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Considerable attention must be given to the selection ofmontages (or derivations), for example, determining thecombination of pairs of electrodes to be recorded. Two dif-ferent montages are currently in use. In the referential (ormonopolar) montage, each of the electrodes is measuredagainst the same reference electrode, which is presumed tobe relatively electrically inactive. Commonly used referencepoints are the ears, other noncephalic regions, or the average

of all other electrodes. In bipolar montages, electrodes in aline along an anatomical region are recorded serially as suc-cessive pairs. The first channel would be from the first andsecond electrodes, the second channel would be from thesecond and third electrodes, and so forth. The most popularbipolar montage is the anteroposterior double bananamontage. Creation of different montages gives various viewsof the electrical activity at different parts of the brain. AllEEGs are analyzed using multiple montages over the samerecording, including both referential and bipolar montages.

A routine EEG is recorded for at least 20 minutes.However, it is possible to record from electrodes that areglued onto the scalp; these will record the patients EEG for

hours, days, and even weeks, if clinically necessary.Before the 1980s, the EEG was recorded on paper through

an analog system. Today, nearly all EEGs are recorded dig-itally and displayed on a computer monitor. The majoradvantage of digital recording is that the EEG can be refor-matted and flexibly reviewed in any montage, allowing thedevelopment of automated seizure detection algorithms.Benefits of other quantitative tools remain to be realized (seeQuantitative EEG, later in this chapter).6

THE NORMAL EEG

The electrical activity from any electrode pair can be described

in terms of amplitude and frequency (Figure 75-1). Ampli-

tude ranges from 5 V to 200 V. The frequency of EEGactivity ranges from 0 Hz to about 20 Hz. The frequenciesare described by Greek letters: delta (0 to 3 Hz), theta (4 to7 Hz), alpha (8 to 13 Hz), and beta (more than 13 Hz).

In the normal awake adult (with eyes closed), alpharhythm predominates in the posterior part of the head. Theamplitude of the alpha waves falls off anteriorly, and it isoften replaced by low-voltage beta activity. Often, some low-

voltage theta activity can be seen in frontocentral or tempo-ral regions. The alpha rhythm, which is prominent posteriorly,disappears (or is blocked) when the eyes open. This reactiv-ity to eye opening/closure is an important aspect of a normalEEG, and is often attenuated with many pathologies.

When a normal adult becomes drowsy, the alpha rhythmgradually disappears, frontocentral beta activity may becomemore prominent, and frontocentrotemporal theta activitybecomes predominant. Drowsiness is stage I sleep. As sleepbecomes deeper, high-voltage single or complex theta or deltawaves, called vertex sharp waves, appear centrally. Stage IIsleep is characterized by increased numbers of vertex sharpwaves, and runs of sinusoidal 12- to 14-Hz beta activity, called

sleep spindles, occur. Deeper sleep (Stage III, slow wavesleep), characterized by progressively more and higher-voltagedelta activity, is not usually seen in routine EEG recordings.

In routine EEG studies, some activation procedures arecarried out to enhance or elicit normal or abnormal EEGactivity. These procedures, such as hyperventilation, photicstimulation, sleep, sleep deprivation, and, rarely, the use ofdrugs, are useful in bringing out epileptic activity.7 The mostcommon activation procedures are 3 minutes of hyperventila-tion and a flashing strobe light (at frequencies between 5 and30 Hz). The normal response to hyperventilation ranges fromno change from baseline to a buildup of high-amplitude deltawaves. A hyperventilation response is particularly marked in

children and young adults. The most specific abnormal

Figure 75-1 A normal EEG in an anterior-posteriorbipolar montage. Each dark line represents 1

second. An eye closure is present during the first

second, which results in a resting backgroundalpha rhythm.

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response to hyperventilation is the production of generalizedspike-wave discharges of a typical absence seizure. Photicstimulation with a stroboscope may produce a drivingresponse, or occipital discharges at a frequency that is a har-monic multiple of the flash frequency. In a small number ofepileptic patients, photic stimulation may elicit electrographicepileptiform activity, or even frank seizures.8 The use of anactivating procedure in patients monitored on video-EEG for

nonepileptic psychogenic seizures is controversial. On theone hand, procedures (such as saline injection or placementof a vibrating tuning fork on the patient) to elicit psychogenicseizures are easy, safe, and potentially diagnostic. However,others believe that the deception involved undermines thecare of the patient. Some have proposed using only standardactivating procedures (e.g., hyperventilation and photic stim-ulation) to elicit psychogenic seizures.9

