Electrodiagnostic Studies

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Chapter 178 Electrodiagnostic Studies

The electrodiagnostic (EDX) is an important adjunct to the neurologic examination for diagnosis and management of disorders affecting the peripheral nervous system. Components of the EDX examination include (1) nerve conduction studies (NCSs), (2) needle electrode examination (NEE, or electromyogram), and (3) special studies (e.g., H reflexes, F waves). Each part of the examination has specific advantages and limitations. Diagnosis is best facilitated when these components are used in combination. Although all complete studies include at least an NCS and NEE, the relative value of each test varies depending on the goal of the examination.

A well-designed EDX study should be individualized to address a specific clinical question. Although many EDX laboratories have routine NCS/NEE protocols established by suspected pathology (e.g., cervical radiculopathy protocol, lumbosacral plexopathy protocol, peripheral polyneuropathy protocol), the patient’s history and examination should influence selection of motor and sensory NCSs and specific muscles to be sampled by NEE. Moreover, the study is often modified as it is being conducted based on important and occasionally unexpected findings. When performed in this manner, the EDX examination can facilitate localization, focus differential diagnosis, estimate lesion severity, and provide information useful for estimating prognosis in neuromuscular disorders.

Key Anatomy for Electrodiagnosis

An understanding of key aspects of peripheral nervous system (PNS) anatomy is required for planning and interpreting the results of an EDX study. The motor division of the PNS begins at the anterior horn cell within the spinal cord, whose axon projects outward into the ventral root. The sensory division begins distally along the dorsal root at the dorsal root ganglion, which is typically found within the ostium of the intervertebral foramen.¹ Thus, the dorsal (sensory) roots within the spinal canal are preganglionic. For this reason a lesion within the intraspinal canal (e.g., compression by an intervertebral disc) may damage the sensory fibers and cause clinical sensory symptoms, but the postganglionic fibers remain intact and unaffected for the purposes of sensory NCSs. By contrast, an intraspinal canal injury causing ventral (motor) root axon loss is postganglionic, and thus loss of sufficient motor fibers is measurable by motor NCSs and NEEs. This arrangement is of considerable value in localizing intraspinal canal injury electrodiagnostically.

The dorsal and ventral roots merge segmentally to form mixed spinal nerves, including 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal.² Once the spinal nerves emerge from the intervertebral foramen, they divide into the posterior primary rami, which supply the skin and intrinsic muscles of the posterior neck and back (including the paraspinal muscles) and the anterior primary rami. The anterior primary rami supply the brachial plexus and peripheral nerves of the arm at the cervical segment (Fig. 178-1), the anterolateral aspect of the trunk and the thoracic level, and the lumbosacral plexus and nerves of the leg at the lumbosacral level. Muscles supplied by a given spinal segment are referred to as a myotome, and sensory regions supplied by each spinal segment are referred to as dermatomes.

FIGURE 178-1 Basic anatomy of the peripheral nervous system.

The motor unit is the basic functional element of the motor PNS. It consists of the anterior horn cell, its axon, and all of the muscle fibers it innervates via neuromuscular junctions. The number of muscles fibers innervated by one motor neuron varies (e.g., 10:1 in the extraocular muscles and 2000:1 in the gastrocnemius muscle) and depends on the degree of fine-motor control required. Muscle is organized into fascicles, with the fibers of a single motor unit distributed randomly over as many as 100 different fascicles. Thus, a skeletal muscle consists of a mosaic fiber from 20 to 50 overlapping motor units.³ Analysis of the electrical activity of the motor units and their muscle fibers is the objective of the NEE.

Nerve Fiber Injury Types and Relevance

The EDX examination tests large myelinated nerve fibers, which can be subject to a range of injury. Regardless of whether nerve fibers are compressed, stretched, mechanically deformed, or lacerated, the damage manifests as either axon loss or demyelination, or a combination of the two. Axon loss produces conduction failure along the affected fibers. Of note, for several days after a focal axon loss lesion (2–3 days for motor fibers and 5–6 days for sensory fibers), the nerve fibers distal to the lesion can conduct an action potential when tested by NCSs, after which wallerian degeneration ultimately results in failure of the entire axon segment distal to the lesion site (5–7 days for motor fibers and 10–11 days for sensory fibers).⁴ In contrast, focal demyelination remains restricted to the injury site and only affects the largest myelinated nerve fibers, including motor fibers, and sensory fibers mediating vibration and proprioception. Focal demyelinating conduction block thus can only be demonstrated with NCS by stimulation proximal to the area of injury.⁵

