normal adult eeg and patterns of uncertain significance

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ORIGINALARTICLES

Normal Adult EEG and Patterns of Uncertain Significance

William O. Tatum IV,* Aatif M. Husain, Selim R. Benbadis,* and Peter W. Kaplan

A thorough understanding of a normal EEG is critical in defining

those patterns that are abnormal. Because EEG is unique in the

ability to support a clinical diagnosis of epilepsy, epileptiform

patterns merit careful consideration. Certain benign patterns maybe

epileptiform, yet can occur in healthy individuals without epilepsy.

Understanding normal EEG and the benign variants will help to

minimize overinterpretation and possibly avoid overtreatment of

patients during routine clinical practice.

Key Words: EEG, Normal, Neurophysiology, Benign, Variants,

Epileptiform.

(J Clin Neurophysiol2006;23: 194207)

Neurophysiology has rapidly advanced since the early20th century pioneered the initial human adult EEGexperiences. Over the last 75 years, EEG has evolved from adiagnostic tool, to an integral part of intensive monitoring notonly for diagnostic purposes, but also for providing informa-tion to deliver therapy via direct brain electrical stimulation.The EEG represents a collection of waveforms containinginformation about the function of the brain. In general hos-

pitals, EEG holds a principal role for routine neurodiagnosticinformation in clinical medicine, while in tertiary care epi-lepsy centers, EEG seeks to identify the epileptogenic zonesin patients with intractable seizures for the purposes ofresective epilepsy surgery. To understand the abnormal EEG,one must understand that which is normal. The followingreview represents the most current assessment of clinicalEEG in the context of performing adult scalp-based record-ing.

NORMAL HUMAN ADULT EEG

The advent of EEG in humans started with Hans Berg-ers discovery of the alpha rhythm in human subjects (Adrian

and Mathews, 1934). The alpha rhythm still remains thestarting point to analyze clinical EEG (Kellaway et al., 2003).

In the normal EEG, a posterior dominant rhythm is repre-sented bilaterally over the posterior head regions and lieswithin the 8 to 13 Hz bandwidth that characterizes the alphafrequency.When this rhythm is attenuated with eye opening,it is referred to as the alpha rhythm (see Fig. 1).

In human development, an 8 Hz alpha frequency nor-mally appears by 3 years of age. More than one site exists togenerate the alpha rhythm within both cortical and subcorticalregions. When the best frequency of the alpha rhythm is only8 Hz, this should raise suspicion for abnormal slowing, as thisfrequency occurs in 1% of normal adult subjects at any age.The alpha rhythm remains stable between 8 to 12 Hz evenduring normal aging into the later years of life (see Fig. 2). Inapproximately one fourth of normal adults, the alpha rhythmis poorly visualized with 6% to 7% of normal adults demon-strating voltages of 15 Hz (Kellaway, 2003). The alpharhythm is distributed maximally in the occipital region andshifts anteriorly during the drowsy state. In one third ofpeople, the alpha rhythm may be atypically diffusely repre-sented or appear maximally in the posterior temporal deriva-tions (apiculate temporal alpha). Voltage asymmetries of50% should be regarded as abnormal especially when theleft side is greater than the right. It is best observed during

relaxed wakefulness and normally differs by 1 Hz fromhemisphere to hemisphere. Unilateral failure of the alpharhythm to attenuate is an ipsilateral abnormality referred to asBancauds phenomenon. Frequencies seen to transiently in-crease immediately after eye closure are known as alphasqueak. Alpha variants include both slow and fast variationsof the alpha rhythm and have a harmonic relationship with asimilar distribution and reactivity. The slow alpha variant(theta frequency) has a frequency one half that of the alpharhythm usually in the range of 4 to 5 Hz (see Fig. 2).

Thefast alpha variant(beta frequency) is usually twicethat of the resting alpha rhythm and ranges from 16 to 20 Hz.Alpha variants may have a notched appearance also. Para-

doxical alphaoccurs when alertness results in the presence ofalpha, and drowsiness does not. Normally the opposite effectoccurs. The mu rhythm is a centrally located arciform alphafrequency (usually 8 to 10 Hz) that represents the sensorimo-tor cortex at rest (see Fig. 3). While it resembles the alpharhythm, it blocks not with eye opening, but instead withcontralateral movement of an extremity. It may be seen onlyon one side, and may be quite asymmetric and asynchronous,despite the notable absence of an underlying structural lesion.Themu rhythm may slow with advancing age, and is usuallyof lower amplitude than the existent alpha rhythm. Whenpersistent, unreactive, and associated with focal slowing,mu-like frequencies are abnormal.

