Johnson’s Practical Electromyography
4th Edition

Chapter 2
The Essentials of the Needle EMG Exam
Vivek Kadyan
Ernest W. Johnson
Denise L. Davis
Why Request an EMG?
An electromyographic (EMG) examination is a functional evaluation of the motor unit. It can assess the location, severity, chronology, and prognosis of injuries, diseases, or other compromises of the motor unit. The motor unit is made up of the anterior horn cell, its axon, and all of the muscle fibers innervated. Some wish to characterize electrodiagnosis as synonymous with EMG, and that is historically and conventionally correct, if not correct technically. Most electromyographers in the United States understand that when an EMG is requested, the referring physician desires a comprehensive electrodiagnostic examination, which is a specialty medical consultation that includes EMG testing. This testing is performed either by or under the personal supervision of the physician, and is guided by the clinical information of the interview and clinical examination. Another important point is that the functional evaluation provided by electrodiagnostic evaluation is complementary to imaging’s structural evaluation, and electrodiagnosis is essential to evaluate any trauma or disease affecting the motor unit.
What Conditions Suggest that EMG Would Be useful in Diagnosis and Management?
If the patient complains of pain, weakness, fatigue, or numbness (paresthesia) that results in a differential diagnosis including problems affecting the motor unit or sensory nerves, then an EMG may be useful. The most frequent complaint of patients presenting in a primary care office is “pain.” Pain is commonly caused by:
  • Radiculopathy
  • Entrapped nerve
  • Neuritis (generalized or localized)
  • A variety of nonneurologic causes
Weakness can be seen as either localized or generalized, and this clinical impression will affect the choice of electrodiagnostic tests. Fatigue is differentiated from weakness as the gradual loss of strength during repeated or continuous use of muscle(s).
Paresthesias (numbness) also can be either localized or generalized to multiple limbs and is a very common condition leading to EMG.
What is Electromyography?
Electromyography literally means recording the electrical activity of the muscle cell membrane. With a needle electrode inserted in the muscle, the motor unit potential (MUP) can be recorded. This represents the summated electrical activity of action potentials of all of the muscle fibers making up that motor unit. In the normal situation, the motor unit (MU) is “all or none” in its expression as a MUP. In certain circumstances the action potential

of individual muscle cell membranes can be recorded. This portion of the EMG is described in more detail below in the section on Needle EMG. In more recent usage, the word “electromyography” encompasses all the techniques used in evaluating the function of the peripheral nervous system, including the lower motor neuron and its innervated muscle fibers (the MU), and the associated sensory nerve fibers. In conditions that affect the muscle fibers primarily, this MUP will be smaller and of shorter duration. If the anterior horn cell or its axon is impaired, then the MUP will be absent. Also, if the axon is damaged or the sheath (myelin) is defective, then the resulting MUP will be delayed in onset, unstable in appearance, or altered in shape (i.e., increased duration or reduced amplitude).
Another alteration in the MUP will occur if there is a disease or injury to the endplate area (where the motor axon terminal synapses on the muscle fiber). This contact of axon to muscle is referred to as the neuromuscular junction, and in certain conditions (e.g., myasthenia gravis, Lambert-Eaton syndrome, or botulism) the nerve impulse can be intermittently delayed or blocked in reaching the muscle fiber, thus changing the MUP’s characteristic stability.
What is Nerve Conduction Velocity?
When the motor nerve is maximally stimulated, all of the MUs in that muscle respond by depolarizing, and a surface electrode will record the electrical activity as a compound muscle action potential (CMAP), which is a fairly good measure of the number of motor axons and their MUAPs responding. Some electromyographers (mostly in Europe) call this procedure “neurography.” While they maintain this is more accurate, in motor conduction it is mostly dependent on the appearance of the CMAP as well as the latency; thus, myography is appropriate. We therefore prefer to use the shortened but historically valid and generally accepted term “electromyography” as a reasonable compromise for all of these neurophysiologic studies. With the inclusion of late waves such as the F wave, H reflex, A wave, blink reflex, and somatosensory evoked potentials (SEP) in some examinations, one must also consider using central and peripheral action potentials in the description.
When a nerve is stimulated the resulting action potentials can be recorded with surface electrodes or with “near nerve” needle recording either proximal or distal to the stimulation site. The conduction velocity can be calculated by dividing the distance by the latency time to onset of the response. A semiquantitative measure of the number of functioning axons is represented by the amplitude of the nerve action potential. If a purely sensory nerve, it is referred to as the sensory nerve action potential (SNAP); if recorded over a mixed nerve, it is referred to as the compound nerve action potential (CNAP). For greater accuracy, one should subtract 0.1 ms from the latency before division—this is the “latency of activation,” technically the time between application of stimulus and activation of the axon (i.e., velocity = distance [in mm]/[latency - 0.1 (in ms)]). This time does not present a significant consideration in adults except in very short distances. However, in newborns it could make a difference in small hands with 1.5- to 2-ms latencies.
Needle EMG
There are over 400 separate muscles in the body that could be investigated with a needle electrode. With knowledge of anatomy and the probable causes of weakness or pain, one can plan the needle

