Electromyography (EMG) and Nerve Conduction Studies 863

Electromyography (EMG) and Nerve Conduction Studies

J M Shefner and L Simionescu, SUNY Upstate Medical University, Syracuse, NY, USA
2009 Elsevier Ltd. All rights reserved.

Definitions
Electromyography (EMG) is a technique whereby extracellular current fluxes are recorded from muscles at rest and during voluntary activation. Most commonly, signals are recorded from an intramuscular concentric needle electrode, but recordings can be made from surface electrodes placed on the skin overlying the muscle to be studied. Signals are amplified and filtered digitally and displayed in real time. When needle electrodes are used, action potentials from single muscle fibers that are spontaneously active (fibrillation potentials) may be recorded, as may the combined response of all muscle fibers innervated by a single motor axon (motor unit potential). Motor unit potentials may occur spontaneously (fasciculation potentials) but usually are seen in response to voluntary, reflex, or electrically stimulated activity of motor neurons within the central nervous system. With appropriate processing, motor unit potentials can sometimes be isolated from signals recorded with surface electrodes, but responses of individual muscle fibers and motor units in deeper muscles usually cannot be seen without intramuscular electrodes. Electromyographic signals are recorded for research purposes to assess the timing and level of voluntary, reflex, or other muscle activation; simultaneous recordings from multiple muscles can also be used to investigate central control of motor activity. However, EMG is primarily a clinical tool used to evaluate a variety of diseases in which the peripheral neuromuscular system is affected. Motor unit potential morphology and discharge patterns are altered by both muscle and nerve disease, usually in opposite ways. Because only muscle membrane activity is recorded (and not force), disorders that primarily affect the contractile apparatus within muscle will not affect individual motor unit potentials but may alter discharge rates. In clinical laboratories, EMG is usually performed in conjunction with nerve conduction studies (NCSs); these studies usually involve electrical stimulation of a mixed sensory and motor nerve bundle with recording of compound sensory responses from cutaneous fibers, or they involve compound motor action potentials from muscle fibers innervated by the nerve being stimulated. Because only current fluxes rather than transmembrane potentials are being recorded, sensory NCSs assess conduction only in the largest

diameter myelinated fibers that produce the greatest current flows, whereas motor studies reflect activity in most or all of the alpha motor axons directed to the muscle being recorded. NCSs are particularly useful to evaluate generalized and focal disorders of nerves rather than primary muscle disorders. Although NCSs have evolved primarily as a clinical tool, research applications continue to appear. One current research application is in the area of excitability testing, in which NCSs are used to evaluate the local sources and time courses of ionic currents that occur in response to an evoked action potential. Finally, neuromuscular transmission can be studied using both EMG and NCS. With a specially designed EMG needle and filters that attenuate spatially remote signals, action potentials from two muscle fibers within the same motor unit may be recorded simultaneously (single-fiber EMG). The precise temporal relationship between the firing patterns of the two fibers provides information about the effectiveness of neuromuscular transmission. In addition, if motor nerves are stimulated repetitively, the extent to which the compound motor action potential amplitude declines with repeated stimulation is a measure of the inability of the neuromuscular junction to sustain transmission. Although EMGs and NCSs are typically used to evaluate processes peripheral to the spinal cord, more central systems may also be studied. The mono/oligosynaptic stretch reflex may be studied electrically by stimulating muscle primary (Ia) afferents and recording motor potentials from the corresponding muscle (H reflex). Prior stimulation or concurrent sensory stimulation to evaluate, in particular, spinal circuitry subserving recurrent, reciprocal, and presynaptic inhibitory pathways may modify this reflex. In addition, the recently developed technique of transcranial magnetic stimulation can be used to evaluate the integrity of motor pathways from cortex to muscle.

