Review of Clinical EEG

Review Of Clinical
Electroencephalography
G.R.Shamsaei
Assistant Professor of Neurology
Jundishapour University of Medical Sciences
Foreword
Thanks God helped me to gather this collection in a electroencephalo-graphy as well as neurology

book. In fact this book contains a series of residents. It is hoped that this book contains sufficient
electroencephalography teaching classes for neurology encyclopedic and practical information on
residents. Of course ,it is gathered from many electroencephalo-graphy so that my colleages will
references and many lectures about EEG, which some find it an invaluable companion.
of them are mentioned at the end of the book. It is
necessary to acknowledge all those ones who
encouranged me, special my dear professor Dr.
pakdaman for his emotional support. This book is G.R Shamsaei
written primarily for clinicians who interpret
iii
Introduction
Electroencephalography is the neurophysiologic Many technical advances have been made in

measurement of the electrical activity of the brain by recording the electrical activity of the brain.
recording from electrodes placed on the scalp, or in Extended tracings lasting hours or days are now
the special cases on the cortex. The resulting traces possible. Radiotelemetry allows the patient to move
are known as an electroencephalogram (EEG) and about in a restricted area while his brain activity is
represent so-called brainwaves. This device is used being recorded. The use of television has improved
to assess brain damage, epilepsy, sleep disorders and the encephalographer,s ability to compare the
other problems. In some jurisdictions it is used to patient,s clinical condition with his or her EEG
assess brain death. Some investigators claim that the activity. The use of cortical and depth electrodes has
EEG can be used to predict abnormal development made it possible to define epileptic foci not seen on
and aid in the evaluation of nonspecific symptoms conventional tracings. It has always been clear to
such as behavioral disorders, anxiety, or learning electroencephalographers that the EEG is a
disabilities. On the other hand, by the addition of the physiological recording that is related to the
averaging computer,electrical potential recording has functioning of large groups of neurons, the
been extended to the whole class of evoked or event- interpretation of which is directly related to the
related potentials,thus improving the clinician,s clinical history. The development of radiologic
ability to diagnose multiple sclerosis and lesions techniques, such as CT or MRI , has served to
located in the optic nerve, brain stem, emphasize the limitations of the EEG as an
cerebellopontine angle, and spinal cord. Finally, instrument for anatomic localization.
EEG can also be used in conjunction with other types
of brain imaging.
v
Physiologial basis of the EEG
Electroencephalographic signals are generated by the directly from disruption of cortical neural networks or
cerebral cortex. Spontaneous electroencephalographic indirectly from modification of subcortical inputs onto
activity is a reflection of currents flowing in the cortical neurons.
extracellular space. These currents are generated by the EEG is not the same as electrocorticography
summation of excitatory and inhibitory synaptic because not all potentials recorded at the cortical
potentials occurring on thousands or even millions of surface are detectable at the scalp. In the case of
cortical neurons. Individual action potentials do not epileptiform activity, it has been estimated that 20-70%
contribute directly to electroencephalographic activity. of cortical spikes do not appear on the
Conventional EEG is a continuous graph of the spatial electroencephalogram, depending on the region of
distribution of changing voltage fields at the scalp cortex involved. This is largely because of the
surface recorded over time that result from ongoing pronounced voltage attenuation that occurs in
synaptic activity in the underlying cortex. In addition overlying cerebrospinal fluid and dura. Large areas of
to reflecting the spontaneous intrinsic activities of cortex must be involved in similar activity for a
cortical neurons, EEG depends on important afferent discharge to appear on the electroencephalogram.
inputs from subcortical structures, including the Furthermore, potentials involving surfaces of gyri are
thalamus and brainstem reticular formation. For recorded more readily than are potentials arising in the
example, thalamic afferents probably are responsible walls and depths of sulci. Activity generated over the
for entraining cortical neurons to produce the rhythmic lateral convexities of the hemispheres is recorded more
oscillations that characterize such normal patterns as accurately than is activity coming from
the alpha rhythm and sleep spindles. Similarly, an interhemispheric, mesial, or basal areas.
electroencephalographic abnormality may result
vii
History of Electroencephalography
Historical background discovery basic to the use of evoked potentials in