examination to minimize the number of muscles explored and narrow the diagnostic probabilities. There are five steps to this needle EMG exam to be performed and analyzed as each muscle is explored with the needle electrode.
Figure 2-1 • A small, isolated fasciculation potential is recorded in a patient with amyotrophic lateral sclerosis. Total time duration of the recording is 2 s (gain = 100 μV, sweep = 50 ms).
Figure 2-2 • Fasciculation potentials recorded from the anterior tibial muscle in a person with amyotrophic lateral sclerosis. In this case many different potentials are recorded at a single needle location (gain = 50 μV, sweep = 10 ms).
Figure 2-3 • Myokymic potentials recorded with a monopolar needle in a patient with chronic radiation-induced brachial plexus injury. The slow rate of firing (5 Hz) would be unusual for a MUP under voluntary control. The first and last potentials are associated with short bursts of complex repetitive discharges (gain = 200 μV, sweep = 100 ms).
Step I: Needle in Quiet Muscle (at Rest)
Note spontaneous electrical activity:
  • Fasciculation potentials: these are recognized by their irregular and slow rate of spontaneous firing (Figs. 2-1 and 2-2) and classified by their shape: simple (usually diphasic or triphasic); complex (either the usual polyphasic MUP or repetitive discharge polyphasic); myokymic discharges (groups of MUPs firing together) (Fig. 2-3).
  • Fibrillation potential: this is spontaneous discharge of a single muscle fiber. It could be the result of denervation (but do not call it a “denervation potential”); other reasons for an unstable muscle cell membrane include inflammation (e.g., myositis), spinal shock, myotonia, local muscle trauma and ischemia, and other causes (Fig. 2-4).
In some central nervous system conditions where the upper motor neurons have lost their influence on the muscle cell membrane (i.e., flaccid limb), the stability of the membrane can be lessened, which results in spontaneous discharges, including fibrillation potentials and positive waves appearing. Examples include spinal shock in spinal cord injuries, cerebral vascular accidents with flaccid muscles, and so forth.
Step II: Insertional Activity
Electrical activity resulting from moving the needle electrode through muscle tissue is called insertional activity. These potentials are also

referred to as injury potentials. This activity represents the disruption of the muscle cell membranes as the exploring needle is moved about and membrane action potentials result. This portion of the examination is most at risk of misinterpretation. The duration of the normal insertional activity is related to the technique of needle movement used by the physician performing the examination. The appearance of the resulting burst of action potentials can last from 40 ms to at least as long as 500 ms. There are a number of pathologic conditions in which insertional activity is increased:
  • Muscle cell membrane is hyperirritable from inflammation (e.g., myositis).
  • Loss of control from motor axon compromise resulting in muscle cell denervation
  • Both 1 and 2 can also result in complex repetitive discharges (CRD); these occur by ephapses

