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EEG Atlas: EEG Artifacts (CME available)

EEG Atlas: Encephalopathic Patterns I - Generalized
(CME available)
Slowing
EEG Atlas: Encephalopathic Patterns II - More Severe
(CME available)
Patterns
EEG Atlas: Encephalopathic Patterns III - Miscellaneous
(CME available)
Patterns
EEG Atlas: Epileptiform Normal Variants (CME available)
EEG Atlas: Focal (Nonepileptic) Abnormalities (CME available)
EEG Atlas: Generalized Epilepsies (CME available)
EEG Atlas: Localization-related Epilepsies (CME available)
EEG Atlas: Normal Awake EEG (CME available)
EEG Atlas: Normal Sleep EEG - Rapid Eye Movement
(CME available)
Sleep
EEG Atlas: Normal Sleep EEG - Stage I (CME available)
EEG Atlas: Normal Sleep EEG - Stage II (CME available)
EEG Atlas: Normal Sleep EEG - Stages III and IV (CME available)
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eMedicine - EEG Atlas: EEG Artifacts : Article by Selim R Benbadis, MD
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EEG Atlas: EEG Artifacts Rate this Article Introduction
Physiologic Artifacts
Email to a Colleague Extraphysiologic
Last Updated: May 30, 2002
Artifacts
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Author Information Introduction Physiologic Artifacts Extraphysiologic Artifacts Pictures Bibliography

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Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor,
Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital Continuing
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INTRODUCTION Section 2 of 6
Although EEG is designed to record cerebral activity, it also records electrical activities arising from sites other
than the brain. The recorded activity that is not of cerebral origin is termed artifact and can be divided into
physiologic and extraphysiologic artifacts. While physiologic artifacts are generated from the patient, they arise
from sources other than the brain (ie, body). Extraphysiologic artifacts arise from outside the body (ie,
equipment, environment).
PHYSIOLOGIC ARTIFACTS Section 3 of 6
Muscle (electromyogram) activity
Myogenic potentials are the most common artifacts (see Images 1-2). Frontalis and temporalis muscles (eg,
clenching of jaw muscles) are common causes. As a general rule, the potentials generated in the muscles are of
http://www.emedicine.com/neuro/topic678.htm (1 of 7) [4/9/2003 2:40:53 PM]

shorter duration than those generated in the brain and are identified easily on the basis of duration, morphology,
and rate of firing (ie, frequency). Particular patterns of electromyogram (EMG) artifacts can occur in some
movement disorders. Essential tremor and Parkinson disease can produce rhythmic 4- to 6-Hz sinusoidal
artifacts that may mimic cerebral activity.
Another disorder that can produce repetitive muscle artifacts is hemifacial spasm. The photomyoclonic response
is a special type of EMG artifact that occurs during intermittent photic stimulation. Some subjects contract the
frontalis and orbicularis muscles. These contractions occur approximately 50-60 milliseconds after each flash,
disappear after eye opening and use of paralyzers, are located mostly frontally, and have no concomitant EEG
changes.
Glossokinetic artifact
In addition to muscle activity, the tongue (like the eyeball) functions as a dipole, with the tip negative with respect
to the base. In this case the tip of the tongue is the most important part because it is more mobile. The artifact
produced by the tongue has a broad potential field that drops from frontal to occipital areas, although it is less
steep than that produced by eye movement artifacts. The amplitude of the potentials is greater inferiorly than in
parasagittal regions; the frequency is variable but usually in the delta range and occurs synchronously when the
patient says “Lah-lah-lah-lah” or “Lilt-lilt-lilt-lilt,” which can be verified by the technologist. Chewing and sucking
can produce similar artifacts. These commonly are observed in young patients. However, they also can be
observed in patients with dementia or those who are uncooperative.
Eye movements
Eye movements are observed on all EEGs and are useful in identifying sleep stages. The eyeball acts as a
dipole with a positive pole oriented anteriorly (cornea) and a negative pole oriented posteriorly (retina). When the
globe rotates about its axis, it generates a large-amplitude alternate current field, which is detectable by any
electrodes near the eye. The other source of artifacts comes from EMG potentials from muscles in and around
the orbit.
Vertical eye movements typically are observed with blinks (ie, Bell phenomenon). A blink causes the positive
pole (ie, cornea) to move closer to frontopolar (Fp1-Fp2) electrodes, producing symmetric downward deflections.
During downward eye movement the positive pole (ie, cornea) of the globe moves away from frontopolar
electrodes, producing an upward deflection best recorded in channels 1 and 5 in the bipolar longitudinal
montage.
Lateral eye movements most affect lateral frontal electrodes F7 and F8 (see Images 3-4). During a left lateral
eye movement, the positive pole of the globe moves toward F7 and away from F8. Using a bipolar longitudinal
montage, maximum positivity in electrode F7 and maximum negativity in electrode F8 is recorded, and artifacts
do not occur in channels 9 and 13 or 10 and 14. A so-called rectus lateralis may be present in electrode F7; it is
observed best in the vertex reference montage. With right lateral eye movement, the opposite occurs.
ECG artifact
Some individual variations in the amount and persistence of ECG artifact are related to the field of the heart
potentials over the surface of the scalp. Generally, people with short and wide necks have the largest ECG
artifacts on their EEGs. The voltage and apparent surface of the artifact vary from derivation to derivation and,
consequently, from montage to montage. The artifact is observed best in referential montages using earlobe
electrodes A1 and A2.
ECG artifact is recognized easily by its rhythmicity/regularity and coincidence with the ECG tracing (each “sharp
wave” equals artifact that synchronizes with each QRS complex of the ECG channel; see Image 5). The
situation becomes difficult when cerebral abnormal activity (eg, sharp waves) appears intermixed with EEG
artifact, and the former may be overlooked. The EEG technologist should apply electrodes routinely to record
the ECG.
Pulse
Pulse artifact occurs when an EEG electrode is placed over a pulsating vessel. The pulsation can cause slow
waves that may simulate EEG activity. A direct relationship exists between ECG and the pulse waves. The QRS
complex (ie, electrical component of the heart contraction) happens slightly ahead of the pulse waves (200-300

millisecond delay after ECG equals QRS complex).
Respiration artifacts
Respiration can produce 2 kinds of artifacts. One type is in the form of slow and rhythmic activity, synchronous
with the body movements of respiration and mechanically affecting the impedance of (usually) one electrode.
The other type can be slow or sharp waves that occur synchronously with inhalation or exhalation and involve
those electrodes on which the patient is lying. Several commercially available devices to monitor respiration can
be coupled to the EEG machine. As with the ECG, one channel can be dedicated to respiratory movements. The
simplest way to monitor respiration is by the EEG technician making notations with a pencil (ie, upward
movement of the pencil for inhalations, downward return for exhalations).
Skin artifacts
Biological processes and/or defects may alter impedance and cause artifacts. Sweat is a common cause (see
Image 6). Sodium chloride and lactic acid from sweating reacting with metals of the electrodes may produce
huge slow baseline sways.
Significant asymmetry also can be observed when a collection (eg, subgaleal hematoma) is under or in the skin.
In this last example, the amplitude of the background rhythm is reduced in derivations from electrodes overlying
the hematoma.
Skull defects also can be the source of asymmetry. In this situation, amplitudes are greater in derivations from
electrodes overlying or adjacent to skull defects.
EXTRAPHYSIOLOGIC ARTIFACTS Section 4 of 6
Electrodes
The most common electrode artifact is the electrode popping. Morphologically this appears as single or multiple
sharp waveforms due to abrupt impedance change. It is identified easily by its characteristic appearance (ie,
abrupt vertical transient that does not modify the background activity) and its usual distribution, which is limited
to a single electrode. In general, sharp transients that occur at a single electrode should be considered artifacts
until proven otherwise (see Image 6). At other times, the impedance change is not so abrupt, and the artifact
may mimic a low-voltage arrhythmic delta wave (see Images 7-11).
Alternating current (60-Hz) artifact
Adequate grounding on the patient has almost eliminated this type of artifact from power lines. The problem
arises when the impedance of one of the active electrodes becomes significantly large between the electrodes
and the ground of the amplifier. In this situation, the ground becomes an active electrode that, depending on its
location, produces the 60-Hz artifact (see Image 12). The artifact presents at exact frequency (60 Hz, as its
name indicates). A better identification can be made by increasing the paper speed (ie, sweep time) to 60 mm/s
and counting it (1 cycle per millimeter).
Movements in the environment
Movement of other persons around the patient can generate artifacts, usually of capacitive or electrostatic origin.
Avoid this type of artifact as much as possible. If avoidance is not possible, as in the ICU and the operating
room, place proper notation on the records.
Another artifact, probably due to electrostatic changes on the drops, can be introduced by a gravity-fed
intravenous infusion. Morphologically this appears as spike transient potentials at fixed intervals that coincide
with drops of the infusion.
With the increasing use of automatic electric infusion pumps, a new type of artifact, infusion motor artifact (IMA),
has arisen. Morphologically, IMA appears as very brief spiky transients, sometimes followed by a slow

component of the same polarity. Its frequency does not relate directly to drop rate. Lininger et al have suggested
that this artifact arises from electromagnetic sources.
The artifact produced by respirators varies widely in morphology and frequency. Monitoring the ventilator rate in
a separate channel helps to identify this type of artifact.
Interference from high-frequency radiation from radio, TV, hospital paging systems, and other electronic devices
can overload EEG amplifiers. The pens may deflect upward or downward to full excursion, and no EEG can be
recorded. The cutting and/or coagulating electrode used in the operating room also generates high-voltage high-
frequency signals that interfere with the recording system. The best thing to do is turn off the EEG machine while
using this instrument.
PICTURES Section 5 of 6
Caption: Picture 1. EEG atlas: EEG artifacts. Electromyogram (muscle) artifact best observed in the left
temporal region. ECG artifact also is present, best observed in the posterior region.
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Picture Type: Photo

Caption: Picture 2. EEG atlas: EEG artifacts. Electromyogram (muscle) artifact. These waveforms represent
motor unit potentials as typically observed on needle electrode examination during electromyogram, with a
frequency of 20-100 Hz. Distribution varies, and in this case it is more prominent on the left side. Such artifact
can be diminished by the judicious use of the high-frequency filter. (This sample has the default setting of high-
frequency filter 70 Hz.)
Picture Type: Photo

Caption: Picture 3. EEG atlas: EEG artifacts. Eye movements such as these usually are observed in frontal
electrodes and not further posteriorly then the midtemporal region. The phase reversals at lateral frontal
electrodes F7 and F8 are of opposite polarity, indicating lateral eye movements. Because the cornea is charged
positively and the retina negatively, the side of the positivity indicates the direction of eye movement. Thus, the
first one here is to the right.
Picture Type: Photo

Caption: Picture 4. EEG atlas: EEG artifacts. Left frontal artifact in the fourth second. This is not limited to a
single electrode and has the morphology of an eye movement, but it is unilateral. This is an eye movement in a
patient who has a glass left eye.
Picture Type: Photo

Caption: Picture 5. Regular (periodic) slow waves best observed at midtemporal and posterior temporal
electrodes T4-T6 and T3-T5. These clearly are related to ECG. The duration and morphology are those of pulse
artifact, but as demonstrated by the marker, no delay occurs between the ECG and the artifact. Thus this is an
ECG artifact with broad QRS complexes.
Picture Type: Photo

Caption: Picture 6. EEG atlas: EEG artifacts. Sweat artifact. This is characterized by very low-frequency (here,
0.25- to 0.5-Hz) oscillations. The distribution here (midtemporal electrode T3 and occipital electrode O1)
suggests sweat on the left side. Note that morphology and frequency are also consistent with slow rolling eye
movements, but distribution is not.
Picture Type: Photo

Caption: Picture 7. EEG atlas: EEG artifacts. Electrode artifact at frontal pole electrode Fp1. The duration is too
short ("narrow") for any cerebral potential, and the distribution is limited to a single electrode (Fp1). In general,
activity that affects a single electrode (ie, without the expected drop off and activity at neighboring electrodes or
"plausible field") should be considered an artifact until proven otherwise.
Picture Type: Photo

Caption: Picture 8. EEG atlas: EEG artifacts. Electrode artifact at occipital electrode O1. The morphology is
very unusual for any cerebral waveform, and the distribution is limited to a single electrode. In general, activity
that affects a single electrode (ie, without the expected drop off and activity at neighboring electrodes or
"plausible field") should be considered an artifact until proven otherwise.

Picture Type: Photo

Caption: Picture 9. EEG atlas: EEG artifacts. Electrode artifact at frontal electrode F3. This should not be
misinterpreted as a spike. This sharply contoured transient clearly occurs at only one electrode, as confirmed
on the referential montage.
Picture Type: Photo

Caption: Picture 10. EEG atlas: EEG artifacts. Electrode (impedance) artifact at parietal electrode P3. Initially,
a slow artifact is followed by a more abrupt one at the seventh second. This commonly is referred to as an
electrode pop. Note again the unusual morphology of the sharp component and that it is at a single electrode.
Also note an eye blink in the third second and slight electromyogram artifact in the frontal regions in the first 2
seconds.
Picture Type: Photo

Caption: Picture 11. EEG atlas: EEG artifacts. Just as electrode artifacts can simulate interictal spikes, they
also can mimic an ictal pattern. This rhythmic artifact may be mistaken for an electrographic seizure or
subclinical rhythmic epileptiform discharges of adults (SREDA; see Normal EEG Variants). However, this is
confined to a single electrode (posterior temporal electrode T6), as can be confirmed on a referential montage.
This artifact often is confirmed by the presence of other definite electrode pops in the same electrode.
Picture Type: Photo

Caption: Picture 12. EEG atlas: EEG artifacts. Ground recording artifact. This is a somewhat less common
electrode artifact, also related to accidentally high impedance. The high impedance at posterior temporal
electrode T6 results in this electrode recording from the ground on the forehead, thus picking up eye
movements (which normally should not be observed at T6).