Studies of Nerve Conduction

Many aspects of axon conductivity may be assessed with nerve conduction studies; in the clinical laboratory, however, only conduction velocity and response amplitude are measured. Motor axons and sensory axons can be evaluated separately, and different subtypes of sensory fibers can be selectively studied. Axon numbers are reduced in a variety of clinical disorders. In generalized neuropathies, axons of many or all modalities are lost, often with a distal-to-proximal gradient, whereas focal neuropathies reduce axon numbers in a particular nerve distribution. More proximal disorders of nerve roots or spinal cord will

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also result in axonal dropout; however, if the site of the disease process is proximal to the dorsal root ganglion, only motor fibers will be affected. Thus the ability to distinguish between loss of motor or sensory axons is of clear clinical importance. Measurements of conduction velocity are useful to evaluate the pathogenesis of different neuropathic conditions. When the primary site of pathology is the nerve cell body or axon itself, the number of functioning axons will be reduced but conduction will be unaffected in those axons remaining. In contrast, other disease processes affect the Schwann cell or the myelin sheath that surrounds large-diameter, rapidly conducting axons. Disruption of the myelin sheath may produce slowing of conduction in some or all myelinated fibers, sometimes with relatively little associated axon loss. In addition, focal areas of demyelination can render an axon locally unexcitable, even though conduction may persist both proximal and distal to the area of damage. Such an axon would be unable to transmit impulses between the spinal cord and the appropriate target organ. Such focal dysfunction is known as conduction block. Clinicians perform nerve conduction studies by applying an electrical current pulse to the skin overlying a mixed (sensory and motor) peripheral nerve. With such stimulation, individual axons can be stimulated to produce action potentials. Nerve fibers are much more sensitive to electrical stimulation than muscle fibers are, so even when a nerve lies beneath muscle it is almost always preferentially stimulated by surface electrodes. So-called direct electrical stimulation of muscle with current pulses less than a few milliseconds in duration actually produces contraction indirectly by stimulating motor axons as they pass through the muscle. Within the nerve itself, certain axons are more apt than others to give rise to action potentials. In general, larger-diameter axons have higher sensitivity (lower thresholds) to external electrical stimulation; therefore, when a mixed nerve is stimulated, large-diameter sensory fibers are activated most easily, followed by axons of alpha motor neurons. Geometric considerations are also very important; fascicles lying closer to electrodes on the skin surface will be stimulated more effectively than will be deeper-lying fascicles. With appropriate stimulus intensities, it is usually possible to stimulate all large-diameter (sensory and motor) axons; to stimulate smaller myelinated sensory fibers and any unmyelinated fibers, extremely strong (and therefore quite painful) stimuli are required.
Motor Conduction Studies

A stimulus of appropriate intensity and location will cause action potentials to arise in all motor axons

present in a mixed nerve, and a compound muscle action potential (M response) can then be recorded using a surface electrode placed over the motor point of a muscle innervated by the stimulated nerve, with an indifferent electrode placed over a bony prominence. The recorded potential can be characterized in a number of different ways; the two clinically most useful measures are (1) onset latency and (2) baseline to peak amplitude. The onset latency reflects conduction in only the fastest few fibers and is a function of nerve conduction velocity, speed of neuromuscular transmission, and conduction along the muscle membrane. If, however, the same nerve is stimulated at a second location, the difference in onset latencies can be used to calculate nerve conduction velocity if the distance between the stimulating electrodes is known. Obviously, the accuracy of such measurements depends on the ability to determine the length of nerve between the two locations. Because motor axons conduct with a fairly restricted range of velocities, and the duration of muscle action potentials is much longer than nerve action potentials, the amplitude of the compound response directly assesses the number of muscle fibers activated. This number is not a direct measure of the number of motor axons responding; in conditions of chronic axon loss, surviving axons reinnervate muscle fibers that have lost synaptic contact. Thus a reduced number of motor axons may still contact all available muscle fibers. Therefore, motor action potential amplitude is not a sensitive measure of axon loss. The compound motor action potential can be studied in a way that more directly assesses both axon loss and resultant terminal reinnervation. This technique, known as motor unit number estimation (MUNE), was first proposed more than 30 years ago, but continues to be refined and is increasingly employed clinically and as an outcome measure in clinical trials. A number of MUNE techniques have been developed and remain in use; all rely on the same basic premise: the response amplitude of an average single motor unit potential (SMUP) is calculated, then it is divided into a maximum response, the compound muscle action potential (CMAP), to derive a number that estimates the total number of units present (the MUNE). Of the MUNE techniques that have been devised (incremental, multiple point stimulation spike-triggered averaging, F wave, and statistical methods), only the method of sampling the SMUP responses varies. Although differences of opinion remain among MUNE investigators as to which method should be used, the statistical and the multiple point stimulation (MPS) MUNEs currently enjoy the most widespread use. In diseases characterized by progressive motor unit loss, such as amyotrophic lateral sclerosis (ALS),

