Author(s): Jason Kiene, MD, Andrew Hiett, MD
Originally published: September 9, 2015 Last updated: June 14, 2023
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Overview and Description

Fundamentals

Nerve Conduction Studies (NCSs) are a method to perform an extracellular recording of the intracellular process of neuron or muscle depolarization and action potential (AP) propagation along the axon or muscle fiber.1 This is performed by recording APs for all the axons that comprise a peripheral nerve. The recording of nerve signal transmission occurs at the surface of the skin using specialized electrodes. A ground electrode is used to help minimize electrical interference from the equipment, ambient surroundings and the patient. Contrary to popular teaching, the ground electrode does not direct stray charges away from the body and serves only to minimize interferences with the recording electrodes.2 The course of the specific peripheral nerve being studied is identified using anatomical landmarks and knowledge of neuroanatomy. A stimulator electrode, consisting of a cathode (negative pole) and anode (positive pole), is used to deliver an electrical stimulus of variable intensity and duration. A stimulus with sufficient strength to cause all of the axons to depolarize and propagate an AP is termed maximal stimulation. A supramaximal stimulation has a stimulus intensity approximately 20% above maximal stimulation to ensure that all axons have been evaluated in the study.1 The depolarization and subsequent AP propagation is detected by a recording electrode, referred to as G1 or “pick up” electrode, and the reference electrode, referred to as G2.1

Several pieces of information are collected from the resulting AP. Typically, a preset distance, the length in centimeters between the cathode of the stimulating electrode and the G1 electrode, is recorded. The time (in ms) that elapses between stimulus and depolarization is called the signal response latency.  The nerve conduction velocity (in m/s) is calculated from the measured distance and signal response latency.  The signal amplitude (measured in µV or mV) represents the maximal AP depolarization and voltage gradient of all depolarized fibers of a peripheral nerve. Amplitude is measured at the G1 electrode and is proportional to the number of axons present.

Motor NCS can be recorded by stimulating a mixed sensorimotor or pure motor nerve and recording over a muscle this nerve innervates. Sensory NCS can be recorded by stimulating a sensorimotor or pure sensory nerve and recording at a separate location on the same nerve. Normal values for each NCS are determined based on recordings and calculations in asymptomatic subjects. Historically, these values have been provider- or lab-specific.  However, in 2016, the American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) formed an initiative known as the Normative Data Task Force (NDTF). The NDTF conducted a study based on a set of rigorous, consensus-based methodological criteria to help standardize nerve conduction reference values across worldwide electrodiagnostic labs.3 As a result of these stringent criteria, a literature search was performed from 1990-2012 of published peer‐reviewed articles for 11 commonly assessed sensory and motor NCS.4 Using only those few studies that met the consensus criteria, the NDTF published what they considered to be a suitable resource for providers in an attempt to standardized NCS. Another advantage to the NDTF data is that it introduced standardized reference values across different demographics, including age, birth gender, height and weight, whereas many labs had only set reference values that did not take these differences into account.4

The summation of the motor neuron AP’s transmission through the neuromuscular junction, and subsequent muscle fiber AP is termed the Compound Motor Action Potential (CMAP). The CMAP includes information about the axon such as the number of afferent motor axons, diameter and degree of myelination. The CMAP can also provide information about the function of the neuromuscular junction (NMJ) and the number of excitable muscle fibers. The signal amplitude reflects the total number of motor neurons and muscle fibers that depolarize. The G1 electrode is placed over the muscle belly at the motor point, while the G2 electrode is placed over an electrically silent area, such as a tendon or bone. A stimulation is provided over the nerve, proximal to the G1 electrode.  The time from the stimulus to the initial deflection (distal or onset latency) is recorded for CMAPs only and reflects the myelin quality of the largest, fastest axons contained in the nerve.1 Because the G1 electrode is placed on the muscle belly, the response latencies include the time it takes for transmission across the unmyelinated, terminal axon and NMJ, as well as AP propagation through the muscle.  In order to calculate a conduction velocity of the CMAP, two stimulation sites (one proximal and one distal) need to be recorded.  The CMAP conduction velocity can be calculated along any proximal region of nerve using this calculation:

                           ddistal – dproximal
vconduction = _________________________
                           ldistal – lproximal

where d is distance in centimeters, and l is response latency in seconds.1

The time traveled through the unmyelinated terminal axon, the NMJ and the muscle AP will be constant between the two sites and subtracted out, allowing calculation of the conduction velocity of the segment of motor nerve between the two stimulation sites.