When nerves are injured, the type and degree of axon loss or demyelination affects prognosis. Clinically useful scales rating the degree of nerve injury have been developed by Seddon ⁶ and Sunderland.⁷ Seddon divides focal nerve injuries into three broad categories by severity: neurapraxia, axonotmesis, and neurotmesis. Neurapraxia, the mildest injury type with the best prognosis, is transient and does not involve loss of nerve continuity. Underlying pathophysiology may include functional conduction block (without demyelination), mild demyelinating lesions, and demyelinating conduction block. Axonotmesis occurs when the nerve axon and myelin sheath are completely interrupted, while the surrounding endoneurium, perineurium, and epineurium remain intact. Prognosis in axonotmesis is better than in neurotmesis (loss of the axon and severance of its supporting connective tissue). Axon regeneration in neurotmesis is limited due to disruption of the conduit through which regenerating axons might extend to reinnervate their target organ. Sunderland’s classification system further divides these injury types, particularly with respect to the degree of supporting structure damage in neurotmesis. EDX testing can differentiate between neurapraxia and axonotmesis, providing useful prognostic information. However, axonotmesis and neurotmesis cannot be differentiated, because they appear identical electrodiagnostically.³

Components of the Electrodiagnostic Examination

Nerve Conduction Studies

NCSs can be divided into motor, sensory, and mixed studies (Fig. 178-2). Motor and sensory NCSs are considered part of a routine EDX evaluation, whereas mixed studies are typically used only in special situations (e.g., median, ulnar, or tibial nerve entrapment). Although both surface and needle electrodes can be used for stimulating and recording, most EDX laboratories select noninvasive surface electrodes for NCSs.

FIGURE 178-2 Basic nerve conduction studies performed on the median nerve. A, Motor nerve conduction studies, measured at the abductor pollicis brevis muscle. B, Sensory nerve conduction study measured at the second digit. C, Mixed study. R, recording site; S₁ and S₂, stimulation sites; X, stimulus artifact on each response tracing.

Motor Conduction Studies

Motor NCSs are typically performed using an “active” recording electrode over the center of a muscle belly and reference electrode distally over the tendon of the muscle (“the belly-tendon montage”). A two-pronged (anode-cathode) stimulator is placed over the nerve supplying the muscle, with the cathode oriented closer to the recording electrode. Current is applied over the nerve to induce an action potential in the underlying nerve fibers. As the current is gradually increased with each subsequent stimulation, action potentials are triggered in more nerve fibers, and in turn more muscle fiber action potentials are generated and recorded distally as a single compound muscle action potential (CMAP). When increases in amperage no longer augment the size of the CMAP (i.e., all axons within the nerve are being stimulated), one final increase in current by 20% is performed to achieve a “supramaximal stimulation,” and the resulting CMAP is recorded for analysis.⁸

Several key aspects of the CMAP waveform are analyzed (Fig. 178-3). First, the distal latency is measured in milliseconds from the stimulus artifact to the initial baseline deflection. This measurement combines the action potential travel time from the stimulus site to the neuromuscular junction (NMJ), time across the NMJ, and time required for the muscle fibers to depolarize. Note that this measurement only reflects the fastest conducting fibers (i.e., those that reach the recording electrode earliest and produce the initial baseline deflection). Second, the duration of the negative phase is assessed as a measure of muscle fiber discharge synchrony in response to the stimulus. Demyelinating lesions not severe enough to cause conduction block may slow motor fiber conduction to varying degrees within a stimulated nerve, resulting in dyssynchrony or “temporal dispersion,” increasing the CMAP duration. Third, the amplitude and area of the negative phase are measured, providing an index of the number of muscle fibers depolarizing within the range of the recording electrode. Although a reduction in CMAP amplitude (and area) is most often attributed to axon loss, demyelinating conduction block between the stimulus and recording site has the same effect.

FIGURE 178-3 Compound muscle action potential (left) and sensory nerve action potential (right) examples, both obtained from the median nerve. Note that by convention, deflection above the line is referred to as the “negative” phase and below the line as “positive.”

Further analysis of motor nerve conduction requires a second, more proximal stimulus over the nerve recording at the same location, using the technique just described. The more proximal stimulation is performed at a measured distance from the first. The difference between the proximal latency (PL) and distal latency (DL) in milliseconds reflects the conduction time along the fastest nerve fibers between the sites, eliminating the travel time from the distal site and across the NMJ, as well as muscle fiber depolarization time. The distance between the sites in millimeters divided by the nerve conduction time (i.e., PL minus DL) is known as the conduction velocity (Fig. 178-4). The configuration of the CMAP generated by the proximal stimulation is also compared with that of the distal CMAP. Assuming supramaximal stimulus at both sites, the CMAPs should be essentially identical. A proximal stimulation CMAP amplitude less than 50% of the distal CMAP amplitude is consistent with conduction block, or a very early focal axon loss lesion in which wallerian degeneration has not yet occurred.

