02 normal ''suspicious'' eeg

DOI 10.1212/WNL.0b013e31827974df 2013;80;S4Neurology

William O. TatumNormal ''suspicious'' EEG

January 14, 2013This information is current as of

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William O. Tatum, DO,FAAN

Correspondence toDr. Tatum:[email protected]

Normal “suspicious” EEG

ABSTRACT

The EEG is a unique measure of electrical brain function and is widely used in patients with seiz-ures. Many normal variants and variations of normal EEG have a predilection for the temporal lobeand mimic epileptiform discharges. The high prevalence of temporal lobe epilepsy and the propen-sity for normal variants to occupy the temporal lobe may result in an undesired bias, leading tomisidentification of normal waveforms. Learning the common pitfalls, such as the variations ofnormal EEG, benign variants, and common artifacts, are essential lessons in EEG. Continuingeducation and acquiring experience in EEG interpretation are the basic tools to ensure patientsafety. Above all, judging the results of the EEG interpretation in light of the patient’s clinicalsymptoms is a prerequisite to ensure proper management. Neurology� 2013;80 (Suppl 1):S4–S11

GLOSSARYED 5 epileptiform discharge; SREDA 5 subclinical rhythmic EEG discharges in adults.

The immediate result incurred by a misinterpreted EEG demonstrating epileptiform discharges(EDs) potentially includes lost driving privileges, impaired quality of life, the potential for com-promised employment and social situations, and adverse effects from antiepileptic drug exposure.To accurately interpret an abnormal EEG, one must first have the ability to identify normalpatterns. Just as a normal EEG does not exclude a clinical diagnosis of epilepsy (i.e., frontal lobeepilepsy), an abnormal EEG finding may not be related to the provisional diagnosis or presentingsymptoms (i.e., dizziness). Unfortunately, an EEG may also be designated as abnormal based onmisinterpretation. Particular “suspicious” waveforms may result in EEG misinterpretation. Thisreview highlights normal EEG that is potentially subject to misinterpretation.

In 29% to 55% of patients with epilepsy, the initial EEG will show EDs. Approximately 15%of these patients have repeatedly “negative” studies or normal-appearing EEG. This demonstratesthe limitations of routine scalp EEG for detecting diagnostic abnormalities.1 Even when clearpathologic EDs with a specific profile are encountered, a spectrum of waveforms exists that rangefrom normal to abnormal (figure 1). Indeed, patients with EDs that do not have epilepsy areencountered at rates ranging from 0.2% to 3.5%.2 Children are far more likely to have asymp-tomatic EDs compared with adults. Focal or generalized EDs have been reported in 3.5% ofchildren without epilepsy; the vast majority of these EEG findings disappeared by early adoles-cence without developing seizures or epilepsy.3 Although EDs are rarely seen in patients who donot experience seizures, these waveforms that appear epileptiform may be seen in chronic non-epileptic states (i.e., cerebral palsy) or are the result of an acute neurologic injury in patientswithout clinical seizures.1

EPILEPTIFORM DISCHARGES According to a longstanding global coalition of societies, which foster advancesin EEG, the International Federation of Societies of Electroencephalography and Clinical Neurophysiology,4 EDsexist as transient potentials that are clearly distinguishable from background activity, have a pointed peak, and aredescribed as a spike or a sharp wave. Spikes typically have a duration of 20 to 70 milliseconds, whereas a sharpwave with a negative surface component typically has a duration of 70 to 200 milliseconds. These criteria alone

From the Department of Neurology, Mayo College of Medicine, Mayo Clinic, Jacksonville, FL.

Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the author, if any, are provided at the end of thearticle.

S4 © 2012 American Academy of Neurology

ª 2012 American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

are not adequate enough to distinguish EDs from otherwaveform types and many EEG readers are not familiarenough with the parameters that distinguish an abnor-mal sharp waveform from a normal variant, eventhough these guidelines exist (table).5 Using these crite-ria, “. the majority of these sharp waveforms or spikeconfigurations may be explained away or ignored; those

withstanding . usually prove to be highly correlatedwith clinical/pathologic actualities.”5 The “suggestion”made 40 years ago to remain conservative when inter-preting is still relevant today and is reinforced by thenumber of patients proven to have been misdiagnosed(based on follow-up video-EEG monitoring) on thebasis of misinterpretation of routine EEGs.6,7 The rate

Table Adapted from Maulsby’s guidelines5 for assessing spikes and sharp waves

1. Every spiky-looking wave is an artifact unless there are one or more good reasons for suspecting otherwise.

2. Spikes and sharp waves of cerebral origin always occupy a definable electrical field on the scalp and should always be seen in 2 or more nearby electrode sites.