Picture Type: Photo

Caption: Picture 13. PowerPoint presentation of Images 1-12.
Click to see detail
Picture Type: Presentation
BIBLIOGRAPHY Section 6 of 6
● Bickford RG, Keith HM: Convulsive effects of light stimulation in children. Am J Dis Child 1953; 86: 170-83.
● Daly D, Pedley T, eds: Current Practice of Clinical Electroencephalography. 2nd ed. New York: Raven Press; 1990.
● Lininger AW, Volow MR, Gianturco DT: Intravenous infusion motor artifact. Am J EEG Technol 1981 Dec; 21(4): 167-73[Medline].
● Luders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000.
● Picton TW, van Roon P, Armilio ML, et al: The correction of ocular artifacts: a topographic perspective. Clin Neurophysiol 2000 Jan;
111(1): 53-65[Medline].
● Redding FK, Wandel V, Nasser C: Intravenous infusion drop artifacts. Electroencephalogr Clin Neurophysiol 1969 Mar; 26(3): 318-
20[Medline].
● Schwab RS, Cobb S: Simultaneous EMG’s and EEG’s in paralysis agitans. J Neurophysiol 1939; 2: 36-41.
● Shaffer MA: Problem record of the month. No. 3: Asymmetrical eyeblink artifact. Am J EEG Technol 1970; 10: 153-6.
● Tyner F, Knott J, Mayer Jr W, eds: Fundamentals of EEG technology. In: Basic Concepts and Methods. Vol 1. NY: Raven Press;
1983.
● van de Velde M, van Erp G, Cluitmans PJ: Detection of muscle artifact in the normal human awake EEG. Electroencephalogr Clin
Neurophysiol 1998 Aug; 107(2): 149-58[Medline].
● Westmoreland BF, Espinosa RE, Klass DW: Significant prosopoglossopharyngeal movements affecting the EEG. Am J EEG Technol
1973; 13: 59-70.
● Young GB, Campbell VC: EEG monitoring in the intensive care unit: pitfalls and caveats. J Clin Neurophysiol 1999 Jan; 16(1): 40-
5[Medline].
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eMedicine - EEG Atlas: Encephalopathic Patterns I - Generalized Slowing : Article by Selim R Benbadis, MD
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EEG Atlas: Encephalopathic Rate this Article Introduction
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Patterns I - Generalized Slowing Email to a Colleague Clinical Correlation
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Medical Director, Shriver Clinical Services Corporation; Assistant Professor, Department of Neurology, Boston
Children's Hospital, Harvard Medical School; Matthew J Baker, MD, Consulting Staff, Collier Neurologic
Specialists, Naples Community Hospital; and Nicholas Lorenzo, MD, eMedicine Chief Publishing Officer,
Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Since the EEG is a test of cerebral function, diffuse (generalized) abnormal patterns are by definition indicative
of diffuse brain dysfunction (ie, diffuse encephalopathy). This article discusses generalized slowing, which is the
most common finding in diffuse encephalopathies. (Focal [localized] slow activity reflects focal dysfunction, not
diffuse dysfunction [ie, encephalopathy].) The next level of severity of diffuse brain dysfunction is discussed in
EEG Atlas: Encephalopathic Patterns II - More Severe Patterns, and other encephalopathic patterns are
discussed in EEG Atlas: Encephalopathic Patterns III - Miscellaneous Patterns.
Generalized slowing can be divided in a clinically useful way into 3 patterns: background slowing, intermittent
slowing, and generalized slowing.
WAVEFORM DESCRIPTION Section 3 of 6

Background slowing: A posterior dominant and reactive background is present, but its frequency is too slow for
the patient’s age. The lower limit of normal generally is considered to be 8 Hz beginning at age 8 years. A
guideline to remember the lower limits of normal is as follows: 5-6-7-8 Hz at ages 1-3-5-8 years, respectively
(see Images 1-2).
Intermittent slowing: This involves bursts of generalized slowing, usually polymorphic delta. More rarely, the
intermittent bursts are in the theta frequency range, and occasionally they can be rhythmic rather than
polymorphic. When rhythmic, this pattern sometimes is referred to as frontal intermittent rhythmic delta activity
(FIRDA). The EEG is still reactive to external stimulation and, for example, may have evidence of state changes
such as drowsiness or sleep. A posterior dominant background is usually present, and it may be normal or slow
in frequency (see Image 2).
Continuous slowing: Polymorphic delta activity (PDA) occupies more than 80% of the record. This is usually
unreactive, and a posterior dominant background is usually absent (see Images 3-4).
CLINICAL CORRELATION Section 4 of 6
Essentially, the 3 levels of slowing described above represent 3 degrees of severity (ie, mild, moderate, and
severe) of diffuse encephalopathy. As usual, this is completely nonspecific as to etiology and most commonly is
observed in metabolic and toxic (including medication-induced) encephalopathies. It also can be observed in
diffuse structural or degenerative processes. However, most slowly progressive neurodegenerative diseases
(eg, dementias of the Alzheimer type) go along with a normal EEG until the very late stages.
Caption: Picture 1. EEG atlas: encephalopathic patterns I – generalized slowing. Background slowing. The
posterior dominant background (alpha rhythm) is at 7 Hz, slower than the alpha frequency range. No other
generalized slow activity is present. Since this patient is older than 8 years, and is clearly awake, this is
abnormal. This represents (electrographically) the mildest degree of diffuse encephalopathy.
Picture Type: Photo

Caption: Picture 2. EEG atlas: encephalopathic patterns I – generalized slowing. (1) Background slowing and
(2) intermittent slowing, generalized. Mild diffuse encephalopathy; a posterior dominant background is present,
but it is only at 6-7 Hz, and bursts of generalized polymorphic delta activity (this one lasting 2-3 s) are present.
Picture Type: Photo

Caption: Picture 3. EEG atlas: encephalopathic patterns I – generalized slowing. Continuous slowing,
generalized. The record is dominated by generalized polymorphic delta activity. When this is "continuous"
(greater than 80% of the recording), it usually goes along with a severe diffuse encephalopathy. This is
nonspecific in regard to etiology and most commonly is due to metabolic or systemic disturbances.
Picture Type: Photo

Caption: Picture 4. EEG atlas: encephalopathic patterns I – generalized slowing. Continuous slowing,
generalized. While some faster frequencies are present, this sample is dominated by generalized polymorphic
delta activity. If this is "continuous" (greater than 80% of the recording), this usually goes along with a severe
diffuse encephalopathy.
Picture Type: Photo

● Geller E: Generalized disturbances of brain function: encephalopathies, coma, degenerative diseases, and brain death. In: Levin KH,
Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders; 2000: 438-455.
● Levin KH, Lüders HO, eds: Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000.
NOTE:
EEG Atlas: Encephalopathic Patterns I - Generalized Slowing excerpt

eMedicine - EEG Atlas: Encephalopathic Patterns II - More Severe Patterns : Article by Selim R Benbadis, MD
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Synonyms and related keywords: brain death, ECI, electrocerebral inactivity, periodic patterns, burst-
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AUTHOR INFORMATION Section 1 of 6

Continuing
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Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, this topic. Click
Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital here to take this
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Selim R Benbadis, MD, is a member of the following medical societies: American Academy of Neurology,
patient education.
Since EEG is a test of cerebral function, diffuse (generalized) abnormal patterns are by definition indicative of
diffuse brain dysfunction (ie, diffuse encephalopathy). Generalized slowing is discussed in EEG Atlas:
Encephalopathic Patterns I - Generalized Slowing, and other encephalopathic patterns are discussed in EEG
Atlas: Encephalopathic Patterns III - Miscellaneous Patterns.
This article reviews patterns that generally are considered the next level of severity beyond generalized slowing.
These patterns include periodic patterns (such as burst-suppression), background suppression, and
electrocerebral inactivity (ECI).

● Periodic patterns (Image 1): Discharges occur at regular intervals (ie, periodicity). The discharges are
typically complex and multiphasic and often are epileptiform in morphology. Thus they are like periodic
lateralizing epileptiform discharges (PLEDs) except that, instead of being lateralized, they are
generalized. They sometimes are referred to as generalized periodic epileptiform discharges (GPEDs).
Their periodicity rather than their morphology sets them apart as a unique and clinically useful entity (as
is true for PLEDs). By contrast, the term bi-PLEDs usually refers to periodic discharges that are
bihemispheric but asynchronous (ie, independent).
● Burst-suppression pattern (Image 2): This subtype of periodic pattern consists of bursts of activity
(mixture of sharp and slow waves) periodically interrupted by episodes of suppression (activity <10 µV).
Typically, the episodes of suppression are longer (typically 5-10 s) than the bursts of activity (typically 1-
3 s).
● Background suppression: This is a “nearly flat” EEG, with very low voltage activity (<10 µV) and no
reactivity, but the activity is still too large to meet criteria for ECI.
● Electrocerebral inactivity (Image 3): ECI is defined by no activity greater than 2 µV; to support a
diagnosis of brain death while avoiding “overcalling” brain death, ECI must be recorded according to
strict guidelines. These requirements specify recording time, double interelectrode distances, testing
reactivity, and the integrity of the system. (See Generalized EEG Waveform Abnormalities for the ECI
Guidelines of the American Clinical Neurophysiology Society.)
● As usual, these severe encephalopathic patterns are completely nonspecific as to etiology but represent
extremely severe degrees of diffuse encephalopathy. Because sedative medications can cause or
aggravate these abnormalities, careful interpretation is warranted when reading these patterns. These
patterns are indicative of very severe brain dysfunction if sedative medications can be excluded with
certainty as their cause.
● Periodic patterns, including burst-suppression patterns, are somewhat more common in anoxic injuries
than in other systemic disturbances. Periodic patterns can be induced by high doses of sedatives such
as barbiturates, benzodiazepines, or propofol. In fact, burst-suppression pattern is typically the goal and
the method used to titrate doses of anesthetics for treatment of refractory status epilepticus.
● In the appropriate clinical context, certain periodic patterns can suggest and support the diagnoses of
Creutzfeldt-Jakob disease (CJD) and subacute sclerosing panencephalitis (SSPE). Classically, the
periodicity for CJD is approximately 1-2 seconds, whereas it is much longer in SSPE (approximately 4-10
s).
● Rhythmicity or periodicity is one of the hallmarks of electrographic seizures; thus periodic patterns quite
often are observed in the context of nonconvulsive status epilepticus. Often the decision whether to
consider a periodic pattern ictal must rely on clinical information or the response to anticonvulsant
treatment.
● ECI is supportive of a clinical diagnosis of brain death. Remembering and emphasizing that brain death
is a clinical diagnosis is important. Contrary to a common misconception, EEG is not required for the
diagnosis of brain death and is considered only as a supportive test.

Caption: Picture 1. EEG atlas: encephalopathic patterns II – more severe patterns. Classification: periodic
pattern, generalized. The periodicity here is approximately 1 second.
Picture Type: Photo

Caption: Picture 2. EEG atlas: encephalopathic patterns II – more severe patterns. Classification: burst-
suppression. Note that this is a 15-second segment, to show the periods of suppression (4-5 s) separated by
the bursts. Suppression periods are characterized by activity less than 10 µV.
Picture Type: Photo

Caption: Picture 3. EEG atlas: encephalopathic patterns II – more severe patterns. Classification:
electrocerebral inactivity. The recording demonstrates no cerebral activity greater than 2 µV. Given the high
sensitivity (2 µV/mm), a combination of ECG and 60-Hz artifact often is present, as observed here.
Picture Type: Photo

● American EEG Society: Guideline three: minimum technical standards for EEG recording in suspected cerebral death. American
Electroencephalographic Society. J Clin Neurophysiol 1994 Jan; 11(1): 10-3[Medline].
Lüders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia: WB Saunders Co; 2000:438-455.
● Husain AM, Mebust KA, Radtke RA: Generalized periodic epileptiform discharges: etiologies, relationship to status epilepticus, and
prognosis. J Clin Neurophysiol 1999 Jan; 16(1): 51-8[Medline].
NOTE:

EEG Atlas: Encephalopathic Patterns II - More Severe Patterns excerpt

eMedicine - EEG Atlas: Encephalopathic Patterns III - Miscellaneous Patterns : Article by Selim R Benbadis, MD
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Patterns III - Miscellaneous Patterns Email to a Colleague Descriptions
Clinical Correlation
Last Updated: June 14, 2002 Pictures
Synonyms and related keywords: alpha coma, beta coma, spindle coma, triphasic waves Bibliography
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Author Information Introduction Waveform Descriptions Clinical Correlation Pictures Bibliography
Continuing
Education
this topic. Click
American Clinical Neurophysiology Society, and American Epilepsy Society Click here for
patient education.
Since EEG is a test of cerebral function, diffuse (generalized) abnormal patterns are by definition indicative of
diffuse brain dysfunction (ie, diffuse encephalopathy). Generalized slowing is discussed in EEG Atlas:
Encephalopathic Patterns I - Generalized Slowing, and more severe patterns (ie, periodic patterns, such as
burst-suppression, background suppression, and electrocerebral inactivity) are discussed in EEG Atlas:
Encephalopathic Patterns II - More Severe Patterns.
This article reviews less common encephalopathic patterns, including alpha coma, beta coma, spindle coma,
and triphasic waves.
WAVEFORM DESCRIPTIONS Section 3 of 6

Unusual special patterns observed in comatose patients include alpha coma (Image 1), beta coma (Image 2),
and spindle coma (Image 3).
● These patterns are characterized by electrical activity that morphologically resembles and sometimes
appears nearly identical to normal waveforms (ie, alpha rhythm, beta activity, spindles).
● To be classified as one of these patterns, the activity should be frankly excessive in amplitude or in
spatial distribution (ie, widespread), appear in unusual spatial distribution, or appear excessive in amount
(ie, near continuous). Although some investigators classify these patterns as abnormal even if the
pattern is reactive, unreactive activity is preferred. The most important criterion is patient coma at the
time of clinical recording.
Triphasic waves are frontally positive sharp transients, usually of greater than 70 microvolts amplitude (see
Image 4). The positive phase usually is preceded and followed by a smaller negative waveform. As a rule, the
first negative wave is of higher amplitude than the second. They are bilateral and occur in bursts of repetitive
waves at 1-3 Hz. No reactivity is the rule, and often an anterior-posterior temporal lag can be observed. The
largest deflection is usually frontal, and in ear referential montage the time lag is usually not present. The usual
clinical correlate of triphasic waves is a metabolic or other diffuse encephalopathy. Thus, a triphasic morphology
(while necessary) is not sufficient to classify a record as "triphasic waves."
Alpha coma, beta coma, and spindle coma are infrequent. They are, like all the encephalopathic patterns,
nonspecific in regard to etiology, although anoxia often is associated with alpha coma and drugs with beta coma.
They are generally indicative of a severe degree of encephalopathy. Reactivity is a good prognostic factor. In
fact, some investigators, including the author, do not classify a record as alpha or spindle coma if it is reactive.
Triphasic waves classically are associated with hepatic encephalopathy. However, they are not specific and can
be observed in uremic encephalopathy and even other types of metabolic derangements. Many other patterns
can have a triphasic morphology. Like periodic patterns, triphasic waves quite often are observed in the context
of nonconvulsive status epilepticus. Often the decision whether to consider triphasic waves ictal must rely on the
clinical information or the response to anticonvulsant treatment.
Caption: Picture 1. EEG atlas: encephalopathic patterns III – miscellaneous patterns. Alpha coma. Unlike a
normal alpha rhythm, the alpha activity observed here is not posterior dominant, is continuous, and is
nonreactive. If the entire record is present and the patient is known to be comatose, this qualifies as alpha
coma.
Picture Type: Photo

Caption: Picture 2. EEG atlas: encephalopathic patterns III – miscellaneous patterns. Beta coma. Prominent
fast (beta) activity is noted at 15-22 Hz. To qualify as "excessive fast" activity, the pattern has to be the
predominant frequency and excessive in amount (ie, nearly continuous and unreactive) and amplitude, ie,
greater than the typical 30 microvolts of the normal beta activity. Note that this pattern could be seen in an
awake patient, so that the term "beta coma" is reserved for patients known to be comatose.

