The electrophysiological tests most commonly used are motor and sensory NCSs, including F-wave and H-reflex latency measurements; repetitive stimulation; somatosensory evoked potential (SSEP) tests; and needle EMG. Most often, a patient referred for electrophysiological testing will undergo at least two motor nerve conduction tests, at least two sensory conduction tests, and at least one limb needle EMG. The American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) has published evidence-based guidelines, which may be found on the AANEM website at www.aanem.org/Practice/Practice-Guidelines.aspx.² A review of the client’s history, a relevant systems review, and a physical examination guide the examiner in the selection and sequencing of appropriate tests. In other words, muscle strength and tone, sensation, range of motion (ROM), neurological signs, and cognition are crucial in selecting and administering electrophysiological tests. Electrophysiological testing is considered by all authors on the subject as an extension of the clinical examination.³^,⁴ It does not replace a careful history and physical examination of the patient. It does, however, establish the precise state of the nerves and muscles and can thus determine the location of a lesion more precisely than the clinical examination alone, particularly in cases of mild weakness or ill-defined sensory changes. In very clearly defined pathologies, electrophysiological tests are not necessary (except perhaps for medicolegal reasons). For example, in the case of a unilateral ankle dorsiflexion weakness coupled with a clearly defined L5 nerve root compression on magnetic resonance imaging (MRI) of the lumbar spine, the electrophysiological test may be of little added value. However, for a similar clinical presentation (foot drop) and no clear-cut imaging, the electrophysiological tests will differentiate between a peroneal palsy, a sciatic nerve neuropathy, a lumbosacral plexopathy, or an L5 radiculopathy.

Finally, evidence-based practice recommends that the practitioner have a good understanding of the implication of the sensitivity and specificity of each test to rule it in or out for a specific condition.⁵

Motor nerve conduction

In motor NCSs the peripheral nerve is stimulated at various sites and the evoked electrical response is recorded from a distal muscle supplied by the nerve (a measure of orthodromic conduction). Surface electrodes are usually used for both stimulating and recording. An example of electrode configuration for a motor NCS is shown in Figure 33-1 (ulnar nerve study). The response represents the electrical activity of muscle fibers under the recording electrodes and is called the compound muscle action potential (CMAP). It is also called the M wave or M response. Measurements are taken of the latency (the time in milliseconds required for the impulse to travel from each stimulus site to the recording site) and the amplitude of the response in millivolts (mV). The shape and duration of the response are assessed, and motor nerve conduction velocity is calculated for each segment of interest by dividing the distance between stimulus sites (in millimeters) by the difference in latency measured at each respective site.

Velocities, latencies, and the shape and amplitude of the responses (Figure 33-2) are studied and compared with established normal values and often with values taken from tests of the uninvolved extremity (when possible). In infants and children, nerve conduction is slower than in adults and reaches adult values by age 4 years.¹³ Nerve conduction velocities gradually slow after age 60 years but generally remain within the outer limits of normal.¹¹^,¹³

Figure 33-2 Velocities, latencies, and the shape and amplitude of the responses.

Sensory nerve conduction

Sensory nerve conduction can be measured from many superficial sensory nerves, such as the superficial radial and sural nerves. It can also be measured from mixed motor and sensory nerves. The stimulus is applied over the nerve in question, and the recordings taken from electrodes placed over a distal sensory branch of the nerve. The recordings are called sensory nerve action potentials (SNAPs). An example of recording and stimulation sites is shown in Figure 33-3. Both orthodromic and antidromic conduction can be assessed. Response latencies and amplitudes are measured, and sensory nerve conduction velocities are calculated for each segment by dividing the distance between two adjacent stimulus and recording sites, or two stimulus sites, by the latency (conduction time) between these same sites. Sensory nerve responses are considerably smaller than motor responses. Their amplitudes are generally measured in microvolts (μV). Sensory recordings are more sensitive than motor recordings in cases of mixed sensory-motor neuropathies.

Figure 33-3 Example of recording and stimulation sites.

