INTRODUCTION — The unique 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 nerves).
The most widely used classification of individual nerve fibers relates to their diameters, myelin properties, and conductivity :
●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, three to five 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 temperature 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 .
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 A-alpha fibers conduct in the range of 65 to 70 m/s, whereas six to seven micron A-alpha 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, the number of muscle fibers innervated by the surviving motor nerve fibers is larger, and stimulation can result in a CMAP where the amplitude is normal or only mildly reduced. In this context, contributions from electromyography and motor unit number estimation techniques may be helpful. (See "Overview of electromyography" and 'Motor unit number estimates (MUNE)' below.)
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 and 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). 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 .
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 . The consensus criteria from the American Academy of Neurology, 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 . The American Association of Neuromuscular and Electrodiagnostic Medicine criteria define it as >30 percent increase in proximal versus distal CMAP duration . The relationship between increasing temporal dispersion and increasing length of nerve segment is approximately linear for motor conduction  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 . 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 . 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 . 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 . 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 .
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 . Sensory conduction is 5 to 10 percent faster than motor conduction for each mixed nerve segment .
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 [16,17]. They then plateau until ages 25 to 30 years and decline slowly thereafter at approximately 1 to 3 percent per decade . Decreases in median and ulnar sensory conduction velocities have been estimated at 0.13 to 0.21 m/s per year . 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 . The decline varies from nerve to nerve and is more pronounced for the SNAP than the CMAP (eg, 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) [15,20].
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 years and younger, whereas loss of responses was common in those aged 70 years and older . The sural nerve SNAP was most vulnerable, being absent in 24 percent of patients in their eighth decade and 40 percent in their ninth . However, in other studies, sural SNAPs were found in all subjects up to age 76  and to age 88 years . In addition, sural SNAPs were found in all normal subjects as old as age 90 years with near-nerve electrodes .
Height, body habitus, and sex — 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 . Conversely, age has a much greater effect than height on evoked potential amplitude .
Female subjects typically have faster conduction velocities than males, possibly due to height differences . The higher sural SNAP amplitudes seen in females may relate to differences in subcutaneous tissue at the ankle .
SNAP amplitudes declined with increasing body mass index in two studies but not in another [21,22,25]. 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 . 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 .
A study of healthy subjects confirmed the aforementioned effects of aging but found that correlations between NCS and height, weight, and sex varied among the nerves tested and that normative values varied among subjects from India, Malaysia, and China .
Temperature — The temperature of nerve segments undergoing testing has a significant effect on nerve conductivity and evoked potential amplitude . 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 
●Increased distal latencies, by 2.52 percent per degree Celsius 
●Decreased conduction velocities, by 1.2 to 2.4 m/s per degree Celsius [2,30]
Because of the large magnitude of these changes and their potential role in confounding result interpretation, standardization of temperature during testing is essential. The arm should be maintained at 34 to 36°C and the leg at 32 to 34°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 . Correction factors to compensate for low limb temperatures during testing are not recommended .
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 more deeply located or diseased nerves and when studying the H reflex.
With increasing stimulus strength, a threshold level for nerve firing 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 delivered through surface electrodes of 100 to 300 V, or 10 to 30 mA with a stimulus duration of 0.1 to 0.2 msec, 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 .
Surface electrodes are convenient to use and do not puncture the skin but require considerable stimulus strength (and hence some degree of discomfort) as they are at a distance from the underlying 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 [2,3,32].
Recording — Surface-recording electrodes are typically used to record the electrical activity resulting from nerve excitation. These electrodes, whether small reusable discs or disposable adhesive 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 distal 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 [33,34]. 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 [35,36]. (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 lower extremity sensory nerves with smaller normal amplitudes, especially in older people and in patients with axonal peripheral nerve disorders.
For clean and accurate recordings of these evoked potentials, neurophysiology instruments require a "ground electrode," usually applied between stimulating and recording electrodes, to serve as a reference point and minimize electrical interference .
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 .
Motor nerve conduction — In the peripheral nervous system, efferent motor nerve fibers are part of the motor unit , 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 . 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 .