today,s clinical neurology.
• From the time of the ancients to 18th century,
electricity was regarded as a strange invisible
power.
• Gradually the role of electricity in relation to the
nervous system was to emerge,first from
observation of the effect of applying it to the
body,and eventually from the discovery that many
tissues such as muscle and nerve could themselves
be sources of this power.
• Luigi galvani, an italian physiologist(1780), was
the first one who showed that the contraction of
the frog,s leg was caused by electricity originating
in the animal tissues themselves.
• Du bois-reymond(a German physiologist) in 1848
showed normal electrical potentials recorded from
surface of a muscle on contraction.It was what we
now know as the action potential of nerve and is
the basis of electroneurography. With Du bois-
Reymond,s demonstration of this in man,
electromyography was born. When, in 1850,
Helmholtz designed an instrument for measuring
the conduction velocity of nerve.
• Richard Caton(1874) in England concluded that in
the brain also this phenomenon should be
occurred. He not only detected these electrical Fig-1 Richard Caton
potentials but noticed that when both of his
electrodes lay on the cortical surface there was a
continuous waxing and waning of potential. This • But the first one who showed the electrical activity
oscillation of the baseline was present in the of brain in human was a German psychiatrist as
unstimulated animal brain and Caton proved it to named Hans Berger. He named this activity as
be unrelated to respiratory or cardiac rhythms. He electro-enkephalogram. He had found not only
also proved these fluctuations to be biologic in the EEG but also described various waves of
origin by showing them to be vulnerable to anoxia brain. He also described different patterns of EEG
and to anesthesia and to be abolished by the death in various pathology such as epilepsy,trauma and
of the animal. He also had found the cerebral tumors.
potential change evoked by sensory stimulation, a
ix
Fig-2 Hans Berger
Among many research interests in neurology, attached to the head by a rubber bandage. As a
Berger studied brain circulation,and psychophysiology. recording device he first used the Lippmann capillary
However his main contribution to medicine and electrometer, but results were disappointing. He then
neurology was the systematic study of the electrical switched to the string galvanometer and later to a
activity of human brain and the development of double-coil Siemens recording galvanometer, which
electroencephalography (EEG), following the allowed him to record electrical voltages as small as
pioneering work done by Richard Caton (1842-1926) one ten thousandth of a volt. The resulting output, up to
in England with animals. In 1924, Berger made the three seconds in duration, was then photographed by an
first EEG recording in man. Using the EEG he was assistant.
also the first to describe the different waves or rhythms
which were present in the normal and abnormal brain,
such as the alpha wave rhythm (8-12 Hz), also known
as Berger's wave; and its suppression (substitution by
the faster beta waves) when the subject opens the eyes
(the so-called alpha blockade). He also studied and
described for the first time the nature of EEG Fig-3 The first EEG recording, obtained by Hans Berger in
alterations in brain diseases such as epilepsy and 1929
tumors.His method involved inserting silver wires
under the patients scalp, one at the front of the head
and one at the back. Later he used silver foil electrodes
x
CONTENTS
Introduction Chapter 7
Physiological basis of the EEG................................vii Activation procedures................................................75
History of electroencephalography...........................ix
Chapter 1 Part Two

Principles in recording of EEG...................................1 Abnormal EEG patterns…..........................................83
Chapter 2
Techniques of EEG recording....................................5 Chapter 8
Special electrodes……………..……………………..9
Derivations………………………………………..…10 Epileptic discharges....................................................85
Montages ……...……………………….…………....10
Polarity conventions…………………...................…11
Methods of derivation…………………..…………..13
Chapter 9
Electroencephalography in common epileptic
Chapter 3 syndromes...................................................................97
Localization and polarity............................................15