F-wave latency

When a motor nerve is stimulated in the periphery, both orthodromic (peripherally to the muscle) and antidromic (centrally toward the spinal cord) impulses are generated. A proportion of the antidromic impulses will, as it were, “bounce off” the axon hillock and return as a recurrent discharge along the same neurons to activate the muscle from which the recording is taken. This activity is termed the F wave (Figure 33-4), and it is observed as a small wave occurring after the M wave.¹¹^,¹³^,¹⁴ No synapse is involved. Thus the F wave is not a reflex response, but rather only a measure of conduction along the motor neuron. Specific conditions of electropotential must exist at the soma-dendritic cell membrane to reactivate the efferent axon; therefore the occurrence of the F-wave response is inconsistent and variable in latency and waveform.¹⁵

The F-wave latency can be useful in evaluating conduction in conditions usually involving the proximal portions of the peripheral neurons (e.g., radiculopathy, Guillain-Barré syndrome [refer to Chapter 17], or thoracic outlet syndrome [refer to Chapter 18]). Its value, however, has been questioned by some authors because of its variability. Normal values of F-wave latency are 22 to 34 ms in the upper extremity (stimulating at the wrist) and 40 to 58 ms in the lower extremity (stimulating at the ankle), depending on the height of the subject, with a bilateral difference in latency of no greater than 1 ms.¹⁶

H-reflex response

The H-reflex response latency (Figure 33-5) is a measure of the time for action potentials elicited by stimulating a nerve in the periphery to be propagated centrally over the Ia afferent neurons to the spinal cord, to be transmitted across the synapse to alpha motor neurons, and then to travel distally over these neurons to activate the muscle. The response therefore measures conduction in both the afferent and efferent neurons.¹¹^,¹³ It is also referred to as a “late” response (the other being the F wave).

The H reflex is constant in latency and waveform, and it occurs with a stimulus usually below the threshold level required to elicit the M-wave response (Ia afferent fibers are larger in diameter than alpha motor neurons and thus more sensitive to electrical stimulation). This monosynaptic reflex response is most easily found by stimulating the tibial nerve at the popliteal area and recording from the soleus muscle. Braddom and Johnson ¹⁷ reported a mean latency of 29.8 ms (±2.74 ms) for the tibial nerve in normal adults, and a bilateral difference of no more than 1.2 ms. The H-reflex latency is a valuable measure of conduction over the S1 nerve root in differentiating suspected proximal plexopathy and radiculopathy from a herniated disc or foraminal impingement. Sabbahi and Khalil¹⁸ have reported a technique for recording the H reflex from the flexor carpi radialis muscle when stimulating the median nerve. In normal human beings older than 1 year, the H reflex is usually seen only in the tibial, femoral, and median nerves. It can be elicited from several nerves in infants and in conditions of CNS dysfunction in adults.

Repetitive stimulation tests

The repetitive nerve stimulation (RNS) test is used to evaluate transmission at the neuromuscular junction (motor synapse) in patients with diffuse weakness. RNS tests are helpful in the differential diagnosis of disorders such as myasthenia gravis and Lambert-Eaton myasthenic syndrome (LEMS). One protocol uses a series of supramaximal electrical stimuli applied to a peripheral nerve at a distal site (e.g., median or ulnar nerve at the wrist) at a rate of three to five per second for five to seven responses. Changes in amplitude of the muscle response are assessed. Precise technical requirements are specified to prevent movement artifacts and other testing errors. Detailed descriptions of the RNS test can be found in other texts.¹¹^,¹⁹ Under normal conditions the amplitude does not change more than 10% from that of the initial response in a series of 10 stimuli recorded before and after resistive exercise. An amplitude decrease in the fifth or sixth response of more than 10% is considered abnormal and is compatible with a physiological defect at the postsynaptic receptor site of the neuromuscular junction, as in myasthenia gravis.