FIGURE 178-4 Motor conduction velocity calculation example, performed on the median nerve. S₁ (distal) and S₂ (proximal) are stimulation sites, (–) is cathode and (+) is anode of the stimulator.

Sensory Conduction Studies

Sensory NCSs are performed with the two-pronged stimulator and pair of recording electrodes over the nerve. These studies may performed antidromically (stimulating proximally and recording adjacent to the sensory receptor) or orthodromically (stimulating distally and recording proximally). These responses are relatively small and are measured in microvolts (μV, 1/1000 of the unit used to measure a CMAP). As with motor NCSs, current is applied over the nerve to induce an action potential and is gradually increased with subsequent stimulations. At supramaximal stimulation, the combined action potentials of the sensory fibers are recorded as a sensory nerve action potential (SNAP). SNAP latency, duration, and amplitude are measured. Latency is measured to onset (representing the conduction of the fastest fibers) or, more commonly, to the peak of the negative deflection (see Fig. 178-3).⁸

Routine sensory NCSs in most laboratories include the median nerve (recorded over digit 2) and ulnar nerve (recorded over digit 5) in the arm and are supplemented by studies of the radial, dorsal ulnar cutaneous, lateral antebrachial cutaneous, medial antebrachial cutaneous, and median sensory responses recorded over digit 1 or 3, as indicated. In the leg the sural sensory response (recorded over the lateral ankle) is routine, and supplemented by the lateral/medial plantar, superficial peroneal, saphenous, and lateral femoral cutaneous sensory responses, depending on the clinical indication for the study. For example, the superficial peroneal SNAP is of particular importance when differentiating between an intraspinal canal lesion affecting the L5 root and a common peroneal mononeuropathy.

Particular advantages of NCSs compared with the NEEs include the ability to perform these studies with minimal patient cooperation (e.g., patients under anesthesia), provide key localizing information with regard to the sensory nerve fibers, and superior potential for identifying demyelinating lesions. It is, however, important to appreciate that NCSs only assess the large myelinated nerve fibers of the PNS, and thus disorders affecting only the smallest nerve fibers (e.g., small sensory fiber peripheral polyneuropathies) will not be demonstrated. NCSs are also relatively insensitive to motor axon loss compared with NEEs, underscoring the complementary nature of NCSs and NEEs.⁵

Needle Electrode Examination

The NEE allows rapid, widespread assessment of the motor component of the PNS. The procedure involves inserting an electrode into individual muscles and evaluating the insertional, spontaneous, and volitional electrical activity present, both visually on an oscilloscope, which displays voltage as a function of time, and aurally. NEE is particularly sensitive for identifying axon loss when compared with a motor NCS. Importantly, an optimal NEE requires patient cooperation and can be uncomfortable for patients, occasionally limiting its usefulness due to poor patient tolerance.

The first step of the NEE of a muscle is to evaluate “insertional activity,” which is generated by needle movement within a muscle at rest. When an electrode is quickly moved through normal muscle, the fibers depolarize, generating a brief burst of electrical activity lasting 100 to 200 msec. This finding confirms that the electrode is in viable muscle. Although increased insertional activity lasting more than 300 msec is nonspecific, it is the earliest NEE finding in a partially denervated muscle, typically consisting of unsustained trains of positive sharp waves. These spontaneous electrical potentials have a characteristic initial positive phase followed by a long negative phase. Conversely, insertional activity may be decreased or absent in chronic neuromuscular conditions because the muscle has been replaced by electrically silent fat and fibrous tissue.

Next, the examiner assesses for spontaneous electrical activity with the needle electrode at rest within the muscle. Normal muscle should be electrically silent during this phase. Fibrillation potentials are an important electrophysiologic marker of denervation. This form of spontaneous activity is characterized by regularly firing potentials, most commonly of a brief sharp spike configuration, derived from a single denervated muscle fiber. Larger-amplitude potentials are observed in acute disease ⁹ and are present in greater density in more severe disorders. Fibrillation potentials are sensitive to denervation because disruption of a single motor axon results in fibrillation of all muscle fibers within that motor unit. They can thus be seen when motor axon loss is insufficient to cause clinical weakness. Although these potentials are most commonly associated with injury to motor axons, they may also be found in inflammatory myopathies and rarely in other neuromuscular disorders. Importantly, in the setting of denervation, fibrillation potentials require an average of 21 days to appear after injury and persist until reinnervation occurs or the muscle fibers degenerate at around 18 to 24 months after axon loss.¹⁰

Other forms of spontaneous activity can be observed during the resting phase. Fasciculation potentials, which are irregularly firing spontaneous discharges of an entire motor unit, are a marker of nerve fiber irritation as opposed to denervation. Complex repetitive discharges, which are recurrent, cyclic discharges of a series of muscle fibers, are a marker of chronicity, typically seen in neurogenic or myopathic disorders of at least 6 months’ duration.³

