Overview of nerve conduction studies

Steven H Horowitz, MD

:Section Editor

Jeremy M Shefner, MD, PhD

:Deputy Editor

April F Eichler, MD, MPH

All topics are updated as new evidence becomes available and our peer review process is
.complete

.Literature review current through: Jan 2020. | This topic last updated: Aug 30, 2018

INTRODUCTION — The unique natural electrical properties of peripheral nerves can be

evaluated in health and disease with externally applied stimuli and analysis of the
consequent neurophysiologic responses. Nerve conduction study (NCS) techniques permit
stimulation and recording of electrical activity from individual peripheral nerves with
sufficient accuracy, reproducibility, and standardization to determine normal values,
.characterize abnormal findings, and correlate neurophysiologic-pathologic features

:These clinical studies are used to

Diagnose focal and generalized disorders of peripheral nerves ●

Aid in the differentiation of primary nerve and muscle disorders (although NCS itself ●
evaluates nerve and not muscle)

Classify peripheral nerve conduction abnormalities due to axonal degeneration, ●

demyelination, and conduction block

Prognosticate regarding clinical course and efficacy of treatment ●

The basic anatomy, physiology, and pathophysiology of the peripheral nervous system, as
reflected in the clinical study of nerve conduction, will be reviewed here. Needle
electromyography is discussed separately. (See "Overview of electromyography".)

ANATOMY AND NORMAL NEUROPHYSIOLOGY — Most peripheral nerves are composed of

nerve fibers with motor, sensory, and autonomic functions; these are "mixed" nerves.
However, certain nerves available for clinical neurophysiologic investigation contain
primarily motor fibers (eg, anterior interosseous branch of the median nerve, posterior
interosseous branch of the radial nerve) or primarily sensory fibers (eg, sural, superficial
.peroneal, superficial radial)

The most widely used classification of individual nerve fibers relates to their diameters,
:myelin properties, and conductivity [1]

A-alpha (or A-alpha beta) are large myelinated fibers, 6 to 15 microns in diameter. The ●
.largest muscle afferent fibers are sometimes classified as 1a fibers
.A-delta are small myelinated fibers, 3 to 5 microns in diameter ●

.C fibers are unmyelinated fibers, 0.5 to 2 microns in diameter ●

Functionally, most efferent motor fibers are large myelinated (A-alpha). Sensory fibers
mediating touch, vibration, and position senses are also large myelinated (A-alpha), while
those that mediate cold and pain sensations are small myelinated (A-delta), and those that
mediate warm, itch, and pain sensations are unmyelinated C fibers. Efferent postganglionic
.sympathetic autonomic fibers are unmyelinated C fibers

Clinical neurophysiologic techniques are able to study only the largest A-alpha fibers; this
poses a problem in clinical situations where strength and vibration and position senses are
unaffected, but pain and temperature sensations are abnormal, a condition frequently
referred to as "small fiber neuropathy." NCS are normal in pure small fiber neuropathies.
(See "Skin biopsy for the evaluation of peripheral nerve disease", section on 'Small fiber
neuropathy'.)

— Compound action potentials

Sensory nerve action potentials (SNAPs) and compound muscle action potentials (CMAPs)  
are compound potentials that represent the summated electrical activity of individual nerve
.fibers simultaneously activated by nerve stimulation

For both SNAPs and CMAPs (recorded from muscle), this electrical activity is generated by
A-alpha fibers. With special techniques, such as digital averaging of many stimulus responses
with near-nerve recording electrodes, electrical activity of sensory A-delta fibers can be
.visualized [2]

Conductivity in myelinated fibers is saltatory, ie, node-to-node (Ranvier) depolarization, and

the speed of conduction is fiber-diameter dependent. The largest fibers conduct the fastest;
the relationship between fiber diameter and conduction velocity of electrical impulses is
roughly linear with a conversion factor of approximately 4.3 m/s/micron in healthy people
[2-5]. Thus, 14 to 15 micron fibers conduct in the range of 65 to 70 m/s, whereas 6 to 7
.micron fibers conduct at approximately 30 to 35 m/s

For the SNAP, the peak-to-peak amplitude and the area under the waveform of the
compound potential reflects the number of nerve fibers activated, while the CMAP
.amplitude more accurately reflects the number of activated muscle fibers than nerve fibers

In acute nerve lesions, when nerve regeneration has not had time to develop, the loss of
motor nerve fibers parallels the loss of muscle fibers capable of being activated, and CMAP
.amplitude is reduced accordingly

In chronic nerve lesions, however, CMAP amplitude is a poor estimate of motor nerve fiber
number because surviving motor units reinnervate previously denervated muscle fibers via
collateral sprouting of terminal motor nerve fiber branches. Subsequent to this process of
reinnervation, there are reduced numbers of motor fibers, each with enlarged motor unit
territories and increased numbers of muscle fibers per motor unit, and stimulation can result
in a CMAP whose amplitude is normal or only mildly reduced. In this context, contributions
.from electromyography and motor unit number estimation techniques may be helpful
 — Temporal dispersion

Differences in conduction speed of A-alpha myelinated fibers contributing to compound

evoked potentials create a temporal dispersion of electrical activities such that the largest
and fastest conducting fibers contribute to the earliest part of the potential and slower
conducting fibers contribute to later parts. Thus, the onset latency of a compound evoked
potential is determined by the conduction speed of the fastest fibers. In addition, the evoked
potential has a measurable duration from the time it first leaves the baseline to when it
.returns

The concept of temporal dispersion can be understood by envisioning an automobile race

over a distance of 120 miles; the fastest cars travel 60 miles per hour, the slowest 40 miles
per hour. Shortly after the start, the cars are bunched together, and their concentration
(representing CMAP amplitude) is greatest, while the spread between the fastest and
slowest cars (representing duration) is shortest. However, as the race proceeds cars splay
out and their concentration at any one point decreases. When the fastest cars reach the
finish line at two hours, the slowest cars are 40 miles behind. There, the concentration
(amplitude) of cars is less than anywhere previously and the distance (duration) between the
.fastest and slowest cars is greatest

With increasing lengths of nerve segment between stimulating and recording electrodes,
.temporal dispersion increases and amplitude decreases (figure 1)
With increasing lengths of nerve segment between stimulating and recording electrodes, temporal dispersion
.increases and amplitude decreases

As an example, one study of upper extremity nerves recorded from hand muscles found
that proximal stimulation at Erb's point in the supraclavicular fossa resulted in a 20 percent
decline in CMAP amplitude and a 10 percent increase in CMAP negative phase duration
.compared with distal stimulation at the wrist [6]