EEG AND AGE

The EEG background is dramatically different in neonates,infants, and children. The EEG plays an important role in the

evaluation of preterm infants, as stereotyped EEG changesare seen in the maturing brain.10 The EEG may be discon-tinuous and asynchronous in premature infants. Sharp activ-ity, not indicative of epileptic activity, may be seen up to age1 month. Posterior background rhythms increase from 5 to 6Hz at age 1 to the normal 9 to 11 Hz by age 15. 11 Alphabackground decreases with age, but should not drop below 8Hz.12

EEG ABNORMALITIES

Abnormalities of the EEG are either focal (involving only onearea of the brain) or generalized (involving the entire brain).

Additionally, abnormalities are either continuous or intermit-

tent. An abnormality that appears and disappears suddenly iscalled paroxysmal.

Nonepileptic EEG AbnormalitiesThe most common focal EEG abnormality consists of slowwave activity. Increased slow activity (i.e., theta and deltaactivity in a waking record) is virtually always abnormal.Almost all conditions that diffusely affect the brain increase

slow activity.In particular, focal delta activity is usually irregular in

configuration and is termedpolymorphic delta activity (PDA)(Figure 75-2). PDA is usually indicative of a focal brain lesion(such as tumor, stroke, hemorrhage, or abscess).13 Before theadvent of modern neuroimaging, focal delta abnormalitieswere used to localize cerebral lesions. Focal cerebral lesionsmay also cause asymmetric slowing of the background alphawaves or asymmetric beta activity.

The EEG may also show generalized abnormalities, par-ticularly in encephalopathies. As a general rule, the EEG is asensitive, though nonspecific, test for encephalopathies. Themost common pattern with metabolic encephalopathies is

generalized moderate- to high-amplitude theta and deltaactivity without an alpha resting background.14 Anothercommon pattern observed with hepatic and renal encepha-lopathies is the presence of triphasic delta waves.15 These arehigh-voltage, diffuse periodic discharges, and are at timesdifficult to differentiate from epileptiform generalized spike/sharp-slow wave discharges.16 In infectious encephalopathies,particularly in encephalitides, an admixture of slow activityand epileptogenic activity is often seen.

Intermittent rhythmic delta activity may be seen focallyor diffusely. Such activity is frequently confined to the frontalregion in adults, and is called frontal intermittent rhythmicdelta activity (FIRDA); in children, this pattern is most often

located posteriorly. Although initially believed to have been

Figure 75-2 Polymorphic delta activity in the lefthemisphere in a patient with a brain tumor.

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Few definite electrographic changes have been reportedwith most typical antipsychotic drugs at therapeutic doses;background slowing and even epileptic activity may be seenat higher doses. Clozapine induces abnormalities (such asslowing and spikes) in more than half of patients.24 Lithiummay produce diffuse slowing and enhance preexisting epilep-tiform activity on the EEG.22 No specific EEG changes areseen with use of antidepressants.

Alcohol and Other Recreational DrugsPatients with alcoholism are vulnerable to falls and to otherhead trauma. In these patients, focal EEG abnormalities andpartial seizures may be seen. During acute intoxication,slowing is seen on the EEG, but it diminishes with tolerance.Alcohol withdrawal seizures are generalized, even in patientswith focal injuries. The EEG in chronic alcoholism is associ-ated with a greater incidence of low-voltage (less than 25 V)recordings with little slowing in more than half the patients(56%) as compared to control subjects without a history ofalcoholism (13.9%).25 This can be helpful in distinguishingdelirium tremens (DTs) from other toxic metabolic enceph-

alopathies that are associated with diffuse theta and deltaslow waves. An increase in beta activity is seen on the EEGwith use of cocaine and other central nervous system (CNS)stimulants.22,26 No clinically useful changes on the EEG areseen with other recreational drugs.