During repetitive nerve stimulation testing, the CMAP amplitude or area is measured after a train of 4 to 10 stimuli is applied. (See "Electrodiagnostic evaluation of the neuromuscular junction", section on 'Repetitive nerve stimulation'.)
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):
●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
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 .
Upper limb position has long been recognized as affecting ulnar nerve motor conduction velocity calculations across the elbow . The standard position for upper limb recording is for the elbow to be flexed at 90 degrees . Lower limb position can also affect fibular motor nerve conduction across the knee and distal to the fibular head . 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, acquired inflammatory demyelinating polyneuropathies ) from those with disproportionate distal nerve conduction slowing (eg, polyneuropathy with antibodies against myelin-associated glycoproteins). The terminal latency index is a measure that combines distal latency and proximal conduction velocity to evaluate whether disproportionate distal slowing is present .
Sensory nerve conduction — Afferent sensory fibers, which have their cell body 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).
Late responses — The late responses are most useful for studying the proximal segments, the plexus and nerve roots, of the peripheral nervous system.
F wave — Electrical activity propagating proximally (antidromically) activates a small percentage of motor neurons (they "backfire"), which then can generate another wave known as the F wave (also called the F response). The F wave is a low-amplitude late potential generated by supramaximal nerve stimulation (waveform 1).
●Recording technique – F waves are recorded using surface electrodes over distal muscles in the same manner as motor nerve conduction studies. Supramaximal nerve stimulation is utilized with the stimulating cathode proximal to the anode to prevent anodal block of the antidromic potential.
It is important to record at least 10 to 20 F waves for analysis because individual F waves arise from different subpopulations of motor neurons and vary in configuration, amplitude, and latency .
If the stimulation site is moved proximally, the F wave latency will decrease by the same amount that the CMAP latency increases because the distance between that stimulation site and the motor neuron decreases while the distance to the recording electrodes increases. With more proximal stimulation sites, the F wave can be lost as it merges into the larger amplitude of the CMAP potential. Voluntary movement and repetitive nerve stimulation may activate F waves in patients with previously absent F waves secondary to immobility .
●Clinical significance – F waves may be the most sensitive electrodiagnostic test for nerve injury, since the potentials must traverse all components (antidromic plus orthodromic) of the motor nerve [47-49]. 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 [50,51].
F wave slowing may be seen in demyelinating, axonal, and mixed polyneuropathies [9,45,52]. In demyelinating polyneuropathies, there is decreased persistence of F waves with absent F waves in the presence of relatively preserved M responses .
The value of F waves in focal nerve lesions, such as radiculopathy, is controversial . F wave conduction along longer normal nerve segments may "dilute" any conduction delay across much shorter radicular segments . Since most peripheral nerves consist of axons from multiple nerve roots, with multiple innervations of the muscles undergoing recording, normal conductivity across unaffected roots may also dilute the abnormalities of the affected root.
Repeater F waves are frequently seen in amyotrophic lateral sclerosis (ALS) and are associated with the degree of lower motor neuron loss [54,55]. F wave latencies and chronodispersion are also increased in ALS .
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). 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 soleus H reflex decreases in amplitude with age but can be elicited in 92 percent of healthy people who are age 60 years and older .
●Recording technique – The amplitude of the H reflex is greatest just below the threshold for the appearance of the compound muscle action potential (CMAP). The H reflex disappears with maximal and supramaximal stimulation, replaced by the F wave, which has a slightly longer latency. The typical soleus H reflex latency is approximately 30 msec.
Stimulus durations of 0.5 to 1 msec are necessary for group 1a afferent fiber activation. As with the F wave, the stimulating cathode is proximal to the anode. Optimal cathode placement for eliciting the tibial H reflex occurs at the midpoint of the popliteal fossa crease . The tibial H reflex amplitude is greatest with the recording electrodes placed over the central soleus region . The median nerve H reflex is best recorded with the patient sitting with forearm pronation .