During the activation phase of the NEE, the muscle is contracted in order to analyze the firing pattern and morphology of voluntarily generated motor unit action potentials (MUAPs). A MUAP represents the summed electrical activity produced by depolarization of the muscle fibers of a single motor unit within the range of the recording electrode. The force generated by a muscle is a function of the number of different MUAPs firing and the rate at which they fire. At minimal contraction, a single MUAP may be observed firing in a semirhythmic pattern at a basal rate of approximately 5 to10 Hz. As the patient is asked to gradually contract the muscle with greater force, a second MUAP is “recruited,” and the firing rates of both MUAPs are increased until a third MUAP is recruited, and so on. A normal ratio of firing frequency to the number of different MUAPs firing is approximately 5:1 (e.g., when the MUAP firing rate reaches 20 Hz, four different MUAPs should be identifiable).⁸ At maximal contraction, MUAPs overlap and create an interference pattern, in which no single motor unit can be distinguished.

The interference pattern is reduced at maximal patient effort when either MUAP activation (ability to increase the firing rate) or recruitment (ability to add motor units as the firing rate increases) is diminished. Reduced activation occurs when MUAPs fire in equally decreased numbers at a slow to moderate rate and is indicative of either suboptimal patient effort (e.g., intentional, or due to pain) or a disease state of the CNS (e.g., stroke, multiple sclerosis, or other upper motor neuron lesion). Conversely, abnormal recruitment is consistent with a lower motor neuron disorder. Reduced MUAP recruitment (i.e., a neurogenic firing pattern) is observed when motor units cannot be activated due to conduction block or axon loss. With fewer MUAPs capable of firing, the intact potentials fire at a faster rate in order to generate the force intended. When a sufficiently large number of motor axons are damaged, reduced recruitment is immediately apparent, unlike fibrillation potentials, which appear after an average of 3 weeks.

Finally, the morphology of the MUAPs is analyzed. In partial or gradual axon loss disorders, chronic neurogenic changes in the MUAP configuration can be appreciated after a period of 4 to 6 months. These changes occur due to collateral sprouting of the surviving motor axons, resulting in a greater number of muscle fibers belonging to each remaining motor unit. As more adjacent muscle fibers join the motor unit, the MUAP increases in duration and amplitude and appears more complex (polyphasic). Once present, these changes persist indefinitely and may be the sole evidence of a remote neurogenic injury.³

Late Responses

H Reflex

The H reflex is the electrophysiologic equivalent of the Achilles tendon muscle stretch reflex (“ankle jerk”) and is unique in its ability to assess the preganglionic sensory fibers of the S1 nerve root. The reflex is elicited by stimulating the tibial nerve within the popliteal fossa at a progressively greater stimulus intensity, while recording the soleus muscle. Beginning at a submaximal stimulus intensity, lower-threshold sensory fibers are discharged first, resulting in an afferent (proximally directed) action potential, which synapses at the anterior horn cells of the S1 root. This initiates an efferent (distally directed) motor action potential, which is recordable as an H response at the soleus muscle. As the strength of the stimulus intensity is increased by the examiner, the tibial motor fibers at the stimulation site are depolarized, directly resulting in a measurable direct motor response, the M wave. Further increases in stimulus intensity depolarize additional motor fibers and thus result in a progressively higher-amplitude M wave. Direct discharge of these motor fibers results in a lower-amplitude H response because the orthodromic H response is blocked by an antidromic motor fiber discharge from the stimulation site. At supramaximal stimulus, only the M wave is apparent.

The H response amplitude and latency can be compared contralaterally and to values in normal controls adjusted for age and height, providing evidence of nerve fiber injury within the S1 reflex arc. Although H reflex abnormalities are considered sensitive for root impingement caused by S1 radiculopathy, the finding lacks specificity, also being found in patients with polyneuropathy, proximal tibial or sciatic mononeuropathies, and lumbosacral plexopathy. Absent H reflexes are also commonly observed in patients older than age 65 and in patients with a history of lumbar laminectomy and are thus of unclear clinical significance in this context.¹¹ Overall, the usefulness of an absent H reflex is limited when the remainder of the EDX examination is within normal limits.