Abnormal temporal dispersion is characterized by an excessive difference in slowing

between individual motor axons within a nerve; it typically results from altered or damaged
myelin [7]. The consensus criteria from the American Academy of Neurology (AAN), created
for research purposes, define abnormal temporal dispersion as >20 percent drop in CMAP
amplitude and >15 percent change in CMAP duration between proximal and distal sites [8].
The American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM)
criteria define it as >30 percent increase in proximal versus distal CMAP duration [9]. The
relationship between increasing temporal dispersion and increasing length of nerve segment
is approximately linear for motor conduction [10], but not so for sensory conduction. (See
'Sensory nerve conduction' below.)
Phase cancellation — Because the recorded potentials of both single motor units and single
sensory fibers have both positive and negative components, phase cancellation can occur
depending on the conduction velocity of individual fibers. Phase cancellation becomes more
.significant with greater distances between stimulating and recording electrodes

Individual sensory and motor nerve fibers contribute differently to compound SNAPs and
CMAPs, respectively. A single large myelinated sensory fiber action potential has a much
shorter duration (typically 2 msec) than a single motor unit potential (typically 5 to 15 msec).
Because of this short duration, a small amount of dispersion will produce a much more
dramatic reduction in SNAP amplitude than CMAP amplitude.Increasing conduction distance
decreases median and ulnar SNAP amplitudes 16 to 17 times more than corresponding
decreases in CMAP amplitudes [6]. However, there are no accepted criteria for the extent to
which SNAP amplitude may decline with increasing distance between stimulating and
recording electrodes. This issue becomes important when considering diagnostic criteria for
.demyelinating diseases of nerve

Saltatory conduction — "Saltatory conduction" is the term used to describe the rapid

propagation of action potentials along myelinated fibers in which nodes of Ranvier are
interspersed between myelinated internodal areas along the axon. Conduction jumps from
node to node along the nerve fiber by activation of inward sodium currents, which generate
an outward capacitive (driving) current at the next node. The nodal membrane is
depolarized to threshold, opening sodium channels and initiating another cycle [11]. When
the driving current exceeds the threshold current of the nerve, conduction occurs. The ratio
of driving current to threshold current is the safety factor, and is normally >5 [12]. Because
of saltatory conduction, the conduction velocity of myelinated fibers is >10 times faster than
.what would be predicted for an unmyelinated axon of the same diameter

Original theories regarding saltatory conduction posited that the myelin sheath acted as an
insulator, preventing current leakage along the internodal axon. However, later evidence
suggested that myelin may actually leak current, and that its major role is to limit nodal
capacitance to a minimum, thereby allowing the node to depolarize rapidly to threshold. In
this model, the most important section of the myelin sheath responsible for maintaining
saltatory conduction is the paranodal area [11]. One report found that reduced nodal and
paranodal ionic conductances in motor and sensory axons in vivo predated clinical
symptoms, signs, and electrophysiologic abnormalities in patients with type 1 diabetes
.mellitus [13]

Physiologic factors affecting nerve conduction

Specific nerves and nerve segments — Normative data for distal latencies, conduction
velocities, and evoked potential measurements vary in regard to specific nerves and nerve
segments. For instance, nerve conduction velocities are 15 to 20 percent faster in upper
extremity nerves than in lower extremity nerves, and 5 to 10 percent faster in proximal
segments compared with distal segments [14]. Sensory conduction is 5 to 10 percent faster
.than motor conduction for each mixed nerve segment [14]

Age — Nerve conduction velocities are approximately half normal adult values in full-term
infants and increase into the adult range by age three to five years [15,16]. They then
plateau until ages 25 to 30 and decline slowly thereafter at approximately 1 to 3 percent per
decade [14]. Decreases in median and ulnar sensory conduction velocities have been
estimated at 0.13 to 0.21 m/s per year [17]. Effectively, this is a change of 10 m/s or less
.even into the ninth decade

There is a negative correlation between age and evoked potential amplitude, probably
related to loss of nerve fibers with aging [18]. The decline can be as much as 50 to 75
percent for the SNAP in the median, ulnar, sural, and superficial peroneal nerves between
the second and ninth decades [14,19]. However, the decline varies from nerve to nerve, and
.is more pronounced for the SNAP than the CMAP

The issue of absent evoked potentials in normal older adult subjects, when recording with
surface electrodes, is unsettled. One study found that responses could not be recorded in <1
percent of patients age 50 and younger, whereas loss of responses was common in those
aged 70 and older [18]. The sural nerve SNAP was most vulnerable, being absent in 24
percent of patients in their eighth decade and 40 percent in their ninth [18]. However, in
other studies, sural SNAPs were found in all subjects up to age 76 [20] and to age 88 years
[21]. In addition, sural SNAPs were found in all normal subjects as old as age 90 with near-
.nerve electrodes [22]

Height, weight, gender — There is a negative correlation between height and nerve

conduction velocity, more so for lower extremity nerves, and the effect of height is greater
than that of age [18]. Conversely, age has a much greater effect than height on evoked
.potential amplitude [18]

Women have faster conduction velocities than men, possibly due to height differences [23].
The higher sural SNAP amplitudes seen in women may relate to differences in subcutaneous
.tissue at the ankle [22]

SNAP amplitudes declined with increasing body mass index in two studies but not in another
[20,21,24]. Body mass index affects specific nerve segments; ulnar conduction velocities
across the elbow directly correlated with body mass index, but not ulnar forearm conduction
velocities [23]. Possible explanations are that nerve length may be overestimated in the
presence of adipose tissue, or that added insulation may produce higher local nerve
.temperatures [25]

A study of healthy Malaysian subjects of different ethnicities confirmed the aforementioned

effects of aging, but found that correlations between NCS and height, weight, and gender
varied among the nerves tested, and that ethnicity affected normative values (eg, Indian
subjects had slower conduction velocities and higher CMAP and SNAP amplitudes than
.Malay or Chinese subjects) [26]

Temperature — The temperature of nerve segments undergoing testing has a significant

effect on nerve conductivity and evoked potential amplitude [27]. In normal subjects, within
a range that excludes very high or very low temperatures, decreased local temperature
:results in the following changes

Increased evoked potential amplitudes, by 1.76 to 2.27 percent per degree Celsius (C) [28]●

