Handbook of Clinical Neurology, Vol.

160 (3rd series)

Clinical Neurophysiology: Basis and Technical Aspects
K.H. Levin and P. Chauvel, Editors
https://doi.org/10.1016/B978-0-444-64032-1.00009-6
Copyright © 2019 Elsevier B.V. All rights reserved

Chapter 9

Normal EEG variants

JOSE MARI-ACEVEDO1, KIRSTEN YELVINGTON2, AND WILLIAM O. TATUM3*
1
Department of Neurology, University of Nevada School of Medicine, Reno, NV, United States
2
Department of Neurology, Mayo Clinic, Jacksonville, FL, United States
3
Department of Neurology, Mayo Clinic College of Medicine and Health Sciences, Jacksonville, FL, United States

Abstract
Understanding common variations of normal EEG and benign variants of uncertain significance is essential
to discern the boundary between normal and abnormal EEG. Wide variation and fluctuation can occur with
normal signals generated by the brain, and these can be a pitfall for less-experienced electroencephalogra-
phers in accurately interpreting the EEG. Normal EEG variants are benign and do not portend specific path-
ological conditions. They can show predilection for the temporal lobes and mimic epileptiform discharges.
These factors, along with the “spiky” appearance of these patterns, can often lead to erroneous interpretation
of the recording and result in misdiagnosis. This chapter reviews the normal EEG variants that may
confound the clinician and lead to misinterpretation that can result in suboptimal patient management.

INTRODUCTION
Electroencephalography is one of the most influential
noninvasive tools available to clinicians for evaluating
a patient’s neurophysiologic function. The EEG signal
maintains a high degree of complexity in normal and
abnormal conditions. The extraction of clinically rele-
vant data is achieved by routine visual analysis. Accurate
interpretation is facilitated by an orderly approach to the
study of waveforms in the recording (Beniczky et al.,
2013). EEG is best suited and most specific in the eval-
uation of patients with epilepsy and those suspected of
manifesting seizures or paroxysmal neurologic events
(Smith et al., 1999; Pillai and Sperling, 2006; Tatum
et al., 2006). However, standard scalp EEG is not without
its limitations. Scalp EEG is a composition of electro-
physiologic activity obtained from billions of neurons
in the brain, and yet it only records one-third of the cere-
bral cortex. Additionally, most clinical decision making
is based upon the routine scalp EEG, which is composed
of 20–30 min of recording (Pillai and Sperling, 2006).
The clinical application of EEG in the diagnosis of
epilepsy is well-established, but the interpretation of a
recording has only moderate interrater reliability using
visual analysis (Beniczky et al., 2013).
Epileptiform discharges (EDs) are relatively specific
abnormal electrophysiological potentials with character-
istic features and are often found in people predisposed
to manifest seizures. EDs tend to stand out from the
ongoing background activity, possess a pointed mor-
phology, and are described as a spike or a sharp wave
(Table 9.1). Furthermore, EDs may appear as a distinct
single wave or a series of waveforms. Spikes in EEG
are epileptiform potentials with durations between
20 and 70ms, whereas sharp waves have longer durations
of 70–200 ms. Duration alone is inadequate to distinguish
EDs from other waveforms and recognizing them can
be confusing (Benbadis and Tatum, 2003; Krauss et al.,
2005; Benbadis and Lin, 2008; Tatum, 2013b). Further-
more, many interpreters may be unfamiliar with the
parameters that distinguish an abnormal sharp waveform
from a normal variant, even though these guidelines exist
(Maulsby, 1971; Sinha et al., 2016).
The importance of understanding normal EEG lies in
appreciating the wide range of normal signals that can
beguile the interpreter. In one study of 324 patients at
an epilepsy center, EEG was one of the two most impor-
tant factors leading to a clinical misdiagnosis (Smith
et al., 1999). Therefore understanding the boundaries