The summation of the sensory neuron APs of a peripheral nerve is termed the Sensory Nerve Action Potential (SNAP). In antidromic recordings, the stimulus is delivered opposite the direction of physiologic nerve transduction. An antidromic response in sensory NCS is proximal to distal. Orthodromic recordings measure AP propagation in the normal physiological direction. An orthodromic response in sensory NCS is distal to proximal. The more common method of recording SNAPs is antidromic, due to larger signal amplitudes and ease of recording.5 The G1 electrode is placed over the skin along the course of the nerve and the G2 electrode is placed 3-4 cm distal to G1 along the same course. In antidromic stimulation, the stimulating electrode is then placed proximal to G1 along the nerve with the cathode closer than the anode to G1.

Similar to a CMAP, the SNAP signal amplitude reflects the total number of neurons that depolarize. However, SNAP amplitudes are several orders of magnitude smaller and are measured in µV rather than mV. Both the onset response latency and peak response latency are useful for SNAPs.5 The peak response latency is helpful because it is more reliable and reproducible, particularly given the overall small amplitudes of a SNAP and reflects a variety of diameters of sensory nerve axons.1 The onset response latency reflects the AP propagation time for the largest, fastest sensory axons and is used to calculate the SNAP conduction velocity. Because the sensory nerve is myelinated and lacks a NMJ, the distance between cathode and G1 electrode is used for the numerator and the onset response latency is used as the denominator.

Proximal, or late, responses evaluate the proximal portions of the peripheral nerves.  Common late responses include the H-reflex and F-wave. The H-reflex is a monosynaptic reflex arc resulting from a submaximal, low intensity and high duration stimulation. Typically, this study is performed on the tibial nerve behind the knee. The H-reflex is orthodromic – starting with sensory fibers that travel proximally, synapsing in the spinal cord, reflexively triggering an AP in motor neurons that travel distally, where the recording electrode obtains the waveform. The H-reflex is typically used to test proximal S1 segments, but also has utility in the assessment of C6 or C7 radiculopathy by evaluating the C7 spinal reflex arc at the flexor carpi radialis.

In contrast, an F-wave is a pure motor study and generated from a supramaximal stimulation of distal motor neurons. The AP is transmitted proximally in an antidromic direction through a motor neuron to the spinal cord. In the spinal cord, the motor neuron synapses with an interneuron, which then sends the signal orthodromically back down the same motor nerve where the stimulus originated. The arrival of the signal at the distal muscle is seen at the recording electrode. F-waves are commonly obtained from ulnar, median, fibular (peroneal), and tibial nerves, but can be obtained from any peripheral nerve in the body that can be stimulated by the nerve stimulator. They have variable latencies, amplitudes and morphologies and may not appear with each stimulus but will generally fall within a set timeframe in healthy patients.

Common errors affecting accuracy

Above all else, technical errors can impact the accuracy of NCS findings. Examples include incorrect electrode placement, measurement errors, poor instrument maintenance, or the incorrect use of filters on the recording equipment. Operator error should be an electrodiagnostician’s first thought when unusual findings are recorded.

Decreased temperature leads to delayed Na+ channel inactivation and prolonged depolarization, which results in a larger voltage change and an increase in CMAP and SNAP signal amplitudes. The delay in Na+ channel inactivation will delay AP propagation and saltatory conduction, thus delaying onset response latencies and conduction velocities.1 These effects tend to be more prominent in SNAPs than in CMAPs.