F waves

F waves ¹² are produced after a distal motor nerve stimulation. They can be measured during routine distal motor nerve conduction after reversing the stimulator orientation (the cathode is positioned proximal and the anode distal) and adjusting recording equipment settings to account for the low amplitude and long latency of these responses. F waves are different from H reflexes because they are conducted solely along motor axons, do not synapse within the spinal cord, and are thus not a measure of a true reflex arc. They are produced when some of the antidromic impulses cause a subpopulation of anterior horn cells to “backfire.” The resulting impulses travel back down the motor axons, and the latency of these late responses can be measured. These can be compared contralaterally and with height-adjusted normal values. A prolonged F wave latency is consistent with demyelination of the motor axon between the stimulus site and the recording muscle, as might be observed in acquired demyelinating polyradiculoneuropathy or demyelination in other causes or radiculopathy.⁵

Electrodiagnostic Localization of Spinal Disorders

Radiculopathy

Assessment for nerve root injury in patients with back pain radiating to a limb is a common reason for referral to EDX laboratories. Whereas imaging studies visualize the nerve roots and their relationship to the intervertebral discs, neuroforamina, and other associated structures, EDX studies provide important functional information, including the presence, severity, and acuity of axon loss and evidence of compensatory reinnervation. Moreover, structural causes of radiculopathy (e.g., a herniated intervertebral disc, impingement from spondylosis, epidural abscess, neoplasm) are most common, but imaging may be normal when the cause is infection, ischemia, inflammation, or microscopic neoplastic infiltration, and thus more effectively demonstrated by EDX studies.

Injury to a single spinal nerve root within the intraspinal canal usually results in normal sensory and motor NCSs. Since the lesion occurs proximal to the dorsal root ganglion (DRG), intact distal sensory fibers yield normal sensory conductions within the distribution of the suspected nerve root injury (Table 178-1). One important exception to this rule can occur at the L5 root, whose DRG can be found within the intraspinal canal in between 10% and 40% of patients.¹³ In these cases, an intraspinal canal lesion affecting the L5 level root (and DRG residing within the canal) causes loss of the superficial peroneal SNAP, complicating localization. Using the NEE to identify denervation changes within nonperoneal-innervated L5 muscles (e.g., gluteus medius, tensor fascia lata, semitendinosus, flexor digitorum longus, and tibialis posterior muscles) is required for proper localization in these cases. Motor NCSs are usually also normal, unless damage to a nerve root supplying the recording muscle results in sufficient axon loss to reduce the CMAP amplitude. Thus, the most important role of NCSs in radiculopathy evaluation is often to exclude mimicking causes, including plexopathy and mononeuropathy.

TABLE 178-1 Sensory Nerve Action Potentials (by Root)

Root	Sensory Response	Recording Site
C5 and C6	Lateral antebrachial cutaneous	Lateral forearm
C6	Radial	Thumb
C6	Median	Thumb
C6 and C7	Radial	Anatomic snuffbox
C6 and C7	Median	Index finger
C7	Median	Middle finger
C7 and C8	Median	Ring finger
C7 and C8	Ulnar	Ring finger
C8	Ulnar	Fifth digit
C8	Dorsal ulnar cutaneous	Dorsal forearm
T1	Medial antebrachial cutaneous	Medial forearm
L4	Saphenous	Medial ankle
L5	Superficial peroneal	Lateral ankle
S1	Sural	Posterior ankle

A lesion affecting the nerve root within the intraspinal canal will not affect the postganglionic sensory nerve action potential.

Abnormalities on NEE are identified in muscles innervated by the same spinal root, or myotome. Finding evidence of neurogenic injury in more than one muscle (ideally both proximal and distal muscles) supplied by different nerves sharing the same spinal root is central to NEE localization. However, only a subset of motor fibers within the nerve root undergoes axon degeneration in all but the most severe radiculopathies, and thus findings on NEE may be limited to a few muscles within the affected myotome. A myotomal map based on systematic studies of the various NEE patterns occurring with single cervical root lesions, as defined by surgical localization for the upper (Table 178-2)¹⁴ and lower (Table 178-3)¹⁵ extremity, is provided, arranged by root. Note that due to overlap, particularly between the C5 and C6, C6 and C7, and L3 and L4 myotomes, the ability to differentiate root lesions at these levels from one another is limited.

TABLE 178-2 Typically Affected Muscles in Cervical Radioculopathy (by Root)

Root	Abnormal Muscle	Nerve
C5 (or C6)	Supraspinatus	Suprascapular
	Infraspinatus	Suprascapular
	Deltoid	Axillary
	Biceps brachii	Musculocutaneous
	Brachioradialis	Radial
C7 (or C6)	Triceps	Radial
	Anconeus	Radial
	Pronator teres	Median
	Flexor carpi radialis	Median
C8	Extensor indicis proprius	Radial
	Flexor pollicis longus	Median
	First dorsal interosseous	Ulnar
	Abductor digiti minimi	Ulnar
T1 (or C8)	Abductor pollicis brevis	Median

TABLE 178-3 Typically Affected Muscles in Lumbosacral Radiculopathy (by Root)

