ORIGINAL ARTICLES

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 Neurophysiol 2006;23: 194207)

europhysiology has rapidly advanced since the early

20th century pioneered the initial human adult EEG
experiences. Over the last 75 years, EEG has evolved from a
diagnostic tool, to an integral part of intensive monitoring not
only for diagnostic purposes, but also for providing information to deliver therapy via direct brain electrical stimulation.
The EEG represents a collection of waveforms containing
information about the function of the brain. In general hospitals, EEG holds a principal role for routine neurodiagnostic
information in clinical medicine, while in tertiary care epilepsy centers, EEG seeks to identify the epileptogenic zones
in patients with intractable seizures for the purposes of
resective epilepsy surgery. To understand the abnormal EEG,
one must understand that which is normal. The following
review represents the most current assessment of clinical
EEG in the context of performing adult scalp-based recording.

NORMAL HUMAN ADULT EEG

The advent of EEG in humans started with Hans Bergers discovery of the alpha rhythm in human subjects (Adrian
and Mathews, 1934). The alpha rhythm still remains the
starting point to analyze clinical EEG (Kellaway et al., 2003).

*Department of Neurology, Tampa General Hospital, University of South

Florida, Tampa, Florida, U.S.A.; Department of Medicine (Neurology),
Duke University Medical Center and Neurodiagnostic Center, Veterans
Affairs Medical Center, Durham, North Carolina, U.S.A.; and Department of Neurology, Johns Hopkins Bayview Medical Center, Johns
Hopkins 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:
WOTIV@aol.com.
Copyright 2006 by the American Clinical Neurophysiology Society
ISSN: 0736-0258/06/2303-0194

194

In the normal EEG, a posterior dominant rhythm is represented bilaterally over the posterior head regions and lies
within the 8 to 13 Hz bandwidth that characterizes the alpha
frequency. 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 normally appears by 3 years of age. More than one site exists to
generate the alpha rhythm within both cortical and subcortical
regions. When the best frequency of the alpha rhythm is only
8 Hz, this should raise suspicion for abnormal slowing, as this
frequency occurs in 1% of normal adult subjects at any age.
The alpha rhythm remains stable between 8 to 12 Hz even
during normal aging into the later years of life (see Fig. 2). In
approximately one fourth of normal adults, the alpha rhythm
is poorly visualized with 6% to 7% of normal adults demonstrating voltages of 15 Hz (Kellaway, 2003). The alpha
rhythm is distributed maximally in the occipital region and
shifts anteriorly during the drowsy state. In one third of
people, the alpha rhythm may be atypically diffusely represented or appear maximally in the posterior temporal derivations (apiculate temporal alpha). Voltage asymmetries of
50% should be regarded as abnormal especially when the
left side is greater than the right. It is best observed during
relaxed wakefulness and normally differs by 1 Hz from
hemisphere to hemisphere. Unilateral failure of the alpha
rhythm to attenuate is an ipsilateral abnormality referred to as
Bancauds phenomenon. Frequencies seen to transiently increase immediately after eye closure are known as alpha
squeak. Alpha variants include both slow and fast variations
of the alpha rhythm and have a harmonic relationship with a
similar distribution and reactivity. The slow alpha variant
(theta frequency) has a frequency one half that of the alpha
rhythm usually in the range of 4 to 5 Hz (see Fig. 2).
The fast alpha variant (beta frequency) is usually twice
that of the resting alpha rhythm and ranges from 16 to 20 Hz.
Alpha variants may have a notched appearance also. Paradoxical alpha occurs when alertness results in the presence of
alpha, and drowsiness does not. Normally the opposite effect
occurs. The mu rhythm is a centrally located arciform alpha
frequency (usually 8 to 10 Hz) that represents the sensorimotor cortex at rest (see Fig. 3). While it resembles the alpha
rhythm, it blocks not with eye opening, but instead with
contralateral movement of an extremity. It may be seen only
on one side, and may be quite asymmetric and asynchronous,
despite the notable absence of an underlying structural lesion.
The mu rhythm may slow with advancing age, and is usually
of lower amplitude than the existent alpha rhythm. When
persistent, unreactive, and associated with focal slowing,
mu-like frequencies are abnormal.