Picture Type: Photo

Caption: Picture 3. EEG atlas: encephalopathic patterns III – miscellaneous patterns. Spindle coma. Note the
prominent spindlelike activity at 13-16 Hz. Typically, spindlelike activity associated with coma is even more
continuous than shown here, and unreactive. The term "spindle coma" is reserved for patients known to be
comatose.
Picture Type: Photo

Caption: Picture 4. EEG atlas: encephalopathic patterns III – miscellaneous patterns. Triphasic waves. Note
the near continuous pattern of periodic triphasic waveforms, with a large frontal positivity (downgoing) preceded
and followed by smaller negative deflections. The wave marked near the middle of the sample illustrates the
classic anterior-posterior lag. This pattern is typically unreactive. Note that a triphasic morphology is necessary
but not sufficient to classify a pattern as "triphasic waves."
Picture Type: Photo

● Benbadis SR, Tatum WO: Prevalence of nonconvulsive status epilepticus in comatose patients. Neurology 2000 Nov 14; 55(9): 1421-
3[Medline].
● Kaplan PW, Genoud D, Ho TW, Jallon P: Etiology, neurologic correlations, and prognosis in alpha coma. Clin Neurophysiol 1999 Feb;
110(2): 205-13[Medline].
● Kaplan PW, Genoud D, Ho TW, Jallon P: Clinical correlates and prognosis in early spindle coma. Clin Neurophysiol 2000 Apr; 111(4):
584-90[Medline].
● Lüders H, Noachtar S, eds: Atlas and Classification of Electroencephalography. Philadelphia: WB Saunders Co; 2000.
NOTE:

EEG Atlas: Encephalopathic Patterns III - Miscellaneous Patterns excerpt

eMedicine - EEG Atlas: Epileptiform Normal Variants : Article by Selim R Benbadis, MD
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EEG Atlas: Epileptiform Normal Rate this Article Introduction
Waveform
Variants Email to a Colleague Descriptions
Synonyms and related keywords: benign epileptiform transients of sleep, midline theta, phantom Bibliography
spikes and waves, psychomotor variants, small sharp spikes, subclinical rhythmic EEG discharges of
adults, wicket spikes, 14- and 6-Hz positive spikes Click for related
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Epileptiform normal variants are EEG patterns that resemble epileptogenic abnormalities. Most of these patterns
initially were thought to be associated with epilepsy or other neurological conditions but subsequently were
demonstrated to have no such significance. They now are considered normal variants of no clinical significance.
Their recognition is important to avoid overinterpretation or misinterpretation with regard to their significance.
This article reviews the following such patterns: small sharp spikes (SSS), wicket spikes, 14- and 6-Hz positive
spikes, phantom spike and waves, psychomotor variants, subclinical rhythmic EEG discharges of adults
(SREDA), and midline theta.
Most of these patterns initially were described in the 1950s. Gibbs and Gibbs described small sharp spikes in
1952, and 14- and 6-Hz positive spikes were described at approximately the same time (Gibbs and Gibbs, 1951;

Grossman, 1954; Kellaway et al, 1959; Nidermeyer and Croft, 1961). The 6-Hz phantom spike-wave was
described by Walter (1950), and the psychomotor variant was described by Gibbs and Gibbs (1952). Wickets
were described in 1977 (Reiher and Lebel).
Small sharp spikes (Images 1-3): Also known as benign epileptiform transients of sleep (BETS), SSSs occur in
light sleep (stages I and II of nonrapid eye movement [NREM] sleep), usually sporadically. Location is temporal,
either unilateral or bilaterally independent, and with a broad field of distribution. Morphology is typically
monophasic, occasionally diphasic, and the decline after the first negative peak is very steep. SSSs rarely may
have a single aftergoing slow-wave component but generally are not disturbing the background. The main
features of SSSs are in their name: duration is short, amplitude is small, and an easy guideline states that SSSs
generally should be less than 50 mV and less than 50 milliseconds.
Wicket spikes (Images 4-6): Wicket spikes occur in both awake state and light sleep. Frequency is 6-11 Hz,
usually in short runs (“wicket rhythm”) but also as single sharp transients. Location is temporal, usually bilateral
and independent. Morphology is archlike or mu-like, sharp, monophasic, and not followed by an aftergoing slow
wave. Amplitude may be high, but the transient arises out of an ongoing rhythm and does not "stand out."
14-Hz and 6-Hz positive spikes: This pattern is observed at any age, but it is expressed maximally in
adolescents, especially those aged 13-14 years (Klass and Westmoreland, 1985). The 6-Hz positive spikes
predominate in children younger than 1 year and in adults older than 40 years, and the 14-Hz positive spikes
predominate or combine with 6-Hz spikes in the other age groups (Gibbs et al, 1963). Both 14- and 6-Hz positive
spikes are observed predominantly during light sleep. These spikes usually appear in short runs lasting less
than 2 seconds, and their frequencies, as the name implies, are 14 Hz and 6 Hz. Location is mostly posterior
temporal, unilaterally or bilaterally. Morphology is a sharply contoured positive spike alternating with rounded
negative component. Amplitude is medium, around 20-60 µV.
Phantom spike and wave (6 Hz): The 6-Hz spike and wave pattern may be observed in both adolescents and
adults. It generally occurs during relaxed wakefulness and stage I sleep and disappears during deeper levels of
sleep. Frequency is 6 Hz, and the bursts last 1-2 seconds. Location is usually diffuse, bisynchronous, and
relatively symmetric. This pattern may predominate in the anterior and posterior head regions. Morphology is a
typically small (<30 µV and <30 ms), evanescent diphasic spike followed by a higher (50-100 µV) slow wave
component. Thus, the spike component may be difficult to see.
Psychomotor variant (Image 7): A more useful and descriptive term is rhythmic midtemporal theta of drowsiness
(RMTD). Frequency is theta (4-7 Hz). Location is maximum midtemporal, unilateral or bilaterally independent or
bisynchronous. Morphology typically is notched, flat topped, or sharply contoured. Bursts may last 1-10 seconds
or longer and thus resemble temporal lobe seizures. Amplitude is medium to high.
Subclinical rhythmic EEG discharges of adults: SREDA is an uncommon pattern observed mainly in older
persons (>50 y). It may occur at rest or during drowsiness. SREDA superficially resembles an EEG seizure
pattern. Frequency is typically 5-6 Hz. Location is widespread or bilateral with a posterior maximum. Morphology
is seizurelike (ie, rhythmic sharply contoured theta). Abrupt onset and termination may help distinguish SREDA
from an EEG seizure. Duration ranges from 20 seconds to minutes (average 40-80 s).
Midline theta rhythm (ie, Ciganek rhythm): Midline theta rhythm may be observed during wakefulness or
drowsiness. As indicated by the name, frequency is 4-7 Hz, and the location is midline (ie, vertex). Morphology
is rhythmic, smooth, sinusoidal, arciform, spiky, or mu-like.
As a whole, these normal variants need to be differentiated from epileptiform discharges (ie, spikes, sharp
waves, spike-wave complexes; see Generalized EEG Waveform Abnormalities). In general, the benign patterns
lack the characteristics of pathological epileptiform discharges, high amplitude and aftergoing slow wave or
suppression, making them “disturbing” to the background activity. By default, assume that sharp transients are

benign variants, and consider them epileptiform and abnormal only if they do not meet criteria for any benign
transients.
SSS are generally easy to distinguish from spikes because of their short duration and small amplitude.
The 14- and 6-Hz positive spikes should not be confused with temporal spikes because of their characteristic
polarity (epileptiform spikes are almost always surface negative in polarity) and typical frequency.
Phantom spike and waves (6 Hz) may be difficult to distinguish from the definitive clinically significant spike and
wave complexes. A helpful way to distinguish them is by the tendency of benign phantom spike and waves (6
Hz) to disappear during sleep; epileptiform discharges (spike and wave complexes) tend to persist or become
more prominent with deeper levels of sleep.
Psychomotor variant differs from a seizure discharge because it is usually a monomorphic or monorhythmic
pattern that does not evolve into other frequencies or waveforms as usually occurs during seizures.
Wicket spikes commonly are misinterpreted as sharp waves, especially when they occur as single sharp
transients. Examining the context and whether they arise out of an ongoing rhythm is important. Wickets
predominate in adults older than 30 years and have an incidence of 0.9% (Reiher and Lebel, 1977).
SREDA is never associated with symptoms, in contrast to a seizure pattern.
Midline theta rhythm does not have any clinical significance and appears to represent a nonspecific variant of
theta activity. As with many others, this pattern initially was believed to occur predominantly in patients with
temporal lobe epilepsy. Later reviews have shown that the Ciganek rhythm represents a nonspecific variant of
theta activity (Mokran et al, 1971; Westmoreland and Klass, 1986).
Caption: Picture 1. EEG atlas: epileptiform normal variants. A small sharp spike is present in the left temporal
region (modified double banana montage). Note the widespread field of distribution (isopotential at F7, T1, and
T3), low amplitude (<50 mA), and short duration (<50 ms).
Picture Type: Photo

Caption: Picture 2. EEG atlas: epileptiform normal variants. Left temporal small sharp spike. Note low
amplitude (<50 mA) and short duration (<50 ms).

Picture Type: Photo

Caption: Picture 3. EEG atlas: epileptiform normal variants. A small sharp spike is present in the right temporal
region. Note the low amplitude (<50 mA) and short duration (<50 ms).
Picture Type: Photo

Caption: Picture 4. EEG atlas: epileptiform normal variants. Wicket spikes in the left temporal region. Note the
sharp transients arising out of an ongoing rhythm and the symmetric up-slope and down-slope giving the
“wicket” morphology.
Picture Type: Photo

sharp transients arising out of an ongoing rhythm and the symmetric up-slope and down-slope, giving the wicket
morphology.
Picture Type: Photo

sharp transients arising out of an ongoing rhythm and the symmetric up-slope and down-slope, giving the wicket
morphology.
Picture Type: Photo

Caption: Picture 7. EEG atlas: epileptiform normal variants. Rhythmic midtemporal theta of drowsiness or
psychomotor variant. Note the seizurelike rhythmicity and notched morphology.
Picture Type: Photo

Caption: Picture 8. PowerPoint presentation, EEG epileptiform normal variants
Click to see detail
● Benbadis SR, Tatum WO IV: Over-intepretation of EEGs and misdiagnosis of epilepsy. In press.
● Ciganek L: Theta-discharges in the middle-line—EEG symptom of temporal lobe epilepsy. Electroencephalogr Clin Neurophysiol
1961; 13: 669-673.
● Daly DD, Pedley TA: Current Practice of Clinical Electroencephalography. 2nd ed. New York, NY: Raven Press; 1990:243-251.
● Engel J Jr: A practical guide for routine EEG studies in epilepsy. J Clin Neurophysiol 1984 Apr; 1(2): 109-42[Medline].
● Garvin JS: Psychomotor variant pattern. Dis Nerv Syst 1968 May; 29(5): 307-9[Medline].
● Gibbs EL, Gibbs FA: Atlas of Electroencephalography. Vol 2. Cambridge, Mass: Addison-Wesley; 1952:346-358.
● Gibbs EL, Gibbs FA: Electroencephalographic evidence of thalamic and hypothalamic epilepsy. Neurology 1951; 1: 136-144.
● Gibbs FA, Gibbs EL: Atlas of Electroencephalography. Vol 3. Reading, Mass: Addison–Wesley; 1964.
● Gibbs FA, Rich CL, Gibbs EL: Psychomotor variant type of seizure discharge. Neurology (Minneap) 1963; 13: 991-998.
● Gibbs FA, Gibbs EL: Fourteen and six per second positive spikes. Electroencephalogr Clinical Neurophysiol 1963; 15: 553-558.
● Grossman C: Laminar cortical blocking and its relation to episodic aggressive outbursts. Arch Neurol Psychiat (Chicago) 1954; 71:
576-587.
● Hughes JR, Schlagenhauff RE, Magoss M: Electroclinical correlations in the six per second spike and wave complex.
Electroencephalogr Clin Neurophysiol 1965; 18: 71-75.
● Kellaway P, Crawley JW, Kagawa NA: A specific electroencephalographic correlate of convulsive equivalent disorders in children. J
Pediatr 1959; 55: 582-592.
● Klass DW, Westmoreland BF: Nonepileptogenic epileptiform electroencephalographic activity. Ann Neurol 1985 Dec; 18(6): 627-
35[Medline].
● Lombroso CT, Schwartz IH, Clark DM: Ctenoids in healthy youths. Controlled study of 14- and 6-per-second positive spiking.
Neurology 1966 Dec; 16(12): 1152-8[Medline].
● Luders HO, Noachtar S: Atlas and Classification of Electroencephalography. Philadelphia, Pa: WB Saunders Co; 2000.
● Marshall C: Some clinical correlates of the wave and spike phantom. Electroencephalogr Clin Neurophysiol 1955; 7: 633-636.