*Correspondence to: William O. Tatum, D.O., Department of Neurology, Mayo Clinic, 4500 San Pablo Road, Mangurian Bldg.,
Fourth Floor, Jacksonville, FL 32224, United States. Tel: +1-904-953-2498, Email: tatum.william@mayo.edu
144 J. MARI-ACEVEDO ET AL.
of normal EEG waveforms and their variants is paramount
in avoiding overinterpretation that may lead to misdiagno-
sis (and subsequently mistreatment) of epilepsy.
In general, when interpreting EEG a conservative
approach is generally recommended, especially in the
presence of epileptiform waveforms (Maulsby, 1971;
Pillai and Sperling, 2006; Tatum, 2013a). Failure to recog-
nize normal variants often leads to misinterpretation of
EEG (Maulsby, 1971; Krauss et al., 2005). Careful analysis
of a waveform’s location, frequency, and morphology in
relationship to the background electrocerebral activity
Table 9.1
Criteria used to interpret epileptiform activity
● Suspicious waveforms confined to a single channel in the
EEG are considered as artifact until proven otherwise
● EDs are electrophysiological potentials that always occupy a
believable spatial field of distribution
● The sharpest or highest voltage component of an ED is
typically surface negative
● Interictal EDs are usually followed by an aftergoing slow
wave discharge
● EDs have abnormal features other than alteration in voltage
or superimposition of background frequencies
● Normal physiologic spikes and sharp waves are common
waveforms and should be familiar to the interpreter
Adapted from Maulsby RL. Some guidelines for assessment of spikes
and sharp waves in EEG tracings. Am J EEG Technol. 1971;11:3–16.
and level of alertness is essential to accurately discern
normal variations and benign variants from abnormal
waveforms. When interpreting an EEG, if a waveform in
question is equivocally epileptiform, a nonepileptiform
interpretation is preferred (Tatum, 2013a). In this case,
a “2-min rule” can be beneficial to avoid overemphasis
of “suspicious” waveforms: if a waveform is in question
for more than 2 min, interpret it as a benign feature
of the EEG (Tatum, 2013a). Finally, EEG findings
should always be interpreted within the clinical context
of the recording (Benbadis and Lin, 2008; Azzam
et al., 2015).
The aftermath of overinterpretation of normal varia-
tions and benign variants in the EEG can include mis-
diagnosis, missed treatment of the true underlying
condition, adverse effects from ASD exposure, loss of
driving privileges, compromised employment and social
situations, and impaired quality of life. In this chapter, we
address the normal variants in EEG and variations of nor-
mal waveforms that may be misidentified as abnormali-
ties and potentially hinder accurate interpretation.
NORMAL EEG
The “Berger band” (i.e., 1–30 Hz) is commonly used for
routine visual analysis. The brain has a limited repertoire
of normal frequencies, durations, and amplitudes that
may vary and fluctuate throughout the course of EEG
recording (Westmoreland and Klass, 1990). These vari-
ations and fluctuations, along with benign variants, can
be misinterpreted as abnormal (Table 9.2). In addition,
waveforms identified in the EEG may be normal in

Table 9.2
The “Berger” band, variations of normal, and normal variants

Rhythm Frequency Normal EEG Variations of normal EEG Normal (benign) EEG variants