A lack of supramaximal stimulation can lead to artificially low signal amplitudes.5 Too intense of a stimulus can lead to co-stimulation of adjacent nerves through volume conduction of the electrical signal in tissues, which may lead to artificially high signal amplitude or faster conduction velocities. A common indicator of volume conduction is a sudden change in waveform morphology from its traditional pattern after the stimulus intensity has been increased.  One typically sees this change after reaching maximum amplitude and increasing the intensity beyond supramaximal stimulation.  However, in smaller or leaner patients, volume conduction can also occur at low stimulus intensities.  In addition, too intense of a stimulus can enlarge the area of depolarization, leading to nerve activation further distal to the cathode at the time of stimulation, resulting in a decreased distal/onset latency.5

Improper electrode placement can lead to error for several reasons. If the G1 is not placed over the motor point, the amplitude will be artificially lowered, which could be misconstrued as an axonal problem. One may also see an initial positive deflection or variation from the typical waveform as evidence of an improperly placed G1 electrode. Additionally, in sensory studies, if G1 and G2 are too close or too far away, the resulting waveform can be affected.

Stimulating with the cathode distal to the anode can also produce error. This mistake, termed polarity reversal or anodal block, can artificially prolong latency and decrease conduction velocity measurements.6

Failure to account for patient height, weight, age and gender can also result in false positive or false negative results error.  Longer nerves, in general, have slower conduction velocities due to the smaller diameter of the nerve as they taper distally. Taller individuals may have slowed conduction velocities due to more tapering of the nerve and the tendency of recording NCS distally in the limbs. Furthermore, longer limbs tend to be cooler than shorter ones due to the physical limitations of euthermia resulting from arterial and venous flow.1 Obesity can also cause technical challenges. NCSs are more difficult to obtain in obese individuals, due to signal attenuation between the nerve and the skin’s surface where the stimulus originates. Conduction velocities tend to slow with age.  If using reference values for younger individuals, these velocities could be artificially construed as prolonged. The NDTF data takes into account all these factors.4

Anomalous innervations can also contribute to errors. Without prompt recognition, the presence of an accessory peroneal nerve, Martin-Gruber anastomosis (a median to ulnar anastomosis in the forearm) or other anatomic variation can lead to the false interpretation of normal findings as pathologic.1,5

Neuropathology – NCS correlation

Nerve conduction studies are commonly used to evaluate for specific nerve injuries or entrapments, but can also help with the diagnosis of polyneuropathies, myopathy or NMJ disorders. Lesions of the motor or sensory axon typically result in loss of CMAP and SNAP amplitudes. Decreased distal latency and conduction velocity is only seen when there is severe large fiber loss. While postsynaptic NMJ disorders tend to have normal latencies, amplitudes and conduction velocities, presynaptic NMJ disorders have variable CMAP amplitudes.

Lesions affecting myelin result in slowed conduction and can present with prolonged distal latencies for distal entrapments. Another feature of diseases or injuries to myelin is conduction block, which is defined as a drop in the amplitude during stimulation proximal to the lesion, but a normal amplitude on distal stimulation.7 This finding indicates that some of the individual axon’s impulses fail to traverse the area of injury, although that nerve is still alive, viable and able to be stimulated distal to the site of entrapment.

Temporal dispersion may also occur with demyelinating lesions. When some axons have slowed APs through a region and others conduct normally, the resultant waveform is one that is wider due to a larger difference between the conduction of the fastest and slowest fibers. Moreover, the spreading of AP velocities results in a lower amplitude, as the APs through the various nerves in the axon arrive at G1 at variable times and do not summate as they would if arriving at a more uniform time.1,5

Relevance to Clinical Practice

There is a wide variety of potential nerve conduction studies available for each patient. A history and physical examination prior to performing the study will lead to a differential diagnosis. The differential diagnosis will guide selection of appropriate sensory and motor nerve conduction studies as well as possible evaluation of proximal responses. Performing a routine nerve conduction “screen” is inappropriate as selection of specific studies should be tailored to each individual patient.8,9 Electrodiagnosticians should never lose sight of the fact that the NCS and EMG are an extension of their physical exams. NCSs are not diagnostic in isolation and should be accompanied by needle EMG.9 Using NCSs to make a diagnosis requires a detailed understanding of the history, physical exam, and interpretation of NCS and EMG findings.10

Nerve conduction studies are useful in evaluating for generalized neuropathies. In axonal neuropathies, the primary abnormality will be the loss of SNAP and CMAP amplitudes with proximal or distal testing. Prolongation of distal latency or decrease in conduction velocity will only occur after extensive large fiber loss and is only a secondary feature. In acquired demyelinating neuropathies, salient nerve conduction findings include prolonged distal latencies, decreased conduction velocities, and the presence of conduction block with proximal stimulation. Loss or prolongation of F-wave latencies and H-reflexes, as well as temporal dispersion, may also be seen. In congenital demyelinating neuropathies, similar findings are seen but without the features of conduction block or temporal dispersion.

