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Overview of electromyography

Overview of electromyography
Literature review current through: Jan 2024.
This topic last updated: Feb 17, 2023.

INTRODUCTION — Electromyography (EMG) is the clinical study of the electrical activity of motor units and their muscle fibers, individually and collectively. EMG typically evaluates electrical activity with the muscle at rest and during periods of voluntary muscle contraction [1].

This topic will review the basic principles of EMG and a summary of its applications to the major categories of neurological disease. The clinical utility of EMG relating to specific diseases are discussed separately in topic reviews.

Nerve conduction studies are discussed separately. (See "Overview of nerve conduction studies".)

ELECTRODES — Electrical activity can be recorded either with intramuscular needle electrodes or surface electrodes placed on the skin overlying the muscle. Both needle and surface electrodes measure the electrical potential difference between two sites of the muscle. Needle electrodes are typically monopolar or concentric [1].

Monopolar electrode – The monopolar needle serves as the active recording site, with the surface electrode serving as the reference electrode.

Concentric electrode – A fine wire in the center of the needle serves as the active recording site. It is surrounded by a needle cannula, which is insulated from the fine wire and serves as the reference electrode.

Monopolar electrodes are smaller in diameter and therefore are less expensive and typically less painful than concentric electrodes. However, they generate larger and more complex potentials with lower resolution. Concentric electrodes provide higher resolution and lower baseline noise because of the shorter fixed distance between wire and cannula. Consequently, concentric needle electrodes are preferred in most EMG laboratories.

Ground electrodes are essential in addition to the primary needle electrode, regardless of which is used. (See 'Electrical injury' below.)

THE MOTOR UNIT — The basic functional component of the muscle is the motor unit [2]. The motor unit consists of an anterior horn cell, its axon, and terminal branches, their neuromuscular junctions, and all the individual muscle fibers they innervate (figure 1).

The size of a given motor unit is determined by the number of individual muscle fibers innervated by its single axon. The number of motor units within a given muscle also varies widely from muscle to muscle. In general, muscles executing fine motor control tasks have smaller motor units with lower number of muscle fibers per axon (ie, low innervation ratios, such as 10:1 to 20:1 in the extraocular muscles), whereas big, bulk-supporting muscles have larger numbers of bigger motor units with high innervation ratios [3,4].

The motor unit territory is the space occupied by the motor unit within the muscle and is typically arrayed in a spherical or ovoid territory. The dimensions are dependent upon muscle fiber number and size, length of nerve terminal branches, and distribution of motor endplates in the muscle's endplate region. An arm muscle motor unit territory typically has an average diameter of 5 to 7 mm, whereas a leg muscle motor unit territory diameter is in the 7 to 12 mm range [4].

Within the territory of a motor unit, muscle fiber density is greater in the center than in the periphery [5]. The muscle fibers in one motor unit overlap with muscle fibers from other motor units. Consequently, a concentric needle EMG recording electrode usually picks up electrical activity from as many as four to six motor units during low to moderate voluntary activation.

Motor unit action potential — When an anterior horn cell is activated, all the muscle fibers belonging to that motor unit are depolarized synchronously. The total electrical activity from all these individual muscle fibers produces a waveform recorded by the EMG needle electrode as the motor unit action potential (MUAP). The MUAP usually has a triphasic configuration resulting from the propagation of depolarization throughout the motor unit and its muscle fibers, as follows (figure 2):

A positive (downward) deflection as the electrical impulse moves along the muscle fiber membrane toward the recording electrode

A negative (upward) deflection when the impulse moves under the electrode

Another positive (downward) deflection as the impulse moves away from the electrode

MUAPs change configuration, size, and activation patterns in neurogenic, myopathic, and other diseases, providing essential data for diagnosis. Reference values for MUAP parameters recorded by both monopolar and concentric needle electrodes and for single muscle fiber potentials recorded by single-fiber EMG electrodes have been published [6]. (See 'MUAP waveform analysis' below.)

MUAP waveform morphology — Characteristics of the motor unit action potential (MUAP) waveform help to identify and discriminate among neuromuscular disease processes. Recording three or more consecutive discharges of a single MUAP enables an accurate waveform evaluation. The morphology of MUAPs in a specific muscle in an individual patient can then be compared with normative data for that muscle.

To be sure that the sample of MUAPs studied is representative of the muscle as a whole, the electromyographer should record and analyze multiple different MUAPs, typically 20 to 30 or more from multiple sites within the studied muscle [7]. As the electrode often records multiple MUAPs at each recording site, interference of different MUAPs with each other is common. Up to six MUAPs can be recruited and visually analyzed at each site with 10 seconds of moderate muscle activity [8].

Needle electromyography and interpretation of MUAPs as well as motor unit recruitment and interference patterns are high-level skills, and results are critically dependent on the experience and skill of the operator. (See 'MUAP waveform analysis' below.)

Specific characteristics of MUAP waveform morphology are important in evaluating the type of disease affecting the motor unit (figure 2):

Rise time and amplitude – Proper needle electrode placement is crucial to MUAP evaluation. The central spike of the MUAP is generated by fewer than 10 fibers within the central part of the recording radius of the electrode tip (0.5 mm) within a normal motor unit. A spike "rise time" of <0.5 ms indicates that the muscle fibers generating the spike are <0.5 mm from the electrode's recording tip and indicates that the electrode is correctly placed for proper capture of the MUAP from that motor unit (figure 3 and figure 4).