●Clinical significance – The H reflex is most commonly used to assess the S1 nerve root in suspected radiculopathies and to assess proximal conduction in polyneuropathies [61,62]. The H reflex improves the diagnostic sensitivity of standard neurophysiological tests in polyneuropathies . Unilateral absence of the H reflex or side-to-side differences of >1.5 to 2 msec support a focal nerve lesion on the affected side, most commonly at the S1 root, but also at the sacral plexus or sciatic nerve. Less frequently, the H reflex is also used to study central nervous system functions . Examples include the evaluation of spinal cord injury, multiple sclerosis, and intraoperative monitoring during thoracic spine and brainstem surgeries [65,66].
Blink reflex — The blink reflex is another true reflex . The afferent sensory arm is the first division of the trigeminal nerve and the efferent motor arm mediated by the facial nerve. The blink reflex can be abnormal in both peripheral and central lesions (eg, lesions of the brainstem or trigeminal or facial nerves). Evaluating the blink reflex may be useful in patients with demyelinating neuropathies where peripheral responses are unable to be obtained .
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 [41,68-70] or when different equipment is used. Special training may minimize intra-observer variability amongst experienced clinical neurophysiologists but does not eliminate inter-observer differences .
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 distribution; it has been suggested that nonparametric methodology using percentiles is more suitable in the determination of reference values [41,70,71]. Other statistical methods for determining reference values for electrodiagnostic tests are under study ; however, large neurophysiology laboratories are encouraged to develop their own normal values for their study population. For nerves with smaller normal amplitudes or less commonly tested nerves, side-to-side comparison can be helpful.
ABNORMAL FINDINGS — There are three main pathologic mechanisms affecting peripheral nerve:
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 largest fibers is manifested as a decrease in compound muscle action potential (CMAP) amplitude and a change in configuration (increased dispersion and increased number of phases) of the compound evoked potentials. In addition, loss of enough of these fibers causes slowing in the maximum conduction velocity and an increase in the distal latency. 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)  or 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 . A greater loss of fast conducting fibers could be responsible for greater conduction slowing. However, in lesions with pure axonal loss, the conduction slowing cannot go below 70 percent of the lower limits of normal , or 60 percent of the normal mean value for that particular nerve and segment . 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 usually 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 . 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 elbow
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) [12,13,75]. (See 'Conduction block' below.)
Unfortunately, the diagnosis of primary demyelination in an individual patient or nerve can be problematic because there is a wide range of normal values for the standard parameters of nerve conduction. In addition, slowed conduction velocities and prolonged distal latencies can also occur in axonal and focal entrapment disorders [52,76].
CMAP amplitude can be normal or reduced in demyelination and conduction block. With focal sites of demyelination and block, electrical stimulation distally will result in normal CMAP amplitudes if the motor 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 in temporal dispersion and conduction block are, in part, dependent upon CMAP amplitude [9,10]. 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 :
●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, and F-wave latency ≥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 .
Prolongation of the distal CMAP duration, due to abnormal temporal dispersion, can be an indication of distal demyelination; in isolation, this finding is not observed in axonal neuropathic disorders or in focal nerve compression syndromes (eg, carpal tunnel syndrome) [78-80]. 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 [78,80].
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) . However, the same report found abnormal distal CMAP prolongation affecting multiple nerves occurred in 39 percent of patients with chronic inflammatory demyelinating polyneuropathy .
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 . 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 [32,83,84]. Ultrasound positioning of the near-nerve recording electrode in sural nerve studies has been found superior to surface electrodes, especially in older adults .
There is no gold standard set of diagnostic criteria for the electrophysiologic identification of demyelination. Such criteria are difficult to devise . Multiple sets of criteria for chronic inflammatory demyelinating polyneuropathy exist, with wide variation in sensitivity and specificity [77,86-88]. (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 . (See "Chronic inflammatory demyelinating polyneuropathy: Etiology, clinical features, and diagnosis", section on 'Diagnostic pitfalls'.)
Conduction block — Conduction block can occur with compressive lesions and 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 .