● Maulsby RL: EEG patterns of uncertain diagnostic significance. In: Klass DW, Daly DD, eds. Current Practice of Clinical
Electroencephalography. NY: Raven Press; 1979:411-419.
● Miller CR, Westmoreland BF, Klass DW: Subclinical rhythmic EEG discharges of adults (SREDA): Further observations. Am J EEG
Technol 1985; 25: 217-224.
● Mokran V, Ciganek L, Kabatnik Z: Electroencephalographic theta discharges in the midline. Eur Neurol 1971; 5(5): 288-93[Medline].
● Nidermeyer E, Croft JR: Uber die bedeutung der 14 and 6 per sec positiven spitzen im EEG. Archiv fur phychiatrie und
Nervenkrankeiter (Berlin) 1961; 202: 266-280.
● Pedley TA: EEG pattern that mimic epileptiform discharges but have no association with seizures. In: Henry CE, ed. Current Clinical
Neurophysiology: Update on EEG and Evoked Potentials. NY: Elsevier Science; 1980:307-336.
● Reiher J, Lebel M: Wicket spikes: clinical correlates of a previously undescribed EEG pattern. Can J Neurol Sci 1977 Feb; 4(1): 39-
47[Medline].
● Silverman D: Phantom spike-waves and the fourteen and six per second positive spike pattern: a consideration of their relationship.
Electroencephalogr Clin Neurophysiol 1967 Sep; 23(3): 207-13[Medline].
● Small JG: Small sharp spikes in a psychiatric population. Arch Gen Psychiatry 1970 Mar; 22(3): 277-84[Medline].
● Small JG, Sharpley P, Small IF: Positive spikes, spike-wave phantoms, and psychomotor variants: A survey of these EEG patterns in
psychiatric patients. Arch Gen Psychiatry 1968; 18: 232-238.
● Thomas JE, Klass DW: Six-per-second spike-and-wave pattern in the electroencephalogram. A reappraisal of its clinical significance.
Neurology 1968 Jun; 18(6): 587-93[Medline].
● Walter WG: Epilepsy. In: Hill D, Parr G, eds. Electroencephalography: A Symposium on Its Various Aspects. London: Mcdonald &
Company; 1950:228-272.
● Westmoreland BF, Klass DW: A distinctive rhythmic EEG discharge of adults. Electroencephalogr Clin Neurophysiol 1981 Feb; 51(2):
186-91[Medline].
● Westmoreland BF, Klass DW: Midline theta rhythm. Arch Neurol 1986 Feb; 43(2): 139-41[Medline].
● White JC, Langston JW, Pedley TA: Benign epileptiform transients of sleep. Clarification of the small sharp spike controversy.
Neurology 1977 Nov; 27(11): 1061-8[Medline].
● Wiener JM, Delano JG, Klass DW: An EEG study of delinquent and nondelinquent adolescents. Arch Gen Psychiatry 1966; 15: 144-
150.
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eMedicine - EEG Atlas: Focal (Nonepileptic) Abnormalities : Article by Selim R Benbadis, MD
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EEG Atlas: Focal (Nonepileptic) Rate this Article Introduction
Waveform
Abnormalities Email to a Colleague Descriptions
Last Updated: March 8, 2002 Pictures
Synonyms and related keywords: slowing, delta slowing, slow activity, amplitude asymmetry, Bibliography
periodic epileptiform lateralized discharges, PLED
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Before the advent of modern neuroimaging, EEG was the best noninvasive tool to use in searching for focal
lesions. In the last few decades, with progress in imaging techniques, the role of EEG is changing; its use for
localization of a brain lesion is being superseded by neuroimaging. The utilization of EEG outside of epilepsy
has declined markedly.
The use of EEG in monitoring brain activity in the operating room and also in intensive care settings needs to be
redefined and its utility reassessed. In clinical situations in which the primary question is the electrical functioning
of the brain and not primarily localization, EEG will remain a necessary test. EEGs are performed routinely in
various clinical situations; therefore the neurophysiologist is expected to be familiar with the EEG findings even
in situations in which they are of relatively limited value.

Like most neurophysiologic tests, EEG is a test of cerebral function; hence for the most part it will be nonspecific
as to etiology. Although at one time authors discussed the application of EEG in differentiating various types of
lesions, this clearly has not been clinically useful in the modern era. The exercise of describing EEG
abnormalities by pathology (eg, stroke, abscess, tumor, even various types of tumors!), which was common in
old EEG texts, is therefore not followed here. Instead, the different patterns of focal (nonepileptic) disturbances
of brain function and their clinical significance are reviewed.
Slow activity
Abnormal slow activity is by far the most common EEG manifestation of focal brain dysfunction. The abnormality
that correlates best with the presence of a structural lesion is polymorphic or arrhythmic (as opposed to
monomorphic or rhythmic) delta (ie, 1-3 Hz) slowing. This is all the more reliable when it is continuous,
unreactive (ie, characterized by lack of change between states, such as wake or sleep, or in response to
external stimuli), of high amplitude, polymorphic, and unilateral. The localization of slow potentials follows the
same rules as that of epileptiform discharges. Thus, “phase reversals” are useful to localize slow potentials and
do not imply abnormality or epileptogenicity.
Amplitude asymmetry
In the classification used here, the term asymmetry refers to asymmetry of amplitude and to normal rhythms. By
contrast, a focal frequency asymmetry would be classified as focal slow (Lüders and Noachtar). Finally, readers
should keep in mind that amplitude asymmetries should be evaluated on referential montages, since amplitude
is highly dependent on interelectrode distances.
Periodic lateralized epileptiform discharges
Described in 1964 by Chatrian et al, periodic lateralized epileptiform discharges (PLEDS) are a special type of
focal abnormality. As implied by their name, they are periodic, lateralized, and epileptiform. Periodicity is the
most characteristic feature, and the one that sets PLEDS apart from other focal abnormalities. Periodicity refers
to a relatively constant interval between discharges, which varies between 0.5 and 3 seconds and most often is
around 1 second. The epileptiform morphology of the discharges is not invariable, as PLEDS are often closer to
slow waves than to sharp waves in morphology.
Slow activity
Continuous focal slow activity is the only nonepileptiform focal abnormality that can be interpreted unequivocally
as abnormal when it is an isolated finding. Other focal abnormalities are quite frequent but are of such low
specificity that they almost never constitute an abnormality in themselves. To be interpreted as abnormal, these
usually require the coexistence of a more definite abnormality such as slowing or epileptiform discharges.
As already outlined, focal slowing is nonspecific as to etiology, and in the era of neuroimaging the EEG has no
role in diagnosing the nature of a lesion. Focal slowing is the most common abnormality associated with focal
lesions of any type, including (but not limited to) neoplastic, vascular, subdural collections, traumatic, and
infectious (see Images 1-4). It occasionally may be seen even in more subtle structural abnormalities such as
mesiotemporal sclerosis or focal malformations of cortical development.
The physiologic basis for focal polymorphic delta activity caused by focal cortical lesions is not fully understood.
It is probably due to abnormalities in the underlying white matter rather than the cortex itself. When present,
focal slow activity correlates highly with the side of the lesion, but it is not reliable for lobar localization. The
likelihood of a structural lesion (ie, specificity) diminishes when the slow activity lacks these characteristics and
is intermittent (see Image 5), in the theta rather than the delta range, and of low amplitude. This type of slowing
may be normal (eg, temporal slowing of the elderly; see the article Normal EEG Variants). This is essentially the

difference between focal “continuous slow” and “intermittent slow” (Lüders and Noachtar).
In a few situations in clinical neurology, the EEG may show clear evidence of focal dysfunction (ie, focal slow)
while no structural abnormality is found. The typical cases in point are the focal epilepsies. A readily
demonstrable structural lesion usually is not found on neuroimaging, typically MRI (see EEG Atlas: Localization-
related Epilepsies).
Focal brain dysfunction without structural abnormalities has been observed in transient ischemic attacks (TIA),
migraine, and postictal states. Polymorphic delta activity in these cases may be indistinguishable from that
caused by a structural lesion, except that it is short-lived (ie, it disappears over time). The postictal state is the
most common cause of nonstructural polymorphic delta activity, but the activity disappears within minutes to
hours after the ictal event. Patients with ongoing TIAs or migraine rarely undergo an EEG during the
symptomatic period, so clinical data are scarce.
Amplitude asymmetry
Destructive lesions clearly can attenuate the amplitude of normal rhythms. However, normal rhythms are never
perfectly symmetric in amplitude, therefore which asymmetries to consider significant is not always clear. (Some
have proposed a greater than 50% side-to-side difference as abnormal.)
A good rule of thumb is that, with very few exceptions, significant focal asymmetries are associated with slowing.
The authors recommend that any amplitude asymmetry associated with slowing of frequency be considered
significant.
Amplitude asymmetry or suppression of normal rhythms is somewhat more likely to be seen in structural
abnormalities that increase the distance or interfere with the conduction of the electrical signal between the
cortex and the recording scalp electrodes. Examples include subdural collections (eg, hematoma, empyema),
epidural collections (eg, hematoma, abscess), subgaleal collections, and calcifications such as those seen in
Sturge-Weber syndrome.
Amplitude asymmetry also may be more common than slowing in subdural hematomas. However, caution must
be exercised before considering isolated nonepileptiform focal findings other than slowing as abnormal. In
general, as with other types of focal EEG abnormalities such as slowing, amplitude asymmetry is nonspecific as
to etiology.
Although asymmetry in amplitude is usually indicative of dysfunction on the side of depressed amplitude, one
notable exception to this rule is the so-called breach rhythm (see Image 6). This is caused by a skull defect,
which attenuates the high-frequency filter function of the intact skull. As a result, faster frequencies (eg, alpha,
spindles, beta) are of higher amplitude on the side of the defect. Since morphology often is sharply contoured,
determining the epileptogenicity of these discharges can be extremely difficult, and in this situation erring on the
conservative side, by not interpreting them as epileptiform, is clearly preferable. Because of a cancellation effect
between frontopolar (Fp1/Fp2) and frontal (F3/F4), eye movements often are not increased on the side of a skull
defect and may indeed be of lesser amplitude on that side.
Periodic lateralized epileptiform discharges
PLEDS are caused by acute destructive focal lesions and are a transitory phenomenon: they tend to disappear
in weeks, even if the causal lesion persists. Over time, the record takes on a less specific focal slow
appearance, which is more likely to persist. By far the most common etiology is an acute cerebrovascular event;
second most common is focal encephalitis such as that caused by herpes. In a clinical context suggestive of
viral encephalitis, the EEG can be of great value for diagnosis and can guide tissue biopsy. Though most often
associated with an acute destructive lesion, PLEDS, like other EEG findings, are not specific as to etiology and
have been described in almost all types of structural lesions, including subdural hematoma and chronic lesions,
especially in the presence of a superimposed systemic disturbance.
In keeping with their epileptiform morphology, PLEDS have a close association with clinical seizures, and on
average about 80% of patients with PLEDS have clinical seizures (see Images 7-8). The transition between
PLEDS and a clear ictal seizure pattern is very gradual, illustrating the hypothesis that PLEDS may represent a
subclinical ictal pattern. In clinical practice, however, PLEDS usually are managed as interictal discharges (ie,
spikes or sharp waves). They indicate a high risk for focal seizures, but usually are not treated with antiepileptic
drugs unless clinical evidence for seizures is noted. This position is endorsed by the authors and others. This is

somewhat controversial, however, and some advocate antiepileptic treatment in all patients with PLEDS.
Periodic patterns in Creutzfeldt-Jakob disease usually are generalized and bisynchronous (see articles on
encephalopathies) but occasionally, especially early in the course, they may be unilateral or markedly
asymmetric, and thus take on the appearance of PLEDS.
Other less common focal patterns
An abnormal response to photic stimulation can be seen in focal lesions. Normal photic driving has long been
known to be potentially reduced on the side of a lesion. Posterior destructive lesions are particularly likely to
attenuate the driving response, but some reports have described an enhanced photic response on the side of
dysfunction. However, since the normal driving response can be quite asymmetric, such a finding should be
accompanied by a more reliable abnormality such as slowing of the waveform frequency in order to be
interpreted as abnormal.
The Bancaud phenomenon refers to the unilateral loss of reactivity of a normal rhythm and initially was
described in the context of the alpha rhythm. It should be considered a pathological finding only when
associated with other more definite abnormalities, such as slowing.
Caption: Picture 1. EEG atlas: focal (nonepileptiform) abnormalities. Continuous slow, lateralized right
hemisphere. While “spilling over” to the left frontal region, the polymorphic delta activity is clearly predominant
over the right hemisphere. This type of slowing almost invariably is associated with a structural hemispheric
lesion. This patient had a large right middle cerebral artery infarct.
Picture Type: Photo

Caption: Picture 2. EEG atlas: focal (nonepileptiform) abnormalities. Continuous slow, lateralized left
hemisphere. This polymorphic delta activity was continuous throughout the record. This patient had a left
hemisphere neoplasm.
Picture Type: Photo

Caption: Picture 3. EEG atlas: focal (nonepileptiform) abnormalities. Continuous slow, regional right temporal.
This polymorphic delta activity is somewhat more focal than that shown in Image 1, with a maximum in the
temporal chain. Little such activity is evident in the central chain, but enough to exclude a T4 electrode artifact.
The slowing shows phase reversals at T4, indicating a maximum at that electrode.

Picture Type: Photo

Caption: Picture 4. EEG atlas: focal (nonepileptiform) abnormalities. Continuous slow, regional left temporal.
This polymorphic delta activity is somewhat more focal than that in Image 2, with a maximum in the temporal
chain. The phase reversals at T3 indicate a maximum at that electrode.
Picture Type: Photo

Caption: Picture 5. EEG atlas: focal (nonepileptiform) abnormalities. Intermittent slow, lateralized left
hemisphere. This brief burst of delta activity is seen in the temporal and central areas. This is a much “weaker”
finding than continuous slowing, and much less reliably associated with a structural lesion. This is indicative of
mild dysfunction in that region.
Picture Type: Photo

Caption: Picture 6. EEG atlas: focal (nonepileptiform) abnormalities. Asymmetry, increased beta, regional right
frontocentral. The beta activity is increased in amplitude in the right frontocentral region. This is a “breach
rhythm” and is caused most often by a skull defect (in this case a burr hole).
Picture Type: Photo

Caption: Picture 7. EEG atlas: focal (nonepileptiform) abnormalities. Periodic lateralized epileptiform
discharges (PLEDS), regional left centrotemporal. The repetitive discharges occur with a periodicity of about 1
second. Polymorphic delta activity is seen over the left hemisphere, but the classification as PLEDS already
implies severe focal dysfunction. In addition, it indicates an acute destructive process and very high (80%) risk
of seizures.