The amplitude is primarily related to the size and density of the muscle fibers in close proximity to the needle electrode. MUAP amplitudes vary from muscle to muscle and also with athletic conditioning (especially muscle-building exercise regimens, such as weightlifting or manual labor) but typically range from 0.5 to 3 mV on average. MUAPs greater than 10 mV are usually abnormal and a sign of denervation/reinnervation and are called "giant units" [7,9,10].

Duration – MUAP duration is determined by several features:

Size of muscle fibers

Muscle fiber density

Motor unit territory (spatial dispersion of the terminal axons of the motor unit in the endplate zone)

Physiologic variability in axon length and neuromuscular junction transmission

These factors result in muscle fiber potentials within a single motor unit reaching the recording electrodes at varying times (despite unitary activation of the parent motor unit) and from varying directions, producing phase additions and cancellations and temporal dispersion of electrical activity within the MUAP. Consequently, although the duration of the electrical potential of a single muscle fiber is fairly constant at 3 to 4 ms, the duration of the summated or compound triphasic MUAP is more variable, usually in the range of 8 to 13 ms or longer.

MUAP duration reflects depolarization of all muscle fibers within the full radius, approximately 2.5 mm. Consequently, the duration of the MUAP is more representative of the overall size of the motor unit. In addition, needle movement has a lesser effect on duration than amplitude (figure 3 and figure 4).

The duration of the MUAP varies from muscle to muscle and increases with age. From childhood to early adulthood, increase in MUAP duration is due to increasing muscle fiber size [7,10,11]. The normal mean duration of MUAPs progressively increases with age (eg, the biceps brachii is 7.7 ms at birth, 10 ms at age 20, 11.1 ms at age 40, 11.9 ms at age 60, and 12.8 ms at age 80 [12] and in the abductor pollicis brevis is 6.2 ms, 9.2 ms, 9.3 ms, 9.5 ms, and 9.5 ms, respectively, according to an older normative aging study). However, a study of the anconeus muscle suggests that age-related collateral reinnervation may have limits and is minimal in male subjects older than 80 years [13].

Another contributor to changes in MUAP duration with aging is neuromuscular instability due to structural changes at the neuromuscular junction, resulting in more asynchronous single muscle fiber firing, as documented by MUAP "jiggle" studies [14], as well as by single-fiber EMG jitter analysis and decomposition-based quantitative EMG [15].

Phases and complexity – A phase is defined as the part of the MUAP waveform between baseline crossings and is normally four or fewer. MUAPs with more than four phases are termed "polyphasic" potentials. Some polyphasic potentials are expected in healthy control subject muscles but should constitute no more than 12 to 15 percent of the total MUAP sample recorded from a single muscle with a concentric electrode (or up to 35 percent with a monopolar electrode).

Directional changes in the waveform that do not cross the baseline are called "turns," and more than five turns is considered abnormal. This complexity may be called either polyphasia or turn number, but their diagnostic significance is the same.

Motor unit recruitment patterns — Healthy muscles are electrically silent at rest. With minimal voluntary activation, a few single motor units (typically the smaller motor units in the muscle) are activated, producing a small amount of contractile force. As voluntary activation increases, the firing rates of the first activated units increases, resulting in greater summation and further increases in force until maximal force is achieved. These motor unit recruitment patterns can be assessed with needle EMG examination.

As a muscle begins to contract at the lowest force levels, the first recruited motor unit begins to fire repeatedly at a specific frequency. As demand for more strength increases, the firing frequency of the motor unit increases until a second motor unit is recruited. The specific firing frequency of the first recruited motor unit at the moment the second motor unit is recruited is the "recruitment frequency." (See 'Recruitment and interference patterns' below.)

As voluntary muscle force increases, each MUAP will begin to obscure waveforms of other active motor units, and this interference among waveforms is call the interference pattern. This response typically appears as a dense band of competing waveform activity at slow sweep speeds, which normally obscures the baseline tracing. At maximal effort, this "envelope amplitude" is between 2 and 4 mV for most muscles. (See 'Recruitment and interference patterns' below.)

Reduced activation occurs with upper motor neuron disorders, pain, and with reduced effort.

Motor unit number estimates — A variety of methods for measuring the number of motor units within a given muscle have been devised, most of which use variations on nerve conduction study techniques. They can help assess disease progression, particularly in neurogenic disorders (eg, amyotrophic lateral sclerosis [ALS]), most neuropathies, and also in some central nervous system conditions [16-18]. Detection of silent motor unit loss in presymptomatic/subclinical motor neuron disorders, either in patients at risk for disease or in muscles still having normal strength in patients with mild or early disease is possible with motor unit number estimates (MUNE) techniques and useful as a measure of treatment efficacy in clinical trials [17,19,20].

Common to all these techniques is the accurate measurement of either the amplitude or area of the compound muscle action potential (CMAP) following supramaximal stimulation of the appropriate nerve. This result is then related to the sum of single motor unit potentials recorded with either surface or concentric needle electrodes, derived from stimulating the nerve at threshold and other submaximal and incremental intensities or during voluntary contractions at various force levels. These digitized and computerized MUNE techniques include incremental stimulation (IS-MUNE) [21,22], high-density surface EMG (HDSEMG) [23,24], multiple-point stimulation (MPS-MUNE) [25], adapted MPS (AMPS-MUNE) [26], MScanFit (MScan-MUNE) [27-29], decomposition-based quantitative EMG with spike-triggered averaging [30], neurophysiological index [31], and motor unit number index (MUNIX) [20,31-33].