Dementia and PseudodementiaObtaining an EEG may be helpful in the process of differen-tiating dementia with secondary depression from depressivepseudodementia. In patients with either depression or depres-sive pseudodementia, the EEG has been shown to be eithernormal or mildly slowed. In contrast, in patients with demen-tia with secondary depression, the majority have abnormal

EEGs; in up to one-third of patients, there may be moderateor severe abnormalities.27

SchizophreniaStudies have demonstrated that patients who demonstratenormal EEG findings with decreased reactivity to stimuli,deemed to be hypernormal, had an unfavorable prognosis.28Increased delta and beta activity, as well as decreased alphafrequencies, have been reported in patients with schizophre-nia.29 Electroencephalography has been used to evaluate thetheory that schizophrenia is the result of functional discon-nections in cerebral networks. Decreased intrahemisphericcoherence in the EEG has been demonstrated in patients withschizophrenia.30 In general, EEG studies in schizophrenicpatients have produced inconsistent results, and it has beendebated whether EEG abnormalities in these patients are dueto the state of the patient or due to the trait of the disease.31

QUANTITATIVE EEG

Quantitative EEG (qEEG) involves the use of computerizedstatistical analysis and graphical representation of EEG data.Common manipulations include spectral analysis, whichinvolves conversion of the time domain into a frequency

domain through Fourier transformation, thus allowing theassessment of the power of a frequency over a given record-ing; source analysis, a technique used to back-project EEGsignals to derive localization of a dipole; and electromagnetictomography, a method of graphing statistical results onto thepatients structural neuroimaging scan (such as a magneticresonance imaging [MRI] scan) to create a map of theseresults. Because of difficulty in replicating studies, over-

enthusiastic usage of statistical manipulation, and aggressivemarketing of qEEG devices in the 1980s, the role of qEEGin a wide range of neuropsychiatric disorders has been castinto doubt by the neurological community.32 The AmericanNeuropsychiatric Association recommends cautious use ofqEEG in attentional and learning disabilities of childhood,and in mood and dementing disorders.32

EVOKED POTENTIALS

Evoked potentials (EPs) can be used to test the integrity ofa pathway in the CNS. A sensory stimulus in any modality(e.g., visual, auditory, or somatosensory) will produce a

change in the EEG. The change is usually small comparedwith the background EEG; the exact configuration of thechange depends on the nature of the stimulus and the site ofthe recording on the scalp. The evoked potential is the changein the EEG that is dependent on, and time-locked to, thestimulus; to see it, the stimulus must be repeated many timesand the EEG averaged.33-35

The most common use of evoked potentials is to test thespeed of conduction in a particular pathway. Multiple sclero-sis is a disease of central myelin; if myelin is damaged, con-duction is slowed and the evoked potentials will be delayed.Although many multiple sclerosis plaques are clinically silentthey often show themselves with this electrical test. Hence,

evoked potentials are quite useful in making the diagnosis ofmultiple sclerosis.36

Visual evoked potentials (VEPs) were the first to becomepopular. They are ordinarily obtained with a checkerboardstimulus that alternates black and white squares repetitively.Each eye is stimulated individually and then responses aremeasured from the occipital area of the scalp. The majorwave measured is a large positive wave at a latency of about100 ms (P100). In multiple sclerosis or optic neuritis, thewave is delayed.36 Delayed or absent VEPs can be seen inmany other conditions, including ocular conditions (e.g., glau-coma), compressive lesions of the optic nerve (e.g., pituitarylesions), and pathological conditions of the optic radiationsor the occipital cortex.

Auditory stimulation produces complex waveforms. Stim-ulation with brief clicks produces six small waves in the first10 ms. Surprisingly, the sources of this electrical activity arein serial ascending structures in the brainstem. It becomespossible to study the integrity of the brainstem with thesewaves, and the test has also been used to assess brainstemdeath in cases suspected of brain death.37 The waves arealso delayed in multiple sclerosis.

Somatosensory evoked potentials (SEPs) are the averagedelectrical responses in the CNS to somatosensory stimulation.

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Like sensory nerve action potentials (SNAPS) in the periph-eral nervous system, most components of SEPs representactivity carried in the large sensory fibers of the dorsal column(medial lemniscus primary sensorimotor cortex pathway).SEPs can be used to test the integrity of the pathway and totest the speed of conduction in the pathway.

SEPs from the upper extremity are commonly producedby stimulation of the median nerve at the wrist. The cerebral

SEP to this type of stimulation was the first EP to be discov-ered. The cerebral SEP to median nerve stimulation is bestrecorded from a site approximately 2 cm posterior to thecontralateral central electrode. SEPs from the lower extrem-ity are produced by stimulation of the posterior tibia1 nerveat the ankle or the peroneal nerve at the fibular head and arerecorded best at the vertex of the head.