    among muscle fibers whose membranes are extra-excitable (Figs. 2-5 and 2-6).
  • Electrolyte disturbance
  • Local muscle trauma or ischemia
Figure 2-4 • Fibrillation potentials (F) and positive sharp waves (PSW) in a photo of storage oscilloscope (gain = 50 μV, sweep = 10 ms; calibration is indicated by the slanted row of dots).
Figure 2-5 • This series of complex repetitive discharges (CRDs) was recorded from a boy with Duchenne muscular dystrophy. The small amplitudes of the action potentials reflect the atrophy of the muscle fibers (gain = 50 μV, sweep = 5 ms).
Figure 2-6 • Complex repetitive discharges (CRDs) recorded from a patient with persistent weakness caused by neuropathy. The presence of CRD suggests that the neuromuscular process has been present for a longer period of time or is chronic (gain = 100 μV, sweep = 10 ms).
Figure 2-7 • Endplate spikes and endplate positive waves are recorded together intermittently as the needle position is changed slightly (gain = 100 μV, sweep = 10 ms).
Figure 2-8 • A continuous recording shown cut into two segments. Endplate spikes are shown in the motor point of a healthy muscle, and as the needle is moved, the endplate spikes are shown to appear as positive sharp wave (PSW) forms. This type of PSW is normal and can be found in any muscle. The endplate PSW is differentiated from the PSW seen in pathology by its relatively sharply pointed negative (upward) phase, its higher frequency rate of occurrence, and especially by its appearance with endplate spikes (gain = 1 mV, sweep = 10 ms).
The most common reason for increased insertional activity is that the needle electrode is in the endplate area of the muscle. This zone, also known as the motor point, is the region where muscle fibers are naturally most vulnerable to irritation and the production of an action potential (Figs. 2-7 and 2-8).
Figure 2-9 • Diagram of the origin of the polyphasic MUP occurring within the first 4 weeks after the onset of radiculopathy. The inflamed nerve tissue allows ephaptic activation of axon membranes, resulting in synchronous MUP appearances.

To perform this portion of the EMG study, move the needle electrode briskly through the muscle tissue at different angles. Normally, there will be an immediate burst of electrical activity with needle movement. If there are a few positive sharp waves after needle electrode movement stops, this is abnormal and represents a mild instability of the muscle cell membrane, as is seen early in neurogenic disease or injury (e.g., radiculopathy). If there is no electrical discharge or activity, then there is edema, fibrous tissue, or no viable muscle tissue (e.g., infarcted muscle due to compartment syndrome).
Step III: Minimal Contraction of the Muscle
With the patient just barely contracting the muscle, one examines the MUP in detail and observes the rate of firing, stability of amplitude, duration, and shape. The shape will include the amplitude, duration, and number of phases (MUP is polyphasic if more than four phases). The stability of the MUAP (shape and amplitude) is critical also for diagnosis. Amplitude instability implies immaturity of a reinnervating MU.
A special type of polyphasic MUAP is the so-called early polyphasic, which would be better

characterized as “pseudo” because it is two or more MUAPs that discharge synchronously but not simultaneously, thus appearing as a polyphasic MUAP (Fig. 2-9).
Figure 2-10 • The recruitment interval (RI) is shown as the time period between sequential onsets of the MUPs just before the occurrence of a secondary MUP. The reciprocal of the recruitment interval is the recruitment frequency (RF). In this example from healthy muscle, RI = 90 ms and RF = 11.1 Hz.
Recruitment of the secondary MU should also be measured. If there are too few MUPs in the recruitment pattern, then the first MU will fire more rapidly before the second one is recruited. In most normal muscles, the secondary MU will appear when the primary MU is firing repeatedly at 10 to 12 Hz. If, as in a myopathy, there are the normal number of MUs but each does not contribute to a normal effort because many muscle fibers are myopathic, the second MU will be recruited early, when the first recruited MU is firing at 6 to 10 Hz. In fact, an early sign of myopathy is the inability to get a single MUP on the screen.
The recruitment frequency is the rate at which the primary MU is firing when the secondary MU appears (Fig. 2-10). This is a fairly good estimate of the number of MUs available. Normal limb muscles have a recruitment frequency of about 10 to 12 Hz, but in neuropathic conditions the recruitment frequency is increased: that is, the first MU will be at a higher rate when the secondary one is activated. For this strength of effort, the primary MU must fire faster because there are not enough MUs.
Step IV: Maximal Contraction
It is difficult, if not impossible, to get a maximal contraction in a two-joint muscle in a recumbent position, so whenever possible explore single-joint muscles. For example, explore the vastus medialis rather than the rectus femoris. Ensure a full effort by noting the firing rate and listen to the audio from the speaker, which will be helpful in estimating the effort and number of MUs recruited as you gain experience in listening.
The screen is filled horizontally and vertically with a normal maximal contraction; the sound is similar to static on the radio. The screen is filled horizontally but not vertically in myopathy; the sound will take on a higher pitch and a hissing quality. The screen is filled vertically but not horizontally in neuropathy, with a thudding quality to the sound as individual, large MUPs stand out from other noise (Fig. 2-11).
Figure 2-11 • Reduced number of MUPs in the recruitment pattern. In this case of neuropathic disease, polio of remote onset, a single MUP is firing at 16.7 Hz. The amplitude varies, suggesting some neuromuscular junction failure that is seen commonly in situations of reinnervation. This type of recruitment is often described as discrete for reporting purposes. Gain = 1 mV, sweep = 100 ms (top) and 20 ms (lower).