Comparisons among MUNE techniques have been performed, and in general all seem capable of quantifying motor unit loss in a variety of denervating disorders, most commonly ALS [26,28,29]. MUNIX may be the best tolerated by patients with respect to discomfort and speed, but it is dependent upon patient compliance and observer technical experience [17,18,20,33].

MUNE is also discussed separately elsewhere. (See "Overview of nerve conduction studies", section on 'Motor unit number estimates (MUNE)'.)

RECORDING STAGES AND PATHOPHYSIOLOGY — Standard diagnostic electromyography includes four major stages, each of which is recorded at multiple sites:

Insertional activity

Spontaneous activity with the muscle at rest

Motor unit action potential (MUAP) analysis

Recruitment and interference patterns

Insertional activity — As the needle electrode passes through the muscle, it transects and mechanically deforms muscle fibers along its track, creating brief bursts of electrical activity that persist during and shortly after cessation of needle movement (for approximately 50 ms). This electrical activity is due to mechanical irritation. It is recorded primarily as fibrillations and positive sharp waves. Once needle movement has ceased, no other electrical activity should appear in a healthy muscle at rest.

Continued firing of potentials for more than a few hundred milliseconds after needle movement has ceased is abnormal and is reported as increased insertional activity. Increased insertional activity suggests excessive irritability of the muscle fiber and is a hallmark of disorders of the motor axon or cell body of the motor neuron, inflammatory myopathies, and some other primary muscle diseases. (See 'Spontaneous activity' below.)

Decreased insertional activity is seen when the needle electrode passes through scar tissue within the muscle, such as in atrophic and/or fibrotic muscle.

Spontaneous activity — Spontaneous firing of potentials in a resting muscle is a hallmark of neuropathic or myopathic processes but some patterns of activity may occasionally be seen in healthy patients (eg, the gastrocnemius).

Denervation discharges — Muscle fibers that have lost innervation through motor axon injury, inflammation, or a myopathic disease process may periodically undergo spontaneous depolarization. These brief spikes and waves with a sharp positive component are identified as fibrillations or positive sharp waves in the resting muscle. They are often scored according to a semiquantitative grading system of 1+ when spontaneous activity is rare to 4+ when spontaneous potentials fill the oscilloscope screen [34].

Following acute nerve injury, denervation discharges first appear after 10 to 14 days and can therefore be used to time the onset of acute denervation with serial studies. The further the tested muscle is from the site of nerve injury, the later the interval to onset, because retraction of the axonal branches of the nerve from muscle fibers is delayed in longer nerves.

Fibrillation potentials – These discharges occur when an individual muscle fiber is denervated (no longer innervated by its nerve terminal) and spontaneously depolarizes. Fibrillation potentials are small (<500 microvolts), short (<5 ms in duration), biphasic or triphasic waveforms with an initial downward (positive) deflection, and fire regularly or sometimes irregularly, producing an audio output likened to "rain on a tin roof."

Positive sharp waves – These waveforms have a sharp initial downward (positive) deflection followed by a longer duration, lower-amplitude upward (negative) phase than fibrillation potentials [35]. The waveform pattern of positive sharp waves may transition to fibrillation potential morphology with slight adjustments of the electrode (waveform 1) [36]. Presumably, the negative spike of a fibrillation potential emerges as the electrode is moved away from the membrane or disappears with electrode/membrane contact.

Endplate potentials — These discharges are the spontaneous electrical activity generated by the activation of the neuromuscular junction in normal muscle. They consist of continuous, rapidly firing, biphasic, small-amplitude (100 to 200 microvolts), short-duration (3 to 4 ms) spikes with upward (negative) onset in the vicinity of the muscle endplate.

Endplate potential activity produces a sound similar to radio static on the audio speaker. The sound of endplate potentials has been likened to "fat in the frying pan". Endplate potentials are recorded when the needle electrode is near the endplate zone of the muscle. Unlike pathological waveforms such as fibrillations or positive sharp waves, endplate potentials are concentrated in the endplate zone and appear as an initial upward (negative). When the needle is moved away from the endplate zone, they disappear. It is also important to avoid the endplate zone during needle electromyography because the region is more highly populated with pain receptors and is more uncomfortable for the patient than examination elsewhere in the muscle.

Electrical artifacts — Electrical artifacts are sometimes found during routine EMG evaluation. Defective needle electrodes or highly sensitive modern EMG equipment may register environmental or other biologic electrical patterns. Electrical wiring in the walls of the examination room, fluorescent lighting, cell phones, transformers, other laboratory equipment, and poor grounding of the patient may be encountered. Electrical current from municipal power grids produces classic 60 Hz sine wave (50 Hz in some countries). Inside the patient, cardiac pacemakers are a common source of artifacts, but, as stimulation devices proliferate, new sources of interference are appearing, including deep-brain stimulators and spinal stimulators [37]. These electrical artifacts resemble spontaneous activity and may interfere with their interpretation but can usually be recognized by their periodicity.

Other spontaneous discharges

Complex repetitive discharges — Complex repetitive discharges (CRDs) are bursts of multiphasic, complex waveforms with up to 10 spike components (turns), having a total duration of up to 100 ms. CRDs represent the firing of groups of muscle fibers within the muscle (rather than firing of the motor units), in which one muscle fiber acts as a pacemaker, driving other muscle fibers [35,36]. CRDs can occur with denervation of any kind but are also prevalent in certain categories of myopathy [38], including inflammatory myopathies, metabolic myopathies (ie, glycogen storage disease II, also known as Pompe disease or acid maltase deficiency), some muscular dystrophies, and the Schwartz-Jampel syndrome.