Alpha 8–13 Hz Posterior dominant Temporal alpha (third rhythm), spiky Wicket waves, frontal arousal rhythm
rhythm alpha, spiky vertex waves in N1
Mu rhythm sleep, spiky mu rhythm
Beta 13–30 Hz Drowsiness and light Fast alpha variant, breach rhythm, 14-and-6 Hz positive spikes, benign
sleep medication effect epileptiform transients of sleep
(benzodiazepines and
barbiturates), myogenic artifact
(i.e., photomyogenic response)
Theta 4–8 Hz Drowsiness Slow alpha variant, lambda waves, Rhythmic midtemporal theta bursts of
Positive occipital sharp spike driving with photic drowsiness, 6 Hz spike-and-waves,
transients (sleep) stimulation, theta (drowsy bursts), subclinical rhythmical EEG discharges
runs of positive occipital sharp in adults, Cigánek rhythm
transients of sleep
Delta 0.5–4 Hz Stage N2 and N3 (slow Posterior slow waves of youth; None
sleep), buildup with hyperventilation response, rare
hyperventilation delta complexes in the elderly
(awake)
 NORMAL EEG VARIANTS
one setting and abnormal in another; for example, alpha
frequencies, part of the normal waking state, may por-
tend demise when the patient is comatose.
Fluctuations of normal waveforms can at times have
an “apiculate” or sharply contoured morphology (i.e.,
spiky alpha rhythm) that may mimic EDs (Benbadis
and Tatum, 2003; Tatum et al., 2006). Normal wave-
forms (predominately in the alpha and beta bands) such
as lambda waves, mu rhythms, positive occipital sharp
transients of sleep (POSTS), vertex sharp waves, drowsy
bursts, and temporal alpha can at times be sharply con-
toured and be confused with an abnormality. Incorrect
EEG interpretation of variations of normal waveforms
can occur when vague, unexplained symptoms have
been elicited from patients evaluated in an outpatient set-
ting (Benbadis and Lin, 2008).
ALPHA
Variants of the normal posterior dominant occipital alpha
rhythm (8–12 Hz) have long been known to occur
(Goodwin, 1947; Aird and Gastaut, 1958), and fluctuations
are common (Westmoreland and Klass, 1990). Typical var-
iations of the alpha rhythm may involve morphology (spiky
or “apiculate” alpha), location (temporal alpha), and fre-
quency (fast/slow alpha variants) (Fig. 9.1). Fluctuations
Fig. 9.1. Slow (subharmonic) alpha variant with muscle artifact. Note the emergence of a 5- to 6-Hz rhythm resolving to a 10- to
11-Hz posterior dominant rhythm (arrows).
145
in normal alpha rhythms have inter- and intravariability
(Haegens et al., 2014) that could be misconstrued as an
abnormal waveform. In one study, a normal alpha rhythm
was misidentified as EDs on a prior EEG in 41 of 127
patients (32%) who later received a definitive diagnosis
of psychogenic nonepileptic attacks following video-
EEG monitoring (Benbadis and Tatum, 2003). For this
reason, the frequency, symmetry, and reactivity of the
alpha rhythm should be noted to avoid confusion and
bring clarity to the interpretation (Beniczky et al., 2013).
Alpha variants may occur as a harmonic of the poste-
rior dominant rhythm and may therefore lie outside of the
alpha frequency. These variants may be confusing when
superimposition of faster frequencies occurs (particu-
larly during slow alpha variant) yet these are readily iden-
tified by their reactivity to eye opening. Mu rhythm
(Fig. 9.2) is a common arciform alpha frequency seen
in about 25% of normal EEGs and represents the resting
rhythm of the rolandic cortex. Mu may be asymmetrical
and appear epileptiform but is nevertheless reactive and
attenuates with contralateral movement (or thought of
moving) of an extremity.
Temporal alpha frequencies comprise a rhythm that
demonstrates no relation to the occipital alpha and the
mu rhythm and has been termed the “third rhythm.” This
alpha frequency is not routinely present on scalp EEG
146 J. MARI-ACEVEDO ET AL.
Fig. 9.2. Mu rhythm with the appearance of an ictal discharge (boxes). Note the bilateral parietal spatial distribution, alpha fre-
quency, and slightly drowsy state.
but may be identified in the presence of a bone defect
(Niedermeyer, 1990). It may be found in the waking state
and, similar to alpha and mu rhythms, may appear spiky
and mimic EDs. Temporal alpha has been observed to
disappear over a resected temporal lobe and appear only
over the normal side in patients with temporal lobe epi-
lepsy (Niedermeyer, 1997). Magnetoelectroencephalo-
graphy has suggested its origin lies in the auditory
cortex (Tiihonen et al., 1991).
BETA
Beta rhythms (13–30 Hz) may be observed bifrontally
and attenuate with eye opening, alerting, or movement.
Beta activity is commonly increased by benzodiazepines,
barbiturates, and chloral hydrate. The patterns involving
the beta frequency range include the fast alpha variant,
spiky beta spindles, and breach rhythm. Fast alpha vari-
ants (supraharmonic) may appear as a “notched” or bifur-
cated waveform appearing at twice the patient’s usual
frequency and may attenuate with eye opening.
A breach rhythm (Fig. 9.3) is a focal or regional state-
independent increase in the amplitude of beta activity that
develops at or near an area of bony defect (Cobb et al.,
1979). Unless associated with spikes or focal slowing, a
breach rhythm is not indicative of brain dysfunction and
may be considered a physiologic byproduct of a bone
defect (Brigo et al., 2011). Nonetheless, when combina-
tions of frequencies are superimposed (alpha, theta, or
mu rhythm) a breach effect may adopt an arciform or spiky
morphology that can be mistaken for EDs and can make
distinguishing a breach rhythm from an underlying abnor-
mality challenging. With breach rhythm, suspicious activ-
ity should be contained within the location of the skull
breach and not spread to adjacent areas.
THETA
Theta rhythms (>3.5 to <8 Hz) may appear normally
during relaxed wakefulness. The patterns of normal
EEG that predominantly involve theta frequencies are
the slow alpha variant, frontal arousal rhythm (children),
rhythmic temporal theta activity of drowsiness, midline
theta rhythms, and focal parietal theta activity
(Westmoreland and Klass, 1990). A slow alpha variant
exists as a subharmonic frequency approximately half
of the patient’s posterior dominant rhythm and attenuates
with eye opening. Midline theta is usually maximal in
the frontal or fronto-central regions and can be facilitated
by focused concentration and drowsiness.
 NORMAL EEG VARIANTS 147

Fig. 9.3. Breach rhythm with “spiky” beta activity mimicking a polyspike (circle).