Increased distal latencies, by 2.52 percent per degree C [28]●

Decreased conduction velocities, by 1.2 to 2.4 m/s per degree C [2,29]●

Because of the large magnitude of these changes and their potential role in confounding
result interpretation, standardization of temperature during testing is necessary. The arm
should be maintained at 34 to 36 degrees C and the leg at 32 to 34 degrees C. The situation
is of particular importance during cold weather and in patients with anxiety-induced
sympathetic overactivity. External infrared heating elements, hot packs, and hot water baths
can be effective in raising limb temperatures, but measured skin temperature may differ
considerably from intramuscular or nerve temperatures [28]. Correction factors to
.compensate for low limb temperatures during testing are not recommended [27]

METHODOLOGY — The essential parameters evaluated during clinical peripheral NCS are the
amplitudes, areas, configurations, and durations of the sensory nerve action potentials
(SNAPs) and compound muscle action potentials (CMAPs) evoked by peripheral nerve
stimulation, and the sensory and motor nerve conduction velocities. All measures are
.dependent upon the integrity of the largest myelinated fibers

Stimulation — Peripheral nerve activation involves placement of a stimulating cathode

(negative pole) and anode (positive pole) over the nerve and generating an electrical pulse
between them. Negative charges accumulate under the cathode and depolarize the nerve.
Simultaneously, the nerve is hyperpolarized under the anode. Modern stimulators generate
a square or rectangular wave pulse, the duration and strength of which can be varied. The
most commonly used durations are 0.1 to 0.2 msec, but pulses with durations of up to 1
.msec may be necessary with diseased nerves and when studying the H reflex

With increasing stimulus strength a threshold level is reached, which is the minimum
stimulus needed to depolarize some individual fibers in the underlying nerve and thereby
generate a propagating action potential. Greater stimulus strength recruits more nerve
fibers and progressively increases the compound action potential until a maximum size is
reached. For motor conduction studies, a maximal stimulus strength can be reached such
that all motor axons within the nerve that can be activated are activated. However,
compared with motor axons, sensory fibers have a greater variability in fiber diameter and
sensitivity to stimulation. Thus, a maximum response may be reached that represents
activation of all large myelinated sensory fibers but that does not include smaller myelinated
.fibers

A supramaximal stimulus, 10 to 20 percent above the maximal stimulus level, is employed to

ensure that variations in stimulus intensity or inadvertent minor changes in the relationship
between stimulator and nerve do not affect the action potential, particularly its amplitude
and onset latency. In normal nerves, stimuli of 100 to 300 V, or 10 to 30 mA, delivered
through surface electrodes, are usually sufficient to provide supramaximal stimulation.
Higher-intensity stimuli may be required at more proximal stimulation sites, especially in
patients with a higher body mass index. In achieving supramaximal stimulation, stimulus
intensity and duration are inversely related; the greater the stimulus intensity, the less the
duration needed, and vice versa. That said, a stimulus duration of 0.2 msec may be preferred
.because it is most acceptable from a pain perspective [30]

Surface electrodes are convenient to use and do not puncture the skin, but require
considerable stimulus strength (and hence discomfort) as they are at a distance from
theunderlying nerve. Needle electrodes placed close to the nerve (ie, near-nerve electrodes)
puncture the skin and have to be positioned properly but use less current and produce less
pain during supramaximal stimulation. Additionally, there is less stimulus artifact and less
stimulus spread along the nerve, so the specific site of nerve excitation and the calculated
conduction velocity can be determined more precisely. Near-nerve electrodes are also able
to record smaller SNAPs in diseases of nerves, especially with digital averaging to increase
.signal-to-noise ratio [2,3,31]

Recording — Surface recording electrodes are typically used to record the electrical activity
resulting from nerve excitation. These electrodes are placed over a muscle, a sensory nerve,
.or a cutaneous nerve distribution

The parameters most often studied are

the time (latency) between the stimulus artifact and the onset of the compound action
potential, and the

,amplitude

,duration

area, and

configuration

.of the compound action potential

In motor nerve studies, recording occurs from muscles. The active electrode is placed over
the motor point (endplate) and the reference electrode over the muscle tendon; they record
summated activity from all activated muscle fibers under the active electrode. The CMAP is
recorded by the active electrode as a near-field potential. Although the reference electrode
is considered electrically silent, it does record far-field or volume-conducted electrical
activity from other concurrently activated muscles (eg, with ulnar nerve stimulation and
activation of multiple hand muscles), or from faster conducting sensory fibers, thereby
contributing to the CMAP and potentially interfering with the interpretation of CMAP
amplitude and onset latency [32,33]. As an example, the reference electrode can record
electrical activity from multiple small foot muscles during lower extremity motor NCS; the
greater distances between the recording electrodes at the foot and the stimulating
electrodes at the popliteal fossa (tibial nerve) or fibular head (fibular nerve) magnify the
effects of temporal dispersion and phase cancellation, which can reduce the proximal CMAP
amplitude enough to give the false impression of a partial conduction block [34,35]. (See
'Conduction block' below.)

For recording of sensory potentials, digital averaging of evoked responses to multiple stimuli
is often employed. This technique increases the signal-to-noise ratio by the square root of
the number of stimuli averaged. Small SNAPs having identical latencies after each stimulus
can be differentiated from baseline, as baseline noise is reduced. This is important when
studying small lower extremity sensory nerves, especially in older people and in patients
.with axonal degenerative peripheral nerve disorders

For clean and accurate recordings of these evoked potentials, electromyography

instruments require a "ground electrode," usually applied between stimulating and
.recording electrodes, to serve as a reference point and minimize electrical interference [36]

Orthodromic and antidromic recording — When a nerve is electrically stimulated, it is

depolarized. Evoked electrical activity in the nerve propagates both proximally and distally
.from the stimulus site
Motor conduction studies are orthodromic, meaning that propagation of the evoked
potential occurs from nerve to muscle in the direction of physiologic conduction. Sensory
potentials can be recorded with either orthodromic (propagation of the evoked potential
away from the sensory receptor) or antidromic (propagation of the evoked potential toward
.the sensory receptor) methods (figure 1)

In clinical practice, sensory responses using antidromic recording techniques (with the
stimulator placed proximal to the recording electrodes) are more frequently employed for
sensory nerve conductions, mainly because the amplitude of the SNAP is larger with
.antidromic than with orthodromic recording [2]

Motor nerve conduction — In the peripheral nervous system, efferent motor nerve fibers
are part of Liddell and Sherrington's motor unit [37], which consists of an anterior horn cell
(motor neuron), its axon (motor nerve), terminal nerve branches, synapses, and all individual
.muscle fibers so innervated

— CMAP latency, amplitude, area, and duration

When the active recording electrode is properly placed over the motor point of the muscle,  
the CMAP is biphasic, beginning with negative (upward) activity as the potential leaves the
.baseline