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FIGURE 1. Normal 9 Hz alpha

rhythm blocked with eye opening
in a 96 y/o with a TIA.

FIGURE 2. Slow alpha variant (note

the reduction of the posterior dominant rhythm to 1/2 that of the 10
Hz alpha rhythm present in the initial portion of the tracing).

Beta rhythms are frequencies that are more than 13 Hz.

They are common, and normally observed within the 18 to 25
Hz bandwidth, less frequently noted at 14 to 16 Hz, and even
rarer at 35 Hz. A normal voltage of 20 uV is found in
98% of normal adults. Electrocorticography demonstrates the
highest voltage in the perirolandic cortex, and precentral beta
activity may attenuate with movement or the thought of
movement much like the mu rhythm (Kozelka and Pedley,
2000). Voltages beyond 25 uV in amplitude are abnormal.
Benzodiazepines, barbiturates, and chloral hydrate are potent
beta activators and activate beta in the 14 to 16 Hz bandCopyright 2006 by the American Clinical Neurophysiology Society

width. Mental, lingual, or cognitive efforts may also activate

beta rhythms. Beta activity normally increases during drowsiness and light sleep. Persistently reduced voltages of 50%
suggests a cortical gray matter abnormality within the hemisphere having the lower amplitude. However, lesser intermittent voltage asymmetries may simply reflect normal physiologic skull asymmetries. Beta activity may have regionally or
hemispheric suppression from a structural lesion of the cortex
or from an extradural fluid collection associated with a
subdural, epidural, or subgaleal accumulation of blood or
cerebrospinal fluid between the surface of the cortex and

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FIGURE 3. Note the prominent

left central mu rhythm during eye
opening.

FIGURE 4.
Breach rhythm in the
right temporal region (maximal at
T4) following craniotomy for temporal lobectomy.

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recording electrode. A skull defect may produce a breach

rhythm (Fig. 4) with focal, asymmetric, higher-amplitude
(relative increase may be threefold) beta activity without the
skull to attenuate the faster frequencies. It is not an abnormality unless associated with spikes or focal slowing, and is
an expected physiologic condition when the voltage dampening effects of the skull have been compromised. Generalized excess fast activity 50 uV for 50% of the waking
tracing is usually due to drug effects. Faster high frequency
oscillations 80 Hz may occur in normal brain (and epileptic) structures, yet ultrafast frequencies above 25 Hz are
rarely seen during scalp-based EEG recording (Khosravani et
al., 2005).
Theta rhythms are electrocerebral activity composed of
4 to 7 Hz frequencies of varying amplitude and morphologies. Approximately 35% of normal young adults show
intermittent 6 to 7 Hz theta of 15 uV during relaxed
wakefulness that is maximal in the frontal or fronto-central
head regions (Kellaway, 2003). In the teenage years and in
the early 20s, central theta may occupy 10% to 20% of the
recording (see Fig. 5). The appearance of frontal theta can be
facilitated by heightened emotional states, and marked frontal-central rhythmic theta during wakefulness has been described during periods of focused concentration and during
the performance of mental tasks (Santamaria and Chiappa,
1987). Theta activity is normally enhanced by hyperventilation, drowsiness, and sleep. When intermittent 4 to 5 Hz
activity is present in the temporal leads bilaterally, or with a
lateralized predominance (usually left right), this may
occur in the asymptomatic elderly population with an incidence of approximately 35% (Klass and Brenner, 1995), and
is not considered an abnormal finding.
Lambda waves have been initially described as surface
positive sharply contoured theta waves appearing bilaterally
in 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 posterior
dominant rhythm. When they occur asymmetrically, they
may create confusion with interictal epileptiform discharges,
and potentially leads to misinterpretation of the EEG. They
are best observed in young adults when seen, though are more
frequently found in children. Lambda waves are best elicited
when the patient visually scans a textured or complex picture
with fast saccadic eye movements (see Fig. 6). When encountered in the EEG laboratory, placing a plain white sheet of
paper in front of the individual will eliminate the visual input
that is essential for their generation.
Delta rhythms are frequencies consisting of all frequencies up to 4 Hz activity that comprises 10% of the normal
waking EEG by age 10 years (see Fig. 7). In the waking
states, delta can be considered a normal finding in the very
young and in the elderly. With advancing age, the normal
elderly population may demonstrate rare irregular delta slowing in the temporal regions (Van Cott, 2002). It is similar to
temporal theta in the distribution often occupying the left
temporal head regions, but normally is present for 1% of
the recording. Delta may be seen normally in individuals
older than 60 years (see Fig. 4), at the onset of drowsiness, in
response to hyperventilation, and is especially prominent
during slow wave sleep. Excessive generalized delta is abnormal and indicates an encephalopathy of nonspecific etiology. Focal arrhythmic delta usually indicates a structural
lesion involving the white matter of the ipsilateral hemisphere
especially when it is continuous and unreactive.