Picture Type: Photo

Caption: Picture 8. EEG atlas: focal (nonepileptiform) abnormalities. Periodic lateralized epileptiform
discharges (PLEDS), lateralized right hemisphere. The repetitive discharges occur with a periodicity of 2-4
seconds. PLEDS are associated with severe focal dysfunction and with acute destructive processes and very
high (80%) risk of seizures.
Picture Type: Photo

Caption: Picture 9. EEG atlas: focal (nonepileptiform) abnormalities. PowerPoint presentation of Images 1-8.
Click to see detail
● Au WJ, Gabor AJ, Vijayan N, Markand ON: Periodic lateralized epileptiform complexes (PLEDs) in Creutzfeldt- Jakob disease.
● Bancaud J, Hécaen H, Lairy GC: Modifications de la réactivité EEG, troubles des fonctions symboliques et troubles confusionnels
dans les lésions hémisphériques localisées. Electroencephalogr Clin Neurophysiol 1955; 7: 179.
● Benbadis S: Focal disturbances of brain function. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology.
Philadelphia: WB Saunders Co; 2000:457-467.
● Brenner RP, Schaul N: Periodic EEG patterns: classification, clinical correlation, and pathophysiology. J Clin Neurophysiol 1990 Apr;
7(2): 249-67[Medline].
● Brenner RP, Sharbrough FW: Electroencephalographic evaluation in Sturge-Weber syndrome. Neurology 1976 Jul; 26(7): 629-
32[Medline].
● Cantor FK, Ilbag F: Facilitation of photic response by focal lesions. Electroencephalogr Clin Neurophysiol 1973 Jan; 34(1): 77-
9[Medline].
● Chatrian GE, Shaw CM, Leffman F: The significance of periodic lateralized epileptiform discharges in EEG: an electrographic, clinical,
and pathological study. Electroencephalogr Clin Neurophysiol 1964; 17: 177-193.
● Chu NS: Periodic lateralized epileptiform discharges with preexisting focal brain lesions. Role of alcohol withdrawal and anoxic
encephalopathy. Arch Neurol 1980 Sep; 37(9): 551-4[Medline].
● Cobb WA, Guiloff RJ, Cast J: Breach rhythm: the EEG related to skull defects. Electroencephalogr Clin Neurophysiol 1979 Sep;
47(3): 251-71[Medline].
● Collice M, Arena O, Fontana RA, et al: Role of EEG monitoring and cross-clamping duration in carotid endarterectomy. J Neurosurg
1986 Dec; 65(6): 815-9[Medline].
● Erkulvrawatr S: Occurrence, evolution and prognosis of periodic lateralized epileptiform discharges in EEG. Clin Electroencephalogr
1977; 8: 89-99.
● Faught E: Current role of electroencephalography in cerebral ischemia. Stroke 1993 Apr; 24(4): 609-13[Medline].
● Fischer-Williams M, Last SL, Lyberi G, Northfield DW: Clinico-EEG study in 128 gliomas and 50 intracranial tumours. Brain 1962; 78:
42-58.
● Furlan AJ, Henry CE, Sweeney PJ, Mitsumoto H: Focal EEG abnormalities in Heidenhain's variant of Jakob-Creutzfeldt disease. Arch
Neurol 1981 May; 38(5): 312-4[Medline].
● Gambardella A, Gotman J, Cendes F, Andermann F: Focal intermittent delta activity in patients with mesiotemporal atrophy: a reliable
marker of the epileptogenic focus. Epilepsia 1995 Feb; 36(2): 122-9[Medline].

● Gilmore PC, Brenner RP: Correlation of EEG, computerized tomography, and clinical findings. Study of 100 patients with focal delta
activity. Arch Neurol 1981 Jun; 38(6): 371-2[Medline].
● Gloor P, Ball G, Schaul N: Brain lesions that produce delta waves in the EEG. Neurology 1977 Apr; 27(4): 326-33[Medline].
● Heye N, Cervos-Navarro J: Focal involvement and lateralization in Creutzfeldt-Jakob disease: correlation of clinical,
electroencephalographic and neuropathological findings. Eur Neurol 1992; 32(5): 289-92[Medline].
● Joynt RJ, Cape CA, Knott JR: Significance of focal delta activity in adult electroencephalography. Arch Neurol 1965; 12: 631-638.
● Maytal J, Novak GP, Knobler SB, Schaul N: Neuroradiological manifestations of focal polymorphic delta activity in children. Arch
Neurol 1993 Feb; 50(2): 181-4[Medline].
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Electroencephalogr Clin Neurophysiol 1979 Mar; 46(3): 256-73[Medline].
● Musil F: Development of focal changes in the EEG of those with cranio-cerebral injury. Electroencephalogr Clin Neurophysiol 1969
Feb; 26(2): 229[Medline].
● Neufeld MY, Vishnevskaya S, Treves TA, et al: Periodic lateralized epileptiform discharges (PLEDs) following stroke are associated
with metabolic abnormalities. Electroencephalogr Clin Neurophysiol 1997 Apr; 102(4): 295-8[Medline].
● Pfurtscheller G, Sager W, Wege W: Correlations between CT scan and sensorimotor EEG rhythms in patients with cerebrovascular
disorders. Electroencephalogr Clin Neurophysiol 1981 Nov; 52(5): 473-85[Medline].
● Pohlmann-Eden B, Hoch DB, Cochius JI, Chiappa KH: Periodic lateralized epileptiform discharges--a critical review. J Clin
Neurophysiol 1996 Nov; 13(6): 519-30[Medline].
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506[Medline].
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Ann Neurol 1986 Dec; 20(6): 703-11[Medline].
● Schwartz MS, Prior PF, Scott DF: The occurrence and evolution in the EEG of a lateralized periodic phenomenon. Brain 1973 Sep;
96(3): 613-22[Medline].
● Snodgrass SM, Tsuburaya K, Ajmone-Marsan C: Clinical significance of periodic lateralized epileptiform discharges: relationship with
status epilepticus. J Clin Neurophysiol 1989 Apr; 6(2): 159-72[Medline].
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Neurophysiol Clin 1971 Jan-Mar; 1(1): 81-3[Medline].
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Electroencephalogr Clin Neurophysiol 1975 Jun; 38(6): 611-22[Medline].
NOTE:
EEG Atlas: Focal (Nonepileptic) Abnormalities excerpt

eMedicine - EEG Atlas: Generalized Epilepsies : Article by Selim R Benbadis, MD
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The International Classification of Epileptic Syndromes and Epilepsies (International League Against Epilepsy
[ILAE],1989) classifies the epilepsies along 2 dichotomies: partial (ie, localization-related) vs generalized, and
idiopathic vs cryptogenic or symptomatic. This double dichotomy conveniently allows the epilepsy classification
system to be presented in a simple 2 x 2 table (Table 1).
Table 1. Classification of the Epilepsies*
Generalized Localization-related

Idiopathic Childhood absence epilepsy Benign focal epilepsy of childhood (2

(genetic) Juvenile absence epilepsy types)
Juvenile myoclonic epilepsy ADNFLE**
Epilepsy with grand-mal seizures Primary reading epilepsy
on awakening
Other idiopathic generalized
epilepsies
Symptomatic West syndrome Mesiotemporal lobe epilepsy

or cryptogenic Lennox-Gastaut syndrome Neocortical focal epilepsy
Other symptomatic generalized
epilepsies
* Adapted from Tich and Pereon (1999)

** ADNFLE - Autosomal dominant nocturnal frontal lobe epilepsy
The term “idiopathic” often is misunderstood in this setting and requires clarification. Whereas the term idiopathic
in medicine usually means “of unknown cause,” idiopathic epilepsies are not truly of “unknown cause” (this
confusing terminology will most likely be corrected in the upcoming International League Against Epilepsy (ILAE)
classification system [Engel 1998]). In epilepsy, idiopathic seizures are genetically determined and have no
apparent structural cause, with seizures as the only manifestation of the condition. Findings of the neurologic
examination and neuroimaging studies are normal, and EEG findings also are normal other than the epileptiform
abnormalities. In some syndromes the genetic substrate has even been identified.
Most idiopathic epilepsies are generalized, but a few genetic epilepsies are focal. Nonidiopathic epilepsies are
by definition not genetic (although some may be associated with a minor genetic predisposition), but are the
result of a brain insult or lesion. If the damage is focal, it results in a localization-related epilepsy; if it is diffuse, it
results in a generalized epilepsy. The difference between symptomatic and cryptogenic is subtle: symptomatic
means that the etiology is known, while cryptogenic means that an underlying etiology is apparent but cannot be
documented objectively. Thus the boundary between the 2 is largely dependent on our diagnostic and imaging
techniques.
This review discusses EEG findings in the generalized epilepsies.
Spikes and sharp waves are sharp transients that have a strong association with epilepsy. The two are
distinguished by their duration (spikes <70 ms, sharp waves 70-200 ms), but no difference is noted in terms of
clinical significance. Several characteristics distinguish these from benign epileptiform variants (see article EEG
Atlas: Focal (Nonepileptic) Abnormalities), including high amplitude that makes them “stand out” from ongoing
background activity and aftergoing slow waves, which give the appearance of their “disrupting” background
activity (see Images 1-2).
Spike-wave complexes (SWC) are the repetitive occurrence of a spike followed by a slow wave. Since any
significant spike or sharp wave usually is followed by a slow wave (see above), a run of 3 seconds is required to
classify a record as SWC, as opposed to the categories already mentioned (spike or sharp wave). SWC can be
divided further into 2 more specific types, as follows:
● 3-Hz SWC: This pattern is characterized by a frequency of 2.5-4 Hz and a very monomorphic (“perfectly
regular”) morphology (see Image 3). It occurs in very discrete bursts, and between bursts the EEG is
normal.
● Slow SWC: This pattern is not only slower (<2.5 Hz) but also more irregular (less monomorphic) than the
3-Hz SWC. Bursts are less discrete than the 3-Hz SWC, and between bursts other abnormalities are
seen in symptomatic/cryptogenic epilepsies of the Lennox-Gastaut type (see Images 4-5).
Polyspikes are multiple repetitive spikes occurring at about 20 Hz (see Image 6).

Generalized epileptiform discharges (ie, spikes, sharp waves, SWCs) are usually maximal in the frontal regions,
with typical phase reversals at the F3 and F4 electrodes (see Image 7).
Hypsarrhythmia is defined as continuous (during wakefulness), high-amplitude (>200 Hz), generalized

polymorphic slowing with no organized background and multifocal spikes (see Images 8-9).
Electrographic seizures
● Electrodecrement consists of abrupt attenuation (“flattening”) of background activity, often preceded by a

high-amplitude transient (see Image 10). This typically is associated with infantile spasms or atonic
seizures.
● Generalized paroxysmal fast activity (GPFA) consists of bursts of fast (10 Hz) activity and typically is
associated with tonic seizures.
Idiopathic generalized epilepsies
These syndromes, formerly called primary generalized epilepsies, are the best known group of idiopathic
epilepsies. They epitomize the meaning of the term idiopathic: genetic basis, normal neurologic examination
findings, and normal intelligence. EEG shows generalized epileptiform discharges and may show
photosensitivity. Seizure types include generalized tonic-clonic (GTC), absence, and myoclonic. Accordingly,
EEG typically shows generalized spikes or sharp waves, 3-Hz or faster SWCs (clinically associated with
absence seizures), and polyspikes (clinically associated with myoclonic seizures). The EEG is normal (ie, no
abnormal slowing) except for the epileptiform abnormalities.
Within the group of idiopathic generalized epilepsies, distinct entities are distinguished, primarily on the basis of
predominant seizure type(s) and age of onset. Some syndromes are very well individualized, while others have
less clear boundaries. The major and well-defined types of idiopathic generalized epilepsies include childhood
absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with grand mal seizures (sometimes referred to as
grand mal on awakening).
Symptomatic generalized epilepsies
These are associated with diffuse brain dysfunction. The cause may be known ("symptomatic"), such as anoxic
birth injury or a metabolic or chromosomal defect, or it may be unknown ("cryptogenic"). Accordingly, clinical
evidence of diffuse brain dysfunction is usually present, either intellectual (ie, developmental delay or mental
retardation) or motor (ie, developmental delay or cerebral palsy). Similarly, the EEG shows evidence of diffuse
brain dysfunction in addition to the epileptiform abnormalities, in the form of slowing. The clinical and EEG
manifestations are not specific as to etiology, but vary tremendously with age, and thus are said to be age
dependent.
West syndrome is the phenotype of symptomatic or cryptogenic generalized epilepsy in the first year of life and
is characterized by infantile spasms, hypsarrhythmia, and developmental delay. It is an age-specific response of
the immature brain to a nonspecific focal or generalized insult. Age of onset peaks between 3 and 7 months of
age.
Lennox-Gastaut syndrome (LGS) has an early childhood onset (age 1-8 years) and consists of multiple seizure
types, mental retardation, and typical EEG findings dominated by generalized slow SWC. Seizure types include
atypical absences, tonic, atonic, myoclonic, and GTC seizures. The atonic, myoclonic, tonic, and GTC seizures
of LGS frequently result in unprotected falls (referred to as “drop attacks”) with injury. Besides the classic EEG
pattern of generalized slow SWC, other frequent but less specific EEG findings include background slowing,
generalized slowing, and multifocal spikes. During sleep, the EEG may show polyspikes and slow waves.
Another typical feature of LGS is generalized paroxysmal fast activity (>10 Hz) during sleep. Many patients with
symptomatic generalized epilepsy do not meet all the criteria for LGS.

Caption: Picture 1. EEG atlas: generalized epilepsies. Spike, generalized. Note the high amplitude and the
aftergoing background suppression and slow wave.
Picture Type: Photo

Caption: Picture 2. EEG atlas: generalized epilepsies. Spike, generalized. Significant spikes usually are
followed by a slow wave, as shown here. This example also illustrates that generalized spikes are typically
maximal frontally. This is typical of the primary (ie, idiopathic, genetic) epilepsies. If the burst lasted 3 seconds
or more, it could be classified as spike-wave complexes.
Picture Type: Photo

Caption: Picture 3. EEG atlas: generalized epilepsies. Sharp waves, multifocal. Sharp waves are seen at T4,
T6, T5, and F3 on this 9-second segment. With other findings, this often is seen in the symptomatic/cryptogenic
epilepsies of the Lennox-Gastaut type.
Picture Type: Photo

Caption: Picture 4. EEG atlas: generalized epilepsies. Slow spike-wave complexes. In addition to being slower,
this is also less monomorphic than the 3-Hz spike-wave complexes. With other findings, this often is seen in the
symptomatic/cryptogenic epilepsies of the Lennox-Gastaut type.

Picture Type: Photo

Caption: Picture 5. EEG atlas: generalized epilepsies. Slow spike-wave complexes (SWC). In addition to being
slower, this is also less monomorphic than the 3-Hz SWC. With other findings, this often is seen in the
symptomatic/cryptogenic epilepsies of the Lennox-Gastaut type.
Picture Type: Photo

Caption: Picture 6. EEG atlas: generalized epilepsies. Polyspike, generalized. Note the aftergoing slow wave.
This is associated with the “primary” or idiopathic (genetic) generalized epilepsies, most typically juvenile
myoclonic epilepsy.
Picture Type: Photo

Caption: Picture 7. EEG atlas: generalized epilepsies. 3-Hz spike-wave complexes (SWC), generalized. This
pattern is very monomorphic, with a maximum (shown here by a phase reversal) frontally, typically at F3/F4.
This is typical of idiopathic (ie, genetic) generalized epilepsies, such as absence epilepsy. The 3-Hz SWC is
often faster at onset (4-5 Hz), as shown here.
Picture Type: Photo

Caption: Picture 8. EEG atlas: generalized epilepsies. Hypsarrhythmia. High-amplitude slowing with no
organized background, and multifocal spikes (left and right frontal in this sample). This is a phenotype of the
first year of life and is associated with West syndrome (ie, infantile spasms).