3. Clinically significant spikes and sharp waves are almost always surface negative in polarity initially, or at least the sharpest or highest voltage component of the waveis usually surface negative.

4. Most spike or sharp wave discharges of clinical import are followed by a slow wave or series of slow deflections. If it does not have a slow after-wave, be moresuspicious of artifact or of a sudden alteration in voltage of physiologic background rhythms.

5. Ignore sharp or spiky events that can be logically explained by simple alterations in voltage of the existing background rhythms or by superimposition of severalcomponents in the background activity of the record.

6. There are several types of physiologic spikes or sharp waves, particularly during sleep; these should be thoroughly familiar to the interpreter and can be discriminatedfrom abnormalities by knowledge of the patient’s age, state of consciousness, location on the scalp, and form or pattern of the wave in question.

Figure 1 Abnormal interictal EEG

Abnormal interictal EEG in several adult patients with localization-related epilepsy demonstrating (A) a burst of repetitive T3 spike-and-slow waves (arrow),with a broad hemispheric field of spread (red arrow); (B) a burst of “suspicious” abnormal left temporal sharp waves (red arrow) and normal right rhythmicmidtemporal theta bursts in drowsiness (black arrow); (C) a burst of bioccipital sharp and slow waves in a patient with right temporal-occipital epilepsy (notethe variability in sharp wave amplitude and morphology); and (D) a positive sharp wave in a patient after left temporal lobe surgery.

Neurology 80 (Suppl 1) January 1, 2013 S5


of such misdiagnoses is even higher for nonspecialists.8

Incorrect designation of EDs contributes to the clinicalissue of misdiagnosis.1,3,5–7 There are guidelines availablefor conducting EEG studies,9 but those available fordefining and identifying EDs do not exist for EEG inter-pretation. To date, studies on interrater reliability ofEEG interpretation are scarce or focus on non-ED topics;furthermore, there is even considerable interreader varia-bility among experts.10 Computer-based spike detectorsaid in recognizing “suspicious” transients but the rateof overidentification is higher than the rate for humaninterpreters.11 Standardizing the parameters for clear elec-tronegative spikes and sharp waves (involving distinctchanges in frequency and amplitude), coupled with con-comitant focal slowing, an after-going slow wave, andoccupying a believable cerebral field in the absence ofan alternative explanation such as an artifact or normalvariant, may help improve our rate of correctly identify-ing EDs that are associated with seizures.

PITFALLS OF PATTERN RECOGNITION Pattern rec-ognition is inherently prone to pitfalls when rules ofpolarity and convention are ignored. The function of abipolar montage is to compare 2 active electrode sites,whereas a reference montage compares an active andcommon electrode site. Phase reversals identify the sitesof maximal electronegativity (or electropositivity). There-fore, the occurrence of a phase reversal may signify a nor-mal finding (figure 2) and is not necessarily synonymouswith an abnormality in the EEG (figure 1A). It is impor-tant to note that a "phase reversal" alone does not signifyan abnormal EEG although it is frequently interpretedthat way. It is well known that phase reversals are present

in almost every normal sleep record (figure 2A). Theelectrical convention relies on the electrophysiologic dif-ference between both electrodes in the pair. When thevoltage of the first electrode is more electronegative thanthe second electrode, the deflection of the waveform is inan upward direction (figure 2A). Similarly, if the voltageof the second electrode is more negative than the firstelectrode, then the deflection of the waveform is in adownward direction.12 Normal and abnormal phasereversals may exist as electronegative events. Infrequently,phase reversals that are electropositive may occur withabnormal spikes and sharp waves (figure 1D).13 Addi-tionally, the superimposition of normal waveforms (orartifact) may appear to be abnormal but instead reflect acombination of innocuous potentials with different fre-quencies (figure 3). Any routine frequency (i.e., alpha,beta, theta, and delta) or waveform (i.e., mu and lambda)in the normal waking EEG may manifest activity thatmimics EDs.