In another RNS protocol, stimuli are applied to a nerve, first at a slow rate, then at a faster rate, usually 10 to 20 per second for up to 10 seconds. Normally, the amplitude can decrease up to 40% from the initial amplitude. In some defects at the presynaptic site, the response may be lower than normal during a slow stimulation rate but show a significant amplitude increase at the higher rate. Increases in amplitude greater than 100% over the initial response are consistent with presynaptic neuromuscular junction defects such as seen in LEMS, which has a strong association with small-cell bronchogenic carcinoma, and in botulism. In 1957 Eaton and Lambert ²⁰ reported this phenomenon as a myasthenic syndrome.

Gilchrist and Sanders ²¹ reported another protocol referred to as a double-step RNS test. This test measures amplitude before and after a temporarily induced ischemia of the extremity. They found the double-step RNS test to be slightly more sensitive than the routine RNS test, but only 60% as sensitive as the SFEMG technique. The RNS test is a good alternative test for neuromuscular transmission when the SFEMG is not available, but the examiner must meticulously adhere to technical details when conducting the test.

Blink reflex

In some conditions (e.g., facial palsy) or to establish the presence of a widespread neuropathy, it may be necessary to assess the conduction in the cranial nerves. The stimulation of the supraorbital nerve (branch of the trigeminal nerve, cranial nerve V) elicits two separate responses of the orbicularis oculi muscles, one early and ipsilateral (R1) and one late and bilateral (R2), via the facial nerve (cranial nerve VII). The early R1 response involves a synapse in the pons, whereas the late bilateral R2 responses involve a more complex pathway involving the pons and lateral medulla. Analysis of the respective latencies of each response will help in determination of the following:

Trigeminal neuralgia (cranial nerve V) or Guillain-Barré: all responses delayed

Acoustic neuroma or Bell palsy (cranial nerve VII): ipsilateral responses delayed

Pontine lesion: absence of R1

Medullar lesion: absence of R2

Others

Hence, the blink reflex is a nerve conduction test that assesses a portion of the CNS and has shown some utility in assisting in the diagnosis of multiple sclerosis (see Chapter 19) and Wallenberg syndrome.⁷

Clinical evoked potentials

Electrical potentials elicited by stimulation of nerves or sense organs in the periphery can be recorded from various sites as the impulses are transmitted centrally along the neuronal pathway and from the representative area of the brain.¹¹^,^22–24 SSEP procedures are particularly useful in assessing the integrity of afferent pathways in the CNS. They are helpful in differentiating among lesions in areas such as the plexus, spinal cord, brain stem, thalamus, and cerebral cortex. Evoked potential tests have the advantage of providing data about the integrity of both peripheral and central neuronal pathways, including transmission across axodendritic synapses.

The SSEP is valuable in assessing damage and continuity of spinal cord tracts in early spinal cord injury (SCI). For example, if an electrical stimulus is applied at the popliteal area over the tibial nerve, responses can be recorded with surface electrodes placed over the spine at the L3 and C7 spinal segments and from the lumbar representation of the contralateral sensory cortical area. Conduction time and other parameters of the response waveforms can be measured from the recordings.

This simplified example of an SSEP illustrates how conduction over sensory peripheral nerves and afferent pathways to the cerebrum can be studied. The median nerve is usually tested to evaluate the integrity of peripheral and central pathways and their synaptic connections as the impulses travel from the upper extremity to the contralateral cortical area.

In visual evoked potential (VEP) procedures, visual stimuli such as variable light flashes of changing patterns are applied to one or both eyes under highly controlled conditions. The response is recorded from the scalp over the representative area of the cerebral cortex.¹¹^,²³^,²⁴ The term pattern reversal evoked potentials (PREPs), a more descriptive term for these procedures, is recommended by the American Electroencephalographic Society.²² These tests and other VEP procedures are useful in assessing pathology of retinal photoreceptors, the optic nerve, and postchiasmal pathways. Abnormal conduction findings have been reported when VEP studies are used in demyelinating disorders such as multiple sclerosis and optic neuritis. The examiner may conclude that the patient is cortically blind because no response is recorded on the visual cortex. Although many causes for a stimulus not reaching the visual cortex are possible, the end result is considered blindness. If the cause for cortical inactivity is swelling or a neurochemical imbalance within a nuclear relay structure, once corrected, the individual may experience normal vision. A change in the reaction of the patient to the visual environment may reflect increased awareness and a change in coma scale rating. Similarly, just because an individual turns toward a light or visual stimulus does not mean an evoked potential reaches the visual cortex. Instead, the eyes as receptors and the visual tract to the brain stem may be intact even though a problem in the synaptic connections between or within the thalamus and visual cortex may exist.