It is possible to localize a lesion in the somatosensorypathway by using short latency SEPs from subcortical struc-tures. Several systems of electrode placement can be used,but the one that seems to produce potentials of greatestamplitude is where the active electrode is placed over thecervical spine and referred to an inactive site such as the

vertex of the head. Four components can be identified.38 Bystimulating leg nerves, it is possible to obtain EPs at all levelsof the neuraxis, including over the spinal cord. SEPs areparticularly useful in evaluation of a comatose patient. Bilat-erally absent SEPs are highly predictive of poor outcome.39

NERVE CONDUCTION

Peripheral Nerve Conduction StudiesSensory Nerve ConductionThe cell bodies of sensory neurons are located in the dorsalroot ganglia. Each neuron has a central process entering thespinal cord through the dorsal horn and a peripheral process

connecting to a sensory receptor in the skin or deep tissuesof the limb. The receptors transduce somatosensory stimuliinto electrical potentials, which eventually give rise to actionpotentials in the axons that are transmitted along the periph-eral process to the central process. This is termed thesensorynerve action potential (SNAP). There are a variety of sensoryneurons, each with a characteristic spectrum of axonal diam-eters. Some neurons are myelinated and others are unmyelin-ated; in routine studies the unmyelinated fibers cannot bemeasured. Many sensory axons with differing function andsize run together with motor axons.

The goals of sensory nerve conduction studies are to assessthe number of functioning axons and to assess the state ofthe myelin of these axons. In the usual sensory nerve conduc-tion study, all of the axons in a sensory nerve are activatedwith a pulse of electric current. The nerve is stimulated atone location while the transmitted signal is recorded atanother location. Electrical stimulation of these nerves canbe performed, either orthodromically (along the direction ofphysiological nerve conduction) or antidromically (along theopposite direction). Action potentials travel along the nerve,and the electric field produced by these action potentials isrecorded at a site distant from the site of stimulation. Eachaxon makes a contribution to the magnitude of the electrical

field, and thus the amplitude of the recorded sensory actionpotential is a measure of the number of functioning axons.Using the distance between the site of stimulation and thesite of recording and the time between stimulation and thearrival of the action potentials at the recording site, it is pos-sible to calculate the conduction velocity, which reflects thequality of myelin of the axons.

In axonal degeneration neuropathies, the primary feature

is reduced sensory action potential amplitudes. The conduc-tion velocity may be slightly slowed, but only to the extentthat the normally largest axons are gone and the measuredconduction velocity reflects the velocity of the largest remain-ing axons. In demyelinating neuropathies, the primary featureis slowing of conduction. In radiculopathies, sensory actionpotential amplitudes and conduction velocities are fullynormal. This is because the lesion is virtually always proximalto the dorsal root ganglion and the cell body and its peripheralprocess remain normal. Sensory action potentials similarlyremain normal with lesions of the CNS.

Motor Nerve Conduction

There are significant differences between sensory and motornerve conduction that depend in large part on the differencesof their anatomy. Motor neurons have cell bodies in the ante-rior horn of the spinal cord and send their axons to innervatemuscle fibers. Motor axons are always intertwined withsensory axons; there are no nerves that are pure motor nerves.Hence, the electrically stimulated compound action potentialof any nerve with motor fibers in it is really a mixed nerveaction potential. Consequently, it is not possible to deducethe number of functioning motor axons by looking at theamplitude of a nerve action potential.

It is possible to study motor nerve axons separately fromsensory axons by electrically stimulating a nerve and by

recording from the muscle fibers innervated by the motoraxons in that nerve. Since each motor axon typically inner-vates hundreds of muscle fibers, the compound muscle actionpotential is much larger than the nerve action potential.

The number of axons can be diminished and the actionpotential normal if the process of collateral reinnervation bythe remaining axons has been complete. The number of axonscan be normal and the action potential diminished if there isa neuromuscular junction deficit or if there is loss of musclefibers. As a neuropathy progresses and collateral reinnerva-tion fails to keep pace, the muscle action potential willdecline.

The interval between delivery of the electrical stimulusand the onset of the muscle action potential may be difficultto interpret. This period is composed of the time it takes forthe motor nerve action potential to travel down the terminalbranches of the axon, the time for the release of acetylcholineinto the neuromuscular junction, the time for the acetylcho-line to produce an endplate potential, the time for generationof a muscle action potential, and, depending on the positionof the recording electrodes, the time for the muscle actionpotential to propagate to the recording electrodes. Calcula-tion of a conduction velocity for these neurons is not asstraightforward as it is for the sensory nerve. The interval

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itself, if obtained under standard conditions, can be a usefulmeasure of the conduction time in the terminal part of theaxon; it is termed the distal motor latency.