*Department of Neurology, Tampa General Hospital, University of SouthFlorida, Tampa, Florida, U.S.A.; Department of Medicine (Neurology),Duke University Medical Center and Neurodiagnostic Center, VeteransAffairs Medical Center, Durham, North Carolina, U.S.A.; and Depart-ment of Neurology, Johns Hopkins Bayview Medical Center, JohnsHopkins University, Baltimore, Maryland, U.S.A.

Address correspondence and reprint requests to Dr. William O. Tatum IV,13801 Bruce B. Downs Blvd. #401, Tampa, FL 33613, U.S.A.; e-mail:[email protected].

Copyright 2006 by the American Clinical Neurophysiology SocietyISSN: 0736-0258/06/2303-0194

Journal of Clinical Neurophysiology Volume 23, Number 3, June 2006194


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Beta rhythms are frequencies that are more than 13 Hz.They are common, and normally observed within the 18 to 25Hz bandwidth, less frequently noted at 14 to 16 Hz, and evenrarer at 35 Hz. A normal voltage of20 uV is found in98% of normal adults. Electrocorticography demonstrates thehighest voltage in the perirolandic cortex, and precentral betaactivity may attenuate with movement or the thought ofmovement much like the mu rhythm (Kozelka and Pedley,2000). Voltages beyond 25 uV in amplitude are abnormal.Benzodiazepines, barbiturates, and chloral hydrate are potentbeta activators and activate beta in the 14 to 16 Hz band-

width. Mental, lingual, or cognitive efforts may also activatebeta rhythms. Beta activity normally increases during drows-iness and light sleep. Persistently reduced voltages of50%suggests a cortical gray matter abnormality within the hemi-sphere having the lower amplitude. However, lesser intermit-tent voltage asymmetries may simply reflect normal physio-logic skull asymmetries. Beta activity may have regionally orhemispheric suppression from a structural lesion of the cortexor from an extradural fluid collection associated with asubdural, epidural, or subgaleal accumulation of blood orcerebrospinal fluid between the surface of the cortex and

FIGURE 1. Normal 9 Hz alpharhythm blocked with eye openingin a 96 y/o with a TIA.

FIGURE 2. Slow alpha variant (note

the reduction of the posterior domi-nant rhythm to 1/2 that of the 10Hz alpha rhythm present in the ini-tial portion of the tracing).

Journal of Clinical Neurophysiology Volume 23, Number 3, June 2006 Normal Adult EEG and Patterns of Uncertain Significance

Copyright 2006 by the American Clinical Neurophysiology Society 195


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FIGURE 3. Note the prominentleft central mu rhythm during eyeopening.

FIGURE 4. Breach rhythm in theright temporal region (maximal atT4) following craniotomy for tem-poral lobectomy.

Tatum et al. Journal of Clinical Neurophysiology Volume 23, Number 3, June 2006

Copyright 2006 by the American Clinical Neurophysiology Society196


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recording electrode. A skull defect may produce a breachrhythm (Fig. 4) with focal, asymmetric, higher-amplitude(relative increase may be threefold) beta activity without theskull to attenuate the faster frequencies. It is not an abnor-mality unless associated with spikes or focal slowing, and isan expected physiologic condition when the voltage damp-

ening effects of the skull have been compromised. General-ized excess fast activity 50 uV for50% of the wakingtracing is usually due to drug effects. Fasterhigh frequencyoscillations 80 Hz may occur in normal brain (and epilep-tic) structures, yet ultrafast frequencies above 25 Hz arerarely seen during scalp-based EEG recording (Khosravani etal., 2005).

Theta rhythms are electrocerebral activity composed of4 to 7 Hz frequencies of varying amplitude and morpholo-gies. Approximately 35% of normal young adults showintermittent 6 to 7 Hz theta of 15 uV during relaxedwakefulness that is maximal in the frontal or fronto-centralhead regions (Kellaway, 2003). In the teenage years and in

the early 20s, central theta may occupy 10% to 20% of therecording (see Fig. 5). The appearance of frontal theta can befacilitated by heightened emotional states, and marked fron-tal-central rhythmic theta during wakefulness has been de-scribed during periods of focused concentration and duringthe performance of mental tasks (Santamaria and Chiappa,1987). Theta activity is normally enhanced by hyperventila-tion, drowsiness, and sleep. When intermittent 4 to 5 Hzactivity is present in the temporal leads bilaterally, or with alateralized predominance (usually left right), this mayoccur in the asymptomatic elderly population with an inci-dence of approximately 35% (Klass and Brenner, 1995), andis not considered an abnormal finding.

