motor units

firing rapidly

Interpretation of the

Electrodiagnostic

Examination

Principles of Localization

Needle electromyography is

con-ventionally used for evaluation of

lesions that are primarily axonal or

so proximal that it is not possible to

stimulate both proximal and distal

to an entrapment site Muscles that

are supplied by multiple peripheral

nerves, roots, or areas of the plexus

are examined, and a localization is

made on the basis of the

distribu-tion of abnormalities A sciatic

nerve lesion in the thigh can be

dis-tinguished from L5 radiculopathy,

for example, if there is evidence of

denervation in muscles supplied by

the superficial and deep branches

of the peroneal nerve but not the

tensor fasciae latae or paraspinal

muscles Thus, localization is based

on finding abnormalities distal to a branch point but normal findings proximally.8,9

Nerve conduction studies are best at localizing the site of patho-logic change when there is demye-lination As mentioned previously, demyelination causes focal slowing and conduction block; the presence

of these findings can precisely lo-calize a focal entrapment Conduc-tion block and slowing is observed only in demyelination and neura-praxia It is not present in lesions with axon loss once wallerian de-generation has occurred (about 7 days after onset); therefore, localiza-tion of purely axonal lesions de-pends primarily on EMG findings

Deducing the Pathophysiology

Neurapraxia and demyelination are best demonstrated when there

is focal conduction block and slow-ing on nerve conduction studies but a large-amplitude CMAP or SNAP is elicited distal to the site of the lesion Purely neurapraxic injuries have no electrophysiologic evidence of axon loss (fibrillation potentials or positive sharp waves)

or reinnervation

Axon-loss lesions (e.g., axonot-mesis and neurotaxonot-mesis10) are usually demonstrated by evidence of de-nervation on needle EMG examina-tion as well as small-amplitude CMAP and SNAP responses with stimulation and recording distal to

the site of the lesion While needle electromyography is a more sensi-tive indicator for motor-axon loss, measurement of CMAP or SNAP amplitude is a better measure of the degree of axon loss and of prognosis Axonotmesis and neurotmesis can-not usually be distinguished on elec-trodiagnostic studies, because the primary difference between the two conditions is integrity of the support-ing structures (which have no elec-trophysiologic function) (Table 1)

Timing of Electrophysiologic Changes

The time course of electrodiag-nostic changes after the onset of a neuropathic lesion is an important consideration that influences the interpretation of the electrophysio-logic examination Neurapraxia, demyelination, and severe axon loss produce electrophysiologic changes immediately at onset if the nerve can be stimulated both proxi-mal and distal to the lesion How-ever, proximal lesions, in which it

is not possible to get proximal and distal to the lesion, do not immedi-ately produce changes on distal nerve conduction studies or elec-tromyography Moreover, distinc-tion between neurapraxia and ax-onotmesis cannot be made until 7 days have passed, allowing time for wallerian degeneration to have progressed to the point that stimu-lation of motor axons elicits no

Table 1

Electrodiagnostic Findings in Various Peripheral Nerve Disorders

Motor nerve amplitude +/− (focal) +/− (diffuse) +/−

Large polyphasic MUAPs + (chronic) + (chronic) +/−(severe) + +/−

motor responses.2 Ten days after

the onset of a complete lesion,

SNAPs will be absent as well

Therefore, 7 to 10 days after onset,

a neurapraxic injury (in which the

distal amplitudes will be normal)

can be differentiated by nerve

con-duction studies from an

axonot-metic lesion (in which the distal

amplitudes will be reduced)

Two to three weeks after the

onset of injury, the needle EMG

study starts to show fibrillation

potentials and positive sharp

demon-strate these abnormalities first;

more distal muscles, later

Radicu-lopathies, for example, may show

paraspinal abnormalities at day 10

to 14 after onset, but distal-limb

muscle changes may not be

appar-ent for 3 to 4 weeks after onset

Fibrillations and positive sharp

waves may persist for several

months or even many years after a

single injury, depending on the

extent of reinnervation

The timing and type of

electro-physiologic changes consequent to

reinnervation will depend in part

on the mechanism of reinnervation

When reinnervation is a result of

axonal regrowth from the site of the

lesion (usually in complete injuries),

the appearance of new MUAPs will

not occur until motor axons have

had sufficient time to regenerate

across the distance between the

lesion site and the muscle (usually

proceeding at a rate of a few

mil-limeters a day) When these new

axons first reach the muscle, they

will innervate only a few muscle

fibers, producing short-duration,

small-amplitude potentials,

some-times referred to as Ònascent

poten-tials.Ó With time, as more muscle

fibers join the motor unit, the

MUAPs will become larger, more

polyphasic, and longer in duration

Motor-unit potential changes

will also develop when

reinnerva-tion occurs by axonal sprouting

Polyphasicity and increased

dura-tion develop first as newly formed, poorly demyelinated sprouts sup-ply the recently denervated muscle fibers As the sprouts mature, large-amplitude, long-duration MUAPs develop and persist indefinitely