.CMAP latency is the time between stimulus onset and onset of negative peak ●

CMAP amplitude is the height of the negative peak from baseline or the difference ●
.between negative and positive peaks

CMAP area is the area under the negative peak waveform [15]. This measurement is ●
.calculated by computerized electronic integration of the CMAP negative waveform

CMAP duration is the time from onset of the negative peak to return to baseline of the end ●
.of the potential

If the CMAP potential starts with a positive (downward) deflection, then either the active
electrode is distant from the motor point, or activity is being recorded from nearby muscles
.[15]

— Conduction velocity

Conductivity of an electrical impulse is fastest along the main axon and slower in terminal  
.nerve branches

At neuromuscular junctions (NMJs; synapses), acetylcholine quanta are released from nerve
terminals; they activate acetylcholine receptors at muscle fiber endplates. There is
depolarization of the muscle membrane, development of a motor action potential, and
muscle fiber contraction. These NMJ activities add an approximately 1 msec delay to motor
unit conductivity, with an additional delay due to electrical transmission along muscle fiber
.membranes

Consequently, the pure conduction velocity of electrical current flowing along a motor nerve
cannot be accurately measured between a single stimulating electrode placed along the
nerve and a recording electrode over the muscle, because the conduction time from
stimulus onset to onset of recorded electrical potential comprises not only nerve
.conduction, but also NMJ transmission and muscle fiber conduction

The conduction time involving all three components (nerve conduction, NMJ transmission,
and muscle fiber conduction) is called the terminal motor latency or distal motor latency.
Normal terminal motor latency values vary from nerve to nerve, being longer in lower
.extremity nerves

Calculation of motor conduction velocity — To measure motor conduction velocity, a motor

nerve must be stimulated at two points, one proximal and one more distal. The conduction
time in the terminal segments of the motor unit are identical for the resulting CMAP
.recordings from both stimulation sites

:The pure motor conduction velocity can be calculated as follows (figure 2)

Stimulation at different proximal sites along the ulnar nerve while recording from the abductor digitiminimi
.muscle allows the conduction velocity (CV) of the motor neurons to be calculated

Measuring the distance (d) between the stimulation sites in millimeters ●

Subtracting the conduction time between the distal stimulus site and the recording site ●
(distal latency) from the conduction time between the proximal stimulus site and the
recording site (proximal latency)

Dividing the distance (d) in millimeters by the difference in conduction times (proximal ●
latency - distal latency) in milliseconds

Thus, motor conduction velocity = d/(proximal latency - distal latency). The units are
.millimeters/millisecond (mm/msec), or meters/second (m/s)

Motor conduction velocity determinations are critically dependent upon accurate

measurements of both distal and proximal latencies and of conduction distances between
these stimulation sites. The standard consensus is that distances of at least 10 cm or more
should be used to minimize measurement errors. However, with modern electrodiagnostic
equipment, accurate conduction velocities can be determined with distances as short as 5 to
.6 cm [38]

Upper limb position has long been recognized as affecting ulnar nerve motor conduction
velocity calculations across the elbow [39]. The standard position for upper limb recording is
for the elbow to be flexed at 90 degrees [40]. Lower limb position can also affect fibular
motor nerve conduction across the knee and distal to the fibular head [41]. The optimal leg
.position for recording is flexion of the hip and extension of the knee

Further evaluation of conduction in the terminal segment of the motor unit may
differentiate demyelinating disorders that have uniform conduction slowing along the entire
length of nerve (eg, hereditary motor and sensory neuropathy type 1A), and those with
multifocal conduction changes and nonuniform conduction slowing (eg, hereditary
neuropathy with pressure palsy, the inflammatory demyelinating polyneuropathies [42]),
from those with disproportionate distal nerve conduction slowing (eg, polyneuropathy with
antibodies against myelin-associated glycoproteins). The terminal latency index (TLI) is a
measure that combines distal latency and proximal conduction velocity to evaluate whether
.disproportionate distal slowing is present [43]

— Sensory nerve conduction

Afferent sensory fibers, which have their cells of origin in the dorsal root ganglia, do not  
have synapses within the peripheral nervous system. Therefore, electrical current flowing
between stimulating and recording sensory electrodes in the periphery occurs solely along
the nerve, and a conduction velocity can be derived by dividing conduction distance by
conduction time between stimulating and recording electrodes. In routine studies, the
.sensory receptors are not evaluated

Whereas the CMAP is measured in millivolts (mV), the SNAP is measured in microvolts
.(microV) (figure 3)
Recording of the sensory action potential is helpful in determining the site of nerve injury particularly in those
with lesions resulting in sensory symptoms. This illustration depicts a sensory nerve conduction study of the ulnar
nerve. Normal latency is seen with lesions of the central nervous system or those that are proximal to the dorsal
root ganglion (arrowhead number 1). A more distal lesion (arrowhead number 2) results in a decreased
amplitude but normal conduction velocity. Either a compressive mononeuropathy (arrowhead number 3) or
generalized demyelinating peripheral neuropathy results in a decrease in both amplitude and conduction
.velocity

— F wave

.F waves are late responses generated by supramaximal nerve stimulation (waveform 1) 
The F wave is visible as a low amplitude late potential following the M response. External stimulation depolarizes
peripheral nerves, triggering electrical potentials that propagate both proximally and distally. With motor nerves,
electrical activity moving distally results in a direct motor response, the compound muscle action potential, also
known as the CMAP or the M response. Electrical activity propagating proximally activates a small percentage of
motor neurons (they "backfire"), which then generate the F wave. The F wave latency varies depending upon the
.conductivity of the subpopulation of motor neurons activated

Electrical activity moving proximally in motor nerves activates or backfires motor neurons,
which can generate an orthodromic response known as the F wave that is visible as a low-
.amplitude late potential

F waves are useful for evaluating peripheral neuropathies with predominantly proximal
involvement, such as the acute and chronic inflammatory demyelinating polyneuropathies,
.in which distal conduction velocities may be normal early in the disease

 — H reflex
The H reflex is a true reflex with an afferent arc mediated by large, fast-conducting group 1a
.fibers, and an efferent arc mediated by alpha motor neurons (waveform 2)
The H reflex with tibial nerve stimulation in the popliteal fossa, recording from the soleus muscle. The H reflex is
visible only with submaximal stimulation. With a slow increase in stimulus strength, the H reflex appears as the
stimulus changes from subthreshold to submaximal. The amplitude of the H reflex is greatest just below the
threshold for the appearance of the compound muscle action potential (CMAP or M response). With increasing
stimulus strength, the H reflex amplitude declines as M response amplitude increases. The H reflex disappears
.with maximal and supramaximal stimulation