The defining characteristics of CRDs is their firing pattern, marked by highly regular, machine-like discharges at an average frequency of 30 to 40 Hz. They have been described as sounding mechanical (at lower frequencies) or like a machine gun on the audio speaker. These trains of discharges stop and start abruptly (rather than tapering off, which distinguishes them from myotonic discharges).

Myotonic discharges — Myotonic discharges are positive waves or brief spikes, which also fire repetitively at a frequency ranging from 20 to 150 Hz. They are produced by the spontaneous discharges of multiple single muscle fibers, typically evoked by needle insertion, needle movement, or voluntary contraction. Myotonic discharges are also seen in a number of hereditary myopathies including myotonic dystrophy, myotonia congenita, paramyotonia congenita, Schwartz-Jampel syndrome, hyperkalemic periodic paralysis, and metabolic myopathies [39,40] and myofibrillar myopathies [41].

Unlike CRDs, myotonic discharges begin and end gradually and continuously vary in amplitude. They produce a waxing and waning sound on the audio speaker output that may be described as sounding like the revving of a motorcycle or outboard engine.

Neuromyotonia — Neuromyotonic discharges are similar to myotonia but fire at higher frequencies (150 to 300 Hz) and begin and end abruptly without waxing and waning amplitudes. They generate audio output that may be described as sounding like the whine of a mosquito or the engine of an automobile.

Neuromyotonia is extremely rare and is associated with Isaacs syndrome and Morvan syndrome as well as rattlesnake envenomation. Myokymia and neuromyotonia probably represent a spectrum of defects in voltage-gated K+ channels [42]. Neuromyotonia is clinically manifested by sustained and visible muscle contractions, often inducing cramps [43].

Fasciculations — Fasciculations are either single motor units or groups of single motor units that spontaneously depolarize. Fasciculations are most commonly a benign and incidental finding in healthy individuals. However, they are also associated with denervation and can be especially prominent in motor neuron disease. In a study using high-density surface EMG recordings in patients with motor neuron disorders, isolated motor unit discharges were much more common than in controls, especially if the isolated discharges came from two or more motor units firing simultaneously [44]. They may also be associated with metabolic disorders such as thyrotoxicosis as well as tetany and drugs, including acetylcholinesterase inhibitors and caffeine.

These potentials discharge at irregular intervals in the resting muscle, often at frequencies less than 1 Hz. They may be identical to a single MUAP or appear as a compound group of MUAPs superimposed on one another.

There are no definitive features to discriminate between benign or pathological fasciculation potentials. However, benign fasciculations may be more likely to arise proximally, whereas pathologic fasciculations associated with chronic denervation are more likely to arise distally [45]. In general, benign fasciculations have faster firing rates and occur in more distal muscles below the knees [12]. Pathological fasciculations may be larger and more complex.

Clinical fasciculations may be observed at the skin surface, but diagnostic modalities such as EMG and ultrasound are much more sensitive assays of fasciculations, detecting deep and small fasciculations that would otherwise not be visible. EMG examination also enables mapping of the extent, quantity, and frequency of fasciculations in muscles throughout the body.

Myokymia — Myokymia consists of spontaneous bursts of groups of 2 to 10 MUAPs. Myokymia can occur in healthy individuals in the orbicularis oculi or oris muscles (eyelid myokymia). Segmental myokymic discharges can occur due to denervation, such as in radiculopathies, but radiation plexopathies are most classically associated with myokymia, typically due to thoracic radiotherapy as may be used to treat breast and lung cancer [46]. Generalized myokymia is seen rarely in metabolic disorders and inflammatory neuropathies.

Clinical myokymia may be seen by visual inspection. By EMG, myokymia has been likened to "marching soldiers". Each myokymia burst fires at an irregular frequency, averaging 0.1 to 3 Hz, with electrical silence between bursts. Intraburst firing frequencies are typically 40 to 60 Hz. The discharge generator is thought to be located along the motor axon. The configuration of myokymic discharges, as well as their comparatively slow and irregular firing frequencies, typically enables clear differentiation from other spontaneous discharges such as CRDs and myotonia.

Cramps — Cramps are sustained involuntary muscle contractions caused by the involuntary activation of multiple motor units. Motor units in cramp discharges usually have a frequency of 40 to 60 Hz, last less than 500 ms, and appear to originate at the motor nerve terminals. Clinically, cramps manifest as acute-onset, palpable, involuntary, strong muscle contractions, which are often painful. They may occur following exercise or during rest or sleep and often respond to passive stretch.

They occur most commonly in healthy individuals, primarily affecting the calf muscles and feet, but are also common in denervating disorders such as radiculopathy, neuropathy, and motor neuron disease. Muscle cramps with electrical silence on needle EMG examination are termed "physiologic contractures" and are the consequence of the failure of metabolic mechanisms necessary for muscle relaxation. They are most strongly associated with McArdle disease (glycogen storage disease type V, or myophosphorylase deficiency), as well as other glycogenoses.

One small study found an inverse correlation between the cramp threshold frequency (the minimum electrical stimulation frequency at which a muscle cramp may be induced) and a history of cramping [47], suggesting that cramp threshold frequency might be useful to identify individuals with an increased risk of cramping.