Lambda waveshave been initially described as surface

positive sharply contoured theta waves appearing bilaterallyin the occipital region. These potentials have a duration of

160 to 250 ms, and may at times be quite sharply contoured,asymmetric, with higher amplitudes than the resting posteriordominant rhythm. When they occur asymmetrically, theymay create confusion with interictal epileptiform discharges,and potentially leads to misinterpretation of the EEG. Theyare best observed in young adults when seen, though are more

frequently found in children. Lambda waves are best elicitedwhen the patient visually scans a textured or complex picturewith fast saccadic eye movements (see Fig. 6). When encoun-tered in the EEG laboratory, placing a plain white sheet ofpaper in front of the individual will eliminate the visual inputthat is essential for their generation.

Delta rhythms are frequencies consisting of all frequen-cies up to 4 Hz activity that comprises 10% of the normalwaking EEG by age 10 years (see Fig. 7). In the wakingstates, delta can be considered a normal finding in the veryyoung and in the elderly. With advancing age, the normalelderly population may demonstrate rare irregular delta slow-ing in the temporal regions (Van Cott, 2002). It is similar to

temporal theta in the distribution often occupying the lefttemporal head regions, but normally is present for1% ofthe recording. Delta may be seen normally in individualsolder than 60 years (see Fig. 4), at the onset of drowsiness, inresponse to hyperventilation, and is especially prominentduring slow wave sleep. Excessive generalized delta is ab-normal and indicates an encephalopathy of nonspecific etiol-ogy. Focal arrhythmic delta usually indicates a structurallesion involving the white matter of the ipsilateral hemisphereespecially when it is continuous and unreactive.

NORMAL SLEEP ARCHITECTURE

Stage 1 sleep is defined by the presence ofvertex waves

typically 200-millisecond diphasic sharp transients with max-imal negativity at the vertex (Cz) electrode. They may be

FIGURE 5. Normal frontocentraltheta in an 18 year-old whileawake.




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FIGURE 6. Bioccipital lambda waves in a 28 year old with dizziness. Notice the frequent horizontal eye movement artifactin the F7 and T8 derivations.

FIGURE 7. Intermittent left mid-temporal delta during transition todrowsiness in a normal 84 year-oldevaluated for syncope.




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seen in stage 1 to 3 sleep. They are bilateral, synchronous,symmetric, and may be induced by auditory stimuli. Vertexwaves can appear spiky (especially in children) but shouldnormally never be consistently lateralized. Other featuresinclude attenuation of the alpha rhythm, greater frontal prom-inence of beta, slow rolling eye movements, vertex sharp

transients. In addition, positive occipital sharp transients(POSTS) are another feature signifying stage 1 sleep. Theseare surface-positive, bisynchronous physiologic sharp waveswith voltage asymmetries that may occur over the occipitalregions as single complexes or in repetitive burst that may bepresent in both stage 1 and 2 sleep.

Stage 2 sleep is defined by the presence of sleepspindles and K complexes (Fig. 8). This stage has the samefeatures as stage 1 with progressive slowing of backgroundfrequencies. Sleep spindles are transient, sinusoidal 12 to 14Hz activity with waxing and waning amplitude seen in thecentral regions with frontal representation by slower frequen-cies of 10 to 12 Hz. A K-complex is a high-amplitude

diphasic wave with an initial sharp transient followed by ahigh amplitude slow wave often associated with a sleepspindle in the fronto-central regions. A K-complex may beevoked by a sudden auditory stimulus. A persistent asymme-try of50% is abnormal on the side of reduction.

Slow wave sleep now best describes nonrapid eyemovement (non-REM) deep sleep and is comprised of 1 to 2Hz delta frequencies occupying variable amounts of thebackground. Stage 3 previously noted delta occupying 20%to 50% of the recording with voltages of75 uV, whereasstage 4 consists of delta present for50% of the recording(see Fig. 9).

Rapid eye movement sleep is characterized by rapideye movements, loss of muscle tone, and sawtooth waves in

the EEG (see Fig. 10). Non-REM and REM sleep alternate incycles four to six times during a normal nights sleep. Apredominance of non-REM appears in the first part of thenight, and REM in the last third of the night. A routine EEGwith REM may reflect sleep deprivation and not necessarilya disorder of sleep-onset REM such as narcolepsy.

