The Electrodiagnostic Examination

CHAPTER13 The Electrodiagnostic Examination

The electrodiagnostic examination comprises two parts: nerve conduction studies (NCS) and needle electrode examination (NEE). Together, they assess the peripheral sensory and motor nervous system. Sensory NCS assess the integrity of dorsal root ganglion (DRG) cells (usually residing within the intervertebral foramina), their axonal projections within mixed sensory and motor nerve trunks, and arborizations into individual nerve fibers innervating sensory organs subserving primarily vibration and proprioception. Motor NCS assess the integrity of anterior horn cells (in the anterior region of the spinal cord), their axonal projections within pure motor or mixed nerve trunks, arborizations into individual motor nerve fibers, the neuromuscular junctions, and attached muscle fibers.

The electrodiagnostic examination is best conceptualized as an extension of the neurologic examination of the peripheral nervous system. In the setting of abnormalities identified in the neurologic history and examination, the electrodiagnostic examination can be valuable in (1) confirming the clinical impression, (2) investigating the presence of other conditions in the differential diagnosis, and (3) localizing the precise site of a focal nerve trunk lesion not clearly defined on clinical examination.

The electrodiagnostic examination can discriminate between the two main types of pathologic responses that can affect nerve fibers: axon loss (neurotmesis and axonotmesis) and demyelinating conduction block (neurapraxia). In cases of axon loss, the electrodiagnostic examination has the potential of discriminating acute, subacute, and chronic nerve lesions. It can identify early evidence of reinnervation and can quantitatively track the reinnervation process over weeks to months. In the setting of diffuse signs and symptoms, the electrodiagnostic examination can discriminate among generalized sensory and motor peripheral polyneuropathy, myopathy, and diffuse motor axon loss processes such as motor neuron disease.

A well-executed electrodiagnostic examination can confirm or refute the presumptive diagnosis and can provide a screening assessment for other peripheral nerve and muscle conditions that could reasonably be the cause of the patient’s symptoms. In that way, the electrodiagnostic examination should be thought of as an electrodiagnostic consultation and not solely a test to rule in a specific diagnosis. Qualified electrodiagnostic consultants usually are board certified in electrodiagnosis, clinical neurophysiology, or neuromuscular medicine, having completed an approved training program and having shown competence by examination. The electrodiagnostic examination must be interpreted by the individual performing the study because there is no single machine-generated tracing (as would be the case for an electrocardiogram or electroencephalogram) that can be interpreted simply by reviewing data collected elsewhere.


The clinical practice of electrodiagnosis is based on numerous precepts that are derived from the pathophysiology of nerve and muscle function. These provide the basic principles that define the clinical utility and limits of this procedure.

Regardless of etiology, most focal nerve lesions—including lesions at the root level—result in either axon loss or demyelination. Axon loss produces nerve transmission failure along the affected fibers, whereas focal demyelination causes either conduction block or conduction slowing at the lesion site, depending on its severity. One fundamental difference between these two types of lesions is that focal demyelination remains localized and does not materially affect the segments of the axon proximal or distal to the lesion. In contrast, an axon loss lesion results in wallerian degeneration that eventually involves the entire course of the nerve affected.

Because axon loss and demyelinating conduction block stop nerve impulse transmission across the lesion site rather than merely slowing it, both can result in clinical weakness and sensory abnormalities whenever they affect a sufficient number of motor and sensory axons. Demyelinating conduction slowing does not affect muscle strength, however. This is because all of the nerve impulses ultimately reach their destination, although slightly later in time than they normally would.1

The electrodiagnostic examination assesses the integrity of large sensory and motor nerve fibers because the electrical fields generated by small nerve fibers are too small to reach the recording electrodes in routine studies. For this reason, pain alone cannot be assessed because that sensory modality is mediated through small C-type nerve fibers. When pain is associated with large nerve fiber dysfunction, such as weakness, electrodiagnostic testing is more valuable.

General Concepts of Electrodiagnostic Examination

Nerve Conduction Studies

NCS are the first component of the electrodiagnostic examination. During NCS, a peripheral nerve is stimulated resulting in an electrical response generated directly by the nerve itself (as in a sensory response) or the muscle it innervates (as in a motor response). The duration and intensity of the stimulus are gradually increased until a maximal response is generated. These responses are recorded using surface electrodes placed over the skin and then analyzed. During each study, valuable information is produced regarding the number of functioning nerve fibers, the speed of conduction along those fibers, and their relative rates of conduction.