MUAP waveform analysis — With minimal voluntary activity, the morphology of individual MUAPs can be analyzed for pathologic evidence of motor unit remodeling. Low levels of voluntary contraction are used to isolate individual motor units for analysis during routine clinical intramuscular needle electromyography. Smaller motor units, having lower excitability thresholds, are activated first at lower levels of voluntary contraction [48,49]. More and larger motor units are recruited as force of contraction increases.

With minimal voluntary activation, a small number of the first activated motor units normally discharge in a semi-rhythmic pattern, separated by variable intervals of 50 to 250 ms at frequencies averaging 5 to 15 Hz.

Average and outlier larger MUAPs can be assessed during interference pattern analysis, but average large MUAP morphology is most accurately assessed with more advanced methods such as macro-EMG, decomposition-based quantitative EMG, and high-density surface EMG. (See 'Recruitment and interference patterns' below.)

MUAP in acute denervation – Following acute axonal injury, fewer motor units are activated at maximal voluntary contraction. The motor units that are activated may fire at a higher-than-normal frequency to compensate for the units paralyzed by the injury. In addition, recruitment and interference patterns are typically reduced. However, MUAP configuration is unchanged in the acute (first three to four weeks) setting because motor unit remodeling has not yet had time to occur.

With complete loss of all axons, such as in total transection of the nerve trunk, no motor units can be voluntarily activated, and voluntary muscle contraction does not occur.

MUAP in chronic denervation – In the chronic stage following axonal injury, the compensatory process of collateral reinnervation begins, usually starting approximately four weeks after injury and continuing over several months. With a progressive denervating disease, such as amyotrophic lateral sclerosis (ALS), collateral reinnervation becomes constant.

During collateral reinnervation, surviving axons send terminal branches to those muscle fibers orphaned by loss of their parent axons, and they are thereby absorbed into functional neighboring motor units. This process enlarges the number of muscle fibers within the reinnervated unit, producing a larger MUAP, with a longer duration, higher amplitude, and more complex morphology. These motor units are called "neurogenic MUAPs."

In the earliest phases of the collateral reinnervation process, some of the normal small motor units in the overall population will also participate and may become complex before enlarging, creating short-duration, low-amplitude complex units known as "nascent MUAPs." In some instances, severely injured axons may revive with recovery and try to reclaim some of their lost connections with muscle fibers through collateral reinnervation, also producing nascent MUAPs. These nascent MUAPs may resemble the complex, low-amplitude, short-duration MUAPs seen in myopathies [10,50,51].

By incorporating muscle fibers from denervated motor units through collateral sprouting, a single motor unit can increase the number of muscle fibers that it innervates by an estimated two to five times normal [52-54]. Another mechanism to compensate for motor unit loss is hypertrophy of surviving muscle fibers, though this is a minor contributor compared with collateral reinnervation, unless intensive physical therapy or exercise is applied during recovery (waveform 2).

When a surviving motor unit reinnervates a distant patch of muscle fibers, it may generate two apparent potentials. This second peak, which may itself have all of the characteristics of a single MUAP, is known as a "satellite potential," or as a late component. In addition to satellite potentials, transmission between separate axons with degeneration of the nerve may produce concurrent firing of different motor units in pairs (doublets), threes (triplets), or more (multiplets). Though these waveforms can rarely occur in normal individuals, they are much more likely in hyperexcitable states (eg, hyperventilation, tetany, Isaacs syndrome [43,50].

In cases of axonal injury with natural recovery or recovery following treatment, reinnervation can occur only by regrowth of axons across a site of injury or from the anterior horn cell, along the original nerve fiber tracts. As axons grow at rates of approximately 1 millimeter each day, reinnervation can be very delayed and incomplete in muscles distant from the site of injury. This regrowth rate also enables rough calculations of when recovery might be expected in specific muscle groups, by measuring the length of the nerve from the anterior horn cell or site of focal injury to the muscle of interest.

MUAP in myopathic disorders – In disorders featuring degeneration of the muscle but not the motor nerve, the number of motor units is normal. However, there is a pathologic loss of muscle fibers within motor units throughout the muscle, resulting in smaller, weaker motor units containing fewer overall fibers. This results in correspondingly smaller MUAPs, having shorter duration and lower amplitude, as well as increased complexity due to muscle fiber dropout, known as "myopathic MUAPs" (waveform 2).

Recruitment and interference patterns — In nerve and muscle disorders, reduced number of motor units are available to respond to volitional activation. Attempts to compensate for the loss of strength due to motor unit dropout occur by recruitment in the spinal cord and central motor system. This occurs through increasing the firing rate or number of available motor units.

Delayed recruitment in neuropathic disorders – In conditions where denervation has occurred, there are fewer voluntary motor units available to respond to central drive. The firing rate of the surviving functional motor units increases, thereby increasing the summated tetanic contraction force of the muscle. During electromyographic recruitment analysis, the first recruited motor units will exceed their normal firing frequency before more motor units are recruited and will fire at up to 30 to 40 Hz, rather than the typical 5 to 15 Hz before additional motor units appear (delayed recruitment).

Early recruitment in myopathic disorders – In conditions primarily featuring pathology of the muscle, the total number of units is normal, but the units are smaller and generate less force. Consequently, the central motor system activates more motor units sooner as volitional contraction increases to compensate for less force per unit. This results in a phenomenon opposite to that of denervation, in which large numbers of motor units rapidly fill the screen, even at low levels of early contraction (early recruitment).