The most common generalized neuropathy is diabetic peripheral neuropathy. While the entirety of the disease is beyond the scope of this review, there have been advances in the literature as it relates to NCS usage. First, an A1c >9% and the presence of neuropathic pain show a strong correlation with NCS pathology.11 Second, the development of pathology in NCS of diabetic neuropathy appear to follow a specific pattern of initially reduced sensory amplitudes and slowed motor velocities, followed by reduced motor and sensory amplitudes and prolonged motor latencies with disease progression.11 Moreover, studies have demonstrated that radial nerve SNAP abnormalities on NCS may be the most strongly correlated with peripheral neuropathy severity. Another study found that sural SNAP amplitudes had excellent utility for diagnosing diabetic peripheral neuropathy and could also be used to assess severity and progression of disease.12 This knowledge could serve as useful with regards to monitoring disease progression treatment response.13 Finally, for every 1% improvement in A1c, conduction velocity will improve by roughly 1.3 m/s.14

While less commonly used, the Blink Reflex is a way to use NCSs to assess the facial nerve.15 The blink reflex, first described by Kimura, has been used primarily for assessment of Bell’s palsy. In essence, it’s the “analogue to the physiologic corneal reflex.”16 One can use the blink reflex NCS to make quantitative assessments regarding the severity of an injury and the prognosis.16

Cutting Edge Concepts / Emerging Issues

Motor unit number estimation is a nerve conduction technique that is used in research settings to allow the estimation of the number of nerve axons in a motor nerve. Although primarily used in ALS research, its application could extend to other motor axonal disorders such as post-polio syndrome and radiculopathy. It might also be useful in evaluating nerve recovery after surgical repair. There are multiple methods of this technique which are time consuming and challenging to complete. Further techniques might be more useful in the clinical setting to be able to follow patients over time.17

There are ongoing studies investigating the total number of limbs required to diagnose a distal symmetric polyneuropathy.  Current practice is to include both lower limbs, but newer evidence suggests that this practice may lead to unnecessary studies and increased cost to health care systems, while providing limited diagnostic utility.18

While it is understood that NCS is the best method for quantitative information regarding the presence, severity, and prognosis of peripheral neuropathy,19 there is emerging evidence that ultrasound may be similar or superior in assessing median neuropathies at the wrist or ulnar neuropathies at the elbow.20,21 Furthermore, there is some suggestion that ultrasound may unveil median neuropathies at the wrist, which were not evident on NCS.21,22

Current research includes focus on developing normative values for more proximal nerve studies, including the axillary nerve,23 accessory nerve23 and medial femoral sensory nerve.24 The goal of these studies is to follow the NDTF guidelines3,4 to develop standardized reference values for these lesser-studied proximal nerves.

There is also research investigating the role of limb position and its affects conduction velocity across different limbs,25 as well as how anodal stimulation affects the waveforms and amplitudes of nerve conductions studies.6

Gaps in Knowledge/ Evidence Based

While the NDTF has published consensus guidelines on NCS standardization, the normative data is based on a relatively small number of studies that met inclusion criteria and much of the data came from a single lab.4 The limited literature should be confirmed via larger multicenter trials. Including few studies in the data means the normative values might not represent a diversified population. Another problem is the lack of normative nerve conduction reference data on patients older than 79 years old. However, the consensus guidelines will serve as an excellent roadmap for future research efforts on NCS standardization. Eliminating variance in how nerve conduction studies are performed and reported will allow for reproducibility and longitudinal evaluation that will allow NCS to be better compared to alternative testing methods.