ACTIVATION PROCEDURES

Hyperventilation is routinely performed for 3 to 5minutes in most EEG laboratories (see Fig. 11). The purposeis to create cerebral vasoconstriction through respiratorymeans of promoting systemic hypocarbia. Hyperventilationnormally produces a bilateral increase in theta and deltafrequencies (buildup) that is frontally predominant, and oftenhigh amplitude. Resolution of the effect occurs normallywithin 1 minute. Activation, or the generation of epileptiformdischarges, is infrequently seen in those with localization-related epilepsy (10%), however, may approach 80% for

those with generalized epilepsies that include absence sei-zures (Gabor and AjmoneMarsan, 1969). Superimpositionof beta and delta frequencies during normal buildup maymimic abnormal generalized spike-and-slow waves, but theinconsistent relationship from complex to complex is a clueto the nonpathological origin of the situation. Hyperventila-tion may produce focal slowing in patients with an underlyingstructural lesion. It should not be performed in patients withsevere cardiac or pulmonary disease, acute or recent stroke,significant large vessel cerebrovascular, sickle cell anemia ortrait, and used with caution during pregnancy.

Intermittent photic stimulation, when used as an acti-vating procedure normally produces rhythmic potentials ex-quisitely time-locked to the frequency of the intermittent light

FIGURE 8. Stage 2 sleep withprominent occipital POSTs and

fronto-central sleep spindles. Notethe single T4 small sharp spike dur-ing the 6th second.




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stimulus, and is referred to as photic driving (see Fig. 12).Response depends on background illumination and the dis-tance of the light source from the patient. Distances of30cm from the patient are used to optimize the effect ofstimulation. Flashes are very brief, and delivered in sequencefrom 1 to 30 Hz flash frequencies for approximately 10

seconds on before stopping the stimulus. Subharmonics andharmonics of the flash frequency may be seen. Photic drivingis usually greatest in the occipital location, in frequenciesapproximating the alpha rhythm, when the eyes are closed.Unilateral driving may be seen and needs to be interpretedwith caution since abnormality usually requires other abnor-

FIGURE 9. Slow wave sleep.Note the intermittent POSTs andsleep spindles.

FIGURE 10. REM sleep with lat-eral rectus (myogenic) spikes inthe anterior-lateral head regionsinduced by rapid eye movements.




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mal features. Photomyoclonic (orphotomyogenic) responsesconsist of frontally dominant muscle artifact that occurs whenthe flash evokes repetitive local contraction of the frontalismusculature (photomyogenic). The periocular muscles arealso usually affected, though single lightening-like head jerks(photomyoclonic) may occasionally be produced. Myogenic

spikes occur 50 to 60 milliseconds after the flash and increasein amplitude as stimulus frequency increases. The response isnormal, though may be seen in withdrawal syndromes orstates of hyperexcitability.

BENIGN ELECTROENCEHALOGRAPHIC

VARIANTS

Both rhythmic and epileptiform waveforms may appearin the human EEG without known clinical significance andare considered to be benign patterns. Interobserver variabilitystill exists between electroencephalographers (Williams et al.,1985). Normal rhythms that appear as variations of normal, or

epileptiform in morphology may serve as the basis for con-fusion and lead some to misinterpretation of the EEG (Ben-badis and Tatum, 2003). Such rhythmic patterns most fre-quently fall within the theta, alpha, and beta frequency ranges(Westmoreland, 2003). Rhythmic temporal theta bursts ofdrowsiness, variants of the alpha rhythm, and sharply con-toured midline theta rhythms are most frequently seen. Pre-viously these EEG patterns were thought to be associatedwith seizures, headaches, abdominal pain, and behavioraldisturbances. However, these anomalies are now consideredbenign variations of normal, and not representative of neu-rovegetative psychopathology nor possess significance spe-cific for epileptic seizures.

Rhythmic temporal theta bursts of drowsiness (see Fig.13) is the preferred term for what was previously described aspsychomotor variant (Hughes and Cayaffa, 1973). This pat-tern occurs in 0.5% to 2.0% of selected normal adults andconsists of bursts or runs of 5 to 7 Hz theta waves that mayappear sharp, flat, or notched in appearance. It is maximal in

the midtemporal derivations and was referred to as rhythmicmidtemporal theta bursts of drowsiness. It is an interictalpattern that does not evolve spatially or temporally thoughmay be represented bilaterally or independently over bothhemispheres. it is seen in adolescents and adults in relaxedwakefulness.