Temporal theta activity is a normal EEG feature in the

temporal delta complexes in the elderly, buildup during
elderly and usually occupies less than 10% of the recording.
hyperventilation (HV), and delta activity during N3 sleep
Variations in theta frequency become more robust during
(slow sleep). PSWY are nonepileptic occipital delta fre-
the transition from the waking to drowsy state. Hypnagogic/
quencies typically seen in children ages 6–14 (but can
hypnopompic hypersynchrony are bursts of theta of vary-
persist to age 20), which can intermix with alpha frequen-
ing amplitude (up to 300 mV) commonly maximal in the
cies and yet react to eye opening (Mizrahi, 1996). Orig-
midfrontal regions and are a normal phenomenon of no
inally, PSWY were thought to be related to immature
clinical significance common in children and young adults
personalities or inappropriate behavior (Aird and
(Mizrahi, 1996). When bursts are mixed with faster frequen-
Gastaut, 1958) but are now recognized as a variation
cies (artifact or beta), they may be mistaken for abnormal
of normal in the EEG during development and are age
generalized spike-and-wave discharges (Fig. 9.4).
dependent. Source localization via dipole modeling sug-
Lambda waves are normal occipital positive sharply
gests a location in the fusiform, lingual, or middle occip-
contoured transients seen with visual scanning of com-
ital gyrus (Ohoyama et al., 2012).
plex images. They may be asymmetrical and may occur
Hyperventilation may generate normal variations of
in repetitive runs with the appearance of sharp waves
EEG and increased delta activity (including intermittent
(Fig. 9.5). Stage 1 sleep may manifest vertex sharp waves
rhythmic delta and theta activity), which resolves within
and POSTS, which are normal physiologic elements of
2 min following cessation of HV. When combined with
sleep in the EEG. Vertex waves may appear spiky (espe-
other frequencies (e.g., artifact or beta), HV may mimic
cially in children) and prominent sharply contoured
spike-and-waves (Fig. 9.6) and may give the appearance
POSTS may mimic pathological sharp waves when taken
of an abnormality.
out of the context of normal sleep and sleep transition.
Photic stimulation may produce rhythmic potentials
at the same frequency of stimulation or a harmonic/
DELTA subharmonic. The “driving” response may appear asym-
Normal activity in the delta range includes frequencies metrical or spiky (i.e., “spike driving”) (Fig. 9.7) at low fre-
such as posterior slow waves of youth (PSWY), rare quencies (especially <4 Hz), which may lead to confusion.
148 J. MARI-ACEVEDO ET AL.

Fig. 9.4. Hypnogogic burst. Note the change in the state of arousal before and after the burst to signify the sleep transition.

Fig. 9.5. Lambda waves during scanning eye movements (arrows). Notice the alpha “squeak” in the 9th second of the EEG sample.
Fig. 9.6. Buildup during hyperventilation in an 18-year-old with migraine.

Fig. 9.7. Spike driving during 1-Hz intermittent photic stimulation in a 54-year-old referred for “passing out.”
150 J. MARI-ACEVEDO ET AL.
NORMAL (BENIGN) EEG VARIANTS clinical significance and can be classified as epileptiform
and nonepileptiform. Most of these patterns were ini-
The importance of identifying normal variations
tially described in the 1950s and were previously thought
(Table 9.3) and benign EEG variants of uncertain signif-
to be associated with epilepsy (Hughes, 1980).
icance (Table 9.4) lies in the ability to distinguish them
When encountered, most normal EEG variants can be
from abnormal waveforms (Tatum, 2013a,b). Recogni-
identified from abnormalities by knowledge of the
tion of benign variants in EEG is just as important as
patient’s age, state of consciousness, anatomic location,
identifying abnormalities, as overinterpretation can lead
and morphology or pattern of the wave in question.
to misdiagnosis. Normal EEG variants are of uncertain

Table 9.3
Common variations of normal in EEG

EEG variant Distribution Morphology Voltage Frequency Generator

Alpha variants Occipital Notched or bifurcated Variable ½ or double patient’s alpha Occipital-parietal
(slow and fast) posterior dominant rhythm (subharmonic, cortex
rhythm harmonic)
Temporal alpha Midtemporal High amplitude, Variable 6–11 Hz Midtemporal lobe/
(third rhythm) rhythmic. L > R auditory cortex
Frontal alpha Frontal High amplitude, bifrontal Variable 7–10 Hz Frontal lobes
sharp waves
Breach rhythm Variable Variable Variable Variable due to harmonics Variable
(skull defect)
Hypnagogic and Bifrontal High amplitude deltaUp to 300 mV 3–5 Hz Presumed frontal
hypnopompic burst lobe
bursts
Posterior slow Posterior Delta frequency waves on Variable 0.5–3 Hz Fusiform, lingual, or
waves of youth nondominant posterior nondominant occipital gyrus
hemisphere hemisphere