Root	Abnormal Muscle	Nerve
L3-4	Iliopsoas	Femoral
	Adductor longus	Obturator
	Rectus femoris	Femoral
	Vastus lateralis	Femoral
	Vastus medialis	Femoral
L5	Gluteus medius	Superior gluteal nerve
	Tensor fascia lata	Superior gluteal nerve
	Semitendinosus	Sciatic (tibial division)
	Flexor digitorum longus	Tibial
	Tibialis posterior	Tibial
	Tibialis anterior	Peroneal (deep branch)
	Peroneus longus	Peroneal (superficial branch)
	Extensor hallucis longus	Peroneal (deep branch)
	Extensor digitorum brevis	Peroneal (deep branch)
S1	Gluteus maximus	Inferior gluteal nerve
	Biceps femoris, long head	Sciatic (tibial division)
	Biceps femoris, short head	Sciatic (peroneal division)
	Medial gastrocnemius	Tibial
	Lateral gastrocnemius	Tibial
	Abductor hallucis	Tibial
	Abductor digiti quinti	Tibial

NEE of the paraspinal muscles is also a routine component of the radiculopathy EDX assessment. Fibrillation potentials in the paraspinal muscles indicate axon loss affecting the posterior primary ramus of the spinal root, consistent with a lesion within or adjacent to the intraspinal canal (i.e., proximal to the brachial or lumbosacral plexus with regard to the arm or leg, respectively).¹⁰ However, due to the overlapping innervation of the paraspinal muscles, findings are not reliably segmental, often occurring caudal to the affected root. They are also not specific for radiculopathy, occurring in patients who have undergone prior spinal surgery via a posterior approach, motor neuron disease, or myopathy and in a portion of normal patients older than age 40. Thus, paraspinal fibrillation potentials cannot be interpreted in isolation and must be considered within the context of the rest of the EDX.¹¹

The specific pattern of neurogenic injury on NEE depends on the lesion duration and severity. During the first 3 weeks after nerve root injury, active motor axon loss changes (i.e., fibrillation potentials) are likely to be absent, particularly in distal limb muscles, resulting in false-negative studies in patients studied too early. Within a few months after localizing changes from active motor axon loss, the process of reinnervation begins. Early compensatory reinnervation is accomplished by collateral sprouting of the remaining intact fibers within a partially affected root and from adjacent nerve roots supplying the same myotome. In the earliest stages, the process is more effective proximally and progresses in a centrifugal fashion, beginning in the most proximal (e.g., paraspinal) muscles and gradually progressing to the distal limb muscles. As muscle fibers are reinnervated, fibrillation potentials cease, unless ongoing axon loss occurs. Thus, in a static radiculopathy (i.e., no additional axon loss), only the most distal muscles of the myotome may appear abnormal after several months. In mild nerve root injuries, the EDX findings may normalize with time. When more severe axon loss has occurred, reinnervation via collateral sprouting results in a larger number of muscle fibers within each motor unit and, in turn, longer-duration, increased-amplitude neurogenic MUAPs within the affected myotome.

Overall, the presence of fibrillation potentials in proximal and distal muscles of a myotome in the absence of chronic neurogenic MUAP changes is most consistent with a recent nerve root lesion. When chronic neurogenic MUAP changes and fibrillation potentials are both prominent within a myotome, either chronic progressive radiculopathy or an acute form superimposed on a more remote root lesion is likely. In contrast, chronic neurogenic motor unit potential changes limited to distal muscles of the myotome are supportive of a static, remote lesion.¹¹

Late responses can also be abnormal in patients with injury to a single nerve root. Since F responses assess conduction both distally and proximally, an abnormal F wave latency in combination with a normal standard distal NCS suggests proximal demyelination affecting the proximal portion of the nerve, plexus, or root supplying the recording muscle. The H reflex can be abnormal in a lesion affecting the S1 nerve root and may be prolonged in latency in demyelinating lesions or absent in patients with demyelinating conduction block or axon loss affecting this level. Importantly, an absent H reflex should not be interpreted in isolation, as this findings may be present in other disorders, including sacral plexopathy and polyneuropathy.

Case Examples

Case 1

A 49-year-old, right-handed woman presented with dysesthesias and weakness in the right upper extremity, starting immediately after a fall onto her outstretched arm 8 weeks prior. No fractures were discerned at the time of the injury. She had pain in the right side of her neck and shoulder, particularly when trying to raise the arm up over her head, and numbness in the right index finger and thumb. Her examination revealed mild weakness of shoulder abduction, elbow extension, and forearm pronation. Triceps reflex was lower on the right. The patient was referred for EDX testing to evaluate for cervical root injury versus brachial plexopathy. See Table 178-4 for EDX results.

TABLE 178-4 Electrodiagnostic Examination: 49-Year-Old, Right-Handed Woman

Impression

Acute right C6-7 radiculopathy was present.