NORMAL SLEEP ARCHITECTURE

Stage 1 sleep is defined by the presence of vertex waves
typically 200-millisecond diphasic sharp transients with maximal negativity at the vertex (Cz) electrode. They may be

FIGURE 5.
Normal frontocentral
theta in an 18 year-old while
awake.

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

FIGURE 7.
Intermittent left midtemporal delta during transition to
drowsiness in a normal 84 year-old
evaluated 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. Vertex
waves can appear spiky (especially in children) but should
normally never be consistently lateralized. Other features
include attenuation of the alpha rhythm, greater frontal prominence of beta, slow rolling eye movements, vertex sharp
transients. In addition, positive occipital sharp transients
(POSTS) are another feature signifying stage 1 sleep. These
are surface-positive, bisynchronous physiologic sharp waves
with voltage asymmetries that may occur over the occipital
regions as single complexes or in repetitive burst that may be
present in both stage 1 and 2 sleep.
Stage 2 sleep is defined by the presence of sleep
spindles and K complexes (Fig. 8). This stage has the same
features as stage 1 with progressive slowing of background
frequencies. Sleep spindles are transient, sinusoidal 12 to 14
Hz activity with waxing and waning amplitude seen in the
central regions with frontal representation by slower frequencies of 10 to 12 Hz. A K-complex is a high-amplitude
diphasic wave with an initial sharp transient followed by a
high amplitude slow wave often associated with a sleep
spindle in the fronto-central regions. A K-complex may be
evoked by a sudden auditory stimulus. A persistent asymmetry of 50% is abnormal on the side of reduction.
Slow wave sleep now best describes nonrapid eye
movement (non-REM) deep sleep and is comprised of 1 to 2
Hz delta frequencies occupying variable amounts of the
background. Stage 3 previously noted delta occupying 20%
to 50% of the recording with voltages of 75 uV, whereas
stage 4 consists of delta present for 50% of the recording
(see Fig. 9).
Rapid eye movement sleep is characterized by rapid
eye movements, loss of muscle tone, and sawtooth waves in