Chapter 10
Epileptiform normal variants....................................125
Chapter 4
Normal adult EEG.......................................................23
Chapter 11
Nonepileptic abnormalities.......................................139
Chapter 5 Abnormalities of the background rhythms............139
Abnormal sleep patterns..........................................145
EEG artifacts..............................................................39 Focal or generalized slow activity.........................147
Abnormal periodic patterns.....................................166
Chapter 6 Chapter 12
Normal sleep EEG......................................................59 Reading and reporting EEG...................................179
xi
Chapter 1
Principles in Recording of EEG
Before describtion of normal EEG some basic 7µV/mm will produce a pen deflection of 1mm or
principles of recording of an EEG should be noticed: an input voltage of 70µV/mm, a pen deflection of
1. First it should be emphasized that a cooperative and 10mm or 1cm. If high amplitude potentials appear
relaxed patient is essential for an ideal EEG study. during recording so that the pens are
An intelligent and trained technician can often overloaded(making a square top), the sensitivity is
obtain maximum cooperation and relaxation even reduced to 10 or 15 so that the wave form of the
from difficult patient such as children or subjects activity can be recognized or vise versa. It should be
who are emotionally disturbed. During electrode kept in mind, that a sensitivity of 2 or 5µV/mm is
placement, the technician should converse with the higher than 7. For example, a 20µV/mm EEG
patient in a friendly manner, asking questions about potential will have a pen deflection of less than
his symptoms and assuring him about the painless 3mm on 7µV/mm setting but 10mm on 2µV/mm
nature of the test.The actual recording should be setting. Some situations that we have a very high
carried out with the subject in the supine position. voltage potentials are:
A bed or a soft easy chair may be used for this i) Infant who have frequent myoclonic jerks may
purpose. have very high amplitude irregularly mixed
2. EEG paper : slow and sharp activity in the EEG, often
In EEG paper the horizontal axis is time and called hypsarrhythmia pattern.
vertical axis is amplitude. This paper is divided by ii) Patients in "petit mal status"(absence
some darker and some lighter lines. The distance status)may show almost continuous high
between two darker lines is 30mm. This vertical voltage 3cps spikewave activity in the EEG.
distance is further subdivided into five equal iii) patients with altered mental state due to
parts(6mm each)by four lighter lines, each encephalitis or various encephalopathies may
subdivision therefore representing 0.2second or show almost continuous high voltage very
200millisecond. slow(delta) activity.
Rarely high amplitude activity may appear in

Instrument settings periodic bursts,typically seen in subacute sclerosing
panencephalitis. In this condition high amplitude slow
Each electroencephalograph has some main controls wave complexes occur every 4-15 seconds throughout
which are: most of the recording, synchronous with body jerks.
a) Sensitivity: sensitivity of system is the magnitude of Using higher sensitivities will be necessary to study the
input voltage required to produce a unit pen low voltage activity, such as the EEG study for
deflection. It is usually denoted as microvolts (µV) determination of cerebral death or electrocerebral
per mm. Common values of sensitivity used in silence. It cannot be overemphasized that any change
routine EEG is 7µV/mm in adults and 10µV/mm in in the sensitivity setting should be noted on the record.
children. This means that an input voltage of
2 Review Of Clinical Electroencephalography
Fig- EEG with high sensitivity(7µV/mm)
Fig-(continued)The same EEG with lower sensitivity(15µV/mm) Note decrease in amplitude in lower sensitivity
Principles in Recording of EEG 3
perfectly aligned. This is of utmost importance if

b) Paper speed:
the phase relationship of an activity(e.g spike)in
two different areas has to be meaningful.
Most EEG instruments have at least three paper speeds, III. The space between the channels should be exactly
15,30 and 60mm/second. EEG records are equal. If one pen is closer to another (above or
conventionally run on a chart speed of 30mm/sec. At below), the mechanical baseline zero for this pen
this speed a distance of 3cm or 30mm, which exists will have to be adjusted so that all the pens should
between two successful dark vertical lines on the EEG be equidistant from the adjoining ones.
paper represents 1 second. This vertical distance is
further subdivided into five equal parts(6mm each)by At the end of the record, calibration should be
four lighter lines, each subdivision therefore performed again at each of the instrument settings of
representing 0.2second or 200millisecond. the amplification and frequency filters used during the
Higher speed than usual (60) and lower speed(15) recording.
is used in special situation, such as use of high speed in
paroxymal activity for distinction between primary or
secondary activity, and low speed in situation such as
periodic phenomena or low amplitude and intermittent
slow activity. Any deviation from the normal paper
speed should be noted on the record at the time the
change is made.
c) Calibration :
In the onset of every EEG study a calibration signal is