Even in normal nerves, the effects of phase cancellation and temporal dispersion can lead to reduction in the CMAP amplitude and area, and increases in conduction velocity, 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 consensus criteria cite normal ranges of CMAP changes between distal and proximal stimulus sites for the more commonly tested nerves as follows :
●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 fibular 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 American Association of Neuromuscular and Electrodiagnostic Medicine consensus criteria for definite partial conduction block in multifocal motor neuropathy, assuming a minimal contribution of temporal dispersion (<30 percent), were the following [10,90]: in median and ulnar nerves, conduction block requires a reduction in CMAP amplitude of >50 percent over wrist to elbow segments, and, in fibular and tibial nerves, conduction block requires a reduction in CMAP of >60 percent over ankle to knee segments.
The American Academy of Neurology criteria are also used for motor nerves, which require only a >20 percent decline in CMAP negative peak-to-peak amplitude with <15 percent change in duration . A change in CMAP amplitude of ≥20 percent is often used in clinical practice. These criteria do not apply to stimulation across Erb's point and the tibial nerve.
While temporal dispersion and its attendant desynchronization and phase cancellation contribute little to the decline in CMAP amplitude and area 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 [16,91]. 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 . 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 . When CMAP area is considered, a drop of >50 percent denotes conduction block, independent of the amount of temporal dispersion .
The diagnosis of conduction block is complicated when distal CMAP amplitude is reduced. 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 most distal stimulus site and the recording electrode placed 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 situations, 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 . 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  or voluntary activity . This activity-dependent, or frequency-dependent, hyperpolarization blocks conduction when the safety factor is reduced . Axonal membrane hyperpolarization was found distal to the site of conduction block in multifocal motor neuropathy . 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) . 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 .
Conduction block can also be caused by mechanisms other than demyelination, such as sodium channel blockade or ischemia . In multifocal motor neuropathy, antibody interference with sodium movement across the nodal membrane may play a role in conduction block .
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 [12,75,95]. 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 [3,7]. Nonetheless, partial sensory conduction block has been demonstrated  and can occur in multifocal acquired demyelinating sensory and motor neuropathy (MADSAM; Lewis-Sumner syndrome) [99,100].
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 loss 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 . In demyelinating disorders, the NCS findings reflect conduction in affected nerve fibers .
The determination of underlying nerve pathology utilizing electrophysiologic studies is heavily dependent upon methodology. Utilizing studies from multiple nerves with both proximal and distal stimulation and including F-wave analysis is important. 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 [102,103]. 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 .
Indications for testing — NCS are invaluable in defining and determining peripheral nervous system function, dysfunction, and disease [104,105]. 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 . However, single nerve measurements may not be an adequate clinical trial outcome measure due to test-to-test variability .
While NCS can distinguish the type of pathophysiologic abnormalities of large myelinated fibers, they mostly 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 . 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 .
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 . The American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) supports use of electrodiagnostic testing in distal symmetric polyneuropathies for the following indications :
●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 [104,105]
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. They are an extension of the clinical evaluation. The AANEM recommends that NCS and electromyography should be performed and interpreted at the same time in the majority of situations . 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".)
Concurrent ultrasound — Concurrent use of neuromuscular ultrasound with nerve conduction studies (and electromyography) may improve diagnostic sensitivity in entrapment neuropathies (eg, median, ulnar, or peroneal nerves) and in localization of focal nerve pathology (eg, nerve enlargement and trauma). Ultrasound can identify abnormalities in vascular supply or overall cross-sectional area, confirm the anatomical course of the nerve, and reveal associated mass lesions or bony defects [109-112].
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 [113,114]. Composite scores may also be useful for the detection of subclinical nerve impairment .
In series of patients with generalized peripheral neuropathies, including patients with diabetes and those with chronic inflammatory demyelinating polyneuropathy, 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  and were the most sensitive indicator of early asymptomatic functional nerve worsening over time .
Motor unit number estimates (MUNE) — Methods to estimate the number of motor units were first developed from standard nerve conduction studies in commonly tested nerves such as the median, ulnar, and peroneal nerves. The size of the amplitude of the total compound muscle action potential (CMAP) represents the total number of motor units and corresponding muscle fibers activated by stimulation of a particular nerve.