Step V: Distribution of Abnormalities
In the diagnosis of a generalized condition, three areas of the body should be tested and seen to be abnormal; this counts the head as an area of the body or “limb.” Needle EMG sampling should be performed in at least three areas in each muscle and eight to ten sites (insertion angles and depths) in each area.
An electrodiagnostic study can be useful in any suspected peripheral nerve injury, radiculopathy, peripheral neuropathy, localized entrapment, or disease of the MU. Chronology is important in assessing nerve injury. Wallerian degeneration occurs within 7 to 10 days, and the electrodiagnostic examination findings will vary as the axon degeneration occurs and results in deterioration of the neuromuscular junction. Generally, it takes 18 to 21 days to develop all of the EMG signs of denervation. However, the nerve will lose its excitability in 7 to 10 days. Thus, motor nerve stimulation studies can give prognostic information after 7 days. If the axon is going to die (Wallerian degeneration), it will lose excitability after 5 to 7 days, a circumstance giving the electromyographer a way to determine the prognosis by the use of the measurement of the amplitude of the CMAP. Stimulation studies can also prove continuity of injured nerves by applying a stimulus proximal to the injury during the first few days after suspected injury and demonstrating a partial response.
Listing of Motor Unit Conditions
The MU comprises the anterior horn cell, axon (passing through rootlets and spinal nerve) and its terminal branches, neuromuscular junctions, and all of the muscle fibers it innervates. Diseases, injuries and other conditions can compromise any or all of these components:
  • Anterior horn cell (AHC) diseases
    • Amyotrophic lateral sclerosis
    • Poliomyelitis, anterior (paralytic)
    • Shingles (sometimes affect the AHC)
    • Infantile progressive muscular atrophy
  • Nerve root injury
    • Herniated nucleus pulposus (with or without radiculopathy)
      • Most herniated discs will compromise the nerve roots proximal to the dorsal ganglion within the spinal canal, so the injury will not alter the SNAP amplitude. An exception is the situation of the cervical root when it is compromised by foraminal encroachment compressing the nerve root at or distal to the dorsal ganglion; this decreases the SNAP amplitude.
    • Dural sheath entrapment
      • This can result in symptoms and electrodiagnostic findings in the posterior primary rami distribution only. Can be seen in diabetic peripheral neuropathy as multiple lumbar radiculopathy and often is the early compromise in Guillain-Barré syndrome.
  • Peripheral nerve (axons)
    • Various peripheral neuropathies affect the axons. If the myelin sheath is affected mostly, conduction will be slow or blocked. If axons are primarily involved, muscle fibers will be denervated, and the electrodiagnostic examination will show fibrillation potentials and positive waves, and nerve conduction velocity testing will show reduced amplitude of the CMAP.
  • Neuromuscular junction
    • Myasthenia gravis
    • Myasthenic syndrome (Lambert-Eaton syndrome)
    • Botulism
    • Immature neuromuscular junctions during reinnervation
  • Muscular diseases
    • Muscular dystrophy
    • Myotonic dystrophy (Steinert disease)
    • Polymyositis
    • Steroid myopathy and type II atrophy
The ABCs of EMG are:
  • Assessment: Diagnosis and prognosis
  • Baseline: Follow the course (getting better or worse?)
  • Complementary: The EMG examination is functional and thus synergistic to all other clinical, imaging, and laboratory evaluations.