Auditory evoked potential tests are used to evaluate neurological function of the cochlear division of the auditory nerve (eighth cranial nerve), central auditory pathways and synapses in the brain stem, and the receptor areas on the cerebral cortex.¹¹^,^22–24 Brain stem auditory evoked potentials are frequently referred to as BAEPs. A series of high-intensity clicks is applied to auditory receptors in the ears through headphones, and several components of the response waveforms are recorded by using surface electrodes over the representative cortical areas. The BAEP is an effective test procedure for localizing and evaluating acoustic neuromas and other space-occupying lesions in the brain stem. This test is also used for assessment of brain damage in patients who are comatose as a result of traumatic brain injury (TBI). Robinson and Rudge²⁵ recommend caution in using BAEP tests for this purpose because other factors, such as defective receptor organs, can cause abnormalities in BAEPs.

The evoked potential tests described in this chapter all require application of appropriate external stimuli that are rapidly repeated many times. The response is electronically averaged to sort out the desired signal from interference signals. The conduction times (latencies), waveform shape and amplitude, and sometimes conduction velocities are measured and compared with normal values. Absence of a response, increased latencies, decreased amplitudes, and slowing of conduction velocities are all abnormal findings. Normal values and details of techniques for the evoked potential tests are described elsewhere.¹¹^,^22–24

Therapists with special interest and training administer the SSEP tests for neurological applications more frequently than other types of evoked potential tests. Because of the highly specialized techniques necessary to administer VEP tests for ophthalmological applications and BAEP tests for hearing dysfunction, they are usually performed by persons who specialize in these procedures.

Needle electromyography

Needle EMG complements the motor and sensory NCSs; it is most sensitive in the detection of denervation.

Unlike NCSs, which use the electrical stimulation of the motor nerves to elicit muscle contraction, the needle EMG is used to record and analyze muscle activity at rest and during voluntary activation. It is particularly useful in identifying pathology of the lower motor neurons and of the muscle itself. EMG can also be used to identify abnormalities of motor neuron recruitment that are associated with certain disorders of the CNS especially when NCS findings are normal—as would be the case in radiculopathies. The primary recording studied is the insertional activity, along with activity at rest and the motor unit action potential (MUAP), which is produced by the depolarization of single motor units during voluntary or reflex activity. Spontaneous electrical activity of single muscle fibers at rest is termed fibrillation and is diagnostic of denervation. For recording of muscle activity, small-diameter needles are inserted within the muscles to be studied. Three electrodes are required: active (negative), reference (positive), and ground. The needles may be monopolar, requiring a second needle or surface electrode for reference, or bipolar, containing both the active and reference electrodes (usually concentric in cross section). The ground electrode is typically placed on the surface of the skin. Most commonly the needles used are disposable. The activity detected in the muscle is displayed on the video display terminal of a computer (and can be stored and printed later). It is simultaneously played through an audio amplifier. The electromyographer can often identify pathological conditions by the characteristic “sounds” of the electrical activity of the muscle. Many excellent resources are available for readers interested in details of the equipment and procedures for EMG.9–11^,²⁶^,²⁷ Details of contraindications and special precautions are described by Currier and colleagues.²⁷