recorded a few times simultaneously in all channels.
Calibration consists of recording the response of the Fig- Calibration deflections in response to three
EEG to a known value of square-wave signal. The signals but with a constant sensitivity. Only the
value of the calibration signal should be according to center calibration has a deflection in a range where
the sensitivity. The calibration signal should usually the pen is not exceeding its limit but is large enough
produce a pen deflection of 5-10mm. Because we for easy and accurate measurement.
commonly use sensitivity of 7 or 10µV/mm , a
50µV/mm calibration signal may be used which should d) EEG filtering:
produce a pen deflection of 7.1mm or 5mm
respectively. It is important that after the calibration Because sensitivity of the recording in EEG instrument
knob has been released to discontinue the calibration are very high, so we have a large series of unwanted
signal, the knob should be pushed in again to record waves such as electricity from scalp muscles, heart ,
another calibration signal only after the pens have and eye muscles. At the other hand, we have many
returned to baseline. Too rapid on-off-on would nonphysiologic waves that originate from media and
overload the pens and the calibration could be electrical instruments. In general,the aims of using of
inaccurate.After calibration signal has been recorded these filtering in EEG instrument are attenuate certain
on all channels,the following should be carried out: frequency component of a signal leaving other
frequencies unaffected. There are two main filtering,
I. Measure the pen deflection for the calibration depending on whether the low or high frequencies are
signal for each channel and make adjustment so affected, the low frequency filter(L.F.F) and high
that each channel responds equally and frequency filter(H.F.F).
appropriately to the signal. In channels showing Low frequency filter(L.F.F): these filters,
less or more deflection, the sensitivity of the control the response of the instrument to lower
amplifier may have to be adjusted to obtain same frequencies while the response to higher frequencies
pen deflection in all channels. remains unaffected.
II. The time axis alignment of all pens should be High frequency filter(H.F.F): these filters
equal. If one or more pens lead or lag behind the attenuate the very high frequencies while the lower
others on the time axis, an adjustment of these frequencies remain unaffected.
pens have to be carried out so that all the pens are
Fig- Note the effect of (H.F.F) on EEG
Fig- Another example of filtering EEG
Duration of recording: the chance of detecting a sample in time from a patient,s life- a very short
specific abnormality is directly proportional to the total sample indeed. Considering this serious limitation, the
recording time. This is especially true of paroxysmal high percentage of epileptiform abnormalities seen in
disorders such as epilepsy. Not less than 15-20 minutes epileptics makes the procedure amazingly valuable
of recording should be made for awake tracing. If the
subject falls asleep an additional 10 minutes of
recording during drowsiness and light sleep should be
obtained. One should remember that the EEG is a
Chapter 2
Techniques of EEG recording:

Electrode placements
When EEG was first carried out on human by Berger, different patients could be compared to each other.
electrodes were placed on the front and back of the There was very wide diversity from place to place in
head and used to record over a number of years; Berger established methods and standard placements. A
viewed much of what he saw as a measure of global committee of the international federation of societies
cortical activity. It was soon discovered by others that, for electroencephalography and clinical
in fact, EEG activity varied in different locations on the neurophysiology recommended a specific system of
head. In 1930,s, as the number of laboratories electrode placment for use in all laboratories under
investigating EEG increased, there was a rapid standard conditions. Their recommendation was the
proliferation of techniques and interpretations of the system now known as the international 10-20 system.
activity recorded and multiple channels allowed Specific measurments from bony landmarks are used to
investigators to record simultaneously from multiple determine the placement of electrodes. Many of the
scalp areas. These observations were in turn followed systems had done this earlier, but they generally used a
by increased attempts to place electrodes at points specific standard interelectrode distance on every
where they might particularly enhance the observation patient. The breakdown of such a system is apparent if
of one or another type of activity that occurred. the application of electrodes to a microcephalic patient
The observation that simultaneous different is compared to application to a hydrocephalic patient
types of activity was occuring in turn encouraged the using the same number of centimeters from landmark
use of more electrodes for more channels of locations or between electrodes.
simultaneous recording. This was followed by attempts
to place electrodes in a standardized manner so that a
patient,s record could be compared over time and
Fig-International 10-20 system placement. Odd number on the left, even on the right, and Z or zero in the midline.
In 1958 the 10-20 system of electrode placement