Picture Type: Photo

Caption: Picture 9. EEG atlas: generalized epilepsies. Hypsarrhythmia. High-amplitude slowing (note the scale)
with no organized background, and multifocal spikes (right frontal and left occipital in this sample). This is a
phenotype of the first year of life and is associated with West syndrome (ie, infantile spasms).
Picture Type: Photo

Caption: Picture 10. EEG atlas: generalized epilepsies. Generalized paroxysmal fast activity and
electrodecrement. This pattern is characteristic of the symptomatic/cryptogenic epilepsies of the Lennox-
Gastaut type and may be subclinical or associated with tonic or atonic seizures.
Picture Type: Photo

Click to see detail
● Appleton RE, Beirne M: Absence epilepsy in children: the role of EEG in monitoring response to treatment. Seizure 1996 Jun; 5(2):
147-8[Medline].
● Beaumanoir A, Bureau M, Deonna T, et al: Continuous spikes and waves during slow sleep. Electrical status epilepticus during slow
sleep. Acquired epileptic aphasia and related conditions. London: John Libbey; 1995.
● Benbadis SR, Luders HO: Epileptic syndromes: an underutilized concept. Epilepsia 1996 Nov; 37(11): 1029-34[Medline].
● Benbadis SR, Luders HO: Generalized epilepsies. Neurology 1996 Apr; 46(4): 1194-5[Medline].
● Benbadis SR, Wyllie E: Pediatric epilepsy syndromes. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology.
● Berkovic SF, Andermann F, Andermann E, et al: Concepts of absence epilepsies: discrete syndromes or biological continuum?
● Brenner RP, Atkinson R: Generalized paroxysmal fast activity: electroencephalographic and clinical features. Ann Neurol 1982 Apr;
11(4): 386-90[Medline].
● Engel J Jr: Classifications of the International League Against Epilepsy: time for reappraisal. Epilepsia 1998 Sep; 39(9): 1014-
7[Medline].

● Grunewald RA, Panayiotopoulos CP: Juvenile myoclonic epilepsy. A review. Arch Neurol 1993 Jun; 50(6): 594-8[Medline].
● Holmes GL, McKeever M, Adamson M: Absence seizures in children: clinical and electroencephalographic features. Ann Neurol 1987
Mar; 21(3): 268-73[Medline].
● Hrachovy RA, Frost JD Jr, Kellaway P: Hypsarrhythmia: variations on the theme. Epilepsia 1984 Jun; 25(3): 317-25[Medline].
● International League Against Epilepsy, Commission on Classification and Terminol: Proposal for revised classification of epilepsies
and epileptic syndromes . Epilepsia 1989 Jul-Aug; 30(4): 389-99[Medline].
● Lancman ME, Asconapé JJ, Brotherton T, et al: Juvenile myoclonic epilepsy: an underdiagnosed syndrome. J Epilepsy 1995; 8: 215-
218.
● Lancman ME, Asconape JJ, Penry JK: Clinical and EEG asymmetries in juvenile myoclonic epilepsy. Epilepsia 1994 Mar-Apr; 35(2):
302-6[Medline].
● Loiseau P, Duche B, Pedespan JM: Absence epilepsies. Epilepsia 1995 Dec; 36(12): 1182-6[Medline].
● Lombroso CT: A prospective study of infantile spasms: clinical and therapeutic correlations. Epilepsia 1983 Apr; 24(2): 135-
58[Medline].
● Markand ON: Slow spike-wave activity in EEG and associated clinical features: often called 'Lennox' or "Lennox-Gastaut' syndrome.
Neurology 1977 Aug; 27(8): 746-57[Medline].
● Reutens DC, Berkovic SF: Idiopathic generalized epilepsy of adolescence: are the syndromes clinically distinct? Neurology 1995 Aug;
45(8): 1469-76[Medline].
● Thomas P, Beaumanoir A, Genton P, et al: 'De novo' absence status of late onset: report of 11 cases. Neurology 1992 Jan; 42(1):
104-10[Medline].
● Tich SN, Pereon Y: Semiological seizure classification. Epilepsia 1999 Apr; 40(4): 531[Medline].
● Wyllie E, Lüders H: Classification of seizures. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. 2nd ed. Baltimore:
Lippincott Williams & Wilkins; 1997:355-357.
NOTE:
EEG Atlas: Generalized Epilepsies excerpt

eMedicine - EEG Atlas: Localization-related Epilepsies : Article by Selim R Benbadis, MD
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EEG Atlas: Localization-related Rate this Article Introduction
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Epilepsies Email to a Colleague Descriptions
Bibliography
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Author Information Introduction Waveform Descriptions Clinical Correlation Pictures Bibliography images.
Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Continuing
Education
Departments of Neurology and Neurosurgery, University of South Florida, Tampa General Hospital
CME available for
Coauthor(s): Diego Rielo, MD, Staff Physician, Department of Neurology, Tampa General Healthcare, this topic. Click
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Editor(s): Leslie Huszar, MD, Consulting Staff, Department of Neurology, Indian River Memorial Hospital; patient education.
The International Classification of Epileptic Syndromes and Epilepsies (International League Against Epilepsy
{ILAE], 1989) classifies the epilepsies along 2 dichotomies: partial (ie, localization-related) vs generalized, and
idiopathic vs cryptogenic or symptomatic. This double dichotomy conveniently allows presentation of the
epilepsy classification in a simple 2 x 2 table (Table 1).
Table 1. Classification of the Epilepsies*
Generalized Localization-related

Idiopathic Childhood absence epilepsy Benign focal epilepsy of childhood (2

(genetic) Juvenile absence epilepsy types)
Juvenile myoclonic epilepsy ADNFLE**
Epilepsy with grand mal seizures on Primary reading epilepsy
awakening
Other idiopathic generalized
epilepsies
Symptomatic West syndrome Mesiotemporal lobe epilepsy

or cryptogenic Lennox-Gastaut syndrome Neocortical focal epilepsy
Other symptomatic generalized
epilepsies
* Adapted from Nguyen et al (1999)

** ADNFLE - Autosomal dominant nocturnal frontal lobe epilepsy
The term “idiopathic” often is misunderstood in this setting and requires clarification. Whereas the term idiopathic
usually means “of unknown cause,” idiopathic epilepsies are not truly of “unknown cause” (this confusing
terminology will most likely be corrected in the upcoming ILAE classification system [Engel, 1998]). Idiopathic
epilepsies are determined genetically and have no apparent structural cause, with seizures as the only
manifestation of the condition. Findings of the neurologic examination and imaging studies are normal, and EEG
is normal other than the epileptiform abnormalities. In some syndromes the genetic substrate has even been
identified.
Most idiopathic epilepsies are generalized, but a few are focal. Nonidiopathic epilepsies are by definition not
genetic, although some may be associated with a minor genetic predisposition; they are the result of a brain
insult or lesion. If the damage is focal, it results in a localization-related epilepsy; if it is diffuse, it results in a
generalized epilepsy. The difference between symptomatic and cryptogenic is subtle: symptomatic means that
the etiology is known, while cryptogenic means that an underlying etiology is apparent but cannot be
documented objectively. Thus the boundary between the two is largely dependent on the capabilities of our
diagnostic and imaging techniques.
This review discusses EEG findings in the localization-related (also known as focal or partial) epilepsies.
Spikes and sharp waves are sharp transients that have a strong association with epilepsy. The two are
distinguished only by their duration (spikes <70 ms, sharp waves 70-200 ms), but they have no differences in
terms of clinical significance. Several characteristics distinguish these from benign epileptiform variants (see
article EEG Atlas: Focal (Nonepileptic) Abnormalities), including high amplitudes, which make them “stand out”
from ongoing background activity, and aftergoing slow waves, which give the appearance of their “disrupting”
background activity (see Images 1-6).
Polyspikes are rarely focal, although focal spikes can at times have a multiphasic “polyspike-like” morphology.
Electrographic seizures: Focal seizures are discharges characterized by rhythmicity and evolution (“build-up”) in
frequency and amplitude. The discharge can consist of rhythmic theta or delta activity, or repetitive spikes or
sharp waves, but the most characteristic features of electrographic focal seizures are rhythmicity and evolution
(see Image 7).
Idiopathic localization-related epilepsies
Benign focal epilepsy of childhood is the main localization-related epilepsy that is idiopathic. Two varieties have

been well described and are in the 1989 ILAE classification: centrotemporal and occipital. A third type has been
described more recently: autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE).
Benign childhood epilepsy with centrotemporal spikes (BECTS) is by far the more common. Age of onset is
between 4 and 12 years (peak age 8-9 years). Seizures are simple partial with motor symptoms involving the
face, and they tend to occur during sleep or on awakening. Though these focal seizures are the most
characteristic seizure types in BECTS, they can be quite subtle and are missed easily, so that the most common
mode of presentation is a (secondary) generalized tonic-clonic seizure. As with all idiopathic epilepsy
syndromes, neurologic examination findings are normal.
EEG findings are characteristic, with stereotyped centrotemporal sharp waves that have a characteristic
morphology. They are activated markedly by non–rapid eye movement (NREM) sleep, often occur in repetitive
bursts, and can be bilateral and independent. Notably, the interictal sharp waves of BECTS often occur in
asymptomatic children. In fact, only a minority of children with these discharges may have seizures.
Childhood epilepsy with occipital paroxysms is less common and less consistently benign. It shares all the
characteristics of an idiopathic syndrome (ie, normal findings on examination, intelligence quotient [IQ] testing,
and neuroimaging studies). Age of onset is 4-8 years. Seizures are rare and primarily nocturnal, and often
involve visual symptoms. Sharp waves have a maximum occipital negativity, often occur in long bursts of spike-
wave complexes, and are activated markedly by eye closure.
ADNFLE is a recently described genetic localization-related epilepsy. Several mutations of the neuronal nicotinic
acetylcholine receptor alpha4 subunit have been identified in association with this epilepsy. It has the expected
features of idiopathic (ie, genetic) epilepsies, including onset early in life and normal imaging findings. Seizures
are nocturnal and occur in clusters, mimicking parasomnias. They are mostly brief tonic seizures and rare
(secondarily) generalized tonic-clonic convulsions, often preceded by a nonspecific aura.
Interictal EEG may show epileptiform discharges with a frontal predominance, often seen only in sleep. Ictal
EEG does not always show definite ictal discharges. Thus the electroclinical features of ADNFLE are not
different from those of symptomatic or cryptogenic frontal lobe epilepsy. Since the genetic findings are variable
(ie, locus heterogeneity), its definite diagnosis is largely one of exclusion.
Cryptogenic focal epilepsies
This is by far the most common type of adult-onset epilepsy. By definition, seizures arise from a localized region
of the brain. If the cause is found, they are said to be symptomatic. If imaging study findings are normal, the
cause remains presumptive and they are said to be cryptogenic. As stated already, the boundary between the
two is largely dependent on our diagnostic and imaging techniques, and etiologies such as low-grade tumors,
hippocampal sclerosis, and subtle cortical dysplasias are identified more and more often owing to advances in
neuroimaging. Clinically, seizures may be simple partial or complex partial, with or without secondary
generalization. Interictal EEG shows focal spikes or sharp waves, and ictal EEG shows a focal or regional
discharge at onset. The main clinical entities are mesiotemporal lobe epilepsy, neocortical focal epilepsies, and
hemispheric syndromes.
Caption: Picture 1. EEG atlas: localization-related epilepsies. Sharp waves, left temporo-occipital region. The
sharp waves are, like any significant epileptiform discharges, followed by slowing and “disruption” of the
background. The referential montage (right panel) confirms that the maximum is at T6, closely followed by O2.
Picture Type: Photo

Caption: Picture 2. EEG atlas: localization-related epilepsies. Sharp waves, left temporal region. The maximum
(phase reversal) is at T3. The small sharp wave in the 4th second may not be sufficient in itself owing to its
small amplitude but, in the context of the definite one, is certainly significant.
Picture Type: Photo

(phase reversal) is consistently at T3. Note the associated slow activity and background attenuation.
Picture Type: Photo

(phase reversal) is at F7 and T1. The small sharp wave that follows would not be sufficient in itself owing to its
small amplitude, but in the context of other definite ones, is most likely significant.
Picture Type: Photo

Caption: Picture 5. EEG atlas: localization-related epilepsies. Sharp wave, left temporal region. The sharp
wave is, like most significant epileptiform discharges, followed by slowing and “disruption” of the background.
The referential montage (right panel) confirms that the maximum is at electrode T2, followed by F8 and T4.

Picture Type: Photo

Caption: Picture 6. EEG atlas: localization-related epilepsies. Spike, left frontal region. Note the typical
aftergoing slow wave. The referential montage (right panel) shows that the maximum is at Fp1 and F7 about
equally, followed by F3.
Picture Type: Photo

Caption: Picture 7. EEG atlas: localization-related epilepsies. EEG seizure, left temporal region. This is
characterized by a rhythmic discharge with “build-up” (ie, evolution in frequency and amplitude).
Picture Type: Photo

Click to see detail
● Benbadis SR: Observations on the misdiagnosis of generalized epilepsy as partial epilepsy: causes and consequences. Seizure 1999
May; 8(3): 140-5[Medline].
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2000 Dec 26; 55(12): 1780-4[Medline].
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● Benbadis SR, Wyllie E, Bingaman W: Intracranial EEG and localization studies. In: Wyllie E, ed. The Treatment of Epilepsy:
Principles and Practice. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001:1067-1075.
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Epilepsia 1993 May-Jun; 34(3): 522-7[Medline].
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MRI, and operative outcome. Epilepsia 1996 Jul; 37(7): 651-6[Medline].
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● Engel J Jr: Classifications of the International League Against Epilepsy: time for reappraisal. Epilepsia 1998 Sep; 39(9): 1014-
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and epileptic syndromes. Epilepsia 1989 Jul-Aug; 30(4): 389-99[Medline].
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Neurology 1995 Apr; 45(4): 780-7[Medline].
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381-9[Medline].
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Sndromes. London: Springer-Verlag; 1987:303-346.
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appraisal of 40 patients and delineation of the epileptic syndrome. Brain 1998 Feb; 121 ( Pt 2): 205-23[Medline].
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Raven Press; 1992:337-347.
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stimulation and outcome in 42 patients treated between 1930 and 1991. Surgery of occipital lobe epilepsy. Brain 1992 Dec; 115 ( Pt
6): 1655-80[Medline].
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surgically between 1929 and 1988. Brain 1995 Jun; 118 ( Pt 3): 607-27[Medline].
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Brain 1995 Feb; 118 ( Pt 1): 61-73[Medline].
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● Wyllie E: EEG atlas. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. 3rd ed. Philadelphia: Lippincott Williams &
Wilkins; 2001.
NOTE:
EEG Atlas: Localization-related Epilepsies excerpt

eMedicine - EEG Atlas: Normal Awake EEG : Article by Selim R Benbadis, MD
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EEG Atlas: Normal Awake EEG Rate this Article Introduction
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Author: Selim R Benbadis, MD, Director of Comprehensive Epilepsy Program, Associate Professor, Continuing
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This article describes the most common features of the normal awake EEG. The images at the end of the article
show representative examples of the features discussed here.
The alpha rhythm is the most prominent feature of the normal mature EEG. It typically is identified first during the
review.
Beta activity refers to a frequency band rather than a distinct (specific) rhythm such as alpha or mu. Beta activity
is commonly present in the EEG of healthy people. However, it is often difficult to see because of its low
amplitude.
Gastaut initially described the mu rhythm in 1952. This morphologically distinct activity is observed in
approximately 17-19% of young adults.