Three basic types of NCS are available: motor, sensory, and mixed (Fig. 13–1). Motor and sensory NCS are generally performed on every patient. Mixed NCS are typically used in the evaluation of specific disorders, such as carpal tunnel syndrome, and are of limited value in the evaluation of spine-related nerve pathology. NCS protocols vary depending on the diagnosis in question and can be tailored to help exclude other diagnoses in the differential. Most electrodiagnostic laboratories have a routine protocol, however, for a general study of the upper extremity (Table 13–1) and lower extremity (Table 13–2).

TABLE 13–1 Nerve Conduction Studies in the Upper Limb

Motor Sensory
Median: thenar (C8, T1) Median: index (C6, C7)
Ulnar: hypothenar (C8, T1) Ulnar: fifth (C8)
Ulnar: first dorsal interosseus (C8, T1) Median: thumb (C6)
Radial: extensor indicis proprius (C8) Median: middle (C7)
Radial: brachioradialis (C5, C6) Ulnar: hand dorsum (C8)
Musculocutaneous: biceps (C5, C6) Radial: thumb base (C6, C7)
Axillary: deltoid (C5, C6) Lateral antebrachial cutaneous: forearm (C6)
  Medial antebrachial cutaneous: forearm (T1)

Note: On each line, the nerve being studied is listed first, followed after the colon by the recording site and then, in parentheses, the root innervation (motor) or derivation (sensory). Underlined root provides major innervation.

TABLE 13–2 Nerve Conduction Studies in the Lower Limb

Motor Sensory
Peroneal: extensor digitorum brevis (L5-S1) Sural: lateral ankle (S1)
Tibial: abductor hallucis (S1)  
Peroneal: tibialis anterior (L5) Superficial peroneal sensory: dorsum ankle (L5)
Tibial: abductor digiti quinti pedis (S1) Saphenous: medial ankle (L4)
Tibial: gastrocnemii (S1)* Lateral femoral cutaneous: lateral thigh (L3, L4)
Femoral: quadriceps (L3, L4)  

Note: On each line, the nerve being studied is listed first, followed after the colon by the recording site and then, in parentheses, the root innervation (motor) or derivation (sensory).

* M component of H response.

Studies technically difficult to perform.

Motor Nerve Conduction Studies

For motor NCS, the recording electrode is placed over the muscle belly, and the reference electrode is affixed over the tendon. The nerve supplying that muscle is stimulated, and the resulting motor nerve response is a compound muscle action potential (CMAP), a biphasic waveform that represents summated muscle fiber action potentials (Fig. 13–2). In routine motor NCS, small muscles of the hand and feet serve as recording muscles, and the nerves supplying them are stimulated at two separate points along their course. For the upper extremity, the wrist (distal) and elbow (proximal) are used as stimulation sites, and for the lower extremity, the ankle (distal) and knee (proximal) are used as stimulation sites.

Numerous parameters are assessed with each CMAP obtained, including amplitude, latency, and conduction velocity (Fig. 13–3). The CMAP amplitude represents the number of nerve fibers that responded to the stimulus and are capable of conducting impulses to the recorded muscle.1,2 It is measured from baseline to negative peak (negative being up) and reported in millivolts. The latency is the time interval between the instant the nerve was stimulated and the onset of CMAPs; these are reported in milliseconds. The conduction velocity is the speed of transmission over the fastest conducting nerve fibers assessed and is reported in meters per second. Conduction velocities are calculated by dividing the distance traveled along a nerve segment (as determined by surface measurements) by the latency difference between the responses to proximal and distal stimulation. Normal conduction velocity in the upper limb is greater than 50 m/sec; in the lower limb, it is greater than 40 m/sec.

Late Responses (H Responses and F Waves)

Two special studies, the H response and the F wave, are NCS used to measure the time in which nerve impulses travel proximally to the spinal cord along the peripheral nerve trunk and then back down the limb to the recorded muscle after distal stimulation of the nerve. Because the potentials seen with both of these techniques are much delayed after nerve stimulation compared with potentials seen with standard NCS, they are referred to as late responses.