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

ACTIVATION PROCEDURES
Hyperventilation is routinely performed for 3 to 5
minutes in most EEG laboratories (see Fig. 11). The purpose
is to create cerebral vasoconstriction through respiratory
means of promoting systemic hypocarbia. Hyperventilation
normally produces a bilateral increase in theta and delta
frequencies (buildup) that is frontally predominant, and often
high amplitude. Resolution of the effect occurs normally
within 1 minute. Activation, or the generation of epileptiform
discharges, is infrequently seen in those with localizationrelated epilepsy (10%), however, may approach 80% for
those with generalized epilepsies that include absence seizures (Gabor and AjmoneMarsan, 1969). Superimposition
of beta and delta frequencies during normal buildup may
mimic abnormal generalized spike-and-slow waves, but the
inconsistent relationship from complex to complex is a clue
to the nonpathological origin of the situation. Hyperventilation may produce focal slowing in patients with an underlying
structural lesion. It should not be performed in patients with
severe cardiac or pulmonary disease, acute or recent stroke,
significant large vessel cerebrovascular, sickle cell anemia or
trait, and used with caution during pregnancy.
Intermittent photic stimulation, when used as an activating procedure normally produces rhythmic potentials exquisitely time-locked to the frequency of the intermittent light

FIGURE 8.
Stage 2 sleep with
prominent occipital POSTs and
fronto-central sleep spindles. Note
the single T4 small sharp spike during the 6th second.

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

FIGURE 10.
REM sleep with lateral rectus (myogenic) spikes in
the anterior-lateral head regions
induced by rapid eye movements.

stimulus, and is referred to as photic driving (see Fig. 12).

Response depends on background illumination and the distance of the light source from the patient. Distances of 30
cm from the patient are used to optimize the effect of
stimulation. Flashes are very brief, and delivered in sequence
from 1 to 30 Hz flash frequencies for approximately 10

200

seconds on before stopping the stimulus. Subharmonics and

harmonics of the flash frequency may be seen. Photic driving
is usually greatest in the occipital location, in frequencies
approximating the alpha rhythm, when the eyes are closed.
Unilateral driving may be seen and needs to be interpreted
with caution since abnormality usually requires other abnorCopyright 2006 by the American Clinical Neurophysiology Society

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FIGURE 11.
Normal buildup during hyperventilation.

mal features. Photomyoclonic (or photomyogenic) responses

consist of frontally dominant muscle artifact that occurs when
the flash evokes repetitive local contraction of the frontalis
musculature (photomyogenic). The periocular muscles are
also usually affected, though single lightening-like head jerks
(photomyoclonic) may occasionally be produced. Myogenic
spikes occur 50 to 60 milliseconds after the flash and increase
in amplitude as stimulus frequency increases. The response is
normal, though may be seen in withdrawal syndromes or
states of hyperexcitability.

BENIGN ELECTROENCEHALOGRAPHIC
VARIANTS
Both rhythmic and epileptiform waveforms may appear
in the human EEG without known clinical significance and
are considered to be benign patterns. Interobserver variability
still 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 confusion and lead some to misinterpretation of the EEG (Benbadis and Tatum, 2003). Such rhythmic patterns most frequently fall within the theta, alpha, and beta frequency ranges
(Westmoreland, 2003). Rhythmic temporal theta bursts of
drowsiness, variants of the alpha rhythm, and sharply contoured midline theta rhythms are most frequently seen. Previously these EEG patterns were thought to be associated
with seizures, headaches, abdominal pain, and behavioral
disturbances. However, these anomalies are now considered
benign variations of normal, and not representative of neurovegetative psychopathology nor possess significance specific for epileptic seizures.
Copyright 2006 by the American Clinical Neurophysiology Society

Rhythmic temporal theta bursts of drowsiness (see Fig.