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MUNE can be used reliably in the longitudinal evaluation of patients. Multiple studies have demonstrated a decline of the number of the motor neurons with disease progression. MUNE has been employed as an outcome measure in several multicenter ALS treatment trials. MUNE can be used for assessing the effects of both neuroprotective therapies and therapies designed to enhance collateral reinnervation as it enables quantitation of motor unit numbers while simultaneously estimating the collateral reinnervation. MUNE may also have a significant potential in clinical decision making, as suggested by studies showing that a single MUNE evaluation and a demonstration of rapid decline of MUNE are both strong predictors of survival in ALS. In addition, it was shown that MUNE could be used to detect motor neuron loss prior to onset of symptoms. In most situations, amplitude and shape of the compound muscle action potential is invariant to changes in stimulating electrode position, so that proximal and distal stimulations produce responses that differ in onset latency only. However, diseases that affect myelin may cause dispersion in conduction velocities, so that the amplitude of the compound response may decrease with proximal stimulation even though the number of stimulated fibers remains the same. This may be confused with true conduction block; however, because the pathophysiology of both events is segmental demyelination, the distinction is not critical.
Sensory Conduction Studies

Sensory conduction studies require recording of nerve action potentials directly. Because electrical current fluxes surrounding nerve are much smaller than those surrounding muscle, up to 1000 times greater amplification is often required to record from the former. Typically a mixed nerve is stimulated, and recordings are made from electrodes placed on the skin over the cutaneous field supplied by the nerve. Conductive gels and mild skin abrasion are used to reduce the impedance between skin and recording electrode. The compound sensory action potential is a more direct reflection of nerve function than is the motor action potential just discussed, because no intervening neuromuscular junction exists and the response amplitude is a more direct reflection of total number of nerve fibers responding. Thus conduction velocity can be calculated from a single recording site. However, given that the distribution of axon diameters is considerably greater for sensory than for motor axons, both onset latency and response amplitude are indicators of conduction in only the largest diameter, fastest conducting axons. Conduction in slower-conducting sensory fibers can be studied in several different ways. Instead of

recording from electrodes applied to the skin surface, needle electrodes may be placed within several millimeters of the nerve (near-nerve recording technique). With appropriate amplification and filtering, recordings from these needle electrodes reflect activity in axons with diameters as small as one-fourth of the largest diameter sensory axons (small myelinated fibers in Ad range). Although many myelinated and all unmyelinated fibers are still left unrecorded, the ability to analyze activity in smaller myelinated sensory axons is very useful in the evaluation of a variety of different neuropathic conditions. To be able to record the response of unmyelinated fibers (C fibers) the technique of microneurography was developed. As unmyelinated fibers have a diameter of less than 1 mm and conduct as slow as 0.5 m s1, the current fluxes generated by action potentials are too small to be recorded by electrodes outside the nerve bundle. With microneurography, a tungsten electrode is inserted directly into the nerve bundle being studied and single unmyelinated C fiber responses can be recorded. Important applications of this technique include analysis of sympathetic efferent activity, as well as investigation of the receptive field properties of different afferents, such as receptive field size and preferred stimulus. Small-diameter sensory and motor axons can also be evaluated using tests of autonomic function. Changes in skin resistance can be measured; they are mediated by activity in unmyelinated autonomic efferent sudomotor fibers to the hand or foot after one or other innocuous stimulus. The latency of this sympathetic skin response is very long, because efferent conduction velocity is about 1 m s1. This response (sometimes called the psychogalvanic reflex) is absent in conditions that interrupt conduction in unmyelinated efferents. Because conduction in unmyelinated fibers cannot be slower than it is normally, abnormalities are manifested by absence of the response rather than increases in its latency. In addition, autonomic afferent and efferent pathways can be studied by recording the variability of heart rate as a function of controlled deep breathing. Axons may be affected by disease or external stress in ways that are reflected by changes in membrane excitability. A noninvasive battery of excitability measures has been developed that yield information about specific ion conductance channels, as well as how such channels are affected by disease processes. Threshold tracking measures, rheobase, and activitydependent axonal conductance measures have been obtained in normal individuals, as well as in patients with neuropathy and motor neuron disease. Results in patients with diabetic neuropathy suggest a defect in inward rectification, while ALS patients tend to