It is visible only with submaximal stimulation and is most consistently seen with tibial
nervestimulation in the popliteal fossa when recording from the soleus and plantar foot
muscles.The H reflex is useful for evaluating the S1 nerve root in suspected radiculopathies
.and proximal conduction in polyneuropathies

— Normative data and reference values

Several studies have emphasized the lack of standardization and reproducibility of NCS,  
especially when repeated for clinical reasons or therapeutic trials [40,44-46]. Special training
may minimize intraobserver variability amongst experienced clinical neurophysiologists but
.does not eliminate interobserver differences [45]

Reliance on previously published normative reference data is problematic because of their

lack of modern statistical and methodologic rigor and the false assumption that these data
follow a bell-shaped (Gaussian) distribution; it has been suggested that nonparametric
methodology using percentiles is more suitable in the determination of reference values
[40,46,47]. Other statistical methods for determining reference values for electrodiagnostic
.tests are under study [48]

— ABNORMAL FINDINGS

:There are three main pathologic mechanisms affecting peripheral nerve  

Axonal degeneration●

Demyelination●

Conduction block●

This pathophysiologic classification is based upon an understanding of the two predominant

neural structures, the axon and its myelin sheath. Peripheral nerve disorders, both focal and
.generalized, can affect either of these structures alone or together

 — Axonal degeneration

The primary feature of axonal degeneration seen with NCS is reduced amplitude. The
conduction velocity may also be reduced to the extent that the largest axons are affected; in
this setting, the measured conduction velocity reflects the velocity of the largest remaining
axons. Nevertheless, the degree of conduction slowing with axonal degeneration is less than
.with demyelination

Pathologic conditions affecting peripheral nerves may produce focal or general loss of axons.
The axons relevant to clinical neurophysiologic studies are A-alpha fibers with diameters of 6
to 15 microns. Loss of these fibers is manifested as a decrease in amplitude and a change in
configuration (increased dispersion and increased number of phases) of the compound
evoked potentials. In addition, loss of these fibers causes slowing in maximum conduction
.velocity

Since the largest fibers contribute to the earliest part of the compound evoked potential,
their loss results in an increase in conductiontimeand a decrease in conduction velocity. As
an example, if all fibers >10 microns in diameter are lost, then the fastest conduction
velocities of the remaining fibers would be in the 40 m/s range. Normally, maximum
.conduction velocities are in the 65 to 75 m/s range

Small A-delta fibers make little if any contribution to the sensory nerve action potential
(SNAP) [3] or compound muscle action potential (CMAP), and C fibers make none. Thus,
these SNAPs and CMAPs are normal in neuropathies that exclusively or predominantly affect
.small fibers

By the "80 percent rule," the conduction velocity should be >80 percent of the lower limits
of normal when the amplitude of the evoked potential is >80 percent of the normal value
.[15]
A greater loss of fast conducting fibers could be responsible for greater conduction slowing.
However, in pure axonal loss lesions, the conduction slowing cannot go below 70 percent of
the lower limits of normal [15], or 60 percent of the normal mean for that particular nerve
.and segment [49]

This is amplitude-dependent slowing, ie, conduction velocity is reduced because a

subpopulation of faster conducting axons has been lost, not because of demyelination of
.conducting axons

Practically, assuming the variables of height, age, and temperature are taken into account,
conduction velocities >30 m/s are compatible with axonal loss, whereas velocities <30 m/s
.most likely reflect demyelination

In acute axonal peripheral nerve injuries, the distal portion of the nerve is separated from
the proximal portion but remains physiologically intact for a period of time despite a
.complete loss of nerve function (Wallerian degeneration)

Few humans with such nerve injuries have been studied electrophysiologically in the early
days postinjury. In the largest human study (16 patients, 20 injured nerves), the injured
nerves were evaluated within three days of injury [50]. All nerves showed CMAP amplitude
decay by day 4, with 85 percent of nerves reaching their CMAP plateau by day 8. Length
dependency was demonstrated by the strong correlation between length of the distal nerve
.segment and CMAP amplitude decay

 — Demyelination

When myelin is disrupted (demyelination), especially in paranodal areas, nodal capacitance

increases, and resistance decreases. It takes longer for the driving current to activate the
next node to threshold, resulting in slowing in internodal conduction and a reduced
.conduction velocity along that segment of nerve

:This slowing in conduction velocities can occur through the several patterns that follow

Uniform (seen in all segments of all nerves), as in hereditary motor and sensory ●
neuropathy type 1

Multifocal (seen in some but not all nerves, or only along certain nerve segments), as in the ●
acute and chronic inflammatory demyelinating neuropathies

Monofocal (one nerve at one site), as in compressive lesions of the median nerve at the ●
carpal tunnel or the ulnar nerve at the ulnar groove

Conduction block occurs (conduction fails at that point of the axon) if the driving current falls
below the threshold current (ie, if the safety factor drops below unity) [11,12,51]. (See
'Conduction block' below.)

Unfortunately, the diagnosis of primary demyelination in any particular patient or nerve can
.be problematic

Slowed conduction velocities and prolonged distal latencies can occur in axonal disorders ●

There is a wide range of normal values for the standard parameters of nerve conduction ●

Secondary demyelination can occur with primary axonopathies [52]●

CMAP amplitude must be considered ●

CMAP amplitude can be normal or reduced in demyelination and conduction block. With
focal sites of demyelination and block, stimulation distally will result in normal CMAP
amplitudes if axons remain intact. However, a definite diagnosis of primary demyelination
may be impossible in the context of marked reductions in distal CMAP amplitudes. That is
why the consensus criteria discussed above are, in part, dependent upon CMAP amplitude
and the amplitude, in part, determines the criteria [8,9]. These criteria are usually
considered sufficiently specific, but insufficiently sensitive to be used in clinical practice. This
raises the risk of not diagnosing and hence, not treating patients who actually have
inflammatory or autoimmune demyelinating disorders that may be responsive to
.immunosuppressive treatments such as intravenous immunoglobulin or plasmapheresis

Multiple studies have attempted to refine the consensus criteria in the hopes of increasing
their sensitivity and specificity. Many such studies have used the electrophysiologic findings
in motor neuron disorders and axonal polyneuropathies as representative of axonal
degeneration, and have defined criteria for primary demyelination in contrast. As an
:example, the following are one set of proposed criteria for primary demyelination [52]

.Motor conduction velocities <70 percent of the lower limit of normal ●

.Prolonged motor distal latency of >150 percent of the upper limit of normal ●

Prolonged F wave latency of >120 percent of the upper limit of normal with distal CMAP ●
negative peak amplitude of >80 percent of the lower limit of normal, with findings present in
at least two nerves. The F wave latency must be prolonged to >150 percent of the upper
limit of normal if the distal negative peak CMAP amplitude is <80 percent of the lower limit
.of normal