Table 9.4
Normal (benign) EEG variants of uncertain significance

EEG variant Distribution Morphology Voltage Frequency Generator

Wicket waves Anterior Monophasic comb-like 60–200 mV 6–11 Hz Temporal lobe

midtemporal appearance. May
occur singly
6-Hz spike- Frontocentral Low amplitude spike in <40 mV 6 Hz Unknown
and-wave spike-and-wave
complex
14-and-6 Hz Posterior 0.5 s unilateral or <150 mV 6–14 Hz range Unknown
positive temporal region bilateral arciform
bursts
BETS Temporal lobe Brief, monophasic or <50 mV Single Posterior insular and
diphasic spike with posterior
broad field temporal-occipital
RMTD Midtemporal Monomorphic burst of 50–200 mV 5–7 Hz Fissures of posterior-inferior
flat, sharp, or notched temporal region
Cigánek Frontal/vertex Sinusoidal or arciform >50 mV 4–7 Hz Mesial-prefrontal, dorsal
rhythm (commonly 6 Hz) anterior cingulate cortex
SREDA Parietal and Bilateral, synchronous, 40–100 mV 5–7 Hz Biparietal
posterior symmetric
temporal monophasic delta
 NORMAL EEG VARIANTS
Normal variants tend to be more prevalent in the early
stages of sleep (N1–2) and thus a similar waveform is
more likely to be considered abnormal when persistent
in deeper stages (N3) of sleep.
EPILEPTIFORM VARIANTS
Most EEG interpretation begins with the use of a bipolar
montage. With this design, phase reversals may be encoun-
tered that help in localizing a focal process (e.g., slowing
or EDs). However, to the inexperienced interpreter, phase
reversals may be falsely equated with abnormality, rather
than indicating a maximal electronegativity or positivity.
The reader is reminded that normal and abnormal phase
reversals may exist as electronegative events in the EEG.
Caution is urged with mere pattern recognition, as it
predisposes the interpreter to error when polarity and con-
vention involving a physiologic field are ignored.
WICKET RHYTHM
Wicket spikes are also termed wicket waves (Fig. 9.8).
They are a normal variant EEG pattern that was first
described in 1977 (Reiher and Lebel, 1977). Wicket
waves consist of bursts or trains of sharply contoured
Fig. 9.8. Burst of wicket waves (oval) in the left midtemporal region mimicking a burst of abnormal spikes. Note the change in
amplitude without change in frequency.
151
6- to 11-Hz monophasic arciform waves maximal in
the midtemporal regions, but they can also occur as frag-
mented single sporadic spikes (Crespel et al., 2009;
Mothersill et al., 2012). They are most often within the
alpha frequency range, of medium amplitude
(60–200 mV) and can occur bilaterally and asynchro-
nously multiple times during the recording (Azzam
et al., 2015). Although sharply contoured or spiky,
wickets are not followed by an aftergoing slow wave
and do not disrupt the background activity (Tatum,
2014). Wicket waves are most prominent during drows-
iness and light sleep (N1–2) but may also occur in the
waking state or during bursts of arousal. This waveform
is most common in middle adulthood (>30 years) and
older adults, with a reported prevalence around
0.04%–0.96%, but this figure varies in different popula-
tion samples (Santoshkumar et al., 2009).
When appearing as isolated waveforms, wickets can
have a high-amplitude spiky morphology that can mimic
a diphasic spike and slow wave complex and discerning
between the two may be challenging (Reiher and Lebel,
1977). Due to their temporal location (which is highly
epileptogenic), wickets may be commonly mistaken
for pathological EDs (Krauss et al., 2005). In one study,
152 J. MARI-ACEVEDO ET AL.
54% (25/46 patients) of wicket rhythms were incorrectly
interpreted as EDs in patients with nonepileptic events
(Krauss et al., 2005).
Wicket waves likely represent fragmented temporal
alpha activity. Wicket waves underlying a breach rhythm
in a patient who had undergone temporal lobe surgery
with seizure freedom have impeded a trial of ASD taper
(Tatum W.O., personal observation 12/1/2012).
Distinction of wicket waves from interictal discharges
may be accomplished by identifying longer sustained
periods of wicket rhythm within a recording, or trains
of fragments with morphologic similarity to a wicket
rhythm. Without the presence of a larger sample, a single
suspicious wave should not be labeled a “fragment” of
wicket rhythm. Previously, wicket rhythms were thought
to have an association with “neurovegetative” symptoms
such as vertigo, headache, migraine, nausea, or epilepsy,
but are now known to be a normal EEG variant with no
association with epilepsy (Reiher and Lebel, 1977).