was established by electroencephalographers
wanting a standard format and common
terminology for electrode locations on the scalp.
The establishment of the International 10-20
System made it possible for
electroencephalographers to not only compare
their patients' serial EEG tracings but allowed for
comparisons between labs in different hospitals,
in different cities and even in different countries.
The initial recommendation was made at the
International Congress of Electroencephalography
and Clinical Neurophysiology in London in 1947
Techniques of EEG recording: Electrode placements 7
The International 10-20 System of Electrode Placement is

a standard procedure for the measured location of equally
spaced electrode positions on the scalp, using identifiable
skull landmarks as reference points. The system allows
for differences in skull sizes by using percentages, either
10% or 20% of the measurements between the landmarks
on the skull. The system is based on the proven
relationship between a measured electrode site and
underlying cortical structures.
The nasion, inion and the two preauricular points are the 4
landmarks on which the 10-20 System is based.
The nasion is the indentation between the forehead and the
bridge of the nose.
The inion is the protrusion of the skull which can be felt as
you run your finger up the neck to the base of the skull.
Individual anatomy may differ slightly and occasionally
the inion is difficult to locate. When a protrusion is not
felt at the inion sight, locate the inion at the same level as
the preauricular points
Fig- Relationship of 10-20 system electrode positions to

the lobes of the brain.
The international 10-20 system of electrode reflect the electrical activity over similar brain areas in
placement is already standard in all EEG laboratories different patients.
worldwide. It is supported by anatomic studies.
Although the actual distance between electrodes varies
with the size and shape of the skull, these electrodes
Alphabetical and Numerical Nomenclature to identify electrodes
The 10-20 System assigns an alphabetical abbreviation to identify the location of the electrode with a particular
lobe or area of the brain under the electrode placement. The alphabetical abbreviations are as follows:
Fp = Frontal Polar
F = Frontal
T = Temporal
C = Central
P = Parietal
O = Occipital
A = Auricular (ear lobes)
M = Mastoid (sometimes used as a substitute for ear lobes, as a reference electrode)
Pg = Nasopharyngeal (These are optional electrodes for recording from the medial aspect of temporal lobe. Placed through the
nostril, the tip resting at the roof of the nasopharynx the tip of the electrode is near the anterior mesial surface of the temporal
lobe and is thought to record from that area).
Technique
The 10-20 system is so named because it divides each length of the line, giving a total of 21 positions. Each
of three lines connecting skull landmarks into segments position is named; it is given both an abbreviation,
the length of which is 10% and 20% of the whole line. such as(Fp) for frontal polar, and a subscript number,
The baselines are the sagittal distance from nasion to such as Fp1(left frontal polar). Odd numbers designate
inion, the horizontal distance from the frontal polar electrodes placed over the left hemisphere, and even
midline(Fpz)to the occipital midline(Oz), and the numbers those placed over the right hemisphere. The
transverse distance from the left to the right subscript Z indicates a midline position, for example
preauricular depression. Electrodes are located along Fz(frontal midline). The left and right ears are
each line at intervals of 10% and 20% of the entire respectively labeled A1 and A2(auricular).
Fig- The term 10-20 is used because the electrodes are placed either 10% or 20% of the total distance between a
given pair of skull landmarks.
Numerical System to further specify location
Brain Area Left Midline Right

Frontal Pole Fp1 Fpz Fp2
Frontal F3 Fz F4
Inferior Frontal F7 F8
Anterior Temporal T1 or F9 T2 or F10
Mid-Temporal T3 T4
Posterior Temporal T5 T6
Central C3 Cz C4
Parietal P3 Pz P4
Occipital O1 (Oz) O2
The 10-20 System assigns a number to further specify the location in the left or right hemisphere. The
"z" is used to indicate that the location of the electrode is in the midline or "zero" meaning that it is
neither left hemisphere or right hemisphere.
* The electrode placed at Cz is said to be the "Vertex" meaning that it is the Mid Central or at the top of
the head.
* Fpz and Oz are not standard placements but are used in achieving the other measurements and can be
used as additional electrode placements for localization of activity. Fpz is sometimes used as the
location of the COM (common) or ground electrode placement.
Special electrodes
The electrical activity of certain portions of the
cerebral cortex, notably the basomedial parts of the
temporal lobe and the orbital and medial parts of the
frontal lobe, is not accessible to the electrodes taken up
thus far. This sometimes leads to problems in
accurately locating seizure foci, particularly in patients
who are being considered for temporal lobectomy. To
overcome such problems, a number of special
electrodes may be used.
T1 and T2 electrodes
The most commonly used additions to the 21 standard