Alpha rhythm
The normal alpha rhythm has the following characteristics:
● Frequency of 8-12 Hz - Lower limit of normal generally accepted in adults and children older than 8 years
is 8 Hz
● Location - Posterior dominant; occasionally, the maximum may be a little more anterior, and it may be
more widespread
● Morphology - Rhythmic, regular, and waxing and waning
● Amplitude - Generally 20-100 mV
● Reactivity - Best seen with eyes closed; attenuates with eye opening
Beta activity
Normal beta activity has the following characteristics:
● Frequency (by definition) greater than 13 Hz - Common 18-25 Hz, less common 14-16 Hz, and rare 35-
40 Hz
● Location - Mostly frontocentral but somewhat variable; some describe various types according to location
and reactivity: generalized, precentral, and posterior
● Morphology - Usually rhythmic, waxing and waning, and symmetric
● Amplitude - Usually range of 5-20 mV
● Reactivity - Most common 18- to 25-Hz beta activity enhanced during stages I and II sleep and tends to
decrease during deeper sleep stages; central beta activity may be reactive (attenuates) to voluntary
movements and proprioceptive stimuli; in infants older than 6 months, onset of sleep marked by
increased beta activity in central and postcentral regions
Mu rhythm
Characteristics of the mu rhythms are as follows:
● Frequency of 7-11 Hz - Generally in alpha frequency band (8-12 Hz)
● Location - Centroparietal area
● Morphology - Archlike shape or like an "m"; most often asymmetric and asynchronous between the 2
sides and may be unilateral
● Amplitude - Generally low to medium and comparable to that of the alpha rhythm
● Reactivity - Most characteristic feature defining the mu rhythm; mu rhythm attenuates with contralateral
extremity movement, the thought of a movement, or tactile stimulation; contrary to the alpha rhythm,
does not react to eye opening and closing
The mu rhythm has been documented on subdural recording of both sensory and motor cortex and shows the
same characteristics as that seen on surface EEG, including distribution, morphology, and reactivity.
Furthermore, some correspondence exists between functional mapping of sensorimotor function and

somatotopic distribution of mu reactivity.
Alpha rhythm
Occasionally the alpha rhythm is of very low amplitude or even not identifiable. This is not abnormal. In addition
to amplitude, other characteristics can vary somewhat without being abnormal, including morphology (eg, spiky),
distribution (eg, widespread), and harmonic frequency (eg, slow or fast alpha variant).
Beta activity
In healthy individuals, beta activity commonly can be mildly different (<35%) in amplitude between the 2
hemispheres, which may be caused by differences in skull thickness. Definite focal, regional, or hemispheric
difference (at least 50%) in amplitude may be significant and may suggest either skull defect (side with higher
amplitude) or a structural lesion (side with lower amplitude). The amount and voltage of beta activity is enhanced
by commonly used sedative medications (benzodiazepines, barbiturates).
Mu rhythm
Asymmetry, unilaterality, or asynchrony of the mu rhythm is generally not abnormal unless associated with other
abnormalities. Very-high-voltage mu activity may be recorded in the central regions over skull defects and may
become sharp in configuration, and thus can be mistaken for epileptiform discharges. When mu rhythm is
detected in an EEG, it should be verified by testing its reactivity.
Caption: Picture 1. EEG atlas: normal awake EEG. A 10-second segment showing a well-formed and well-
regulated alpha rhythm at 9 Hz. Note that it is very regular, rhythmic, waxing and waning, and posterior
dominant. The contrast between the first and second halves of the page illustrates the reactivity of a normal
alpha rhythm, with attenuation upon eye opening.
Picture Type: Photo

Caption: Picture 2. EEG atlas: normal awake EEG. Fleeting alpha. At times, as shown here, the alpha rhythm
can be identified only in very brief bursts and often immediately after eye closure. If normal in frequency, this is
normal.

Picture Type: Photo

Caption: Picture 3. EEG atlas: normal awake EEG. This is an example of an alpha rhythm with a wider
distribution than is typical. If frequency and reactivity are normal, this is another variation of normal. A similar
EEG pattern can be seen in patients in a coma (ie, alpha coma), but in these situations it is usually unreactive.
Picture Type: Photo

Caption: Picture 4. EEG atlas: normal awake EEG. This is an example of "slow alpha variant." The patient's
alpha rhythm at 12 Hz is seen in the second half of the sample. The first half shows a subharmonic at half that
frequency, and this is the "slow alpha variant."
Picture Type: Photo

Caption: Picture 5. EEG atlas: normal awake EEG. A sample of awake EEG showing the normal or usual
amount of beta activity. As shown here, beta activity is often easier to identify during relaxed wakefulness or
early drowsiness.
Picture Type: Photo

Caption: Picture 6. EEG atlas: normal awake EEG. Mu rhythm over the left (greater than right) central region.
To be absolutely certain that this is a mu rhythm, reactivity should be tested. However, morphology (not
absolutely typical but fairly so), frequency, and distribution strongly suggest that this is a mu rhythm.

Picture Type: Photo

Caption: Picture 7. EEG atlas: normal awake EEG. An example of a typical normal alpha rhythm, showing clear
attenuation upon eye opening (second half of page)
Picture Type: Photo

Caption: Picture 8. EEG atlas: normal awake EEG. This is the normal amount of beta activity, frontally
predominant, with waxing and waning amplitude.
Picture Type: Photo

Caption: Picture 9. EEG atlas: normal awake EEG. Alpha rhythm with somewhat "spiky" or sharply contoured
morphology. When fragmented (eg, in drowsiness), this can be misinterpreted as sharp waves.
Picture Type: Photo

● Arroyo S, Lesser RP, Gordon B, et al: Functional significance of the mu rhythm of human cortex: an electrophysiologic study with
subdural electrodes. Electroencephalogr Clin Neurophysiol 1993 Sep; 87(3): 76-87[Medline].
● Benbadis SR: Focal disturbances of brain function. In: Levin KH, Lüders HO, eds. Comprehensive Clinical Neurophysiology.


● McFarland DJ, Miner LA, Vaughan TM, et al: Mu and beta rhythm topographies during motor imagery and actual movements. Brain
Topogr 2000 Spring; 12(3): 177-86[Medline].
● Pfurtscheller G, Stancak A Jr, Edlinger G: On the existence of different types of central beta rhythms below 30 Hz.
Electroencephalogr Clin Neurophysiol 1997 Apr; 102(4): 316-25[Medline].
● Pfurtscheller G, Neuper C, Krausz G: Functional dissociation of lower and upper frequency mu rhythms in relation to voluntary limb
movement. Clin Neurophysiol 2000 Oct; 111(10): 1873-9[Medline].
● Pineda JA, Allison BZ, Vankov A: The effects of self-movement, observation, and imagination on mu rhythms and readiness
potentials (RP's): toward a brain-computer interface (BCI). IEEE Trans Rehabil Eng 2000 Jun; 8(2): 219-22[Medline].
NOTE:
EEG Atlas: Normal Awake EEG excerpt

eMedicine - EEG Atlas: Normal Sleep EEG - Rapid Eye Movement Sleep : Article by Selim R Benbadis, MD
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EEG Atlas: Normal Sleep EEG - Rate this Article Introduction
Waveform
Rapid Eye Movement Sleep Email to a Colleague Descriptions
Last Updated: May 3, 2002 Pictures
Synonyms and related keywords: EEG desynchronization, REM sleep, saw tooth wave Bibliography
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Loomis provided the earliest detailed description of various stages of sleep in the mid-1930s, and in the early
1950s Aserinsky and Kleitman identified rapid eye movement (REM) sleep. Sleep generally is divided in 2 broad
types: nonrapid eye movement sleep (NREM) and REM sleep. On the basis of EEG changes, NREM is divided
further into 4 stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles, each
lasting approximately 90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult NREM
sleep accounts for 75-90% of sleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV). REM
sleep accounts for 10-25% of sleep time.
REM sleep normally is not seen on routine EEGs, because the normal latency to REM sleep (100 min) is well
beyond the duration of routine EEG recordings (approximately 20-30 min). The appearance of REM sleep during
a routine EEG is referred to as sleep-onset REM period (SOREMP) and is considered an abnormality. While not
observed on routine EEG, REM sleep commonly is seen during prolonged (>24 h) EEG monitoring.
Representative examples of waveforms described here can be seen in the images at the end of this article.

By strict sleep staging criteria on polysomnography, REM sleep is defined by (1) rapid eye movements; (2)
muscle atonia; and (3) EEG “desynchronization” (compared to slow wave sleep). Thus, 2 of the 3 defining
characteristics are not cerebral waves and theoretically require monitoring of eye movements (electrooculogram
[EOG]) and muscle tone (electromyelogram [EMG]). Fortunately, muscle activity and eye movements can be
evaluated on EEG, thus REM sleep is usually not difficult to identify. In addition to the 3 features already named,
“saw tooth” waves also are seen in REM sleep.
● EEG desynchronization: The EEG background activity changes from that seen in slow wave sleep (stage
III or IV) to faster and lower voltage activity (theta and beta), resembling wakefulness. Saw tooth waves
are a special type of central theta activity that has a notched morphology resembling the blade of a saw
and usually occurs close to rapid eye movements (ie, phasic REM). They are only rarely clearly
identifiable.
● Rapid eye movements: These are saccadic, predominantly horizontal, and occur in repetitive bursts.
Despite the lack of a dedicated EMG channel, the muscle atonia that characterizes REM sleep is usually
apparent as a general sense of “quiet” muscle artifacts compared to wakefulness.
The duration of REM sleep increases progressively with each cycle and tends to predominate late in the sleep
period into early morning. The occurrence of REM too soon after sleep onset, referred to as SOREMP, is
considered pathological. However, newborns and infants enter REM more rapidly and spend a higher proportion
of sleep in REM (this is true in most species and supports the theory that REM sleep is involved in brain
development).
Caption: Picture 1. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. REM sleep with rapid
(saccadic) eye movements. While muscle “atonia” cannot be proven without a dedicated electromyogram
(EMG) channel, certainly EMG artifact is absent with a “quiet” recording. Also, no alpha rhythm is present that
would suggest wakefulness.
Picture Type: Photo

Caption: Picture 2. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. Typical saccadic eye
movements of REM sleep are shown, with lateral rectus “spikes” seen just preceding the lateral abducting eye
movements.

Picture Type: Photo

Caption: Picture 3. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. In addition to rapid eye
movements, this REM sleep record is characterized by brief fragments of alpha rhythm (first half) and central
saw tooth waves (second half).
Picture Type: Photo

Caption: Picture 4. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. This is a good example
of saw tooth waves seen in REM sleep and their “notched” morphology.
Picture Type: Photo

Caption: Picture 5. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. This is a good example
of saw tooth waves seen in REM sleep and their “notched” morphology, best seen here in the Cz-Pz (last)
channel.
Picture Type: Photo

Caption: Picture 6. EEG atlas: normal sleep EEG – rapid eye movement (REM) sleep. This illustrates the
typical appearance of saw tooth waves on a polysomnogram (PSG) display, equivalent to 1 cm/s.

Picture Type: Photo

Caption: Picture 7. EEG atlas: normal sleep EEG – rapid eye movement sleep. PowerPoint presentation of
pictures 1-6
Click to see detail
● Aserinsky E, Kleitman N: Two types of ocular motility occurring in sleep. J Appl Physiol 1955; 8: 1-10.
● Benbadis SR, Wolgamuth BR, Perry MC, et al: Dreams and rapid eye movement sleep in the multiple sleep latency test. Sleep 1995
Feb; 18(2): 105-8[Medline].
● Chockroverty S: An overview of sleep. In: Chokroverty S, ed. Sleep Disorder Medicine: Basic Science, Technical Considerations, and
Clinical Aspects. Boston: Butterworth-Heinemann; 1999:7-20.
● Dement W, Kleitman N: Cyclic variations of EEG during sleep and their relation to eye movements, body motility and dreaming.
● Loomis AL, Harvey EN, Hobart GA: Potential rhythms of the cerebral cortex during sleep. Science 1935; 81: 597-598.
● Loomis AL, Harvey EN, Hobart GA: Brain potentials during hypnosis. Science 1936; 83: 239-241.
● Loomis AL, Harvey EN, Hobart GA: Cerebral states during sleep, as studied by human brain potentials. J Exp Psychol 1937; 21: 127-
144.
● Loomis AL, Harvey EN, Hobart G: Distribution of disturbance patterns in the human electroencephalogram with special reference to
sleep. J Neurophysiol 1938; 1: 413-430.
● Reynolds CF 3rd, Kupfer DJ, Taska LS, et al: EEG sleep in elderly depressed, demented, and healthy subjects. Biol Psychiatry 1985
Apr; 20(4): 431-42[Medline].
● Sakai T, Kohsaka S, Kohsaka M: Functional changes of the brainstem triggering vertex sharp wave with spindle. Psychiatry Clin
Neurosci 1999 Apr; 53(2): 167-9[Medline].
● Steriade M: Neurophysiological mechanism of non-rapid eye movement (resting) sleep. In: Chokroverty S, ed. Sleep Disorders
Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Boston: Butterworth-Heinemann; 1999:51-62.
● Vignaendra V, Matthews RL, Chatrian GE: Positive occipital sharp transients of sleep: relationships to nocturnal sleep cycle in man.
NOTE:
EEG Atlas: Normal Sleep EEG - Rapid Eye Movement Sleep excerpt

eMedicine - EEG Atlas: Normal Sleep EEG - Stage I : Article by Selim R Benbadis, MD
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Stage I Email to a Colleague Descriptions
Synonyms and related keywords: drowsiness, presleep, sleep stages Bibliography
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patient education.
1950s Aserinsky and Kleitman identified rapid eye movement (REM) sleep. Sleep generally is divided in two
broad types: nonrapid eye movement sleep (NREM) and REM sleep. On the basis of EEG changes, NREM is
divided further into 4 stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles,
each lasting approximately 90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult
NREM sleep accounts for 75-90% of sleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV).
REM sleep accounts for 10-25% of sleep time.
Stage I sleep also is referred to as drowsiness or presleep and is the first or earliest stage of sleep.
Representative EEG waveforms are shown in the images at the end of this article.