Within the limited repertoire of recorded frequencies,durations, and amplitudes, some waveforms may be nor-mal in one setting (i.e., alpha during wakefulness), butabnormal in others (alpha coma). Scenarios in whichconfusion exists between normal and abnormal wave-forms (misidentified EDs on a prior EEG) occurred in41 of 127 patients (32%) with psychogenic nonepilepticattacks who were incorrectly treated for epilepsy becauseof overinterpretation of normal fluctuations in alpharhythm (figure 4).14 In an outpatient epilepsy clinic set-ting, incorrect abnormal EEG designations frequentlycorrelated with multiple unexplained symptoms.15 Dur-ing sleep, V waves and positive occipital sharp transientsof sleep may be incorrectly identified as sharp waves

Figure 2 Adult EEG

Adult EEG demonstrating (A) normal vertex “sharp waves” in a transverse bipolar montage. Note the downward and upward deflections that comprise aphase reversal (boxes). The arrow denotes the site of maximal electronegativity seen in channels Fz and Cz. (B) Breach rhythm after a right frontotemporalcraniotomy with a series of phase reversals in the right midtemporal region that are spiky (box) and reflect a breach rhythm and not abnormal epileptiformdischarges.

S6 Neurology 80 (Suppl 1) January 1, 2013


(figure 2A). This is particularly important during drows-iness and light sleep in youth, because many vertex wavesand positive occipital sharp transients of sleep may appear“spiky,” mimicking EDs. Drowsiness tends to producenormal paroxysmal features that look like generalizedEDs (figure 5).16 Additionally, sharp transients are iden-tified in .90% of normal drowsy patients, which canalso result in misidentification of EDs.17

Typically, identification of normal physiologic Vwaves is not difficult if montages other than a longitu-dinal bipolar are used, but the spatial distribution may“catch the reader’s eye” and lead to overidentificationof EDs (figure 2A). Breach rhythms that emerge aftercraniotomymay appear spikier because of superimposedbeta activity, but are a normal expected finding for suchconditions (figure 2B). Normal variants such as wicketspikes (figure 6) have been previously detailed,12,14,15,18

although there are robust examples of wicket spikes that

mimic EDs. These nonevolving rhythmic bursts repre-sent a normal finding that is unrelated to seizure man-ifestations. Benign epileptiform transients of sleep andrhythmic midtemporal theta bursts of drowsiness mayalso appear similar to an ED (figure 7). Positive bursts,measured at 14 and 6 Hz and often low-amplitude6-Hz (phantom) spike-and-wave patterns, althoughindeed epileptiform, reflect benign waveform variantsof uncertain significance.12 Wicket waves are amongthe most frequently misread pattern of uncertain signif-icance with 25 of 46 (54%) interpreted as EDs, oftenon the basis of single discharges.18

Single potentials or brief trains of sharply contouredwaveforms recorded over the temporal regions duringdrowsiness are usually symmetric in their rate of riseand fall. These waveforms are identical in frequencyto their fellow waveforms and do not have an after-goingslow wave, nor are they associated with other abnormal

Figure 3 A normal burst of theta in the EEG of an adult during drowsiness

The findings were reported as “suspicious” for atypical spike-and-wave patterns that were due to normal superimposition of background frequencies andartifact. Note the prominent intermixed beta activity and electrode artifact at F7 and F3 that combine to make the appearance “spikier.”



features such as complex EDs or focal slowing in thesame region of their occurrence. The occurrence of suchwaveforms underscores the need for conservative inter-pretation. Dramatic subclinical rhythmic EEG dis-charges in adults (SREDA) resemble an electrographicseizure, although it bears no relationship to epilepsyand is rare, occurring in less than 0.05%.12 Most inter-preters will never encounter a SREDA, so misinterpre-tation of a SREDA as seizure activity is unanticipated.