13) is the preferred term for what was previously described as
psychomotor variant (Hughes and Cayaffa, 1973). This pattern occurs in 0.5% to 2.0% of selected normal adults and
consists of bursts or runs of 5 to 7 Hz theta waves that may
appear sharp, flat, or notched in appearance. It is maximal in
the midtemporal derivations and was referred to as rhythmic
midtemporal theta bursts of drowsiness. It is an interictal
pattern that does not evolve spatially or temporally though
may be represented bilaterally or independently over both
hemispheres. it is seen in adolescents and adults in relaxed
wakefulness.
Midline theta was initially described by Ciganek as a
focal sinusoidal or arciform 4 to 7 Hz rhythm over the vertex
region (Ciganek, 1961). While morphologically, it may resemble a mu rhythm, it is not similarly reactive, is slower in
frequency, and occurs both in drowsiness or the alert state.
Although initially felt to be a projected rhythm in temporal
lobe epilepsy, it has been seen in a heterogeneous population
and is therefore of nonspecific clinical significance.
Some benign patterns may have an epileptiform morphology but are not associated with seizures, and therefore do
not represent interictal epileptiform discharges (Stern and
Engel, 2005). This may include normal rhythms (i.e., spiky
alpha in the temporal regions), or include superimposition of
background frequencies giving the appearance of epileptiform discharges (i.e., HV with delta and superimposed beta
simulating generalized spike-and-wave).
Spike-and-wave discharges at 6 Hz were first described
by Gibbs, and later referred to as phantom spike-and-wave
(see Fig. 14). Initial descriptions included two forms. The
acronym WHAM (wakefulness, high amplitude, anterior,

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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 temporal
theta of drowsiness. Note the
sharply contoured morphology.

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FIGURE 14.
Six-Hz (phantom)
spike-wave burst with frontal predominance in a patient with headaches.

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 discharges range from 5 to 7 Hz, though with a typical repetition
rate of 6 Hz lasting briefly for 1 to 2 seconds. The spike is
often of very low amplitude, at times difficult to appreciate
during routine interpretation of the EEG by qualitative visual
analysis. When the spikes are of low amplitude and occur
during drowsiness this is usually reassuring for a benign
findings. When they are seen with high amplitude spikes and
occur with less than a 6 Hz frequency, or occur during
wakefulness 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 called ctenoids.
There can be an association with 6 Hz spike-and-wave that
may occur in the same person (Silverman, 1967). They
appear in the EEG as a burst of positive comb-like spindles
over the posterior temporal head regions. They are present
most frequently at a rate of 14 Hz or 6 to 7 Hz lasting 0.5 to
1 second in duration. The 14 Hz frequency is most prevalent,
and the 6 Hz burst may appear with or without the faster
frequencies (see Fig. 15). They are most common during
adolescence though may persist into adulthood, decreasing
with age. The bursts are usually unilateral or bilaterally
asynchronous with shifting predominance involving one
hemisphere to a greater degree. A contralateral ear reference
montage, and greater interelectrode distance best demonstrate
these bursts (Blume et al., 2002).
The original reference to small sharp spikes or benign epileptiform transients of sleep or benign sporadic
sleep spikes of sleep (Fig. 16) depict a low-voltage (50
uV) brief duration (50 milliseconds) simple waveform with
a monophasic or diphasic spike that has an rapidly ascending
limb and steep descending limb best seen in the anterior to
midtemporal derivations during non-REM sleep. They may
have a slightly higher voltage, or longer duration, and may
appear with an after-going slow wave usually of lower
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amplitude than the spike. They are not associated with focal
slowing, do not occur in runs, and disappear in slow wave
sleep. They are most common in adults and occur with
approximately 20% to 25% incidence. They occur as a
unilateral discharge but are almost always bilateral and independent or reflected to the homologous derivations with a
field that may correspond to an oblique transverse dipole
resulting in opposite polarities over opposite hemispheres.
Wicket spikes (see Fig. 17) are seen in adults 30
years of age and occur within the 6 to 11 Hz band but can
obtain amplitudes of up to 200 uV. They are seen over the
temporal regions during drowsiness and light sleep and are
bilateral and independent. They usually occur in bursts,
though may be confused with interictal epileptiform discharges especially when they occur independently or as
isolated waveforms (Krauss et al., 2005). Comparing the
frequency and morphology of the bursts to the isolated
waveforms a means of demonstrating similar waveforms and
supports the nonepileptogenic origin of the waveform. While
wicket spikes are considered an epileptiform normal variant,
when selecting patients for EEG, they may still appear on the
EEG of patients with a clinical diagnosis of epilepsy ( Krauss
et al., 2005). No focal slowing or after-going slow-wave
component is seen and they likely represent fragmented
temporal alpha activity (Reiher and Lebel, 1977).
In contrast to many of the patterns of uncertain significance that mimic interictal epileptiform discharges (IEDs), a
subclinical rhythmic electrographic discharge in adults
(SREDA) is a pattern that appears to as a paroxysmal burst on
the EEG that mimics the epileptiform characteristics of a
subclinical seizure. However, there are no clinical features
that coexist with it, including neither subjective nor objective
findings, and no association with epilepsy has yet been
demonstrated. In contrast to most benign variants that occur
maximally in younger age ranges during drowsiness, SREDA
is more likely to occur in the population over 50 years of age,
and also occurs while the person is awake. It may exist in two
forms: either as a bilateral episodic burst of rhythmic sharply