There is some concern about the safety of EMG/NCS in patients with central lines due to the use of electricity. Most of the studies researching this question have low power, and more research is needed to confirm electrical safety in these patients.  Additionally, there is little data for electrical safety in patients with Swan-Ganz catheters.2

While newer research is investigating the use of ultrasound as a supplement to electrodiagnostic testing, this practice is limited to larger, tertiary centers. Routine use of ultrasound in conjunction with EMG/NCS may not be practical or cost-effective for an individual practitioner.  Additionally, ultrasound studies tend to have few participants.  More multi-center, high-powered studies are needed to determine use of ultrasound in obese individuals and to confirm previous studies performed on non-obese study participants.26

There remains concern about fraud, waste and the quality of nerve conduction studies.9,27 The use of handheld devices and mobile labs worsened these concerns as large numbers of nerves were tested without adherence to standardized protocols.8 Articles published by AANEM provide definitions as well as appropriate technique for electrodiagnostic studies. These articles also provide rationale for performance of NCSs and highlight that NCS should rarely be performed without subsequent needle EMG.9

Future directions

As mentioned previously, the current normative values are based around relatively few studies. A recent study examining cohorts with different ethnicities (Northern European, Northern Plains Indian, Latino), cohort did not appear to influence CMAP or SNAP amplitudes or distal latencies.28 Future studies should continue to investigate the role of ethnicity, age and birth gender in normative values for NCSs.

Over the last several decades, surgeons have made significant advances in using nerve transfers to treat denervated muscle from a variety of pathologies. Traditionally, electrodiagnosticians have assisted with diagnosis, localization, assessment of severity and prognosis of nerve injuries. As treatment options for these nerve injuries evolve, the electrodiagnostician will play an important role in monitoring nerve injury, determining surgical candidacy and tracking recovery after surgery.29