derivations are the T1 and T2 electrodes. These are
located by first finding the point that is one third of the
way from the external auditory meatus to the outer
canthus of the eye, and locating a point 1cm directly Fig- Placement of T1 and T2 electrodes. As you see,
above. T1 and T2 are closer to the anterior part of the From this surface electrode, electrical activity from the
temporal lobes than F7 and F8, which are actually anterior inferior tip of the temporal lobe can be
recorded. Patients with symptoms of temporal lobe
located over the inferior frontal area.
seizures should have these additional electrode
placements applied for routine EEG recordings.
Zygomatic electrodes Because two connections are needed to complete

an electrical circuit, two electrodes have to be
connected to each channel (amplifier)of the machine. A
These are located over the easily palpated zygomatic
particular pair of electrodes connected to a single
arch, below and anterior to the T1 and T2 electrodes.
amplifier is referred to as a derivation.
Zygomatic electrodes are useful for picking up activity
Experince has shown that a machine that displays
from the tips of the temporal lobes.
at least eight derivations simultaneously is necessary to
adequately study the spatial characteristics of the
brain,s electrical activity. However, the larger
Nasopharyngeal (NPG) electrodes machines and more derivations are capable of
gathering more data in the same amount of time as well
The tips of these electrodes are placed in contact with as providing better resolution of the spatial
the roof of the nasopharynx, so that activity from the characteristics of the brain,s electrical activity.
uncus, hippocampus, and orbitofrontal cortex may be With the use of 21 electrodes, one can have a total
picked up. of 210 different derivations. But in actual practice, all
possible combinations of electrodes are seldom used.
There is an important reason for this. Since
interpretation of the EEG ultimately involves
comparison of different derivations, it is essential to
use derivations having comparable interelectrode
distances. Indeed, most routine EEG only use a few
derivations.
Montages
The particular arrangements whereby a number of

different derivations is displayed simultanously in an
EEG record is termed a montage.
A large number of different montages can be
disgned. The main reason for using different montages
is to make EEG interpretation as easy and accurate as
possible. For this purpose, certain guidelines have to be
followed, and the american EEG society has given
some recommendations in this regard.
First of all, a montage should be simple and easy
to comprehend. Montages should follow some kind of
Fig- Basal view of the brain showing the
anatomical order or pattern. For example, channels
approximate locations of special electrodes
representing the more anterior electrodes should be
arranged on the recording chart above those from the
more posterior regions. Derivations from the left side
should be located on the chart above derivations from
the right side. This may be accomplished either by
Derivations alternating the derivations,i.e; left,right,left,right, and
so, or by placing derivations from the different sides in
With a total of 21 electrodes to work with, how should blocks,e.g; left,left,left,left; right,right,right,right. It is
the electrodes be arranged to best display the brain,s advantageous for a laboratory to use a few common or
electrical activity? In other words, what combinations standard montages so that records from different
of electrodes should be connected to the various laboratories can be compared with ease.
channels of the EEG machine?
Fig- montages for routine EEG
The American Electroencephalographic Society 5-Use simple montages that allow for easy
Guidelines in EEG, Evoked Potentials, and visualization of the spatial orientation of the
Polysomnography (1994) have made basic waveforms - for example, bipolar montages should
recommendations for montages as well as other be in straight lines with equal inter-electrode
technical aspects of performing routine EEG. These distances.
will be called the Guidelines, for the rest of this text.
6-Have the anterior and left-sided channels above the
The guidelines recommend the following:
posterior and right-sided channels.
1-Record at least 8 channels. 7-Use at least some montages that are commonly used
in other laboratories.
2-Use the full 21-electrode array of the 10-20 System.
3-Every routine recording session should include at
least one montage from each of the following
groups: referential, longitudinal bipolar, and
Polarity conventions
transverse bipolar.
4-Label each montage in the recording. The EEG study is essentially an attempt to record the
distribution of electric potentials on the scalp as they
fluctuate with time. It would have been a very simple or input1 (G1) and the other connected to the second
procedure if an area of zero electric potential was grid or input2(G2).
available on the body or elsewhere so that the electric Conventionally , the EEG amplifiers are so designed
potential at different electrodes on the scalp could have that whenever the G1 input of a channel is relatively
been easily measured with respect to this indifferent negative to G2, the pen of that channel deflects
electrode. Because such an ideal in different electrode upward. With the same token, when G1 is relatively
having zero potential does not exist, all EEG positive to G2 the pen moves downward.
measurements essentially indicate potential differences This concept is extremely important for the
between pairs of electrodes, rather than an absolute understanding of localization and polarity of a normal
electrical potential at any electrode position. or an abnormal cerebral activity. A few example are
Essentially each EEG amplifier is connected to two shown in the accompanying diagram (see below fig
electrodes on the scalp and it measures the potential A,B,C) showing the direction and amplitude of pen
differences between these two inputs. In other word, it deflection with varying inputs of grid 1 and grid 2.
has two sources of input, one connected to the first grid
Fig- Symbol for the differential amplifier
Fig- symbol for the differential