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

contoured 5 to 7 Hz theta frequencies appearing maximal

over the temporoparietal derivations and may be asymmetric,
or as an abrupt mononphasic repetitive sharp or slow waveforms appear focally at the vertex that recur in progressively
shorter intervals until a sustained burst is noted that mimics
the evolution seen with an electrographic seizure. The bursts
usually last 40 to 80 seconds and appear without postictal
slowing (see Fig. 18). Single photon emission computed
tomography during SREDA does not demonstrate the corresponding regional cerebral hyperperfusion that occurs during
electrographic seizures in patients with epilepsy (Thomas et
al., 1992).
There is a finite, but subjective difference between
normal 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 between
a pattern of interictal and ictal origin (Chong and Hirsch,
2005). The greatest difficulty appears with the periodic patterns often most evident in the critically ill. These patterns
challenge the electroencephalographer to differentiate those
waveforms that are abnormal, and whether these patterns
reflect the epiphenomenona of dysfunctional brain, or imply

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ongoing seizures. Although technology has made huge advances in the ability to record and continuously monitor EEG
(Kull and Emerson, 2005), our understanding of the underlying pathophysiologic mechanisms, and means to distinguish potentially ictal patterns still remains limited. Because
the impact on treatment is predicated by understanding the
challenges that face the electroencephalographer when presented with abnormal patterns, the essence of distinguishing
normal EEG cannot be overstated.
Our knowledge and utilization of normal EEG have
evolved. The basic waveforms, frequencies, physiologic, developmental and sleep architectures are known. The earlier
association of epileptiform normal variants with neurovegetative symptoms and psychiatric conditions (Boutros et al.,
2005) have been superseded by their identification as patterns
without clinical significance. They are important to identify
because they may serve to impart misdiagnoses in patients
without epilepsy and carry ramifications that include overly
aggressive treatment. The advent of long-term monitoring has
broadened our understanding of EEG, and in the future will
become commonplace with recording during anesthesia, in
the intensive and critical care units, and perhaps even in the
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FIGURE 16.
A right temporal
small sharp spike is present in
drowsiness. Note the 50 microvolt amplitude and simple diphasic
morphology.

FIGURE 17.
Wicket waves maximal at T3 and T4.

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FIGURE 18.
SREDA in a 73 year
old during HV. No clinical signs
were present.

emergency department for acute neurologic care (Tatum,

2001). New waveforms are still being identified (Hirsch et al.,
2004). Coregistration with EEG and other neuroimaging
techniques have facilitated greater source localization of
epileptiform abnormalities. EEG continues to remain at the
forefront in neurologic evaluations, as well as during neurologic monitoring for the systemic effects of general medical
conditions (see Fig. 17). Normal EEG remains at the foundation of interpretation for those that hope to identify abnormal patterns. While 2006 has seen advances in clinical EEG,

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

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