References

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  2. London ZN, Mundwiler A, Oral H, Gallagher GW. Nerve conduction studies are safe in patients with central venous catheters. Muscle Nerve. Aug 2017;56(2):321-323. doi:10.1002/mus.25497
  3. Dillingham T, Chen S, Andary M, et al. Establishing high-quality reference values for nerve conduction studies: A report from the normative data task force of the American Association Of Neuromuscular & Electrodiagnostic Medicine. Muscle Nerve. Sep 2016;54(3):366-70. doi:10.1002/mus.25204
  4. Chen S, Andary M, Buschbacher R, et al. Electrodiagnostic reference values for upper and lower limb nerve conduction studies in adult populations. Muscle Nerve. Sep 2016;54(3):371-7. doi:10.1002/mus.25203
  5. Dumitru D, Amato A, Zwarts M. Electrodiagnostic Medicine. Elsevier; 2001.
  6. Kanbayashi T, Yamauchi T, Miyaji Y, Sonoo M. Interaction of cathodal and anodal stimulations in nerve conduction studies. Muscle Nerve. Jun 2019;59(6):713-716. doi:10.1002/mus.26467
  7. Olney RK, Medicine AAoE. Guidelines in electrodiagnostic medicine. Consensus criteria for the diagnosis of partial conduction block. Muscle Nerve Suppl. 1999;8:S225-9.
  8. Committee PP. Proper Performance and Interpretation of Electrodiagnostic Studies: AANEM Position Statement. 2014. https://www.aanem.org/getmedia/bd1642ce-ec01-4271-8097-81e6e5752042/Position-Statement_Proper-Performance-of-EDX_-2014.pdf
  9. Proper Performance and Interpretation of Electrodiagnostic Studies. Muscle Nerve. May 2020;61(5):567-569. doi:10.1002/mus.26835
  10. Bland JDP. Nerve Conduction Studies for Carpal Tunnel Syndrome: Gold Standard or Unnecessary Evil? Orthopedics. Jul 01 2017;40(4):198. doi:10.3928/01477447-20170627-01
  11. de Souza RJ, de Souza A, Nagvekar MD. Nerve conduction studies in diabetics presymptomatic and symptomatic for diabetic polyneuropathy. J Diabetes Complications. Aug 2015;29(6):811-7. doi:10.1016/j.jdiacomp.2015.05.009
  12. Lai YR, Huang CC, Chiu WC, et al. Sural nerve sensory response in diabetic distal symmetrical polyneuropathy. Muscle Nerve. Jan 2020;61(1):88-94. doi:10.1002/mus.26739
  13. Zis P, Hadjivassiliou M, Rao DG, Sarrigiannis PG. Electrophysiological determinants of the clinical severity of axonal peripheral neuropathy. Muscle Nerve. Apr 2019;59(4):491-493. doi:10.1002/mus.26425
  14. Bansal V, Kalita J, Misra UK. Diabetic neuropathy. Postgrad Med J. Feb 2006;82(964):95-100. doi:10.1136/pgmj.2005.036137
  15. Kimura J. Assessment of Individual Nerves. Electrodiagnosis in Diseases of Nerve and Muscle. 2013.
  16. Hartmann JE. Blink Reflex. Encyclopedia of Otolaryngology, Head and Neck Surgery. Springer; 2013.
  17. Gooch CL, Doherty TJ, Chan KM, et al. Motor unit number estimation: a technology and literature review. Muscle Nerve. Dec 2014;50(6):884-93. doi:10.1002/mus.24442
  18. Dupuis JE, Li J, Callaghan BC, Reynolds EL, London ZN. Bilateral nerve conduction studies in the evaluation of distal symmetric polyneuropathy. Muscle Nerve. Sep 2019;60(3):305-307. doi:10.1002/mus.26616
  19. Shabeeb D, Najafi M, Hasanzadeh G, Hadian MR, Musa AE, Shirazi A. Electrophysiological measurements of diabetic peripheral neuropathy: A systematic review. Diabetes Metab Syndr. Jul 2018;12(4):591-600. doi:10.1016/j.dsx.2018.03.026
  20. Omejec G, Žgur T, Podnar S. Diagnostic accuracy of ultrasonographic and nerve conduction studies in ulnar neuropathy at the elbow. Clin Neurophysiol. Sep 2015;126(9):1797-804. doi:10.1016/j.clinph.2014.12.001
  21. Borire AA, Hughes AR, Lueck CJ, Colebatch JG, Krishnan AV. Sonographic differences in carpal tunnel syndrome with normal and abnormal nerve conduction studies. J Clin Neurosci. Dec 2016;34:77-80. doi:10.1016/j.jocn.2016.05.024
  22. Pelosi L, Leadbetter R, Mulroy E. Utility of neuromuscular ultrasound in the investigation of common mononeuropathies in everyday neurophysiology practice. Muscle Nerve. Apr 2021;63(4):467-471. doi:10.1002/mus.27124
  23. Day TJ. Optimal reference electrode placement for accessory and axillary nerve conduction studies. Muscle Nerve. May 2020;61(5):632-639. doi:10.1002/mus.26847
  24. Geney-Castro DE, Vanegas-Muñóz J, Plata-Contreras J, Salinas-Duran F. Medial femoral cutaneous nerve conduction study with distal recording: A novel technique. Muscle Nerve. Mar 2020;61(3):383-386. doi:10.1002/mus.26788
  25. Simon NG, Walker S. The role of limb position in the interpretation of nerve conduction studies. Muscle Nerve. Sep 2017;56(3):353-354. doi:10.1002/mus.25657
  26. Cartwright MS, White DL, Hollinger JS, Krzesniak-Swinarska M, Caress JB, Walker FO. Ultrasound guidance for sural nerve conduction studies. Muscle Nerve. Jun 2019;59(6):705-707. doi:10.1002/mus.26465
  27. Committee APP. Establishing standards for acceptable waveforms in nerve conduction studies. Muscle Nerve. Mar 2020;61(3):280-287. doi:10.1002/mus.26751
  28. Alhammad R, Davies J, Litchy WJ, Carter R, Dyck PJB, Dyck PJ. Variable differences of nerve conduction amplitudes versus velocities and distal latencies of healthy subjects assessed in ethnic cohorts. Muscle Nerve. Feb 2022;65(2):162-170. doi:10.1002/mus.27418
  29. Robinson LR, Binhammer P. Role of electrodiagnosis in nerve transfers for focal neuropathies and brachial plexopathies. Muscle Nerve. Feb 2022;65(2):137-146. doi:10.1002/mus.27376

Original Version of the Topic

Anthony Chiodo, MD, Michael Wheaton, MD. Nerve conduction velocities. 9/9/2015

Previous Revision(s) of the Topic

Jason Kiene, MD, David Sherwood, DO, Benjamin Westerhaus, MD. Nerve conduction velocities. 7/27/2020

Author Disclosure

Jason Kiene, MD
Nothing to Disclose

Andrew Hiett, MD
Nothing to Disclose