The H response is the electrophysiologic correlate of the Achilles tendon reflex and is named after Hoffmann, who first described it in 1918. To obtain the H response, the tibial nerve is stimulated in the popliteal fossa using low voltage to activate sensory fibers (as opposed to motor fibers), which carry the nerve impulse proximally to the spinal cord (Fig. 13–4). The fibers synapse there with motor neuron cells to complete a monosynaptic reflex arc. The nerve impulse travels down the motor efferent nerve to the gastrocnemius where the recording electrode captures the response. Although the amplitude and the latency of the H response are analyzed, the amplitude is more reliable for diagnostic purposes in the authors’ laboratory.

The F wave was first described by Magladery and McDougall in 1950 and was named the F wave because it was first recorded from muscles in the foot. In contrast to H responses, F waves are not a component of a reflex arc because the nerve impulses recorded travel only along motor axons. F waves are produced when, after distal motor nerve stimulation, some of the impulses passing antidromically up the motor axons cause a few of the motor cell bodies in the anterior horns to backfire; the resulting nerve impulses travel back down the motor axons to produce submaximal muscle activations that are recorded several milliseconds after the initial CMAP as F waves. Several consecutive responses from the same muscle are elicited, and the shortest latency time usually is used for diagnosis. Also in contrast to H responses, F waves can be elicited with any of the standard motor NCS with consistency.

Needle Electrode Examination

NEE is the second and oldest component of the basic electrodiagnostic examination. During this procedure, a recording needle electrode is inserted into various muscles, and the electrical activity being generated in them is evaluated on a visual and audio display system via a differential amplifier. NEE records activity in muscle (1) at rest during needle insertion, (2) at rest without needle movement, and (3) during voluntary muscle activation.

At-Rest Phase

During the at-rest phase, electrical silence ordinarily is noted. Various types of spontaneous activity may appear, however, with neuromuscular pathology. Only three of these are relevant to spine-related nerve disease: fibrillation potentials, fasciculation potentials, and complex repetitive discharges.24

Fibrillation potentials are spontaneous, usually regularly firing action potentials of individual muscle fibers. Although nonspecific in that they can be seen with neuropathic and myopathic disorders, their presence indicates denervation. Fibrillation potentials typically appear in the form of a biphasic spike if the tip of the recording needle electrode is near the denervated muscle fiber; alternatively, they may appear as a positive sharp wave if the needle has injured the abnormal muscle fiber. In the setting of nerve lesions, fibrillation potentials are not present at the onset of motor axon loss. Instead, they are first seen 14 to 35 days after axon degeneration has been initiated; the most widely cited average time is 21 days. When established, fibrillation potentials persist until the denervated muscle fibers generating them either reinnervate or degenerate for lack of a nerve supply; the latter usually occurs 18 to 24 months after the initial nerve fiber injury.

Fibrillation potentials are the most reliable and objective manifestation of active or recent motor axon loss. They can be neither produced nor abolished voluntarily by the patient. They are very sensitive indicators of such loss because the degeneration of a single motor axon can result in hundreds of individual muscle fibers fibrillating within a given muscle, depending on the innervation ratio of the latter. Fibrillation potentials objectively can show that motor axon loss has occurred, when the lesion is far too mild in degree to produce clinical muscle weakness, atrophy, or loss of CMAP amplitude on motor NCS.3 Showing fibrillation potentials in a myotome distribution has been the principal method of identifying root lesions in the electrodiagnostic laboratory for more than half a century.5,6

Fasciculation potentials are spontaneous action potentials of an individual motor unit. In contrast to fibrillation potentials, they are indicative of motor unit irritation, rather than denervation; only intact motor unit potentials (MUPs) can generate them. They are encountered far less often than fibrillation potentials, being restricted essentially to radiculopathies, anterior horn cell disorders, radiation-induced plexopathies, a few entrapment neuropathies, polyneuropathies, and, most often, the syndrome of generalized benign fasciculations.

Complex repetitive discharges are produced when a single muscle fiber is depolarized and that depolarization is spread by ephaptic transmission to adjacent muscle fibers, which reactivate the initial muscle fiber. A recurrent cycle of firing is established. These potentials have a bizarre configuration and fire at high frequency. For many years, they were known as bizarre high-frequency discharges. Although they are abnormal, they are nonspecific, being seen with neuropathic and myopathic disorders. Generally, they appear when there is grouped atrophy (i.e., denervation, reinnervation, and subsequent denervation) and are evidence of chronicity. Although these potentials are not helpful in localization, they are frequently encountered on NEE of the cervical paraspinal muscles in patients with chronic cervical root lesions.3

Activation Phase

After the muscle is evaluated at rest, the patient is asked to contract the muscle. This contraction results in the generation of MUPs, which represent the summated electrical activity produced by contracting muscle fibers of a single motor unit. MUPs are assessed in regard to their recruitment pattern and appearance.