SUSPICIOUS MINDS Focal epilepsy is the most com-mon human adult epilepsy with two-thirds of cases orig-inating in the temporal lobe.19 Temporal waveforms inthe EEG are also the most common potentials misinter-preted as EDs.20 Therefore, even without prior knowl-edge of the reason the EEG is performed, the interpretermay be subconsciously suspicious because of the preva-lence of temporal lobe epilepsy.12,14,15,18 When the reasonfor referral is a “spell” or “seizure,” there might be aninherent bias to identify EDs in the EEG that “help”support the diagnosis of epilepsy biasing the reader tofoster overinterpretation. Coupled with a lack of training

and inexperience, the correct electroclinical diagnosis thatis averted by a misinterpreted EEG may defy “correc-tion” of the mistreatment of epilepsy and remain anundisclosed problem unless video-EEG is performed.14

The problems of fluctuation in the accuracy of EEGinterpretation may vary from person to person and evenin the same person over time.21 When controversialor epileptiform waveforms are encountered based onthe appearance of the waveform alone, a conservativeapproach is always warranted (figure 8). True EDs maybe encountered during EEG interpretation, although thisshould not be equated with an automatic clinical associ-ation with epilepsy and the finding interpreted within theclinical context of the symptoms.22 For diagnostic pur-poses when identifying EDs, I use the 2 minute rule: if2 minutes after review of the EEG, a “discharge” isunable to be clearly categorized as an ED, a conservativeinterpretation should apply, and the waveform inter-preted as nonepileptiform. Results that use words suchas “borderline” to represent the impression of the EEGfeatures are noncommittal and suggest that the inter-preter is unable to distinguish normal from abnormal.

Figure 4 Normal alpha in an adult EEG with a phase reversal at the T6 electrode derivation that was identified as “suspicious” for anepileptiform discharge (arrows)



Figure 5 Normal EEG in an 18-year-old showing a hypnagogic (“drowsy”) burst (oval) of paroxysmal theta and delta frequencies that appearssharply contoured

This reflects normal electrocerebral activity during sleep transition. Note the change in the EEG immediately after the burst to reflect the change in state.The “MARK” applied by the technologist signifies a “suspicious” burst.

Figure 6 Wicket spikes appearing in repetitive bursts during the awake state in a 57-year-old (circles)



Figure 7 Rhythmic midtemporal theta bursts of drowsiness in the EEG of a young adult

Note the sharply contoured waveform that mimics the appearance of bilateral bursts of repetitive temporal sharp waves(boxes).

Figure 8 Adult EEG demonstrating lambda waves during scanning eye movements (black arrows)

Although the pattern may appear morphologically as a “sharp wave,” the location, positive polarity, and the relationship toscanning eye movements (reading) are distinctive. Note the disappearance of the lambda waves after eye closure (redarrows) with return of the normal alpha rhythm that further identifies this feature as a normal finding.



Reporting reliability is reinforced if a confident descrip-tion of ED distribution, morphology, frequency, dura-tion, and field is encountered. If the report is confusingto the clinician, then experience and reliability may bequestionable, especially when the report is at odds withthe clinical state of the patient. In the age of digital EEG,including an image of the “abnormal” waveforms wouldhelp to provide the clinician a chance to validate “suspi-cious” findings that might carry serious and long-termclinical ramifications.

CONCLUDING STATEMENTS Designating an EEG asnormal when the waveform is abnormal will probablynot lead to harmful treatment. However, an incorrectlyidentified “abnormal” EEG based on the presence ofEDs may lead to a misdiagnosis and mistreatment asepilepsy. Some neurologists have no formal training inEEG, no board certification in clinical neurophysiology,no affiliation with EEG education, nor routinely interpretEEGs, yet provide care to patients with seizures.23 Guide-lines for interpreting abnormal waveforms are needed toprevent misinterpreted EEGs from imparting long-termdiagnostic and treatment delays that may be masked foryears before recognition of the underlying problem.24

Therefore, it is incumbent upon all physicians interpret-ing EEGs to remain conservative in their interpretation.

AUTHOR CONTRIBUTIONSW.O. Tatum: drafting/revising the manuscript, contribution of vital

reagents/tools/patients, study supervision.

ACKNOWLEDGMENTThe author thanks Dr. Barbara Westmoreland for her helpful review and sug-

gestions and Mrs. Kelly Viola for her editorial assistance with the manuscript.

DISCLOSUREThe author reports no disclosures relevant to the manuscript. Go to Neurology.

org for full disclosures.

Received November 16, 2011. Accepted in final form September 25,2012.

REFERENCES1. Pillai J, Sperling MR. Interictal EEG and the diagnosis of

epilepsy. Epilepsia 2006;47(suppl 1):14–22.

2. Zivin L, Ajmone Marsan C. Incidence and prognostic signif-

icance of “epileptiform” activity in the EEG of non-epileptic

subjects. Brain 1968;91:751–778.