The conduction velocity of motor axons can be determinedfor parts of the axon proximal to the distal portion. If thenerve is stimulated supramaximally in two places, virtuallyidentical muscle action potentials will result; the major differ-ence will be the different latencies from the time of stimula-

tion. The difference in the latencies is due to the differencein the distances from the sites of stimulation to the muscle.Dividing the difference in the distances by the difference inthe times produces a conduction velocity for the segment ofnerve between the two sites of stimulation. Similar to themeasurement of the sensory action potential, measurementsof the muscle action potential are ordinarily made to the timeof onset; hence, the calculated conduction velocity refers tothe fastest (and largest) axons in the nerve.

In axonal degeneration neuropathies, motor nerve conduc-tion studies are not significantly abnormal until the processis moderately advanced. Total reliance on motor nerve con-duction would result in failure to detect many significant

neuropathies. Typically, there will be a slight slowing of con-duction velocity and prolongation of the distal motor latencysince the largest axons are lost. There may be loss of actionpotential amplitude when the process is advanced. In demy-elinating neuropathies, there will be slowing of conductionvelocity and prolongation of distal motor latency.

A focal lesion of a nerve will lead to slowing of conductionand to a decrement of amplitude across the segment, includ-ing the area of the lesion, but studies of the nerve distal to thelesion will be fully normal. Studies of nerve segments proxi-mal to the lesion will show normal conduction velocity withan unchanging and reduced action potential amplitude. Quitedramatic nerve conduction findings are seen with a focal, total

lesion. The nerve is fully normal below the lesion, but electri-cal stimulation proximal to the lesion produces no response(similar to the patients attempts to activate the muscle).40

In radiculopathy (lesion of the nerve roots), motor nerveconduction studies will ordinarily be normal. There may beslight slowing of conduction velocity in direct relation to theamount of loss of large fibers. In CNS disease, there willordinarily be no change in motor nerve conduction unlessthere is involvement of anterior horn cells.

Late ResponsesStudying the most proximal segments of nerves is difficult,because they are deep and not easily accessible as they leavethe spinal column. However, it is useful to study the proximalsegments of nerves since processes such as radiculopathiesfrom disc protrusion and certain neuropathies (e.g., Guillain-Barr) predominantly affect this segment. The so-called lateresponses (the H-reflex and the F-response) provide a rela-tively easy technique for study of the proximal segments ofnerves. These responses are produced in certain circum-stances after an electrical stimulus to a peripheral nerve, andare late with respect to the muscle response (the M-response)produced by the orthodromic volley of action potentials trav-eling to the muscle directly from the electrical stimulus.

The H-reflex is a monosynaptic reflex response similar inits pathway to that of the tendon jerk. The electrical stimu-lus activates the I-a afferents (coming from the muscle spin-dles) and action potentials travel orthodromically to thespinal cord. In the cord, the I-a afferents make excitatorymonosynaptic connections to the alpha motor neurons;a volley of action potentials is set up in the motor nerve,which runs orthodromically the entire length of the nerve

from the cell bodies to the muscle. Hence, action potentialstravel through the proximal segment of the nerve twiceduring the production of the H-reflex (once in the sensoryportion of the nerve and once in the motor portion). Obtain-ing an H-reflex depends on the ability to stimulate theI-a afferents. If a motor axon is electrically stimulated, anaction potential will travel along the axon antidromicallytoward the spinal cord, as well as orthodromically towardthe muscle. The antidromic action potential will collideeither in the proximal motor axon or in the cell body withthe developing H-reflex in that axon and nullify it. In routineclinical practice, it is possible to get this differential stimula-tion and to produce E-reflexes only in the posterior tibia1

division of the sciatic nerve while recording from the tricepssurae.

The F-response or F-wave has an advantage over the H-reflex in that it can be found in most muscles. It is a mani-festation of recurrent firing of an anterior horn cell after ithas been invaded by an antidromic action potential. After amotor nerve is stimulated, an action potential runs antidrom-ically as well as orthodromically; a small percentage of ante-rior horn cells that have been invaded antidromically willproduce an orthodromic action potential that is responsiblefor the F-response. Thus, to produce an F-response, actionpotentials must travel twice through the proximal segmentof the motor nerve.41

ELECTROMYOGRAPHY

The Physiology Underlying ElectromyographyUnderstanding the concept of the motor unit is central to theunderstanding of the physiology of electromyography (EMG).A motor unit is composed of all the muscle fibers innervatedby a single anterior horn cell. In most proximal limb muscles,there are hundreds of fibers in each motor unit. In the normalsituation, the muscle fibers from the same unit are notclumped together, but are intermingled with fibers fromother motor units. When a motor axon fires, each musclefiber in its motor unit is activated in a constant time relation-ship to the other fibers in the unit.