amplifier
Fig- Some examples of pen deflection with varing inputs

One should note that the pen deflection upwards of the
same magnitude occurs in th first two examples even
though the activity is electronegative in the first and
electropositive in the second example. In the first
example G1 is 80µV more negative than G2 whereas in
the second example G2 is 80µV more positive than
G1(or G1, 80µV less positive than G2), both producing
similar pen deflections.
Summarizing 3. If there is no deflection of the pen, again two

1. If pen moves upwards in a channel. One of the two possibilities exist:
possibilities exist: No activity at G1 and G2 or
G1 more negative than G2(example 1) or Equal activity at G1 and G2 (G1 and G2
G2 more positive than G1(example 2) equipotential, Example 5 ,6)
2. If pen moves downward in a channel, one of the More details on polarity and localization are described
two possibilities exist: in next chapter.
G2 more negative than G1(example 3) or
G1 more positive than G2(example 4)
Fig- According to the standard polarity convention, an

upward signal deflection results if input1(G1) is more
negative than input2(G2) or if input2(G2) is more positive
than input1(G1). Conversely, a downward signal deflection
results if input1(G1) is more positive than input2(G2) or if
input2(G2) is more negative than input1(G1).
Methods of derivation all because each channel is measuring the potential

There are essentially two methods of recording the difference between the scalp electrode (G1) and the
potential fields on the scalp. These are commonly reference electrode (G2). The latter electrode though
known as monopolar(or referential) and bipolar often called "inactive" or "indifferent" may have
derivations. appreciable normal or abnormal cerebral activity. In
In monopolar (referential) technique, one other words there is no true monopolar measuring
reference electrode is selected and the potential under device, all measurments are bipolar. Because of this the
other electrodes on the scalp is measured with respect best term for this technique is referential recording In
to this common reference electrode. Usually the scalp the bipolar technique, there is no common reference
electrodes are connected to G1 and the reference electrode for G2 of all channels. One measures the
electrode connected to G2 of the channels. The term potential difference between each pair of neighboring
monopolar is misleading because it may imply that in electrodes going serially in an anterior-posterior or
this technique one is measuring the absolute potential transverse planes.
under different scalp electrodes, but this is not true at
Fig- Examples of referential montages
Fig- Examples of bipolar montages

Chapter 3
Localization and Polarity
1-Referential or monopolar technique and A1 is connected to Grid 2. Remaining 3 channels