866 Electromyography (EMG) and Nerve Conduction Studies

show a pattern of abnormalities suggesting a persistent sodium conductance not seen in normal persons. Such insights are not available using traditional methods of clinical neurophysiology; thus, excitability testing holds the promise for more detailed study of membrane processes in a variety of peripheral nerve disorders.
H Reflex and Late Responses

To study conduction in more central segments of peripheral nerve, including plexus and roots, volleys of impulses produced by peripheral stimulation pass centrally into the spinal cord and then back out to muscles where the activity can be recorded. Tendon reflexes are produced by activity traveling toward the cord in large-diameter Ia sensory fibers and then back to muscles in alpha motor axons. Their neurophysiologic counterpart is the H reflex, in which afferent volleys are produced by electrical stimulation of spindle primary afferents rather than by mechanical stimulation of their intramuscular endings, and the compound muscle action potential is recorded rather than the clinically observed joint movement. Absence of the H reflex or marked prolongation of its latency usually reflects abnormalities in peripheral nerve conduction, but it may not be possible to separate sensory from motor abnormalities. Supramaximal stimulation of a mixed nerve produces, in addition to impulses in sensory axons and in motor axons conducted distally to the muscle, impulses in the same motor axons that travel antidromically through the ventral roots into the motor neuron pool. An impulse in some of these axons, once it reaches its motor neuron, fails to die out and, in that motor neuron, gives rise to another impulse that is then conducted orthodromically back out, where it can be recorded from muscle as an F wave. Neural activity responsible for F waves travels both to the spinal cord and back out again through motor axons: F waves are therefore not reflexes their afferent arcs are not made up of sensory fibers. The F wave latencies are nevertheless useful, because they are inversely proportional to conduction velocity throughout the entire length of a motor axon.

Clinical EMG
EMG provides invaluable information about the functional status of individual motor units, including, of course, their spinal motor neurons. Electromyographic evaluation of a single muscle involves investigation of three distinct properties. First, electrical activity present during complete relaxation is studied. Normal muscles are silent; that is, no significant spontaneous activity occurs in the motor neuron or muscle fibers. However, any process that causes loss

of motor axons will, at least acutely, result in the presence of some denervated muscle fibers. Initially, such fibers are silent; however, over the course of 23 weeks (and associated with the proliferation of postsynaptic acetylcholine receptors along the sarcolemmal surface), they become spontaneously active and generate action potentials called fibrillation potentials. Once established, fibrillations from a denervated muscle will persist until contact with another motor axon is established. In addition, if a motor axon is damaged but not destroyed, spontaneous activity may also occur, the origin of which is the axon itself; such potentials are called fasciculations. Muscle diseases usually do not involve destruction of motor axons, so it might be expected that spontaneous activity would be absent. However, in many (particularly inflammatory) myopathic processes, muscle fibers split. Under those conditions, part of the fiber may remain connected to a motor axon but the other part is functionally denervated. If an axonal connection is not rapidly established, fibrillation potentials will occur in this latter part. In addition to analyzing spontaneous activity, EMG involves the study of voluntarily activated motor units. Mild voluntary contraction usually results in the activation of one to three different motor units within the region being recorded by the needle electrode. The morphology of an individual motor unit potential is a product of the number of muscle fibers in that unit and the spatial distribution of those fibers with respect to the recording electrode. Within a muscle, a normal motor unit includes some but not all muscle fibers in a specific location (Figure 1). The amplitude of the recorded potential from that unit will be a reflection of both the number of fibers activated and their proximity to the electrode. The duration will reflect primarily the spatial extent of the motor unit. Diseases that produce a loss of motor axons will, after 23 months, also be associated with remodeling of existing motor units, so that more muscle fibers are innervated by a single axon. This will produce the electrical changes shown in Figure 1; motor unit potentials will be larger and more prolonged than normal. In contrast, diseases that are primarily directed at muscle itself will not alter the number of motor units but will reduce the number of functioning muscle fibers; motor unit potentials will then be abnormally small in amplitude and short in duration. In most clinical laboratories, evaluation of motor unit morphology remains a subjective task; electromyographers view the potentials in real time on a computer screen and derive an impression of whether potentials are small or large, brief or prolonged.