In an EMG examination, four conditions are evaluated at each location: (1) activity during needle insertion (normally a brief burst (250 ms) of high-frequency activity that abates when the needle ceases motion), (2) activity during rest (electrical silence is normal unless an electrode is placed directly over a motor endplate), (3) activity during minimal and gradually increasing voluntary contraction (biphasic or triphasic MUAPs of small amplitude composed of slow-twitch type I fibers that increase in frequency and are joined by higher-amplitude potentials as larger, predominantly fast-twitch type II motor units are recruited), and (4) activity during maximal activation (an interference pattern caused by the blending of potentials in which individual MUAPs cannot be identified), characterized as full (complete), reduced, or absent. Several locations in an individual muscle may be studied. The specific muscles to be studied are determined by clinical findings, and results must always be interpreted in the context of the total complex of signs and symptoms. In determining the specific location of a lesion, muscles located both proximally and distally to the suspected lesion site must be assessed. Studies may be repeated at intervals to determine if changes consistent with recovery (such as reinnervation) or exacerbation are present. EMG is typically used to help determine the presence (and extent) of the following:

Denervation

Reinnervation

Myopathic or neuropathic signs

Distribution or specific location of peripheral nerve pathology

Needle EMG is sensitive in determining the state of the axons. When axons are interrupted, there is denervation of the muscle cell. The findings in denervation and partial denervation include increased insertional activity, fibrillation potentials or positive sharp waves at rest, and a reduced or absent interference pattern. CNS dysfunction can result in no resting potentials, but if motor control was impaired a decreased or abnormal interference pattern might be apparent because of difficulty in recruitment (Figure 33-6). Needle EMG also informs the clinician about muscle cell disorders such as myopathies. The primary finding in the case of a myopathy is fibrillation potentials and small-amplitude polyphasic MUAPs.

Figure 33-6 Typical findings in lower and upper motor neuron disorders and myogenic lesions. Myotonia shares many features common to myopathy in general in addition to myotonic discharges triggered by insertion of the needle or with voluntary effort to contract the muscle. Polymyositis shows combined features of myopathy and neuropathy, including (1) prolonged insertional activity, (2) abundant spontaneous discharges, (3) low-amplitude, short-duration, polyphasic motor unit potentials, and (4) early recruitment leading to a low-amplitude, full-interference pattern. (From Kimura J: *Electrodiagnosis in diseases of nerve and muscle: principles and practice,* ed 3, New York, 2001, Oxford University Press.)

Although client cooperation during EMG testing is important, some aspects of muscle electrical activity can be studied in the client who is very young (infant), who is unable to move, or who has only involuntary or reflex activity. Insertional and resting potentials can always be evaluated. MUAPs appear during the contraction of muscle fibers activated both voluntarily and involuntarily in both isotonic or isometric conditions. In normal conditions MUAPs are seen with voluntary movement; however, reflex activation of muscle also produces MUAPs with certain normal characteristics. In CNS disorders hypertonic or spastic muscles will produce recognizable MUAPs when they are actively contracting. The electromyographer can elicit a contraction by tapping on the muscle or tendon. For example, consider a client who is recovering from a traumatic head injury with residual spastic hemiplegia. She is unable to cooperate with the EMG exam. The client has abnormal extensor responses in the lower extremity with the exception of the ankle and foot, which appear flaccid. An EMG of the leg and foot muscles detects abnormal resting potentials, including fibrillation and positive sharp waves in muscles innervated by the peroneal nerve. Tapping on the muscles fails to elicit MUAPs. Muscles in the tibial nerve distribution have no resting potentials and respond with bursts of identifiable MUAPs when the tendon is tapped. These findings would guide the physician and therapist in looking for a possible peripheral nerve lesion in addition to the CNS dysfunction. The treatment program in this situation would differ from that for a client without peripheral nerve pathology.

In summary, results of the needle EMG are best presented in the form of a table that indicates the following:

Insertional activity: may be increased in acute denervation and myopathic processes

Spontaneous activity at rest: present (positive sharp waves and fibrillation potentials) in denervation

Fasciculations: may be present in motor neuron disorders

Analysis of MUAPs:

• Amplitude: Low amplitude is seen in myopathy or nascent potential; large amplitude is a sign of chronicity.

• Phases: Normal MUAPs are biphasic or triphasic. Polyphasia is indicative of denervation-reinnervation.

• Recruitment pattern: A less-than-full recruitment is indicative of fewer motor units discharging, as can be seen in axon loss.