As voluntary muscle force increases, each MUAP will begin to obscure waveforms of other active motor units, and this waveform display is called the interference pattern. With attempted maximal recruitment in the setting of denervation, the interference pattern is reduced. The waveform pattern demonstrates fewer overlapping units, and, in advanced cases, a "picket fence" pattern with large gaps. The envelope amplitude of the interference pattern, however, is increased, and also some very large motor units may be seen outside the envelope (another marker of collateral reinnervation, this time of the full population of surviving motor units) (waveform 2).

DIAGNOSTIC ELECTROMYOGRAPHY — Electrodiagnosis plays a key role in the proper identification of a wide variety of neuromuscular diseases. As with other diagnostic tests, an appropriate and careful history and directed physical examination are critical to generating a differential diagnosis and developing a diagnostic plan. EMG examination is useful for assessing motor neuronopathies, radiculopathies, plexopathies, polyneuropathies, focal neuropathic syndromes, neuromuscular junction disorders, and myopathies. Accurate interpretation of data from EMG requires a detailed knowledge not only of nerve and muscle anatomy but also of the pathophysiology of normal and diseased nerve and muscle. When properly performed, needle EMG provides invaluable information, enabling the proper diagnosis and management of a host of neuromuscular disorders [55-61].

Electrophysiologic investigation of the peripheral nervous system typically includes a series of nerve conduction studies followed by needle EMG and may be supplemented by more specialized studies involving a number of other techniques. Nerve conduction studies are discussed in detail elsewhere. (See "Overview of nerve conduction studies".)

Motor neuronopathies — The motor neuronopathies are those diseases affecting principally the anterior horn cell, with subsequent distal degeneration of the motor axon. Motor neuronopathies are much more common than their sensory counterparts and typically spare extraocular muscle function and bowel and bladder function. The major categories of motor neuronopathy include amyotrophic lateral sclerosis (ALS) and the spinal muscular atrophies. (See "Spinal muscular atrophy", section on 'Diagnosis' and "Diagnosis of amyotrophic lateral sclerosis and other forms of motor neuron disease", section on 'Diagnosis'.)

Needle EMG in ALS reveals both active and chronic changes of denervation and reinnervation. Insertional activity is increased. Spontaneous fibrillations and positive sharp waves are typically widespread, and fasciculations may be prominent. Motor units are neuropathic in morphology and the mean motor unit action potentials (MUAPs) amplitudes are increased and prolonged, often with polyphasia. These conditions are discussed in greater detail separately. (See "Diagnosis of amyotrophic lateral sclerosis and other forms of motor neuron disease", section on 'Electromyography'.)

Radiculopathies — Radiculopathies often result from a compressive lesion such as a herniated disc or spondylitic foraminal encroachment. However, ischemic radiculopathies from occlusion of the vaso-nervorum may also be seen in numerous vasculopathies (including diabetic small-vessel disease). Traumatic injuries, such as cervical nerve root avulsion following a motor vehicle accident, infectious disorders such as cytomegalovirus polyradiculitis, and inflammatory disorders such as chronic inflammatory demyelinating polyneuropathy may also affect the motor nerve root. (See "Clinical features and diagnosis of cervical radiculopathy" and "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis" and "Chronic inflammatory demyelinating polyneuropathy: Etiology, clinical features, and diagnosis".)

In acute compression of mild to moderate severity, focal demyelination may be seen. Because axonal integrity is preserved, typically no abnormal spontaneous activity or changes to motor unit morphology are observed. However, with significant demyelination, conduction block will prevent activation of some axons and an immediate increase in recruitment frequency may be noted. Acute severe compression causes axonal destruction and the subsequent development of fibrillations and positive sharp waves within 10 to 21 days after the initial injury. Because of the delay in the development of spontaneous activity, at least 21 days after an acute injury is required for an optimal electrodiagnostic study. The development of neuropathic motor units, the electrical signature of reinnervation, may not appear for weeks to months after the initial injury. These features are discussed in greater detail separately. (See "Clinical features and diagnosis of cervical radiculopathy", section on 'Electrodiagnostic studies' and "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis", section on 'Neurodiagnostic testing'.)

Plexopathies — Plexopathies may result from compression, stretch injury, trauma, inflammatory syndromes (eg, idiopathic brachial plexitis), or microvascular ischemia in diabetic amyotrophy. It may also follow radiation treatment of a malignancy. (See "Brachial plexus syndromes" and "Lumbosacral plexus syndromes" and "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)

Denervation in plexopathies is similar to radiculopathy, and localization is dependent upon identifying the innervation patterns associated with different portions of the plexus from both nerve conduction studies and EMG. Testing of specific proximal muscle groups such as the rhomboids may assist in localization. These patterns are discussed in greater detail separately. (See "Brachial plexus syndromes", section on 'Nerve conduction studies and needle electromyography' and "Lumbosacral plexus syndromes", section on 'Electrodiagnostic studies' and "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on 'Electrodiagnostic studies'.)

Neuropathies — Several conditions may feature impairment in the function of peripheral nerves, individually, in regionally restricted groups, or in a widespread pattern. The evaluation of patients with polyneuropathies or mononeuropathies is discussed in greater detail elsewhere. (See "Overview of polyneuropathy" and "Overview of upper extremity peripheral nerve syndromes" and "Overview of lower extremity peripheral nerve syndromes" and "Traumatic peripheral neuropathies".)