Alternatively, in hereditary motor and sensory neuropathy type 1, a condition with

pathologically proven demyelination, conduction velocities are <60 percent of the normal
.mean for that particular segment of that particular nerve [49]

Prolongation of the distal CMAP duration, due to abnormal temporal dispersion, can be an
indication of distal demyelination; this finding is not observed in axonal neuropathic
disorders or in focal nerve compression syndromes (eg, carpal tunnel syndrome) [53-55].
One group of investigators determined that distal CMAP durations (from onset of the first
negative deflection to return to baseline of the last negative deflection) are abnormal and
indicative of demyelination when >8.5 msec in acute inflammatory demyelinating
polyneuropathy and >9 msec in chronic inflammatory demyelinating polyneuropathy
.[53,55]

Nevertheless, this phenomenon cannot be used to distinguish between acquired and

hereditary demyelinating polyneuropathies, since one study found that distal CMAP
prolongations of >9 msec occur in a clinically significant proportion of patients with
hereditary demyelinating neuropathies (eg, hereditary motor and sensory neuropathy type
1A) [56]. However, the same report found abnormal distal CMAP prolongation affecting
multiple nerves occurred in 39 percent of patients with chronic inflammatory demyelinating
.polyneuropathy [56]

In another study, a linear correlation between CMAP and SNAP action potential amplitude
and conduction velocity was present in most nerves affected by axonal or demyelinating
polyneuropathy [57]. Thus, the relationship between amplitude reduction and conduction
slowing did not seem useful for distinguishing the degree of demyelination versus axonal
.loss in an individual patient with polyneuropathy

Near-nerve studies of distal sensory nerves may be helpful in diagnosing peripheral

neuropathies and sensory inflammatory demyelinating neuropathies when routine surface
electrode studies are either normal or nondiagnostic [31,58,59]. Ultrasound positioning of
the near-nerve recording electrode in sural nerve studies has been found superior to surface
.electrodes, especially in older adults [19]

Given the many possible electrophysiologic expressions of demyelination, it is no wonder

that confusion exists. There is still no gold standard set of diagnostic criteria for the
electrophysiologic identification of demyelination. Such criteria are difficult to devise [60].
Multiple sets of criteria for chronic inflammatory demyelinating neuropathy exist, for
example, with wide variation in sensitivity and specificity [61]. (See "Chronic inflammatory
demyelinating polyneuropathy: Etiology, clinical features, and diagnosis", section on
'Diagnosis'.)

Misdiagnosis of demyelination is not uncommon, most often due to interpretive errors when
amplitude-dependent conduction velocity slowing occurs (as in length-dependent axonal
neuropathies or motor neuron disease) or when amplitude-independent conduction slowing
.is limited to known compressible sites [62]

 — Conduction block
Conduction block can occur with acquired demyelinating nerve lesions. The key information
for identifying conduction block is the amount of drop in CMAP amplitude and/or area when
stimulating from more proximal, compared with distal, sites. Criteria for conduction block
are specific for individual nerves, since normative data for CMAP amplitude, area, and
.duration vary from nerve to nerve [9]

Even in normal nerves, the effects of phase cancellation and temporal dispersion can affect
compound potentials and lead to reductions in amplitude and area, and increases in
duration, when stimulating from successively more proximal sites. These changes are more
pronounced for SNAPs than CMAPs. The criteria for conduction block must account for these
normal changes. The American Association of Neuromuscular and Electrodiagnostic
Medicine (AANEM) consensus criteria cite normal ranges of CMAP changes between
:stimulus sites distal and proximal as follows [9]

For the median and ulnar nerves, with stimulation at the elbow versus the wrist, CMAP ●
amplitude and area are reduced by no more than 25 and 20 percent, respectively, while
duration increases by no more than 25 percent

For the peroneal nerve, with stimulation at the knee versus the ankle, CMAP amplitude ●
and area are reduced by no more than 30 and 25 percent, respectively, while duration
increases by no more than 30 percent

For the tibial nerve, with stimulation at the knee versus the ankle, CMAP amplitude and ●
area are reduced by no more than 50 and 30 percent, respectively, while duration increases
by no more than 30 percent
With these normal findings in mind, the AANEM consensus criteria for definite partial
conduction block, assuming a minimal contribution of temporal dispersion (<30 percent), are
:as follows [9]

In median and ulnar nerves, conduction block requires a reduction in CMAP amplitude of ●
>50 percent over wrist to elbow segments

In peroneal and tibial nerves, conduction block requires a reduction in CMAP amplitude of ●
>60 percent over ankle to knee segments

The American Academy of Neurology (AAN) criteria require only a >20 percent decline in
CMAP negative peak area or peak-to-peak amplitude with <15 percent change in duration
[8]. Others have proposed a 30 percent CMAP amplitude drop, except with stimulation at
Erb's in the supraclavicular fossa point, for which a >50 percent amplitude drop was used
.[63]

Of note, any reduction in CMAP amplitude of >20 to <50 percent is abnormal according to
.the AAN criteria [8], but not those of the AANEM [9]

While temporal dispersion and its attendant desynchronization and phase cancellation
contribute little to the decline in CMAP amplitude and area over distance in normal
conduction, they can make a significant contribution to CMAP amplitude or area decline in
segmental demyelination, giving a false impression of conduction block [15,64]. Excessive
CMAP desynchronization and phase cancellation, rather than conduction block, should be
considered when a prominent reduction in CMAP amplitude is accompanied by good motor
unit recruitment and strength [15]. Alternatively, abnormal temporal dispersion is an
intrinsic electrophysiologic feature of multifocal motor neuropathy, independent of
conduction block, and, when present, should not preclude this diagnosis whether
conduction block is present or not [65]. When CMAP area is considered, a drop of >50
.percent denotes conduction block, independent of the amount of temporal dispersion [7]

The diagnosis of conduction block is complicated when distal CMAP amplitude is reduced.
The AANEM consensus criteria are valid when the negative phase of the distal CMAP is >20
percent of the lower limit of normal [9]. Reduced distal CMAP amplitudes may be due to
distal axonal loss as seen in conditions with length-dependent axonal degeneration, distal
demyelination, or distal conduction block, that is, a block in conduction between the distal-
most stimulus site and the recording electrode over muscle. (Distal conduction block may be
considered when muscle weakness exists without muscle atrophy or denervation activity on
electromyography.) If a reduced distal CMAP amplitude is due to axonal loss, then greater
desynchronization and phase cancellation can produce further reductions in CMAP
.amplitude with proximal stimulation and obscure possible conduction block