6-HZ SPIKE-AND-WAVE
The 6-Hz spike-and-wave (phantom spike-and-wave) is a
benign EEG variant initially described in 1950 (Walter,
1950). “Phantom” is derived from the low-amplitude spike
within a burst of spike-and-slow wave activity (Fig. 9.9).
The amplitudes of the discharge are low with the spike
component usually <40 mV, and the aftergoing slow wave
Fig. 9.9. 6-Hz “phantom” spike-and-wave (FOLD variety) in a 24-year-old female evaluated for spells.
<50 mV. Phantom spike-and-wave is fronto-centrally pre-
dominant and typically bisynchronous with short bursts
lasting up to 2 s (Tharp and Arsenal, 1966). This is in con-
trast to 3-Hz spike-and-slow wave bursts, which are gen-
eralized and of slower frequency (5–7 Hz vs 3 Hz).
Phantom spike-and-wave has been classified into two
groups (Hughes, 1980): WHAM, for wakefulness, high-
amplitude spike, anterior, in males; and FOLD, for
female, occipital, low-amplitude spike, drowsiness. In
WHAM, the spike is usually >45 mV, whereas in FOLD
amplitudes <40 mV predominate (Hughes, 1980). Of
these two subtypes, FOLD is more benign, with a prev-
alence of 30% in epilepsy patients. In contrast, WHAM
has a prevalence of 90% in epilepsy patients.
14-AND-6 HZ POSITIVE BURSTS
14-and-6 Hz positive bursts are a normal EEG variant
described in the early 1950s (Gibbs and Gibbs, 1951).
They comprise brief bursts (0.5–2 s) of repetitive arci-
form positive spikes in the posterior temporal region,
with a broad field of distribution (Fig. 9.10). Bursts
may be bisynchronous, unilateral, or bilaterally asyn-
chronous (Beydoun and Drury, 1992). When unilateral,
a right-sided predominance is often seen. This pattern
is most common between the ages of 8–14, declines in
adolescence, and is rare by early adulthood (Wegner
and Struve, 1977; Santoshkumar et al., 2009). It is most
 NORMAL EEG VARIANTS
Fig. 9.10. Shows 14-Hz (circle) and 6-Hz (arrow) positive bursts delineated by the ipsilateral ear montage of the EEG. Note the
right hemisphere predominance, prominent 14-Hz component, and the higher amplitude in the central head regions due to montage
selection.
likely to occur in drowsiness and light sleep (N1–2) and
should be absent in wakefulness and deep sleep (N3).
While the most common frequencies for the burst are
14 and 6 Hz, a range of other frequencies may be
observed: typically, 13–17 and 5–7 Hz, with amplitudes
about 75 mV. 14-and-6 Hz positive bursts can be distin-
guished from focal EDs by their shorter duration (rarely
>1 s), bilateral location, and positive polarity. Overlap of
other benign EEG variants (i.e., 6 Hz spike-and-wave)
may occur with 14-and-6 Hz positive bursts.
When present in large numbers, 14-and-6 Hz positive
bursts may indicate an underlying metabolic encephalop-
athy. Various etiologies may be encountered, and the
EEG background typically coexists with diffuse slowing
or triphasic waves in this scenario. This benign EEG var-
iant may also be elicited by administration of
diphenhydramine.
BENIGN EPILEPTIFORM
TRANSIENTS OF SLEEP
Benign epileptiform transients of sleep (BETS) occur
mainly in adults between drowsiness through N2 sleep
(Fig. 9.11) and were initially described by Gibbs and
153
Gibbs (1952). Also known as “small sharp spikes” and
“benign sporadic sleep spikes,” BETS are a benign variant
unassociated with epilepsy (Koshino and Niedermeyer,
1975; White et al., 1977). BETS are usually low voltage
(<50 mV), brief duration (<50ms), simple monophasic
or diphasic spikes with a broad distribution maximally
centered in the temporal lobes (Zumsteg et al., 2006a,b).
Due to their low amplitude, they may be missed by
EEG interpreters. Nevertheless, BETS can demonstrate
higher voltage (>50 mV), longer duration (>50 ms), or a
small aftergoing slow wave that is typically of lower
amplitude than the spike (Tatum, 2013a).
BETS disappear in N3 sleep and should not be seen dur-
ing wakefulness. Sleep deprivation can increase the fre-
quency of BETS in a recording, due to shifting the
NREM-to-REM sleep ratio. Medications that affect REM
sleep cycling (antidepressants, antipsychotics) may also
increase the likelihood of observing BETS (Zumsteg
et al., 2006a,b). Two distinct sources have been suggested
for each component of the waveform in BETS: the first
electronegative component from a presumptive posterior
insular source, and the second electropositive component
(using an ear reference) from the ipsilateral posterior
temporo-occipital region (Zumsteg et al., 2006a,b).
154 J. MARI-ACEVEDO ET AL.