• Firing rate: If elevated, fewer motor units are contracting more often to provide the same tension in a denervated muscle.

Justification and analysis of the basic principles and results after EMG studies should assist therapists managing clients with neurological dysfunction in planning and modifying therapeutic management programs. As electrical tests are being conducted, the findings are continuously studied and used by the physician and examiner as a guide in continuing with or modifying the plan for future tests based on whether they fit the characteristics usually identified with specific pathological conditions. As previously stated, the results of the electrodiagnostic tests must be correlated with other clinical findings and data.

Summary of clinical electroneuromyographic and nerve conduction studies

Instruments with computer-assisted analysis are now commonplace for studying electromyographic signals in great detail.¹¹^,^28–30 Parameters of the waveform, including amplitude, duration, frequency spectrum, number of turns, or phase polarity reversals and area (the integral or total voltage of the waveform) can be automatically analyzed. The data are then compared electronically with predetermined patterns of electrical changes, which correlate with categories of neuromuscular disorders such as myelopathies and neuropathies.

The following is a summary of the more characteristic EMG and nerve conduction changes associated with selected groupings of neurological disorders. The intent is to assist in the understanding of reports of these studies and recognize changes that may be seen in sequential tests during the course of the disorders. The following is a simplified grouping of electrical changes; actual electrodiagnostic studies show considerably more detail and frequent variations of these findings.9–11^,²⁶^,²⁷

Electrical testing in CNS disorders typically shows normal motor and sensory nerve conduction. In the EMG, spontaneous activity is typically not seen, and individual motor units seen on muscle contraction usually have normal parameters. The recruitment pattern may show a slower-than-normal MUAP discharge frequency with an incomplete and irregular interference pattern. In the presence of tremor and other involuntary movements, bursts of MUAPs occur, consistent with the muscle contraction pattern. In cases involving the brain stem, the blink reflex may show abnormalities.⁷ The tests are important in differential diagnosis between a CNS and a PNS problem, but often they are not used when clinical examinations demonstrate the problem to be definitively in the CNS.

In myelopathies, which include upper and lower motor neuron disorders (e.g., amyotrophic lateral sclerosis [ALS], poliomyelitis, cervical spondylitis, and syringomyelia), motor and sensory nerve conduction is usually normal, although mild slowing may be present.¹¹ The characteristic EMG changes, which usually appear in the more chronic stages of the disorders, are increased amplitude and duration of MUAPs because of the variable impulse conduction time in sprouting axon terminals. An increased number of polyphasic potentials with increased duration is usually found. Spontaneous activity is often seen, and on strong contraction fewer rapidly firing large MUAPs are recruited, resulting in a single-unit or partial interference pattern. In ALS, fasciculations and denervation potentials are typically found. The distribution of the EMG abnormalities determines the extent of the condition.

Peripheral neuropathies show a variety of electrical changes depending on the type and location of the pathology. In a proximal pathology (e.g., radiculopathy), motor and sensory nerve conduction generally remain normal, except F waves and H-reflex responses in specific spinal segments. If motor nerve roots are compromised, spontaneous activity and increased polyphasic potentials appear, and reduced recruitment of MUAPs results in an incomplete interference pattern. In more chronic stages MUAP amplitude and duration can be increased. As the lesion improves, spontaneous activity decreases and the recruitment patterns become more normal. If only sensory roots are injured, no EMG changes occur. Again, the distribution of the EMG abnormalities (all in one myotome) is pathognomonic, especially in the presence of denervation potentials in the corresponding paraspinal muscles.³¹

Lesions of peripheral nerves, which range from a focal mononeuropathy to plexopathy, frequently show abnormalities in motor and sensory nerve conduction depending on which components of the nerve are involved. In the EMG, spontaneous activity, particularly fibrillation and positive sharp waves, is common. If the lesion is complete, no MUAPs are found. The presence of even a few MUAPs suggests a more optimistic prognosis. Often the location of the lesion can be identified by the distribution of the electrical changes. With regenerating axons, low-amplitude polyphasic MUAPs gradually appear. In the chronic stage, the amplitude and duration of MUAPs are often increased. Spontaneous activity decreases with reinnervation, but it may persist for several years.