Midline theta was initially described by Ciganek as afocal sinusoidal or arciform 4 to 7 Hz rhythm over the vertexregion (Ciganek, 1961). While morphologically, it may re-semble a mu rhythm, it is not similarly reactive, is slower infrequency, and occurs both in drowsiness or the alert state.Although initially felt to be a projected rhythm in temporallobe epilepsy, it has been seen in a heterogeneous population

and is therefore of nonspecific clinical significance.Some benign patterns may have an epileptiform mor-

phology but are not associated with seizures, and therefore donot represent interictal epileptiform discharges (Stern andEngel, 2005). This may include normal rhythms (i.e., spikyalpha in the temporal regions), or include superimposition ofbackground frequencies giving the appearance of epilepti-form discharges (i.e., HV with delta and superimposed betasimulating generalized spike-and-wave).

Spike-and-wave discharges at 6 Hz were first describedby Gibbs, and later referred to as phantom spike-and-wave(see Fig. 14). Initial descriptions included two forms. Theacronym WHAM (wakefulness, high amplitude, anterior,

FIGURE 11. Normal buildup dur-ing hyperventilation.




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FIGURE 12. Photic driving at 20 Hz seen in the P3-O1, P4-O2, T5-O1, and T6-O2.

FIGURE 13. Rhythmic temporaltheta of drowsiness. Note thesharply contoured morphology.




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male), and FOLD (female, occipital, low amplitude, drowsy)were used to describe the two primary subtypes (Hughes,1980). Bilateral, synchronous, 6 Hz spike-and-wave dis-charges range from 5 to 7 Hz, though with a typical repetitionrate of 6 Hz lasting briefly for 1 to 2 seconds. The spike isoften of very low amplitude, at times difficult to appreciateduring routine interpretation of the EEG by qualitative visualanalysis. When the spikes are of low amplitude and occurduring drowsiness this is usually reassuring for a benignfindings. When they are seen with high amplitude spikes andoccur with less than a 6 Hz frequency, or occur duringwakefulness and persist into slow wave sleep, there is a

greater association with seizures.Positive bursts of 14 Hz and 6 Hz (originally called 14

Hz and 6 Hz positive spikes) have also been calledctenoids.There can be an association with 6 Hz spike-and-wave thatmay occur in the same person (Silverman, 1967). Theyappear in the EEG as a burst of positive comb-like spindlesover the posterior temporal head regions. They are presentmost frequently at a rate of 14 Hz or 6 to 7 Hz lasting 0.5 to1 second in duration. The 14 Hz frequency is most prevalent,and the 6 Hz burst may appear with or without the fasterfrequencies (see Fig. 15). They are most common duringadolescence though may persist into adulthood, decreasingwith age. The bursts are usually unilateral or bilaterally

asynchronous with shifting predominance involving onehemisphere to a greater degree. A contralateral ear referencemontage, and greater interelectrode distance best demonstratethese bursts (Blume et al., 2002).

The original reference to small sharp spikes or be-nign epileptiform transients of sleep or benign sporadicsleep spikes of sleep (Fig. 16) depict a low-voltage (50uV) brief duration (50 milliseconds) simple waveform witha monophasic or diphasic spike that has an rapidly ascendinglimb and steep descending limb best seen in the anterior tomidtemporal derivations during non-REM sleep. They mayhave a slightly higher voltage, or longer duration, and mayappear with an after-going slow wave usually of lower

amplitude than the spike. They are not associated with focalslowing, do not occur in runs, and disappear in slow wavesleep. They are most common in adults and occur withapproximately 20% to 25% incidence. They occur as aunilateral discharge but are almost always bilateral and inde-pendent or reflected to the homologous derivations with afield that may correspond to an oblique transverse dipoleresulting in opposite polarities over opposite hemispheres.

Wicket spikes (see Fig. 17) are seen in adults 30years of age and occur within the 6 to 11 Hz band but canobtain amplitudes of up to 200 uV. They are seen over thetemporal regions during drowsiness and light sleep and are

bilateral and independent. They usually occur in bursts,though may be confused with interictal epileptiform dis-charges especially when they occur independently or asisolated waveforms (Krauss et al., 2005). Comparing thefrequency and morphology of the bursts to the isolatedwaveforms a means of demonstrating similar waveforms andsupports the nonepileptogenic origin of the waveform. Whilewicket spikes are considered an epileptiform normal variant,when selecting patients for EEG, they may still appear on theEEG of patients with a clinical diagnosis of epilepsy ( Krausset al., 2005). No focal slowing or after-going slow-wavecomponent is seen and they likely represent fragmentedtemporal alpha activity (Reiher and Lebel, 1977).