Notes

The NCSs are within normal limits. Additional sensory NCSs were performed for exclusion of a brachial plexus lesion, including the lateral and medial antebrachial cutaneous SNAPs. Changes in the sensory NCS are the most sensitive indicator of axon loss affecting the brachial plexus (Fig. 178-5) and are useful for differentiating a brachial plexopathy from a radiculopathy. The NEE revealed fibrillation potentials and decreased recruitment throughout the proximal and distal C6 and C7 myotome, consistent with an acute lesion. There is no evidence of early compensatory reinnervation (i.e., increased duration MUAPs), consistent with a lesion of less than 3 months in duration.

FIGURE 178-5 Variations in compound muscle action potentials and sensory nerve action potentials. Comparing normal findings (1) with axon loss lesions of varying severity affecting the brachial plexus (2–4) and the roots within the intraspinal canal lesion (5).

Case 2

A 68-year-old, right-handed man presented with long-standing low back pain and more recent numbness of the top of the left foot of 4 weeks’ duration. Examination revealed mild weakness of the left ankle dorsiflexion, eversion, and toe extension and sensory loss over the dorsum of the left foot. The gait appeared normal, but the patient had some difficulty walking on his heels. The patient was referred for EDX testing to evaluate for lumbar root injury versus peroneal mononeuropathy. See Table 178-5 for the EDX results.

TABLE 178-5 Electrodiagnostic Examination: 68-Year-Old, Right-Handed Man

Impression

Subacute left L5 radiculopathy (bilateral chronic L5 radiculopathy) was present.

Notes

Superficial peroneal and sural sensory responses are within normal limits, the former reducing the odds of a significant axon loss lesion affecting the postganglionic fibers of the peroneal nerve on either side. The left peroneal CMAP (measured at both the extensor digitorum brevis and tibialis anterior muscles) is comparable to the right with regard to amplitude, and there is no evidence of conduction block or slowing across the fibular head, suggestive of a peroneal mononeuropathy at the knee segment. The NEE revealed decreased MUAP recruitment and neurogenic MUAPs in the L5 myotome bilaterally. There are fibrillation potentials in the distal left L5 myotome. These findings are consistent with long-standing bilateral L5 radiculopathies, with a more subacute lesion affecting the left L5 root.

Polyradiculopathy

Injury to multiple nerve roots within the intraspinal canal is associated with extensive degenerative changes affecting multiple spinal levels, as well as diabetes mellitus, infection (e.g., cytomegalovirus infection), or spinal root infiltration by a neoplastic process, among other causes. The pattern of abnormality is similar to that described for single-level radiculopathies; most importantly, the sensory NCSs are expected to be normal. However, motor NCSs are more likely to be reduced in amplitude when contiguous roots are injured, proportionate to the severity of axon loss to the root supplying the recording muscle. NEE reveals neurogenic changes in the affected myotomes.

Cervical Root Avulsion

Root avulsions in which the nerve root is severed from the spinal cord at one or more levels typically affect the cervical region and are associated with violent trauma in adults. Motor NCSs are severely reduced in amplitude or absent within the distribution of the avulsion. Similarly, the NEE reveals profuse fibrillation potentials and reduced to absent motor unit potential recruitment. Sensory NCSs from the same segment are normal in a “pure avulsion” because the injury occurs proximal to the dorsal root ganglia. However, relatively reduced sensory responses can occur due to presumed coincident damage to the postganglionic sensory fibers resulting from stretch injury. In these cases, precise localization is complex; however, complete segmental motor fiber axon loss and relatively mild or absent sensory fiber involvement are suggestive of avulsion within the proper clinical context.

Lumbar Canal Stenosis

There is no characteristic EDX finding indicative of stenosis of the lumbar canal. Abnormalities depend entirely on the severity and duration of axon loss present. Findings can range from evidence of severe bilateral (most often asymmetrical) lumbosacral radiculopathies to a relatively normal study. Due to potential involvement of the cauda equina, H reflex recordings and lower-extremity NEE should be performed bilaterally in cases of suspected lumbar canal stenosis.¹¹

Postoperative Electrodignostic Examination

EDX examinations are often obtained in patients who have already undergone spine surgery. When using the EDX examination in the postoperative setting, it is important to keep in mind that the diagnostic utility of an NCS and NEE changes with time from surgery.

Immediately after surgery (10–14 days), a new, severe axon loss lesion can be evidenced by an absent or significantly reduced amplitude motor response (ideally with a preoperative study comparison). A normal CMAP amplitude recorded from a clinically weak muscle (e.g., the tibialis anterior muscle in a patient with footdrop) can exclude motor axon loss as the cause. The remaining possibilities at this stage include proximal conduction block, a lesion affecting the CNS, and nonorganic causes. Active motor axon loss changes identified on NEE during this period must be attributed to lesions predating surgery because sufficient time has not passed for new changes to become apparent.