Needle examination in generalized polyneuropathy is abnormal provided axonal injury has occurred, but minimal to no changes are seen in the early phases of purely demyelinating disorders. In axonal neuropathies, the distal muscles are the earliest and most dramatically affected. Neurogenic motor units are seen in chronic disorders and spontaneous activity is seen in more acute or active processes. The distal predominance is related to the phenomenon of length dependent nerve injury described in diffuse neuropathic disease. (See "Overview of polyneuropathy", section on 'Electrodiagnostic testing'.)

Needle EMG may help determine the type of nerve injury (principally demyelinating or axonal), the timing of onset of the injury, and the severity the nerve injury. EMG may be useful in assessing the degree of nerve injury in mononeuropathies and to help determine the prognosis for recovery. Serial EMG will show progressively increasing numbers of activated motor units as the nerve improves, though some neurogenic motor unit remodeling may be permanent. (See "Overview of upper extremity peripheral nerve syndromes", section on 'Overview of diagnostic testing' and "Overview of lower extremity peripheral nerve syndromes", section on 'Electrodiagnostic studies' and "Traumatic peripheral neuropathies", section on 'Electrodiagnostic testing'.)

Neuromuscular junction disorders — In neuromuscular disorders, needle EMG may occasionally show myopathic-appearing motor units due to neuromuscular junction blockade. These units may change morphology each time they discharge due to fluctuations in the number and locations of neuromuscular junctions blocked within the studied motor unit. This motor unit variability is most easily seen as variation in amplitude of the MUAP. Neuromuscular junction disorders are discussed in detail separately. (See "Electrodiagnostic evaluation of the neuromuscular junction".)

Myopathies — EMG is used to identify and manage disorders primarily affecting the muscle. These myopathies are discussed in detail separately. (See "Overview of and approach to the idiopathic inflammatory myopathies" and "Approach to the metabolic myopathies" and "Myopathies of systemic disease" and "Drug-induced myopathies".)

In many myopathies, myopathic motor units typically appear with low amplitude, short duration, and increased complexity compared with normal motor units. The distribution of MUAP abnormalities is often proximal and may require assessment of both proximal and paraspinal muscles. Recruitment is typically early, as the first recruited motor units are smaller due to diffuse muscle fiber atrophy. Unlike the pattern seen in the neuropathic disorders, the interference pattern is typically quite dense and full, although the envelope amplitude is usually decreased; polyphasia may be prominent. Spontaneous activity is variable, depending upon the specific categories of myopathy (detailed below) but may be most prominent in inflammatory disorders. (See "Overview of and approach to the idiopathic inflammatory myopathies", section on 'Electromyography' and "Approach to the metabolic myopathies", section on 'Electromyography'.)

COMPLICATIONS OF NEEDLE EMG

Pain — EMG is an invasive procedure that is widely used and usually well tolerated. However, needle-related pain is common and may cause studies to be prematurely discontinued [62]. Use of a smaller diameter needle may be less painful than larger diameter needles. In a series of 1781 muscles studied with needle EMG in 304 patients, the muscles associated with the highest levels of patient-reported pain were the thenar, intrinsic foot, and distal leg muscles, correlating with the abundance of pain receptors in these regions [63].

One study in children found needle EMG pain to be equivalent to that of a venipuncture [64]. Others recommend topical anesthetic use for children undergoing EMG [65]. Attention to techniques to minimize pain during needle EMG and studying alternative but similarly innervated muscles may be more comfortable and allow for a more successful EMG study [63].

Serious adverse events — Serious complications of needle EMG are very rare but include bleeding, infection, nerve injury, pneumothorax, and other local traumas [66]. Electrical injury due to stray leakage currents, due principally to nerve conduction study stimulation, is extraordinarily rare, but, in case reports, proximal nerve stimulation at Erb's point has precipitated cardiac arrythmias through an indwelling catheter in the subclavian vein in the intensive care unit setting.

Bleeding — Patients with a potentially increased risk of bleeding from EMG include those with the following conditions [67]:

Thrombocytopenia (platelets <50,000/mm3, and particularly <20,000/mm3)

Chronic renal failure, due to dysfunctional platelets

Coagulopathies, including acquired (eg, liver failure, disseminated intravascular coagulation) and inherited (eg, hemophilia)

Anticoagulant medications (eg, heparin, warfarin, other vitamin K antagonists, direct thrombin inhibitors, and factor Xa inhibitors)

Antiplatelet agents, nonsteroidal anti-inflammatory agents, and certain herbal medications

In a prospective case-control study, the rate of hematoma formation after routine needle EMG was acceptably low in patients taking either antiplatelet agents (1 of 116 muscles examined [0.9 percent]) or oral anticoagulants (1 of 107 muscles [0.9 percent]) compared with controls (0 of 100 muscles) [68]. Both hematomas were small and subclinical, and differences between groups were not statistically significant. Clinical experience and expert consensus suggest that EMG can be performed safely on patients taking antiplatelet agents, nonsteroidal antiinflammatory agents, and herbal medications without a need to stop these agents before the procedure [67,69].

While the risk of bleeding with anticoagulants is higher than with antiplatelets, some experts continue therapeutic anticoagulation when performing EMG in patients with an international normalized ratio (INR) <3.0 [62,69,70]. Others advise stopping anticoagulation several days before the procedure and resuming immediately afterward. The risk of stopping anticoagulation (ie, thromboembolism) must be weighed against the risk of bleeding associated with a minimally invasive procedure such as EMG. (See "Perioperative management of patients receiving anticoagulants".)

We use the following approach to reduce bleeding complications for patients on anticoagulation who undergo needle EMG [67]:

Use the smallest EMG needle available (eg, 30 gauge).