Recruitment of MUPs refers to the orderly increase in number and firing rate of activated motor units as force is increased during contraction of muscle. On initial activation of the muscle with minimal force, a single motor unit fires at its basal rate of 5 to 10 Hz. As the force is increased, additional units are recruited, and the firing rate gradually increases by 5 Hz with each additional unit—up to 20 to 30 Hz. With progressively increasing force, spatial and temporal recruitment occurs, resulting in a full interference pattern in which the screen is obscured by the firing patterns of several MUPs.

Reduced MUP recruitment, also known as a neurogenic MUP firing pattern, is observed whenever numerous motor units in the muscle being sampled cannot be activated on maximal effort because either conduction block or axon loss affects their axons. The fewer MUPs seen on maximal effort, the weaker the muscle is clinically. MUPs that are capable of firing are noted to do so in decreased numbers and often faster than their basal firing rate of 5 to 10 Hz.3,7 The rapid rate of firing of the still functioning motor units is important because, similar to fibrillation potentials, it is unequivocal evidence of involuntary interruption of motor axon impulse transmission. Conversely, if the muscle was weak because of an upper motor neuron lesion or because voluntary effort was simply submaximal (e.g., because of malingering or pain on activation), incomplete MUP activation would be seen—that is, MUPs would fire in equally decreased numbers but at a slow to moderate rate.


The amplitude, duration, and configuration of MUPs are important morphologic characteristics that are assessed during the activation phase. Together, these features reflect the number and size of muscle fibers within a motor unit and their ability to fire in synchrony. Patient age, technical details (e.g., filter setting, type of needle used), and the specific muscle being examined are some of the factors that affect the appearance of MUPs. Based on quantitative analyses, normal ranges for MUP morphology are available for comparison, which vary depending on the patient age and proximity of the muscle to the trunk. A normal MUP has a triphasic waveform appearance.

With chronic nerve lesions, the process of reinnervation of denervated muscle fibers can occur as the result of regeneration of the nerve trunk from the point of nerve transection or (when the nerve transection is not total) by collateral nerve branch sprouting from remaining intact nerve fibers close to the denervated muscle fibers. The latter process is much faster because nerve fiber regeneration occurs at the rate of about 1 mm/day. On NEE, manifestations of reinnervation include resolution of fibrillation potentials; return of activation of motor unit action potentials with voluntary muscle contraction; and appearance of polyphasic, enlarged (so-called neurogenic) motor unit action potentials, reflecting the increased number of muscle fibers attached to surviving nerve fibers owing to collateral sprouting.

Chronic neurogenic MUP changes generally develop about 4 to 6 months after an axon loss injury has occurred because it takes this much time for such configurational remodeling to occur. After chronic neurogenic MUP changes develop, they can persist indefinitely. With many remote, proximal neurogenic lesions (e.g., radiculopathies and particularly poliomyelitis), they are the sole electrical residuals detected during the entire electrodiagnostic examination.3,7,8

Electrodiagnostic Findings in Radiculopathy

The electrodiagnostic examination has been used to assess patients with possible radiculopathies for more than 50 years. Root lesions were one of the first focal peripheral nerve fiber disorders for which the diagnostic utility of NEE was shown.5,6 For many years, lumbosacral radiculopathies were the most common reason for referral to the electrodiagnostic laboratory.9,10 Although several other electrodiagnostic procedures have been introduced over the past half-century, NEE remains the mainstay for diagnosing radiculopathies. The amplitudes of motor NCS are also helpful when root damage is severe, extensive, or both.8,9

Radiculopathies are most commonly caused by nerve root compression secondary to degenerative spine changes, disc herniation, or rupture. The type of nerve pathology at the lesion site depends on the nature of the injury and degree of nerve compression. When the injury results in significant motor axon loss, NEE shows numerous abnormalities, including the presence of fibrillation potentials in corresponding myotomes. Demyelinating conduction block may also be inferred by findings on the electrodiagnostic examination. In many cases of nerve root disease, the electrodiagnostic examination can provide invaluable information regarding localization, severity, age of the lesion, and nerve pathophysiology.

Nerve Conduction Studies

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Jul 28, 2016 | Posted by in ORTHOPEDIC | Comments Off on The Electrodiagnostic Examination

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