In the appropriate clinical situation, with both distal and proximal CMAP amplitude
reductions, critical illness neuromyopathy should be considered, especially in association
with prolonged distal and proximal CMAP durations and relatively preserved motor
conduction velocities (not to demyelination levels) in two or more nerves [66]. This
reduction in CMAP amplitudes and prolonged CMAP durations may be secondary to muscle
fiber inexcitability. (See "Neuromuscular weakness related to critical illness", section on
'Electrodiagnostic testing'.)
Conduction block is significantly influenced by membrane hyperpolarization when an axon
conducts a rapid train of impulses either via external stimulation [67] or voluntary activity
[68]. This activity-dependent, or frequency-dependent, hyperpolarization blocks conduction
when the safety factor is reduced [51]. Axonal membrane hyperpolarization was found distal
to the site of conduction block in multifocal motor neuropathy [69]. In multifocal motor
neuropathy, the electrophysiologic features of the block may change depending on disease
duration; depolarizing blocks were seen in patients with shorter disease duration (two years)
and hyperpolarizing blocks in patients with more chronic disease (five or more years) [70].
Frequency-dependent conduction block has also been found in patients with carpal tunnel
syndrome and significantly prolonged motor latencies. It may explain grip weakness
.associated with this condition [71]

Conduction block can also be caused by mechanisms other than demyelination, such as
sodium channel blockade or ischemia [11]. In multifocal motor neuropathy, antibody
interference with sodium movement across the nodal membrane may play a role in
.conduction block [69]

Sensory fibers are much less susceptible to conduction block than motor fibers for various
physiologic reasons, including protection against hyperpolarization due to greater inward
rectification, a more active sodium-potassium pump, greater expression of persistent
sodium channels, and a higher safety factor for impulse transmission [11,51,68].
Additionally, partial sensory conduction block may be more difficult to define because of the
effects of normal temporal dispersion and phase cancellation on the SNAP [3,6].
Nonetheless, partial sensory conduction block has been demonstrated [3] and can occur in
multifocal acquired demyelinating sensory and motor neuropathy (MADSAM, Lewis-Sumner
.syndrome) [72,73]

 — Electrophysiologic-pathologic correlations
Electrophysiologic studies attempt to characterize abnormalities according to which
mechanism predominates in a particular disorder and patient. However, this division is
simplistic and not absolute; complex axon/myelin interactions exist, many diseases have
both axonal loss and demyelination (eg, hereditary motor and sensory neuropathy 1, severe
carpal tunnel syndrome), and axonal changes can occur secondary to disorders of myelin. In
some patients, the results do not allow distinction. Further, in conditions with axonal loss,
NCS findings come from conduction in fibers that are still functional, and there is no
contribution from the most affected degenerated fibers [74]. In demyelinating disorders, the
.NCS findings reflect conduction in affected nerve fibers [74]

The determination of underlying nerve pathology utilizing electrophysiologic studies is

heavily dependent upon methodology. Motor conduction studies are better for this purpose
than sensory conduction studies, but concurrent histopathologic correlation and
confirmation is not possible as motor nerves are not biopsied. However, a few studies of
patients with suspected peripheral neuropathy compared sural nerve sensory conduction
results obtained from surface electrodes versus those obtained from on-nerve needles
placed on exposed sural nerves during biopsy [75,76]. When the electrophysiologic data
were correlated with histopathologic findings, the diagnostic sensitivity for demyelination or
axonal degeneration with surface sensory electrode studies was low (26 percent), whereas
the diagnostic sensitivity with the on-nerve technique was much higher (69 percent), and
.comparable to the near-nerve technique [2]
CLINICAL APPLICATION

Indications for testing — NCS are invaluable in defining and determining peripheral nervous
system function, dysfunction, and disease [77,78]. They are used clinically in four major
:ways

Diagnose focal and generalized disorders of peripheral nerves ●

Aid in the differentiation of primary nerve and muscle disorders (although NCS itself ●
evaluates nerve and not muscle)

Classify peripheral nerve conduction abnormalities due to axonal degeneration, ●

demyelination, and conduction block

Prognosticate regarding clinical course and efficacy of treatment ●

Some conditions (eg, conduction block) can only be diagnosed with conduction studies.
Conduction studies can also provide the electropathophysiologic diagnoses in other
.conditions, such as axonal damage versus demyelination

NCS may also be helpful in determining therapies, such as when to do surgery in the carpal
tunnel syndrome, or when to use immunosuppressive therapy in polyneuropathies. They
have been thought to be reliable and reproducible, thereby providing objective evidence of
efficacy with therapy and in clinical trials [79]. However, single nerve measurements may not
.be an adequate clinical trial outcome measure due to test-to-test variability [80]

While NCS can distinguish various types of electropathophysiologic abnormalities of large

myelinated fibers, they most often cannot determine specific etiologies. Since conduction
studies evaluate large myelinated fiber functions, they are often normal in polyneuropathies
with predominant small fiber involvement, and in neuropathic pain conditions.
Nevertheless, one study found electrodiagnostic evidence that small fiber sensory
neuropathy progresses to large fiber involvement 5 to 10 years after onset of pain [81]. NCS
are also of limited value for quantifying the clinical severity of muscle weakness and large
fiber sensory loss; thus, some authors view them as surrogate measures of polyneuropathy
.[45]

Although there is evidence of both over- and under-utilization of electrodiagnostic testing in

the evaluation of suspected distal symmetric polyneuropathies, one review concluded that
test results change either diagnosis or treatment in over 40 percent of patients [77]. The
American Academy of Neuromuscular and Electrodiagnostic Medicine (AANEM) supports
use of electrodiagnostic testing in distal symmetric polyneuropathies for the following
:indications [78]

Determination of primary and alternative diagnoses ●

Determination of severity, duration, and prognosis of disease ●

Evaluating risk of associated problems ●

Determination of the effect of medications ●

Evaluating the effect of toxic exposures [77,78]●

The use of electrodiagnostic testing in the evaluation of polyneuropathy is reviewed
separately. (See "Overview of polyneuropathy", section on 'Diagnostic evaluation'.)

Concurrent electromyography — NCS should not be performed or interpreted in isolation.

The AANEM recommends that NCS and electromyography should be performed and
interpreted at the same time in the majority of situations [82]. This is critically important in
patients with suspected radiculopathy, plexopathy, myopathy, motor neuropathy, or motor
neuron disease. In addition, the complementary information derived from
electromyography is useful to ensure that an underlying disease process is not missed (eg,
radiculopathy in a patient with suspected carpal tunnel syndrome). (See "Overview of
electromyography".)