Limit the study to superficial muscles where prolonged compression over a puncture site can be performed if necessary.

Avoid deep muscles that cannot be manually compressed or could result in a compartment syndrome if a hematoma were to develop. Most important among these are the arm muscles close to the antecubital fossa (ie, pronator teres and flexor carpi radialis) and the leg muscles such as the tibialis posterior and flexor digitorum longus. The last two muscles are known to be associated with multiple veins, potentially increasing the risk of bleeding during the procedure [68].

Avoid muscles where a hematoma theoretically could compress adjacent neurologic structures. Most important among these are the gluteal muscles near the sciatic nerve and the paraspinal muscles near the exiting spinal nerves.

Be cautious with muscles situated near large arteries or veins. Most important among these are the flexor pollicis longus near the radial artery, the iliacus near the femoral artery/vein, and the antecubital fossa muscles near the brachial artery.

Pneumothorax — Pneumothorax is a rare but potentially serious complication of needle EMG studies [62,66,71]. This complication may occur with needle EMG involving the following muscles:

Diaphragm

Supraspinatus

Serratus anterior

Lower cervical and thoracic paraspinal muscles

Rhomboids

Ultrasound may be used in the anatomic localization of muscles at risk [62]. The development of chest pain or dyspnea during or after needle EMG suggests the possibility of pneumothorax, which should prompt urgent evaluation and imaging with chest radiography or computed tomography. Initial management is dictated by the severity of the patient's symptoms and the size of the pneumothorax. (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children".)

Electrical injury — Safety procedures are necessary to minimize electrical leaks and injury with EMG [66,67]. Most important are measures to ensure proper grounding. In addition, electrodiagnostic studies should not be performed on patients with external cardiac pacer wires. Additional safety measures are discussed separately. (See "Overview of nerve conduction studies", section on 'Measures to avoid electrical injury'.)

SUMMARY

Definition and clinical utility – Electromyography (EMG) is the clinical study of the electrical activity of motor units and their muscle fibers, individually and collectively. EMG typically evaluates electrical activity with the muscle at rest and during periods of voluntary muscle contraction. (See 'Introduction' above.)

EMG provides invaluable information, enabling the proper diagnosis and management of a host of neuromuscular disorders. These include motor neuronopathies, radiculopathies, plexopathies, polyneuropathies, focal neuropathic syndromes, neuromuscular junction disorders, and myopathies. (See 'Diagnostic electromyography' above.)

Neurophysiology

Motor unit – The basic functional component of the muscle is the motor unit which consists of an anterior horn cell, its axon and terminal branches, and all the individual muscle fibers it innervates (figure 1). The size of the motor unit, which is the number of muscle fibers innervated by a single anterior horn cell, varies with each muscle. (See 'The motor unit' above.)

Motor unit action potential – The total electrical activity from activated muscle fibers produces a waveform recorded by the EMG needle electrode as the motor unit action potential (MUAP). The MUAP usually has a triphasic configuration resulting from the propagation of depolarization throughout the motor unit and its muscle fibers (figure 2 and figure 4). MUAPs change configuration, size, and activation patterns in neurogenic, myopathic, and other diseases, providing essential data for diagnosis. (See 'Motor unit action potential' above.)

Recording stages of EMG – The electromyographic study of each muscle consists of four separate stages, each evaluated at multiple recording sites (see 'Recording stages and pathophysiology' above):

Insertional activity – Needle electrode insertion is normally accompanied by brief bursts of electrical activity that persist during and shortly after cessation of needle movement. (See 'Insertional activity' above.)

Spontaneous activity – Spontaneous firing of potentials in a resting muscle is a hallmark of neuropathic or myopathic processes but some patterns of activity may also be seen in healthy patients. Patterns of spontaneous activity include (see 'Spontaneous activity' above):

-Denervation discharges (fibrillations and positive sharp waves)

-Endplate potentials

-Electrical artifacts

-Complex repetitive discharges (CRDs)

-Myotonic discharges and neuromyotonia

-Fasciculations

-Myokymia

-Cramps

MUAP waveform morphology – The morphology of individual MUAPs can be analyzed for pathologic evidence of motor unit remodeling (waveform 2). (See 'MUAP waveform analysis' above.)

-Following acute axonal injury, fewer motor units are activated at maximal voluntary contraction. The units that are activated may fire at a higher-than-normal frequency to compensate for the units paralyzed by the injury.

-In the chronic stage after axonal injury, the compensatory process of collateral reinnervation begins, producing a larger neurogenic MUAP, with a longer duration, higher amplitude, and more complex morphology.

-In disorders featuring degeneration of the muscle, there is a pathologic loss of muscle fibers within motor units throughout the muscle. Myopathic MUAPs are small and have a shorter duration and lower amplitude as well as increased complexity compared with neuropathic MUAPs.

Recruitment and interference – Attempts to compensate for the loss of strength due to motor unit dropout occur by increased firing rate and delayed recruitment in nerve disorders and early recruitment in muscle disorders. (See 'Recruitment and interference patterns' above.)

Complications of testing – EMG is an invasive procedure that is widely used and usually well tolerated. However, needle-related pain is common. Serious complications of needle EMG are very rare but include bleeding, infection, nerve injury, pneumothorax, and electrical injury. Safety procedures are necessary to minimize these risks. (See 'Complications of needle EMG' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledges Steven H Horowitz, MD, who contributed to earlier versions of this topic review.

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References

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