Fig. 9.11. Benign epileptiform transients of sleep in a 40-year-old female with spells following a motor vehicle accident. A low-
amplitude, right fronto-temporal region spike (around 50 ms) without aftergoing slow wave is present (oval) during drowsiness.

BETS occur in adults of ages 30–60 and are not seen Table 9.5
in children before age 10. BETS have an incidence of
1.36%–2.4% in adult EEG recordings (Santoshkumar BETS vs epileptiform discharges
et al., 2009), and usually multiple occurrences are noted
Epileptiform
within a single tracing. When recurrent, BETS may be
BETS discharges
contralaterally homotopic and occasionally occur syn-
chronously in the bilateral temporal regions. Overall, Occur during light sleep (N1–2) State independent
shifting asymmetry should not present a significant pre- Maintains identical morphology Morphology varies
dilection for one side. At times, BETS may follow an Broad Field Narrow field
oblique transverse dipole that extends across the midline, Aftergoing slow wave is variable Slow waves of equal or
with electronegativity in one hemisphere and electropo- greater amplitude
sitivity in the other.
Due to their epileptiform morphology, occurrence
during light sleep, and temporal location, BETS may electrographic discharge of adults (SREDA) is a benign
be commonly mistaken for interictal EDs. Differentiating rare electrographic pattern that simulates an electrographic
BETS from EDs can be accomplished by keeping the seizure (Fig. 9.12). This is the rarest of benign variant,
characteristics shown in Table 9.5 in mind. with an incidence of 0.05%, and commonly occurs during
wakefulness (Dash and Ashalatha, 2013). It is a broadly
distributed rhythm across parietal-posterior-temporal
SUBCLINICAL RHYTHMIC
regions and demonstrates frequency evolution.
ELECTROGRAPHIC DISCHARGE
Onset may be abrupt or consist of high-amplitude
OF ADULTS
monophasic or diphasic sharp waves that coalesce and
Seizures are rarely recorded during routine scalp EEG evolve to a continuous delta rhythm. This subsequently
recording (Angus-Leppan, 2007). Subclinical rhythmic demonstrates evolution from delta to theta and persists
Fig. 9.12. EEG from 60-year-old female with a history of seizures evaluated with EEG following a motor vehicle accident. Note
SREDA at the onset (A) with a normal awake background transitioning to a generalized, synchronous theta frequency rhythm involv-
ing the bilateral temporal–parietal regions (B) without evolution throughout its duration (C) of 40 s. No postictal slowing was present.
156 J. MARI-ACEVEDO ET AL.
Fig. 9.12—Cont’d
as a sharply contoured 5–7 Hz activity for 40–80 s,
although ranges of 10 s to 5 min have been reported
(Westmoreland and Klass, 1997; Zumsteg et al.,
2006a,b). Amplitudes lie between 40 and 100 mV but
can be as high as 500 mV. Once established, SREDA does
not evolve in frequency, distribution, or morphology. It is
commonly bilateral, synchronous, and symmetric. Reso-
lution may be gradual or abrupt.
SREDA is most common in the elderly and individ-
uals older than 50 (Westmoreland and Klass, 1997). Indi-
viduals who demonstrate SREDA are likely to manifest it
again in future EEGs. The only known trigger for
SREDA is hyperventilation (Westmoreland and Klass,
1997; Zumsteg et al., 2006a,b; Tatum, 2013a). Rarely,
SREDA may have variants that remain in the delta fre-
quency, have a notched contour, or are frontally predom-
inant (Dash and Ashalatha, 2013).
SREDA is distinguished from an ictal pattern by its
lack of temporal-spatial evolution, and its sparing of
the alpha rhythm when the posterior head regions
are unaffected. Upon resolution, baseline EEG activity
is rapidly reestablished without postictal slowing.
Source localization of SREDA using low-resolution
electromagnetic tomography demonstrated a biparietal
focus, overlying watershed areas by the anterior, mid-
dle, and posterior cerebral arteries (Zumsteg et al.,
2006a,b). This led to proposing that it may be related
to vascular causes due to its prevalence in older popu-
lations and provocation by hyperventilation (relative
hypoxia from vasoconstriction), although this remains
controversial.
NONEPILEPTIFORM VARIANTS
Nonepileptiform variants do not typically resemble EDs
and tend to be more rhythmic; they may resemble slow
waveforms. Some nonepileptiform normal EEG variants
may have more than one morphological variant that can
mimic EDs.
RHYTHMIC MIDTEMPORAL THETA
DISCHARGES OF DROWSINESS
Rhythmic midtemporal theta discharge of drowsiness
(RMTD) was previously known as psychomotor variant
due to the belief that it was associated with “psychomotor”
seizures (Lipman and Hughes, 1969). This pattern occurs
in 0.5%–2% of normal adults and is present in around 10%
 NORMAL EEG VARIANTS 157

Fig. 9.13. Rhythmic midtemporal theta discharges in the EEG of a 25-year-old with cognitive changes. Note the bilateral inde-
pendent distribution, 5-Hz frequency, and sharp morphology in drowsiness.