Evaluation of Common Clinical Entities

Hand Numbness (Case 1)

A 50-year-old woman presents with a 3-month history of progres-sive right-hand numbness The numbness involves all digits of the hand but is restricted to the palmar aspect She reports mild chronic neck pain but denies symptoms in the feet Physical examination demonstrates normal strength and muscle stretch reflexes; sensation is normal to pin prick and light touch

There is a positive Tinel sign over the median nerve at the wrist and

at the ulnar groove bilaterally, but

no Phalen sign

The differential diagnosis in this case includes median neuropathy

at the wrist (e.g., carpal tunnel syn-drome), cervical radiculopathy, and ulnar neuropathy Electrodiag-nostic studies are therefore oriented toward looking for evidence of slowing in peripheral nerves or evi-dence of denervation in the mus-cles of the upper limb A notable finding is slowing in the median nerve at the wrist, with prolonged latencies compared with both radial and ulnar nerves (Fig 5) It has recently been shown that it is better (in terms of sensitivity, specificity, and reliability) to perform the three comparisons of median and ulnar nerves illustrated and then to add the median-ulnar and median-radial nerve latency differences, rather than looking at individual tests alone (Fig 6).11 There is no evi-dence of slowing in the ulnar nerve, nor is there evidence of de-nervation in the C5 to T1 myotomes

of the upper limb; thus, the

find-Nerve Conduction Studies

Stimulate Record Latency (msec) Amplitude Velocity (m/sec) Median nerve (sensory) Wrist Ring finger 4.8 12 µ V

Ulnar nerve (sensory) Wrist Ring finger 3.5 8 µ V Median nerve (sensory) Wrist Thumb 4.1 21 µ V Radial nerve (sensory) Wrist Thumb 2.8 11 µ V Median nerve (sensory) Palm Wrist 3.1 20 µ V Ulnar nerve (sensory) Palm Wrist 2.1 22 µ V Median nerve (motor) Wrist APB 4.5 (<4.3) 6.7 (³5.0) mV

Elbow APB 6.1 (³5.0) mV 51 (³50) Ulnar nerve (motor) Wrist ADM 3.6 (<3.8) 8.3 (³5.0) mV

Below elbow ADM 8.1 (³5.0) mV 57 (³50) Above elbow ADM 7.7 (³5.0) mV 61 (³50)

Needle EMG

Spontaneous Activity Motor Unit Action Potentials Muscle Myotome Ins Act Fibs/PSWs Amplitude Duration Phasicity Recruitment Deltoid C5,6 Normal None Normal Normal Normal Full Biceps C5,6 Normal None Normal Normal Normal Full Pronator teres C6,7 Normal None Normal Normal Normal Full ECR C6,7 Normal None Normal Normal Normal Full FCR C6-8 Normal None Normal Normal Normal Full Triceps C7,8 Normal None Normal Normal Normal Full APB C8,T1 Normal None Normal Normal Normal Full FDI C8,T1 Normal None Normal Normal Normal Full Cervical paraspinals C5-T1 Normal None

Figure 5 Findings from nerve conduction and needle EMG studies in case 1 Normal val-ues are shown in parentheses Abbreviations: ADM = abductor digiti minimi; APB = abduc-tor pollicis brevis; ECR = extensor carpi radialis; FCR = flexor carpi radialis; FDI = first dorsal interosseous; Fibs/PSWs = fibrillations/positive sharp waves; Ins Act = insertional activity.

ings are consistent with carpal

tun-nel syndrome but are not

sugges-tive of ulnar neuropathy or cervical

radiculopathy

Pain in the Low Back and Lower

Limb (Case 2)

A 45-year-old man reports low

back pain extending into the left

lower limb, with pain and

numb-ness in the posterolateral thigh

and leg and the lateral aspect of the foot This started after an injury at work when he was lifting and rotating a heavy object He had a similar episode 4 years pre-viously, which resolved with con-servative management Physical examination demonstrates normal strength and sensation but a de-creased left ankle jerk The diag-nostic questions in this case are whether a radiculopathy is present and, if so, at what level and of what duration