Utility of composite scores — Composite scores made up of several NCS attributes may be

better diagnostic measures of nerve impairment than the individual NCS tests [83,84].
.Composite scores may also be useful for the detection of subclinical nerve impairment [85]

In a series of patients with generalized peripheral neuropathies, including patients with ●

diabetes (n = 396) and those with chronic inflammatory demyelinating polyneuropathy (n =
55), composite scores that incorporated nerve conduction velocities, distal latencies, and F
waves of individual or multiple nerves were generally more sensitive and more reproducible
.than individual NCS tests for the detection of neuropathy [84]

In another study involving patients with diabetes but without a diagnosis of ●

polyneuropathy at baseline, composite scores of NCS tests were the most sensitive indicator
of early asymptomatic functional nerve worsening over time [85]. In addition, composite
scores demonstrated latent nerve dysfunction before nerve conduction criteria for diabetic
.polyneuropathy were met, and showed a statistically significant worsening over time [85]

Complications — NCS employing surface electrodes are noninvasive. The major risks involve
possible electrical injury from stray leakage currents. Intensive care unit settings predispose
to increased risk when patients are attached to multiple electrical devices plugged into
different power outlets. In addition, the normal protective barrier of intact, dry skin may be
.breached by intravenous lines, external wires, and fluid spills [86]

NCS can be safely performed in patients with implanted cardiac pacemakers and
cardioverter-defibrillators [87,88]. There is the theoretical possibility that nerve stimuli can
be mistaken as arrhythmias and trigger or inhibit demand pacemakers and cardioverter-
defibrillators or induce atrial or ventricular fibrillation. However, in a study of NCS at routine
sites, including the left supraclavicular fossa, electrical impulses were not detected by the
.bipolar sensing systems of these cardiac devices [87]

Pain during the procedure can be problematic [88]. One study found that providing patients
with written information about the procedure beforehand reduced pain and anxiety during
.NCS [89]

Measures to avoid electrical injury — Safety procedures are necessary to minimize electrical

leaks and injury with electrodiagnostic studies [86,90]. Most important are measures to
.insure proper grounding

Additional measures for patients with cardiac pacemakers and implanted cardioverters-
:defibrillators include the following [88,90]
Do not perform electrodiagnostic studies on patients with external (transcutaneous) pacer ●
.wires

.Ensure all ground electrodes are functional ●

.Limit all electrodes, including the ground, to the limb of interest ●

Extension cords should not be used and patients should be disconnected from nonessential ●
.electrical equipment prior to electrodiagnostic studies

Keep all electrodes as far away from the heart as possible, without crossing cardiac devices ●
.or their wires

Do not stimulate within 6 inches (15 cm) of pacemakers or implantable cardioverter- ●

defibrillators, and avoid ipsilateral proximal stimulation sites such as the axilla, Erb's point,
.and nerve roots

Use a stimulus duration of ≤0.2 ms and a stimulus rate of ≤1 Hz. These parameters exclude ●
.the typical repetitive stimulation done during neuromuscular junction (NMJ) testing

Consult with a cardiologist before performing studies on patients with an implantable ●

.automatic cardioverter-defibrillator

.Medical emergency carts should be available ●

SUMMARY AND RECOMMENDATIONS

The sensory nerve action potential (SNAP) and compound muscle action potential (CMAP) ●
are compound potentials that represent the summated electrical activity of individual nerve
fibers simultaneously activated by nerve stimulation. Normal differences among individual
nerve fibers in action potential conduction speed and duration can affect the amplitude and
duration of compound potentials via temporal dispersion and phase cancellation. Normal
nerve conduction parameters also vary with regard to specific nerves, nerve segments,
individual patient characteristics, and temperature. (See 'Anatomy and normal
neurophysiology' above.)

Surface recording electrodes are typically used to record the electrical activity resulting ●
from nerve excitation. These electrodes are placed over a muscle, a sensory nerve, or a
cutaneous nerve distribution. The essential parameters evaluated are the amplitudes, areas,
durations, and configurations of the SNAPs and CMAPs, and the conduction velocities of
sensory and motor nerves. They are dependent upon the integrity of the largest myelinated
fibers. (See 'Methodology' above.)

F waves are late responses generated by supramaximal nerve stimulation. Electrical activity ●
moving proximally in motor nerves activates or backfires motor neurons, which can generate
an orthodromic response known as the F wave that is visible as a low-amplitude late
potential. F waves are useful for evaluating peripheral neuropathies with predominantly
proximal involvement. The F wave is reviewed in detail separately. (See "Nerve conduction
studies: Late responses", section on 'F waves'.)

The H reflex is a true reflex with an afferent arc mediated by large, fast-conducting group ●
1a fibers, and an efferent arc mediated by alpha motor neurons. It is visible only with
submaximal stimulation and is most consistently seen with tibial nerve stimulation in the
popliteal fossa when recording from the soleus and plantar foot muscles. The H reflex is
useful for evaluating the S1 nerve root in suspected radiculopathies and proximal
conduction in polyneuropathies. The H reflex is discussed in detail elsewhere. (See "Nerve
conduction studies: Late responses", section on 'H reflex'.)

The three main pathologic mechanisms that affect peripheral nerve are axonal ●
:degeneration, demyelination, and conduction block (see 'Abnormal findings' above)

.The primary feature of axonal degeneration is reduced amplitude of SNAPs or CMAPs •

.The primary feature of demyelination is reduced conduction velocity •

Conduction block can occur with acquired demyelinating nerve lesions. The key information •
is the amount of drop in CMAP amplitude and/or area when stimulating from more proximal
.compared with distal sites

Nerve conduction studies (NCS) are invaluable in defining and determining peripheral ●
nervous system function, dysfunction, and disease, both focally, as in entrapment
neuropathies, and generally, as in polyneuropathies. In addition, they are often useful in the
assessment of the degree of axonal damage versus demyelination. Because they evaluate
large myelinated fiber functions, conduction studies are often normal in polyneuropathies
with predominant small fiber involvement. (See 'Clinical application' above.)

NCS and electromyography should be performed and interpreted at the same time in the ●
majority of test situations. This is particularly important in patients with suspected
radiculopathy, plexopathy, myopathy, motor neuropathy, or motor neuron disease. (See
'Concurrent electromyography' above.)

The major risk of NCS is electrical injury from stray leakage currents. Safety procedures are ●
necessary to minimize electrical leaks and injury. (See 'Complications' above.)