of healthy adults over 60 (Santoshkumar et al., 2009). It
consists of bursts of 5–7 Hz theta with a monomorphic pat-
tern that may appear sharp, flat, or notched (Fig. 9.13)
depending on superimposed harmonics (Tatum, 2013a).
The pattern is medium to high amplitude (50–200 mV),
regular, and replaces the preceding background. RMTD
does not vary in frequency but may vary in amplitude
observed in the rise and fall of the burst.
As the name implies, RMTD is maximal in the mid-
temporal region and does not evolve temporally or spa-
tially. It may be represented bilaterally or independently
among both hemispheres. RMTD has a classic duration
of 10 s but may occur in long runs and can last more than
1 h (Fawaz et al., 2015). It is commonly seen in adoles-
cents and young adults in the relaxed wake state, but has
been observed in sleep (Beiske et al., 2016).
Source localization of RMTD using magnetoenceph-
alography suggests an origin within the cortices of the
posterior-inferior temporal regions (Lin et al., 2003).
RMTD has been noted to occur in both epileptic and
nonepileptic patients, and it remained present in epileptic
patients who underwent anterior temporal lobectomy.
Sharply contoured RMTD may be distinguished from
interictal EDs by its lack of evolution in both frequency
and distribution.
CIGÁNEK RHYTHM
Cigánek rhythm is a midline or frontal-midline theta
rhythm (Cigánek, 1961). Cigánek rhythm consists of a
sinusoidal or arciform pattern maximal over the vertex
region (Fig. 9.14). Anterior or posterior displacement
may be seen, with the anterior location being more com-
mon. It has a frequency of 4–7 Hz (commonly 6 Hz), with
an amplitude greater than 50 mV and duration of 3–20 s.
While resembling a mu rhythm, Cigánek is not reactive,
occurs during drowsiness or concentration, and has a
slower frequency (4–7 Hz vs 8–13 Hz). Cigánek was
originally thought to be an abnormal rhythm associated
with temporal lobe epilepsy (Cigánek, 1961), but is
now considered a benign variant of uncertain signifi-
cance (Westmoreland and Klass, 1990; Tatum, 2013a).
Cigánek rhythm is more prevalent in early adulthood
(Mokráň et al., 1971).
158 J. MARI-ACEVEDO ET AL.
Fig. 9.14. Central theta associated with the Cigánek rhythm noted in drowsiness and wakefulness in this patient with recurrent
spells.
Frontal midline theta has been associated with multiple
cognitive tasks such as memory processing, arithmetic,
problem solving, and sustained attention required for
working memory (Miller et al., 2015; Kieffaber and
Hershaw, 2016). Source localization with magnetoen-
cephalography has demonstrated an association with the
medial prefrontal and dorsal anterior cingulate cortex
(Ishii et al., 2014). Some associations have been found
between increased frontal midline theta power and better
performance in cognitive tasks (Kieffaber and Hershaw,
2016) and this has become a potential therapeutic target
for transcranial magnetic stimulation (Miller et al., 2015).
Frontal midline theta has also been described as asso-
ciated with use of personal electronic devices (Tatum
et al., 2016).
ARTIFACT
Artifacts are a common occurrence in the normal record,
though they are composed of signals that are not gener-
ated by the brain (Klass, 1995). Some artifacts may be a
useful component in identifying levels of alertness and
cycling between wakefulness and sleep (eye blinks,
myogenic). Artifacts may be differentiated from physio-
logic waveforms by their lack of conformation to a
believable spatial field of distribution.
One source of nonphysiologic artifact commonly
encountered is electrodes that “pop,” or have a compro-
mised scalp-electrode contact that may simulate EDs.
Myogenic artifact is often prominent during scalp
EEG, with muscle “spikes” that commonly occur over
the temporalis and frontalis muscles and may be confused
with abnormal EDs (Fig. 9.15) or other pathologic wave-
forms (Tatum, 2013a). Artifacts may be generated by a
variety of sources, and when combined (e.g., myogenic
and eye flutter) may create the illusion of generalized
spike-and-slow waves (Fig. 9.4). Sweat and glossokinetic
artifacts have “infraslow” frequencies, and “high-frequency
oscillations” may be simulated by technical artifacts,
although these are easily differentiated by other features
of the scalp EEG recording.
CONCLUSION
Normal EEG variants and variations of normal
waveforms have been known for years, and newer
waveforms are still being identified with as of yet
unknown significance (Tatum et al., 2016). While some
EEG variants are nonepileptiform, others can give the
appearance of EDs and may deceive the interpreter.
Recognizing the wide range of normal physiologic fea-
tures and normal EEG variants remains essential to
accurate EEG interpretation and avoiding the clinical
consequences of overinterpretation. Given the high
prevalence of temporal lobe epilepsies and the penchant
for normal variations, benign variants, and artifactual
waveforms to involve the temporal regions, it is crucial
for interpreters to take a conservative approach to avoid
EEG overinterpretation.
 NORMAL EEG VARIANTS 159

Fig. 9.15. Artifact in the right temporal electrode (at 70 Hz) in (A) and after it was filtered at 15 Hz (B). See the effect of filtering on
the appearance of artifact to mimic a focal epileptiform discharge. From Schomer DL, Lopes da Silva FH, eds. Niedermeyer’s
Electroencephalography. Seventh edition. With permission from Oxford University Press.

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FURTHER READING
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Clin EEG Neurosci 30 (1): 16–20.