The features of drowsiness are as follows:
● Slow rolling eye movements (SREMs)
● Attenuation (drop out) of the alpha rhythm
● Central or frontocentral theta activity
● Enhanced beta activity
● Positive occipital sharp transients of sleep (POSTS)
● Vertex sharp transients
● Hypnagogic hypersynchrony
Slow rolling eye movements
SREMs are usually the first evidence of drowsiness seen on the EEG. SREMs of drowsiness most often are
horizontal but can be vertical or oblique, and their distribution is similar to eye movements in general (see EEG
Atlas: EEG Artifacts). However, they are slow (ie, typically 0.25-0.5 Hz). SREMs disappear in stage II and
deeper sleep stages.
Alpha dropout
Drop out of alpha activity typically occurs together with or nearby SREM. The alpha rhythm gradually becomes
slower, less prominent, and fragmented.
Positive occipital sharp transients of sleep
POSTS start to occur in healthy people at age 4 years, become fairly common by age 15 years, remain common
through age 35 years, and start to disappear by age 50 years. POSTS are seen very commonly on EEG and
have been said to be more common during daytime naps than during nocturnal sleep. Most characteristics of
POSTS are contained in their name. They have a positive maximum at the occiput, are contoured sharply, and
occur in early sleep (stages I and II). Their morphology classically is described as "reverse check mark," and
their amplitude is 50-100 µV. They typically occur in runs of 4-5 Hz and are bisynchronous, although they may
be asymmetric. They persist in stage II sleep but usually disappear in subsequent stages.
Vertex sharp transients
Also called vertex waves or V waves, these transients are almost universal. Although they often are grouped
together with K complexes, strictly speaking, vertex sharp transients are distinct from K complexes. Like K
complexes, vertex waves are maximum at the vertex (central midline placement of electrodes [Cz]), so that,
depending on the montage, they may be seen on both sides, usually symmetrically. Their amplitude is 50-150
µV. They can be contoured sharply and occur in repetitive runs, especially in children. They persist in stage II
sleep but usually disappear in subsequent stages. Unlike K complexes, vertex waves are narrower and more
focal and by themselves do not define stage II.
Hypnagogic hypersynchrony
Hypnagogic hypersynchrony (first described by Gibbs and Gibbs, 1950) is a well-recognized normal variant of
drowsiness in children aged 3 months to 13 years. This is described as paroxysmal bursts (3-5 Hz) of high-
voltage (as high as 350 µV) sinusoidal waves, maximally expressed in the prefrontal-central areas, that brake
after the cerebral activity amplitude drops during drowsiness.

The importance of normal sleep patterns is that they should not be mistaken for pathologic sharp waves. Several
normal stage I patterns easily can be mistaken for epileptic sharp waves or spikes, including vertex sharp
transients, POSTS, and even fragments of alpha rhythm as it drops out.
Caption: Picture 1. EEG atlas: normal sleep EEG - stage I. The earliest indication of transition from
wakefulness to stage I sleep (drowsiness) is shown here and usually consists of a combination of (1) drop out of
alpha activity and (2) slow rolling eye movements.
Picture Type: Photo

Caption: Picture 2. EEG atlas: normal sleep EEG - stage I. Slow rolling (lateral) eye movements during stage I
sleep. Like faster lateral eye movements, slow ones are best seen at the F7 and F8 electrodes, with the corneal
positivity indicating the side of gaze.
Picture Type: Photo

Caption: Picture 3. EEG atlas: normal sleep EEG - stage I. On this transverse montage, typical vertex sharp
transients are seen. In contrast to K complexes, these are narrow (brief) and more focal, with a maximum
negativity at the mid line (Cz and to a lesser degree Fz). These are seen in sleep stages I and II.
Picture Type: Photo

Caption: Picture 4. EEG atlas: normal sleep EEG - stage I. Vertex waves are focal sharp transients typically
best seen on transverse montages (through the midline) and would be missed on this longitudinal bipolar
montage if it did not include midline channels (Fz-Cz-Pz). Vertex waves are seen in sleep stages I and II.

Picture Type: Photo

Caption: Picture 5. EEG atlas: normal sleep EEG - stage I. Positive occipital sharp transients of sleep (POSTS)
are seen in both occipital regions, with their typical characteristics contained in their name. They also have
morphology classically described as “reverse check mark” and often occur in consecutive runs of several
seconds, as shown here.
Picture Type: Photo

Caption: Picture 6. EEG atlas: normal sleep EEG - stage I. PowerPoint presentation of Images 1-5.
Click to see detail
● Aserinski E, Kleitman N: Two types of ocular motility occurring in sleep. J Appl Physiol 1955; 8: 1-10.
● Benbadis SR, Perry MC, Wolgamuth BR, et al: The multiple sleep latency test: comparison of sleep onset criteria. Sleep 1996 Oct;
19(8): 632-6[Medline].
● Chatrian GE, White LE Jr, Daly D: Electroencephalographic patterns resembling those of sleep in certain comatose states after
injuries to the head. Electroencephalogr Clin Neurolphysiol 1963; 15: 272-280.
● Gibbs FA, Gibbs EL: Atlas of Electroencephalography. Normal Controls. Vol 1. Cambridge, Mass: Addison-Wesley; 1950.
144.
Apr; 20(4): 431-42[Medline].
NOTE:

EEG Atlas: Normal Sleep EEG - Stage I excerpt

eMedicine - EEG Atlas: Normal Sleep EEG - Stage II : Article by Selim R Benbadis, MD
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Stage II Email to a Colleague Descriptions
Synonyms and related keywords: K complex, sleep spindle, sleep stages Bibliography
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Loomis provided the earliest detailed description of various stages of sleep in the mid 1930s, and in the early
Stage II is the predominant sleep stage during a normal night's sleep. The distinct and principal EEG criterion to
establish stage II sleep is the appearance of sleep spindles or K complexes. The presence of sleep spindles is
necessary and sufficient to define stage II sleep. Another characteristic finding of stage II sleep is the
appearance of K complexes, but since K complexes typically are associated with a spindle, spindles are the

defining features of stage II sleep. Except for slow rolling eye movements, all patterns described under stage I
persist in stage II sleep (see EEG Atlas: Normal Sleep EEG – Stage I).
Representative examples of the waveforms described here are shown in the images at the end of this article.
Sleep spindles normally first appear in infants aged 6-8 weeks and are bilaterally asynchronous. These become
well-formed spindles and bilaterally synchronous by the time the individual is aged 2 years. Sleep spindles have
a frequency of 12-16 Hz (typically 14 Hz) and are maximal in the central region (vertex), although they
occasionally predominate in the frontal regions. They occur in short bursts of waxing and waning spindlelike
(fusiform) rhythmic activity. Amplitude is usually 20-100 µV. Extreme spindles (described by Gibbs and Gibbs)
are unusually high-voltage (100-400 µV) and prolonged (>20 s) spindles located over the frontal regions.
K complexes (initially described by Loomis) are high amplitude (>100 µV), broad (>200 ms), diphasic, and
transient and often are associated with sleep spindles. Location is frontocentral, with a typical maximum at the
midline (central midline placement of electrodes [Cz] or frontal midline placement of electrodes [Fz]). They occur
spontaneously and are elicited as an arousal response. They may have an association with blood pressure
fluctuation during sleep.
The stigmata of stage II sleep, spindles and K complexes, are usually easy to identify and are less subject to
overinterpretation or misinterpretation than the patterns of stage I sleep.
Caption: Picture 1. EEG atlas: normal sleep EEG - stage II. PowerPoint presentation.
Click to see detail
Caption: Picture 2. EEG atlas: normal sleep EEG – stage II. This shows a K complex, typically a high-
amplitude long-duration biphasic waveform with overriding spindle. This is a transverse montage, which shows
the typical maximum (manifested by a "phase reversal") at the midline.
Picture Type: Photo

Caption: Picture 3. EEG atlas: normal sleep EEG – stage II. Typical sleep spindles with short-lived waxing and
waning 15-Hz activity maximum in the frontocentral regions. Note the associated slow (theta) activity that also
characterizes stage II sleep.

Picture Type: Photo

Caption: Picture 4. EEG atlas: normal sleep EEG – stage II. Vertex sharp transients. This transverse montage
illustrates the maximum negativity (manifested by a negative phase reversal) at the midline. The location is
similar to that of K complexes, but these are shorter (narrower) and more localized.
Picture Type: Photo

Caption: Picture 5. EEG atlas: normal sleep EEG - stage II. K complex, with its typical characteristics: high-
amplitude, widespread, broad, diphasic slow transient with overriding spindle. On the longitudinal montage
(left), the K complex appears to be generalized. However, the transverse montage clearly shows that the
maximum (phase reversal) is at the midline (Fz and Cz).
Picture Type: Photo

Caption: Picture 6. EEG atlas: normal sleep EEG - stage II. A mixture of spindles (ie, bicentral short-lived
rhythmic 14 Hz bursts) and positive occipital sharp transients of sleep (POSTS) can be seen. POSTS occur in
stage I, but the presence of spindles is “diagnostic” of stage II.
Picture Type: ECG

Caption: Picture 7. EEG atlas: normal sleep EEG - stage II. A mixture of positive occipital sharp transients of
sleep (POSTS) and spindles (fronto-central short-lived rhythmic 14-Hz bursts) can be seen.

Picture Type: Photo

● Aserinsky E, Kleitman N: Two types of ocular motility occurring in sleep. J Appl Physiol 1955; 8: 1-10.
● Cote KA, de Lugt DR, Langley SD, et al: Scalp topography of the auditory evoked K-complex in stage 2 and slow wave sleep. J Sleep
Res 1999 Dec; 8(4): 263-72[Medline].
● Gibbs EL, Gibbs FA: Extreme spindles: correlation of electroencephalographic sleep pattern with mental retardation. Science 1962;
138: 1106-1107.
● Hughes JR: Sleep spindles revisited. J Clin Neurophysiol 1985 Jan; 2(1): 37-44[Medline].
● Jankel WR, Niedermeyer E: Sleep spindles. J Clin Neurophysiol 1985 Jan; 2(1): 1-35[Medline].
● Loomis AL: Harvey EN and Hobart GA Cerebral states during sleep, as studied by human brain potentials. J Exp Psychol 1937; 21:
127-144.
● Monstad P, Guilleminault C: Cardiovascular changes associated with spontaneous and evoked K- complexes. Neurosci Lett 1999
Mar 26; 263(2-3): 211-3[Medline].
● Naitoh P, Antony-Baas V, Muzet A, et al: Dynamic relation of sleep spindles and K-complexes to spontaneous phasic arousal in
sleeping human subjects. Sleep 1982; 5(1): 58-72[Medline].
NOTE:
EEG Atlas: Normal Sleep EEG - Stage II excerpt

eMedicine - EEG Atlas: Normal Sleep EEG - Stages III and IV : Article by Selim R Benbadis, MD
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Stages III and IV Email to a Colleague Descriptions
Synonyms and related keywords: delta sleep, delta waves, sleep stages, slow wave sleep, SWS Bibliography
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patient education.
Total sleep time in the healthy young adult approximates 7.5-8 hours. In the full-term newborn, sleep cycles last
approximately 60 minutes (50% NREM, 50% REM, alternating through a 3-4 h interfeeding period). The
newborn sleeps approximately 16-20 hours per day; these numbers decline to a mean of 10 hours during
childhood.

Stages III and IV usually are grouped together as “slow wave sleep” or “delta sleep.” Slow wave sleep (SWS)
usually is not seen during routine EEG, which is too brief a recording. However, it is seen during prolonged (>24
h) EEG monitoring. Representative examples of SWS EEGs are shown in the images at the end of this article.
Men aged 20-29 years spend about 21% of their total sleep in SWS, those aged 40-49 years spend about 8% in
SWS, and those aged 60-69 spend about 2% in SWS (Williams et al, 1974). Notably, elderly people's sleep
comprises only a small amount of deep sleep (virtually no stage IV sleep and scant stage III sleep). Their total
sleep time approximates 6.5 hours.
SWS is characterized by relative body immobility, although body movement artifacts may be registered on
electromyogram (EMG) toward the end of SWS.
SWS, or delta sleep, is characterized, as the name implies, by delta activity. This typically is generalized and
polymorphic or semirhythmic. By strict sleep staging criteria on polysomnography, SWS is defined by the
presence of such delta activity for more than 20% of the time, and an amplitude criterion of at least 75 µV often
is applied.
The distinction between stages III and IV is only a quantitative one that has to do with the amount of delta
activity. Stage III is defined by delta activity that occupies 20-50% of the time, whereas in stage IV delta activity
represents greater than 50% of the time. Sleep spindles and K complexes may persist in stage III and even to
some degree in stage IV, but they are not prominent.
As mentioned above, SWS usually is not seen during routine EEG, which is too brief a recording. However, it is
seen during prolonged EEG monitoring. One important clinical aspect of SWS is that certain parasomnias occur
specifically out of this stage and must be differentiated from seizures. These “slow wave sleep parasomnias”
include confusional arousals, night terrors (pavor nocturnus), and sleep walking (somnambulism).
Caption: Picture 1. EEG atlas: normal sleep EEG – stages III and IV. Slow wave sleep with predominantly delta
activity, especially in the first half.
Picture Type: Photo

Caption: Picture 2. EEG atlas: normal sleep EEG – stages III and IV. Slow wave sleep with predominantly delta
activity.

Picture Type: Photo

Caption: Picture 3. EEG atlas: normal sleep EEG – stages III and IV. PowerPoint presentation of pictures 1-2
Click to see detail
● Aserinski E, Kleitman N: Two types of ocular motility occurring in sleep. J Appl Physiol 1955; 8: 1-10.
● Daly DD, Pedley TA: Current Practice of Clinical Practice of Electroencephalography. 2nd ed. New York: Raven Press; 1990: 574-
575.
144.
Apr; 20(4): 431-42[Medline].
● Williams RL, Karacan I, Hursch CJ: EEG of Human Sleep: Clinical Applications. New York: John Wiley & Sons; 1974.
NOTE:
EEG Atlas: Normal Sleep EEG - Stages III and IV excerpt

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EEG Atlas: EEG Artifacts (CME available)

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PHYSIOLOGIC ARTIFACTS Section 3 of 6

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Muscle (electromyogram) activity

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millisecond delay after ECG equals QRS complex).

EXTRAPHYSIOLOGIC ARTIFACTS Section 4 of 6

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Alternating current (60-Hz) artifact

Movements in the environment

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