EMG activity is ordinarily recorded with a needle placedinto the muscle. Because the muscle fibers of a single motorunit are not packed closely together, the EMG needle recordsfrom only about 10 fibers from each motor unit. The ampli-tude, duration, and configuration of the electrical activityrecorded from a motor unit vary as the needle changes itsorientation to the muscle fibers. Despite its variability it ispossible to specify a normal range for the amplitude, dura-tion, and configuration of motor unit action potentials(MUAPs) for each muscle and each age.

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When an EMG needle is placed in a normal muscle at rest,there is no electrical activity. With weak effort, first one andthen several motor units are activated. At this low level ofactivation, it is possible to see the individual MUAPs andevaluate their parameters. With maximal effort so many unitsare brought into action that individual MUAPs cannot bediscerned; all that can be seen is a dense electrical pattern,called an interference pattern, which can be characterized by

its density and peak-to-peak amplitude. The normal densitywould be either full, if there are no gaps, or highly mixed,if there are a few, short gaps. Some people are not willing orable to exert a maximal effort and the pattern will be lessdense as a result. Hence, the degree of effort has to be takeninto account when assessing the interference pattern.

Findings on the ElectromyogramAcute Partial Injury (e.g., Partial Laceration of a Nerve)Motor axons that are injured undergo Wallerian degenerationover the course of about 5 days, leaving muscle fibers previ-ously innervated by those axons in a denervated state. Withinapproximately 10 to 14 days, denervated muscle fiber action

potentials are recorded by the EMG needle as fibrillationsand positive sharp waves. There is nothing different aboutfibrillations and positive sharp waves other than a slightdifference in the particulars of the recording; both aresimply small, diphasic potentials beginning with a positivephase.

The motor units that can be activated will be normal; itwill not be possible to voluntarily activate the denervatedmuscle fibers. Descriptive terminology for these patterns ishigh mixed, mixed, low mixed, and single unit, inorder of decreasing density.

Chronic Partial Injury

After weeks to months, there will be collateral sproutingfrom surviving motor axons to innervate denervated musclefibers. Spontaneous activity will cease. Motor units will nowcontain more muscle fibers than normal; hence, MUAPs willbe long-lasting, high, and more complex in shape or polypha-sic. The density of the interference pattern may improve, butwill probably remain less than full although the amplitudewill increase.

Complete InjuryIn this circumstance no voluntarily initiated motor nerveaction potentials can reach the muscle due to a focal demy-elinating injury. Muscle fibers will not be denervated so theywill not fibrillate. EMG examination will reveal no spontane-ous activity, no MUAPs, and no interference pattern. Thisis no different from the first few days of a total injury;after these first days the denervated muscle fibers begin tofibrillate.

MyopathyThe simple model of myopathy is characterized by dropoutof individual muscle fibers from their motor units. In activemyopathies, especially polymyositis, there may be some seg-mental muscle necrosis. This process divides a muscle fiberinto an innervated segment and an uninnervated segment.The uninnervated segment might fibrillate and, hence, resultin active myopathies, some fibrillation, and positive sharpwaves; most commonly spontaneous activity is lacking.

Neuromuscular Junction Studies

The most common abnormality at the neuromuscular junc-tion is myasthenia gravis. The standard neurophysiologicalstudies for myasthenia gravis are the repetitive nerve stimula-tion test and the single-fiber EMG. During the repetitivestimulation test, the nerve is stimulated with rates of stimu-lation of 2 to 10 Hz. In normal patients, the action potentialis the same, but in those with myasthenia gravis, the ampli-tude of the action potentials might decline on successivestimulations. In the inverse myasthenic syndromeEaton-Lambert syndromethe repetitive stimulation test showsa progressive increase in amplitude of the muscle actionpotential.

Single-fiber EMG is highly sensitive for the diagnosis of

myasthenia gravis. In this test, a small needle is used that candetect the action potentials from single muscle fibers. Thetime between the firing of two muscle fibers from the samemotor unit should be very stable. In myasthenia gravis, dueto the slow and uncertain function of the neuromuscular junction, there may be an increase in the variability of thetime between firing of these two muscle fibers; this is calledincreased jitter.42

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