Electromyography (EMG) and Nerve Conduction Studies 867

Normal

Myopathic

Reinnervated

c
Figure 1 A single motor unit branches terminally to innervate some but not all muscle fibers within an area of muscle. The action potential produced by each motor unit is seen in the upper right of each section. The normal-appearing but unshaded fibers belong to other motor units. (a) In a normal motor unit, some but not all muscle fibers in a local area are innervated by the same axon. (b) In a myopathic unit, terminal axons are attempting to innervate dysfunctional muscle fibers, resulting in an action potential that is reduced in amplitude and duration. (c) In a reinnervated motor unit occurring as a consequence of chronic axon loss, a single axon innervates more muscle fibers than in the normal situation, resulting in an action potential that is larger in amplitude and longer in duration.

Usually the signals are stabilized by a triggering mechanism. Quantification of duration and amplitude using either weighted averaging or templatematching algorithms is available in most EMG machines, but is not often used in routine studies. In addition to analysis of spontaneous activity and motor unit morphology, EMG also evaluates the pattern of motor unit activation. The central nervous system encodes an increase in muscle activation in two ways: (1) motor units that are initially active at low levels of force production increase their firing rates and (2) motor units that had previously been

silent are recruited into activity. Thus an EMG needle recording from a muscle with increasing activity should note these two parallel processes. If the number of motor units is reduced because of motor axon loss, the EMG should show the normal increase in firing rate in those motor units available to discharge, but a reduction in the number of additional motor units recruited as force is increased. This reduced motor unit recruitment occurs immediately after nerve injury preceding the development of fibrillation potentials or changes in motor unit morphology. In contrast, if the number of motor units is normal but the number of muscle fibers is reduced because of muscle disease, an attempt to increase muscle activation will result in both the increase in firing rate of previously active units and a rapid involvement of other units, because the force generated by a single unit will be less than normal. Thus muscle disease is characterized by early recruitment of smaller than normal motor units. To further obtain accurate data regarding motor unit potential (size, configuration, and firing characteristics), a number of quantitative EMG techniques have been developed. An automated method of decomposition-based quantitative electromyography (DQEMG) can be applied to interference patterns recorded simultaneously from intramuscular and surface electrodes. The EMG-interference pattern can be decomposed into its constituent motor unit potentials. Both motor unit morphology and firing pattern may be studied. Surface-recorded motor unit potentials derived from decomposition may be averaged to yield an average motor unit size, from which a motor unit number estimate may be calculated. Currently, decomposition techniques are primarily research tools; however, the potential exists for DQEMG to provide a reliable method for evaluating the disease progression as well as the response to treatment interventions. The MUPs recorded via concentric needle electrodes reflect the electrical activity of a portion of a motor unit. To obtain information regarding the entire motor unit, another technique using macro needle electrodes was developed. By using a modified single-fiber EMG needle electrode, a single-fiber potential is first recorded and then used as a trigger for recording and time-locking surface potentials, which are averaged to determine the surface electrical activity of a whole motor unit. The parameters measured are the amplitude, area, and duration of the averaged SMUPs. Comparing the macro-EMG with a concentric-needle EMG, regarding their sensitivity in detection of neuromuscular disorders, it was shown that the techniques appear to have similar sensitivities and that by combining the results of both methods additional increase in sensitivity can be achieved.

868 Electromyography (EMG) and Nerve Conduction Studies

Studies of Neuromuscular Transmission

Single-Fiber EMG

A standard concentric needle EMG electrode has a large recording surface, designed to record potentials from at least 20 neighboring muscle fibers. However, by reducing the size of the recording area and by filtering out distant potentials, it is possible to record from a small number of individual muscle fibers within the same motor unit (single-fiber EMG). The average number of fibers from the same motor unit seen with repeated electrode penetrations is called the fiber density, and is a measure of the geographic concentration of single muscle fibers belonging to a given unit. In addition, when two to three fibers from one motor unit are recorded simultaneously, variability in the temporal relationship between activation of both fibers can be studied. This variability is called jitter and is extremely small under normal conditions. However, diseases of the neuromuscular junction, such as myasthenia gravis, cause variability in the time taken by neuromuscular transmission and therefore increase the jitter. Occasionally, neuromuscular transmission is so tenuous that one of the fibers being recorded fails to fire at all; this is called blocking and is a sign of severe disease. Jitter is the most sensitive measure of dysfunction at neuromuscular junctions but it is not specific, and increased jitter can be seen with neuropathic processes as well.
Repetitive Stimulation