Needle electromyography was performed on the muscles of the left lower limb, evaluating com-monly affected myotomes (L3 to S2) to look for evidence of either acute denervation or prior dener-vation and reinnerdener-vation The findings shown in Figure 7 indicate both recent denervation (fibrilla-tions and positive sharp waves) and reinnervation (large, long-duration MUAPs) in the left S1 dis-tribution These findings allow one

to infer that there is both a new-onset S1 radiculopathy and a pre-existing radiculopathy at the same level Asymmetry of the H waves (smaller amplitude and longer latency on the left) confirms the presence of an abnormality at the S1 level

Combined Upper- and Lower-Motor-Neuron Findings (Case 3)

A 70-year-old retired cardiac sur-geon complains of progressive weakness in the upper and lower limbs and muscle atrophy in the upper limbs He has only vague sensory symptoms of numbness in the upper limbs He denies bowel

or bladder dysfunction There is a history of chronic mild neck pain with no difficulty speaking or swal-lowing He reports intermittent muscle twitching in the pectoral muscles, worse with cold (he is not sure if this is shivering) On physi-cal examination, there is marked muscle atrophy in the upper limbs but normal muscle bulk in the lower limbs Strength is diffusely weak (4/5 on MRC scale) in the upper and lower limbs Sensation is nor-mal Muscle stretch reflexes are hyperactive in the upper and lower limbs Cervical spine radiographs reveal marked degenerative changes (spondylosis)

The diagnostic question in this case is whether cervical myelopathy

or motor neuron disease is the cause of the patientÕs symptoms Although the clinical features could

be consistent with either diagnosis, the electrodiagnostic features are usually different Cervical

spondy-Figure 6 Nerve conduction studies in

case 1 Note prolongation of peak latencies

(values in parentheses) in median nerves

compared with ulnar and radial nerves.

The combined sensory index is calculated

by adding the peak latency differences

between median and ulnar nerves to the

ring finger (4.8 Ð 3.5 = 1.3 msec), the median

and radial latency differences to the thumb

(4.1 Ð 2.8 = 1.3 msec), and the median and

ulnar latencies with stimulation in the

palm and recording over the wrist (3.1 - 2.1

= 1.0 msec); this difference totals 3.6 msec.

Values of 1.0 msec or above are considered

abnormal and consistent with median

neu-ropathy at the wrist.

Median

ring

(4.8)

Ulnar

ring

(3.5)

Median

thumb

(4.1)

Radial

thumb

(2.8)

Median

palm

(3.1)

Ulnar

palm

(2.1)

Nerve Conduction Studies

Stimulate Record Latency, msec Amplitude, mV

(Normal side-to-side difference for latency is 1.2 msec, with normal amplitude difference up to 40%.)

Needle EMG

Spontaneous Activity Motor Unit Action Potentials Muscle Myotome Ins Act Fibs/PSWs Amplitude Duration Phasicity Recruitment Vastus medialis L3,4 Normal None Normal Normal Normal Full Adductor longus L3,4 Normal None Normal Normal Normal Full Tibialis anterior L4,5 Normal None Normal Normal Normal Full Tensor fasciae latae L4-S1 Normal None Normal Normal Normal Full Biceps femoris L5,S1 Increased 1+/2+ Increased Increased Normal Full Peroneus longus L5,S1 Increased 1+/1+ Increased Increased Normal Full Soleus S1,2 Increased 2+/2+ Increased Increased Normal

Lumbar paraspinals L3-S1 Normal None

Figure 7 Findings from nerve conduction and needle EMG studies in case 2 Abbreviations: Fibs/PSWs = fibrillations/positive short waves; Ins Act = insertional activity.