By gradually increasing the stimulation intensity, the CMAP amplitude increases as additional motor units are recruited. Because of the phenomenon of phase cancellation, the increments cannot be simply counted and because the true number of motor units in a nerve is difficult to determine (eg, it is not possible to biopsy motor nerves), and a number of methods have been studied to reflect the number of motor units [118-120]. Normal values for the number of motor units in different nerve muscle-combinations have been determined for a number of different MUNE methods and, with most methods, a longitudinal decline in the number of motor units can be shown in diseases such as amyotrophic lateral sclerosis (ALS) [118,119].
In diseases such as ALS and other motor neuropathies and with normal aging, loss of motor units occurs with a compensatory process of collateral reinnervation occurring, which means the CMAP size does not fall linearly with loss of motor units. Knowledge of the number of remaining motor units represents a means of determining the pathology of motor unit loss, and MUNE is an active area of research with the potential to be used in clinical trials as a direct biomarker of motor unit loss.
There are several methods for determining the number of motor units using standard nerve conduction techniques. These include:
●Motor unit number index (MUNIX) [121-123]
●Multipoint incremental method 
●MScan-Fit and other techniques measuring the CMAP scan as the stimulus intensity is gradually increased 
●The neurophysiological index 
At present, no method has achieved widespread use nor has a method been incorporated in any of the multicenter international ALS trials.
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 .
NCS can be safely performed in patients with implanted cardiac pacemakers and cardioverter-defibrillators [128,129]. 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 .
Pain during the procedure can be problematic . One study found that providing patients with written information about the procedure beforehand reduced pain and anxiety during NCS . Using a stimulus duration of ≤0.2 msec and a stimulus rate of ≤1 Hz can reduce discomfort (these parameters exclude the typical repetitive stimulation done during neuromuscular junction testing).
Measures to avoid electrical injury — Safety procedures are necessary to minimize electrical leaks and injury with electrodiagnostic studies [127,131]. Most important are measures to insure proper grounding.
Additional measures for patients with cardiac pacemakers and implanted cardioverters-defibrillators include the following [129,131]:
●Do not perform electrodiagnostic studies on patients with external (transcutaneous) pacer wires and consider consulting with a cardiologist before performing studies on patients with an implantable automatic cardioverter-defibrillator.
●Do not stimulate within 6 inches (15 cm) of pacemakers or implantable cardioverter-defibrillators (eg, avoid ipsilateral proximal stimulation sites such as the axilla, Erb's point, and nerve roots).
●Ensure all ground electrodes are functional and 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.
●Medical emergency carts should be available.
SUMMARY AND RECOMMENDATIONS
●Neurophysiology – 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 nerve conduction parameters also vary with regard to specific nerves, nerve segments, individual patient characteristics, and temperature. (See 'Anatomy and normal neurophysiology' above.)
●Testing parameters – 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. (See 'Methodology' above.)
•Motor nerve conduction – Stimulation of motor fibers includes the anterior horn cell (motor neuron), its axon (motor nerve), terminal nerve branches, synapses, and all individual muscle fibers innervated by a motor unit. Motor nerve testing includes assessment of conduction velocity as well as CMAP latency, amplitude, area, and duration. (See 'Motor nerve conduction' above.)
•Sensory nerve conduction – Sensory nerve testing includes assessment of SNAP latency, amplitude, area, and duration. Conduction velocity in sensory nerves is derived by dividing conduction distance by conduction time between stimulating and recording electrodes because afferent sensory fibers do not have synapses within the peripheral nervous system. (See 'Sensory nerve conduction' above.)
•Late responses – The F wave and H reflex are late responses that are useful for studying the proximal segments, the plexus and nerve roots, of the peripheral nervous system. F waves are useful for evaluating peripheral neuropathies with predominantly proximal involvement in which distal conduction velocities may be normal early in the disease. The H reflex is useful for evaluating the S1 nerve root in suspected radiculopathies and proximal conduction in polyneuropathies. (See 'F wave' above and 'H reflex' above.)
•Concurrent electromyography – 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.)
●Abnormal findings – 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.
●Clinical applications – 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.)
●Complications – 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.)
ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledges Steven H Horowitz, MD, who contributed to earlier versions of this topic review.
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