presynaptic potentiation increases acetylcholine release. Because many more quanta are normally released than are necessary for maximal postsynaptic depolarization (a large safety factor), quantal rundown is only seen when neuromuscular transmission is compromised. In contrast, presynaptic neuromuscular junction disorders (such as botulism or EatonLambert (myasthenic) syndrome) may show some decrement with 23 Hz of stimulation but show striking increases in response amplitude at either rapid rates (3050 Hz) of stimulation or immediately after a short period of maximum voluntary exertion.

Central EMG/NCSs
Historically, EMG and NCSs have been used as aids to the diagnosis of peripheral nervous system disorders. However, they can provide insight into central processes as well. By recording either needle or surface EMG signals from multiple muscle groups simultaneously, movement disorders such as tremor and dystonia can be studied. Different types of tremors are characterized by distinct patterns of EMG activity in agonist and antagonist muscle groups. For example, parkinsonian tremor is electromyographically alternating; that is, one set of muscles is active during relative silence of its antagonists. Enhanced physiologic tremor and essential/familial tremor, in contrast, are characterized by co-contraction; agonist and antagonist muscle groups are active simultaneously. EMG also aids analysis of dystonias, allowing clinicians to determine which muscle groups are active during the assumption of specific postures. This information is of critical importance in planning treatment, which frequently consists of weakening individual muscle groups with local injections of botulinum toxin. In addition to evaluation of conduction in peripheral nerve, it has recently become possible to stimulate brain or spinal cord directly and record peripheral responses. This can be done with high-voltage electrical stimuli applied to the scalp or spinal column; perhaps not surprisingly, this is an uncomfortable procedure. Magnetic stimulation is a less painful alternative, with stimulators that produce brief, powerful magnetic fields. When coils producing these magnetic fields are placed over the skin near nervous tissue, these fields in turn induce in that tissue an electrical field that can stimulate neighboring cortical, spinal cord, or peripheral nerves, therefore providing a method for testing the functional integrity of the corticospinal tract as well as the motor cortex excitability. By using transcranial magnetic stimulation (TMS), motor-evoked potentials can be recorded from arm or leg muscles and, after estimates of peripheral conduction time are subtracted, an estimate of central conduction time can be made. Central conduction

Compound motor action potential response area is positively correlated with the number of muscle fibers activated and, if neuromuscular transmission is intact, with the number of motor axons activated. Repetitive supramaximal stimulation of motor nerves is used clinically to assess function at neuromuscular junctions. With supramaximal electrical stimuli (all alpha motor axons being stimulated), changes in M amplitude, duration, or area with repetitive stimulation reflect disturbances in neuromuscular transmission. Disorders such as myasthenia gravis produce a typical decremental pattern of M response amplitude/area, but only in an affected muscle, when the motor nerve is stimulated at 23 Hz. The first M response is usually not as large as normal, but each subsequent one becomes smaller until the fourth or fifth response is reached, at which time the decrement ceases; subsequent responses often become slightly larger. This pattern (because of reduction in number of functional postsynaptic acetylcholine receptors) reflects normal quantal rundown; the number of quanta of acetylcholine released by each successive impulse decreases, as does the postsynaptic response, until