losis may produce

lower-motor-neuron loss in the upper limbs due

to root or anterior horn cell

involve-ment, but it should not cause

lower-motor-neuron loss in other regions

of the body In contrast, motor

neu-ron disease produces widespread

evidence of upper- and

lower-motor-neuron loss and

fascicula-tions Electromyographic diagnosis

of amyotrophic lateral sclerosis

re-quires evidence of denervation in

three of the following four ÒregionsÓ:

bulbar, cervical, thoracic, and

lum-bosacral

The needle EMG findings in this

case (Fig 8) demonstrate evidence of

denervation in the upper limbs,

con-sistent with two processes There is

denervation of C6-innervated

mus-cles, consistent with a C6

radicu-lopathy Additionally, the distal

muscles of the upper and lower

limbs demonstrate denervation,

suggesting a distal peripheral

poly-neuropathy However, extensive

evaluation of other body regions

(including the tongue, thoracic

paraspinal muscles, and proximal

lower limbs) did not show evidence

of denervation Fasciculations were

limited to two distal hand muscles

and were not widespread

Nerve conduction studies

dem-onstrate slowing of conduction

dif-fusely (in the sural, peroneal, and

ulnar nerves) but more severe

ab-normalities in the median nerve

(with absent sensory response and

very prolonged motor latency)

These findings confirm the

pres-ence of a peripheral

polyneuropa-thy and also suggest a

superim-posed median neuropathy at the

wrist

Thus, the findings are more

con-sistent with cervical spondylosis

and myeloradiculopathy than with motor neuron disease A peripheral polyneuropathy with focal median neuropathy is also present Surgi-cal decompression of the cerviSurgi-cal spine resulted in rapid improve-ment

Summary

The electrodiagnostic examination is

a useful tool for detecting problems affecting the peripheral nervous sys-tem Clinical assessment and

defini-tion of the quesdefini-tions to be answered are essential to tailor the electrodiag-nostic examination for each patient Potential pitfalls include performing tests in a standardized manner with-out examining the patient, not form-ing a differential diagnosis, technical errors, examining too few areas, and overinterpretation of minor devia-tions from Ònormal.Ó However, when performed appropriately, elec-trodiagnostic studies contribute sig-nificantly to the evaluation of patients with peripheral nervous system com-plaints

Nerve Conduction Studies

Stimulate Record Latency, msec Amplitude Velocity, msec Median nerve (sensory) Wrist Thumb Absent response

Radial nerve (sensory) Wrist Thumb 3.7 (²2.7) 3 µV (³5) Sural nerve (sensory) Leg Ankle 6.0 (²4.0) 1 µV (³5) Median nerve (motor) Wrist APB 5.1 (<4.3) 8.8 mV (³5.0)

Elbow APB 7.5 mV (³5.0) 49 (³50) Ulnar nerve (motor) Wrist ADM 3.6 (<3.8) 8.3 mV (³5.0)

Below elbow ADM 8.1 mV (³5.0) 50 (³50) Above elbow ADM 7.7 mV (³5.0) 49 (³50) Peroneal nerve (motor) Ankle EDB 8.6 (²6.0) 2.5 mV (³2.0)

Knee EDB 2.5 mV (³2.0) 35 (³40)

Needle EMG

Spontaneous Activity Motor Unit Action Potentials Muscle Myotome Ins Act Fibs/PSWs Fasc Amplitude Duration Phasicity Recruitment Deltoid C5,6 Normal None None Normal Normal Normal Full Biceps C5,6 Normal None None Normal Normal Normal Full Extensor carpi radialis C6,7 Increased 2+/2+ None Normal Normal Normal Central Pronator teres C6,7 Increased 1+/1+ None Normal Normal Normal Full Triceps C7,8 Normal None None Increased Increased Normal Reduced APB C8,T1 Increased 1+/1+ 1+ Increased Increased Normal Reduced FDI C8,T1 Increased 1+/1+ 1+ Increased Increased Normal Reduced Pectoralis major C5-T1 Normal None None Normal Normal Normal Full Cervical paraspinals C5-T1 Normal None None

Vastus medialis L3,4 Normal None None Normal Normal Normal Full Adductor longus L3,4 Normal None None Normal Normal Normal Full Tibialis anterior L4,5 Normal None None Normal Normal Normal Full Tensor fasciae latae L4-S1 Normal None None Normal Normal Normal Full Biceps femoris L5,S1 Normal None None Normal Normal Normal Full Soleus S1,2 Increased 2+/2+ None Increased Increased Normal Lumbar paraspinals L3-S1 Normal None None

Tongue XII Normal None None

Figure 8 Findings from nerve conduction and needle EMG studies in case 3 Normal val-ues are shown in parentheses Abbreviations: ADM = abductor digiti minimi; APB = abductor pollicis brevis; EDB = extensor digitorum brevis; Fasc = fasciculations; FDI = first dorsal interosseous; Fibs/PSWs = fibrillations/positive short waves; Ins Act = insertional activity.

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