Generalized, systemic peripheral polyradiculoneuropathies can be divided into primarily demyelinating, primarily axon loss, or mixed axonal-demyelinating polyneuropathies. Some involve mostly sensory nerves (e.g., hereditary sensory neuropathy types I to IV, Sjögren syndrome, Friedreich ataxia), and others mostly motor nerves (e.g., chronic inflammatory demyelinating polyneuropathy [CIDP], lead neuropathy), but most involve both sensory and motor nerves. In the primarily demyelinating type, such as Guillain-Barré syndrome, motor and sensory nerve conduction and F waves become markedly slow. EMG changes usually do not occur, except for a reduced recruitment pattern consistent with weak muscle contraction or conduction block (when the demyelination is such that the impulse does not propagate). With primarily axonal polyneuropathies, such as uremic neuropathy, isoniazid or cisplatin toxicity, and lead poisoning, motor and sensory nerve conduction is mildly slowed or may remain normal. The duration and amplitude of the response, however, decrease. During advanced stages, many polyneuropathies develop both demyelinating and axonal pathology (e.g., diabetic neuropathy, which is by far the most commonly encountered polyneuropathy). On EMG, spontaneous activity is commonly seen. These electrical changes generally become more severe with worsening of the pathology, but they also improve if the pathology is reversed. From a patient management standpoint, remyelination occurs at a much more expedient pace than reinnervation.32–34

Again, the scope of the NCS electromyographic test is to determine the presence and extent of a neurological dysfunction. Attributing a cause to the dysfunction (e.g., diabetes versus alcoholism) requires other tests.

With myopathic disorders, motor and sensory nerve conductions are generally normal unless neural tissue is also affected. In advanced stages, however, severely atrophied muscles can produce decreased amplitude and distorted nerve conduction responses. The characteristic findings on EMG are short-duration, low-amplitude potentials. Some spontaneous potentials, particularly fibrillations and positive sharp waves, may be found but are much more frequent in the inflammatory myopathies such as polymyositis. Specific myotonic potentials appear in certain myopathic disorders (e.g., myotonia congenita). The recruitment pattern shows many low-amplitude MUAPs, appearing in a full pattern, with little voluntary effort. This type of recruitment pattern is referred to as early recruitment.

Neuromuscular junction disorders involve the synapse between axons and myocytes. In LEMS the pathology is in the presynaptic membrane (decreased release of acetylcholine [ACh]), whereas in myasthenia gravis the pathology involves the postsynaptic membrane. The two are differentiated by the response to RNS or jitter with single-fiber EMG (see later). In LEMS the amplitude of the responses increases with repetitive stimulation (more quanta of ACh released), whereas in myasthenia gravis the responses decrease (all ACh receptors saturated). Sensory NCS findings are typically normal.

Table 33-1 provides a summary of typical findings.

TABLE 33-1

SUMMARY OF TYPICAL FINDINGS

DISORDER	MOTOR CONDUCTION	SENSORY CONDUCTION	ELECTROMYOGRAPHY
Motor neuron disease (e.g., amyotrophic lateral sclerosis [ALS])	Reduced amplitudes	Normal	Acute plus chronic neurogenic changes, fasciculations
Radiculopathies	Normal	Normal	Acute neurogenic changes in myotome
Plexopathies	Reduced amplitudes	Reduced amplitudes	Acute neurogenic changes in specific pattern
Axonal neuropathy	Reduced amplitude in affected nerve(s)	Reduced amplitude in affected nerve(s)	Acute neurogenic changes in affected nerve
Demyelinating neuropathy	Reduced conduction in affected nerve	Reduced conduction in affected nerve	Normal
Neuromuscular junction disorder	Decrement (myasthenia gravis [MG]) or increment (Lambert-Eaton myasthenic syndrome [LEMS]) with repetitive stimulation	Normal	Occasional myopathic motor unit action potentials (MUAPs)
Myopathies	Normal	Normal	Small-amplitude polyphasic MUAPs