Electromyography (EMG) and Nerve Conduction Studies 869

has been demonstrated to be abnormal in a variety of neurologic diseases, including multiple sclerosis and amyotrophic lateral sclerosis, even prior to onset of symptoms. Therefore, TMS represents a useful investigational tool, allowing early diagnosis, monitoring of disease progression, and estimating prognosis. In addition, a newer TMS technique, repetitive transcranial magnetic stimulation (rTMS), has been developed as a promising therapeutic tool, by modifying the excitability of the cerebral cortex. Tentative therapeutic applications at this time include Parkinsons disease, epilepsy, stroke, and depression. Spasticity, another central disorder, has also proved amenable to study with methods adapted from routine NCSs. As discussed previously, the H reflex is analogous in many ways to a deep tendon reflex; as such, it provides a qualitative measure of upper motor neuron abnormalities. More information about spinal cord processing can be obtained by conditioning the H reflex in a variety of ways. Rapid tendon vibration effectively stimulates primary afferent fibers and acts as a potent stimulus for presynaptic inhibitory pathways; H reflexes conditioned by tendon vibration therefore vary in size as a function of amount of presynaptic inhibition. Prior activity in motor neurons activates Renshaw cells; H reflexes obtained at certain intervals after such activity can therefore be used to evaluate inhibitory activity in recurrent pathways. Thus although EMG/NCSs are primarily tools for evaluation of the peripheral nervous system, they also provide information about central nervous system function.
See also: Cognition: An Overview of Neuroimaging Techniques; Cognitive Neuroscience: An Overview; Electroencephalography (EEG); Glutamate Regulation of Dendritic Spine Form and Function; Neuromuscular Junction (NMJ): Presynaptic Stretch Effects on Neuromuscular Transmission; Transcranial Magnetic Stimulation.

Further Reading
Aggarwal A and Nicholson G (2002) Detection of preclinical motor neuron loss in SOD1 mutation carriers using motor unit number estimation. Journal of Neurology, Neurosurgery & Psychiatry 73(2): 199201.

Alisauskiene M, Truffert A, Vaiciene N, et al. (2005) Transcranial magnetic stimulation in clinical practice. Medicina 41(10): 813824. Armon C and Brandstater ME (1999) Motor unit number estimatebased rates of progression of ALS predict patient survival. Muscle and Nerve 22: 15711575. Boe GS, Stashuk DW, and Doherty TJ (2004) Motor number estimation by decomposition-enhanced spike-triggered averaging: Control data, testretest reliability and contractile level effects. Muscle and Nerve 29: 693699. Boe GS, Stashuk DW, and Doherty TJ (2006) Within-subject reliability of motor unit number estimates and quantitative motor unit analysis in a distal and proximal upper limb muscle. Clinical Neurophysiology 117: 596603. Bostock H, Cikurel K, and Burke D (1998) Threshold tracking techniques in the study of human peripheral nerve. Muscle and Nerve 21(2): 137158. Buchthal F and Rosenfalck A (1966) Evoked action potentials and conduction velocity in human sensory nerves. Brain Research 3: 1122. Burke D, Kiernan M, and Bostock H (2001) Excitability of human axons. Clinical Neurophysiology 112: 15751585. Doherty TJ and Stashuk DW (2003) Decomposition-based quantitative electromyography: Methods and initial normative data in five muscles. Muscle and Nerve 28: 204211. Eisen A (2001) Clinical electrophysiology of the upper and lower motor neuron in amyotrophic lateral sclerosis. Seminars in Neurology 21(2): 141154. Finsterer J and Fuglsang-Frederiksen A (2001) Concentric-needle versus macro EMG. II Detection of neuromuscular disorders. Clinical Neurophysiology 5: 853860. Mogyoros I, Kiernan MC, and Burke D (1996) Strengthduration properties of human peripheral nerve. Brain 119(2): 439447. Olney R, Yuen E, and Engstrom J (1999) The rate of change in motor unit number estimates predicts survival in patients with amyotrophic lateral sclerosis. Neurology 52(supplement 2): A3. Shefner JM (2001) Excitability testing in clinical neurophysiology what, why and when? Muscle and Nerve 24: 845847. Shefner JM (2002) Peripheral sensory conduction. In: Brown WR, Bolton CP, and Aminott MJ (eds.) Neuromuscular Function and Disease, vol. 1, chapter 6. Philadelphia: WB Saunders. Shefner JM and Gooch C (2003) Motor unit number estimation. Physical Medicine and Rehabilitation Clinics of North America 14: 243260. Shefner JM, Preston DC, and Logigian EL (1996) Activity-dependent conduction in single motor units. Neurology 46(5): 13871390. Stalberg E (1980) Macro EMG, a new recording technique. Journal of Neurology, Neurosurgery & Psychiatry 43: 475482. Stalberg E (1990) Macro EMG. Methods in Clinical Neurophysiology 1: 114. Vallbo AB, Hagbarth KE, and Wallin G (2004) Microneurography: How the technique developed and its role in the investigation of the sympathetic nervous system. Journal of Applied Physiology 96: 12621269.