3. Cavazutti GB, Cappella L, Nalin A. Longitudinal study of

epileptiform EEG patterns in normal children. Epilepsia

1980;21:43–55.

4. IFSECN. A glossary of terms commonly used by clinical

electroencephalographers. Electroencephalogr Clin Neuro-

physiol 1974;37:538–548.

5. Maulsby RL. Some guidelines for assessment of spikes and sharp

waves in EEG tracings. Am J EEG Technol 1971;11:3–16.

6. Stroink H, Van Donselaar CA, Geerts AT, Peters ACB,

Brouwer OF, Arts WFM. The accuracy of the diagnosis of

paroxysmal events in children. Neurology 2003;60:979–982.

7. Uldall P, Alving J, Hansen LK, Kibaek M, Buchholt J. The

misdiagnosis of epilepsy in children admitted to a tertiary epi-

lepsy center with paroxysmal events. Arch Dis Child 2006;91:

219–221.

8. Leach JP, Lauder R, Nicolson A, Smith DF. Epilespy in the

UK: misdiagnosis, mistreatment, and undertreatment? The

Wrexham area epilepsy project. Seizure 2005;14:514–520.

9. American Clinical Neurophysiology Society. Guideline 1:

minimum technical requirements for performing clinical

electroencephalography. Available at: http://www.acns.

org/pdfs/Guideline%201.pdf. Accessed November 5, 2011.

10. Halford J, Pressly WB, Benbadis SR, et al. Web-based col-

lection of expert opinion on routine scalp EEG: software

development and inter-rater reliability. J Clin Neurophysiol

2011;28:178–184.

11. Webber WR, Litt B, Lesser RP, Fisher RS, Bankman I.

Automatic EEG spike detection: what should the computer

imitate? Electroencephalogr Clin Neurophysiol 1993;87:

364–373.

12. Tatum WO, Husain A, Benbadis SR, Kaplan PW. Normal

human adult EEG and patterns of uncertain significance.

J Clin Neurophysiol 2006;23:194–207.

13. Matsuo F, Knott JR. Focal positive spikes in electroenceph-

alography. Electroencephalogr Clin Neurophysiol 1977;42:

15–25.

14. Benbadis SR, TatumWO. Overinterpretation of EEGs and

misdiagnosis of epilepsy. J Clin Neurophysiol 2003;20:

42–44.

15. Benbadis SR, Lin K. Errors in EEG interpretation and

misdiagnosis of epilepsy: which EEG patterns are overread?

Eur Neurol 2008;59:267–271.

16. Santamaria J, Chiappa KH. The EEG of drowsiness in

normal adults. J Clin Neurophysiol 1987;4:327–382.

17. Beun AM, van Emde Boas W, Dekker E. Sharp transients

in the sleep EEG of healthy adults: a possible pitfall in the

diagnostic assessment of seizure disorders. Electroencephalogr

Clin Neurophysiol 1998;106:44–51.

18. Krauss GL, Abdallah A, Lesser R, Thompson RE,

Niedermeyer E. Clinical and EEG features of patients with

EEG wicket rhythms misdiagnosed with epilepsy. Neurology

2005;64:1879–1883.

19. Semah F, Picot MC, Adam C, et al. Is the underlying cause of

epilepsy a major prognostic factor for recurrence? Neurology

1998;51:1256–1262.

20. Markand O. Pearls, perils, and pitfalls in the electroenceph-

alogram. Semin Neurol 2003;23:7–46.

21. van Donselaar CA, Stroink H, Arts SF; for the Dutch Study

Group of Epilepsy in Childhood. How confident are we of

the diagnosis of epilepsy? Epilepsia 2006;47(suppl 1):9–13.

22. Itil TM, Soldatos C. Epileptogenic side effects from psycho-

tropic drugs: practical recommendations. JAMA 1980;244:

1460–1463.

23. Fountain NB, Freeman JM. EEG is an essential tool: pro and

con. Epilepsia 2006;47(suppl 1):23–25.

24. LaFrance WC Jr, Benbadis SR. Avoiding the costs of unrec-

ognized psychological nonepileptic seizures. Neurology 2006;

66:1620–1621.



DOI 10.1212/WNL.0b013e31827974df 2013;80;S4Neurology

William O. TatumNormal ''suspicious'' EEG

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