In the 3-week to 4-month postoperative period, evidence of new perioperative motor axon loss changes becomes apparent on NEE. This may not address whether a nerve root decompression was “successful,” because the typical EDX abnormalities caused by the preoperative root compression, including fibrillation potentials, may still be present during this period. However, any conduction block at the root level may resolve after decompression, resulting in a more normal MUAP recruitment pattern on NEE. In the case of an S1 radiculopathy, a previously absent H reflex may be found during this period.

In the remote postoperative period, active motor axon loss changes and their distribution in a given myotome can provide some helpful information. In particular, abundant fibrillation potentials within proximal and distal muscles of a myotome suggest the presence of ongoing or recurrent radiculopathy. As a general principle, the longer the time that has passed since surgery, the more likely that fibrillation potentials are caused by a progressive or postsurgical lesion. In contrast, chronic neurogenic motor unit potential changes may be permanent, particularly within the distal muscles, and may be the manifestation of a root injury 6 months to years prior.¹¹

Recommendations for the Referring Physician

To get the most out of an EDX examination, the following recommendations are offered for referring physicians:

1. Refer with a specific question in mind. A patient should be referred after a complete history and neurologic examination. The EDX examination can then be focused to facilitate localization and attempt to answer the clinical question of interest. Referring for a general survey of a limb may result in more extensive testing than is required and is less likely to yield useful results.

2. Keep the limitations of the test in mind. In particular, with regard to radiculopathies, the EDX examination cannot detect all compressive radiculopathies and therefore cannot be used to exclude the diagnosis. In this context, the examination is more useful for establishing the presence of a radiculopathy, estimating its acuity/severity, and excluding other potential localizations as described earlier.

Other important limitations apply to patients with extensive peripheral edema and morbid obesity. In these cases, an NCS may be unelicitable due to increased distance between the recording electrode and the target muscle or nerve, and ability to access certain muscles may not be possible even with the longest-needle electrode. In these cases, the diagnostic utility of the EDX examination is limited.

Finally, EDX localization can be more difficult in elderly patients. In particular, a portion of normal individuals older than age 60 have bilaterally unelicitable sural and superficial peroneal SNAPs.³ In these cases, differentiation between an intraspinal and extraspinal canal localization can be challenging, particularly in the absence of localizing active motor axon loss changes (e.g., fibrillation potentials) throughout a particular myotome. Thus, in older patients, normal aging, a mild chronic peripheral polyneuropathy, and mild bilateral chronic L5 and S1 radiculopathies may appear electrodiagnostically similar, even with contralateral comparison and evaluation of an upper extremity to assess for evidence of a gradient (i.e., suggestive of a length-dependent polyneuropathy).

3. Consider the onset of symptoms and timing of the examination. A 3-week waiting period after symptom onset is recommended prior to EDX examination in order to allow fibrillation potentials to develop, maximizing the localizing value of the test. Studying the patient as soon as feasible after the initial waiting period is also advisable, due to the tendency for the EDX examination to normalize with time.

4. Prepare patients for the test. Although testing is generally well tolerated by most patients, some degree of discomfort is inherent to both NCSs and NEEs. Patients should be made aware of this prior to their arrival at the EDX testing site. Also, the EDX laboratory should be contacted in advance to determine their procedures for managing special situations such as coagulation abnormalities, use of the medication warfarin, and patients with implantable electronic devices (e.g., spinal cord stimulators), as protocols vary.

Key References

Levin K.H. Electrodiagnostic approach to the patient with suspected radiculopathy. Neurol Clin. 2002;20:397-421. vi, 2002

Levin K.H., Lüders H. Comprehensive clinical neurophysiology. Philadelphia: WB Saunders; 2000.

Levin K.H., Maggiano H.J., Wilbourn A.J. Cervical radiculopathies: comparison of surgical and EMG localization of single-root lesions. Neurology. 1996;46:1022-1025.

Preston D.C., Shapiro B.E. Electromyography and neuromuscular disorders: clinical-electrophysiologic correlations, ed 2. Philadelphia: Butterworth-Heinemann; 2005.

Wilbourn A.J. AAEE case report #12: Common peroneal mononeuropathy at the fibular head. Muscle Nerve. 1986;9:825-836.

Wilbourn A.J. Nerve conduction studies. Types, components, abnormalities, and value in localization. Neurol Clin. 2002;20(305):38.

Wilbourn A.J., Aminoff M.J. AAEM minimonograph 32: the electrodiagnostic examination in patients with radiculopathies. American Association of Electrodiagnostic Medicine. Muscle Nerve. 1998;21:1612-1631.

References

The complete reference list is available online at expertconsult.com.