In contrast to many of the patterns of uncertain signif-icance that mimic interictal epileptiform discharges (IEDs), asubclinical rhythmic electrographic discharge in adults(SREDA) is a pattern that appears to as a paroxysmal burst onthe EEG that mimics the epileptiform characteristics of asubclinical seizure. However, there are no clinical featuresthat coexist with it, including neither subjective nor objectivefindings, and no association with epilepsy has yet beendemonstrated. In contrast to most benign variants that occurmaximally in younger age ranges during drowsiness, SREDAis more likely to occur in the population over 50 years of age,and also occurs while the person is awake. It may exist in twoforms: either as a bilateral episodic burst of rhythmic sharply

FIGURE 14. Six-Hz (phantom)spike-wave burst with frontal pre-dominance in a patient with head-aches.




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contoured 5 to 7 Hz theta frequencies appearing maximalover the temporoparietal derivations and may be asymmetric,or as an abrupt mononphasic repetitive sharp or slow wave-forms appear focally at the vertex that recur in progressivelyshorter intervals until a sustained burst is noted that mimicsthe evolution seen with an electrographic seizure. The burstsusually last 40 to 80 seconds and appear without postictalslowing (see Fig. 18). Single photon emission computedtomography during SREDA does not demonstrate the corre-

sponding regional cerebral hyperperfusion that occurs duringelectrographic seizures in patients with epilepsy (Thomas etal., 1992).

There is a finite, but subjective difference betweennormal and abnormal EEG patterns (Williams et al., 1985).Abnormal EEG patterns may at times reflect a continuum,ill-defined enough to prevent the essential distinction betweena pattern of interictal and ictal origin (Chong and Hirsch,2005). The greatest difficulty appears with the periodic pat-terns often most evident in the critically ill. These patternschallenge the electroencephalographer to differentiate thosewaveforms that are abnormal, and whether these patternsreflect the epiphenomenona of dysfunctional brain, or imply

ongoing seizures. Although technology has made huge ad-vances in the ability to record and continuously monitor EEG(Kull and Emerson, 2005), our understanding of the under-lying pathophysiologic mechanisms, and means to distin-guish potentially ictal patterns still remains limited. Becausethe impact on treatment is predicated by understanding thechallenges that face the electroencephalographer when pre-sented with abnormal patterns, the essence of distinguishingnormal EEG cannot be overstated.

Our knowledge and utilization of normal EEG haveevolved. The basic waveforms, frequencies, physiologic, de-velopmental and sleep architectures are known. The earlierassociation of epileptiform normal variants with neuroveg-etative symptoms and psychiatric conditions (Boutros et al.,2005) have been superseded by their identification as patternswithout clinical significance. They are important to identifybecause they may serve to impart misdiagnoses in patientswithout epilepsy and carry ramifications that include overlyaggressive treatment. The advent of long-term monitoring hasbroadened our understanding of EEG, and in the future willbecome commonplace with recording during anesthesia, inthe intensive and critical care units, and perhaps even in the

FIGURE 15. Fourteen and 6 Hz positive bursts are present in an ambulatory EEG coincidentally during push-button activa-tion. Note the phase reversal between T3-T5 and T5-O1 in seconds 4-8.




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FIGURE 17. Wicket waves maxi-mal at T3 and T4.

FIGURE 16. A right temporalsmall sharp spike is present indrowsiness. Note the 50 micro-volt amplitude and simple diphasicmorphology.




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emergency department for acute neurologic care (Tatum,2001). New waveforms are still being identified (Hirsch et al.,2004). Coregistration with EEG and other neuroimagingtechniques have facilitated greater source localization ofepileptiform abnormalities. EEG continues to remain at theforefront in neurologic evaluations, as well as during neuro-logic monitoring for the systemic effects of general medicalconditions (see Fig. 17). Normal EEG remains at the foun-dation of interpretation for those that hope to identify abnor-mal patterns. While 2006 has seen advances in clinical EEG,

the future promises to bring even greater and more wide-spread applicability of adult EEG to clinical medicine.

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