do not show any pen deflection(fig.A).
As mentioned in the previous chapter, the referential
recording involves the measuring of potentials under
different scalp electrodes as against one or two
reference electrodes which are usually so placed that
they are least contaminated with cerebral activity. The
scalp electrodes which are often referred to as "active"
electrodes are connected to Grid 1 of the input of each
channel and the common reference often called
"inactive" or "indifferent " electrode is connected to
Grid 2. The referential recording therefore attempts to
measure more or less local activity under different
scalp electrodes in a fairly "absolute" manner.
Various reference points have been used, the common
being left and right ear lobules, midcentral(Cz),
nose,chin,mastoid,neck,etc. One should bear in mind Fig-A
that whatever reference point is used, it can not and
never should be regarded as an "indifferent" or What can we say about the origin of this spike and
"inactive" point because it will be affected by cerebral its polarity? Because the spike is seen from the channel
activity to a variable extent. Noncephalic electrodes recording from FP1 and A1, the spike must arise at or
like the one placed on the neck is markedly "noisy" in close to either FP1 or A1. By looking to this channel
terms of EKG activity. Again, in spite of their distance alone, one cannot automatically say that the spike is
from the brain these noncephalic electrodes may pick definitely arising from FP1, it might very well
up appreciable activity arising from base of the brain. originate from an area close to A1 electrode. However
In the following discussion, it will become obvious that the fact that the lower three channels also having input
any one reference is not ideal for all cases. Use of from A1 do not record the spike would strongly favour
montages employing either simultaneously two or FP1 as the site of origin of the spike seen in channel 1.
more different references give more clarification There is also another possibility that spike might be
regarding localization than obtained by the use of a arising close to A1 but it is not recorded in the last 3
single reference. First let us study a few theoretical channels because spike potential in C3, T3 and O1 is
examples to explain how one may determine equipotential with A1. This , however, is an extremely
localization and polarity of an activity in referential remote possibility. The study of the activity
technique. simultaneously in 4 channels therefore suggests that
In the following example, there is a spike recorded spike is most probably originating under FP1 electrode.
in the first channel where FP1 is connected to grid 1 The next question is what is the polarity of the spike
potential. Once the location is known the polarity A1, the downward deflection in channel T3-A1 would
usually poses no problem. Because the spike potential suggest that T3 is more positive and more active than
is arising under FP1, which is connected to Grid 1 and A1. In other words the area of maximum
because the pen moves up, the spike potential is electropositivity is under the T3 electrode. It is then
surface negative. conceivable that the A1 electrode being quite close to
It is therefore obvious from this example, that in T3 is picking up the activity quite appreciably. In the
the study of any type of cerebral activity one has to first 3 channels(FP1-A1, C3-A1, and O1-A1), there is
first detrermine the localization of the activity before upward deflection of the pen because the relatively
correct conclusions can be drawn about its polarity. electropositive A1 electrode is connected to Grid 2 of
This working rule will be more clear in the next these 3 channels.
example shown in fig(B). The most logical and the correct interpretation of
the events in fig(B) can be summarized by stating that
there is a spike potential arising from left
midtemporal(T3) region, that it is surface positive in
polarity and that the potential fields spread to A1
therefore more positive than other electrodes on the left
side such as FP1, C3 and O1.
Fig(C) shows a very similar situation but in this
instant the spike is negative in polarity and originates
again in left midtemporal(T3) region.
Fig-B
Here the first three channels show upward deflection of

pens at the time of spike potential, but the 4th channel
shows downward pen movement. One may interpret
that there is a negative spike of widespread distribution
on the left side seen under FP1, C3 and O1 but a
posiotive spike at left temporal(T3) region. Fig-C
By looking at the first 3 channels, in which there is
upgoing spike, two interpretations are possible: The first 3 channels show downward deflection
I. That spike is arising in fairly diffuse manner over because it is the A1 in Grid 2 of these 3 channels which
left hemisphere, seen under FP1,C3, and O1, is most active and is relatively more negative. In the 4th
electrodes and that it is an electronegative spike and channel the spike deflects upward because T3 is more
that A1 electrode is relatively less active. active (and more negative)than A1. Again it is the
II. That the spike is arising close to A1 which is the negative spike recorded in all 4 channels though it
most active electrode in these three channels and deflects downward in the first 3 and upwards in the
that it is an electropositive spike. last channel.
In summary therefore , one should clearly remember
Now study the fourth channel which records that:
between T3 and A1 and shows a downgoing spike. If 1. upward deflection in a recording channel such as
the explanation (1) was correct that we are dealing with FP1-A1, doesnot automatically mean that it is an
an electronegative spike then downward deflection in activity of negative polarity and similarly a
T3-A1 channel would suggest that T3 is less negative downward deflection doesnot always mean a
than A1. In otherwords of the five electrodes positive activity.
FP1,C3,O1, T3and A1 the least negative(and least 2. if an activity is seen in a recording channel such as
active) in T3 which would be difficult to conceive FP1-A1, it cannot be simply assumed that the
considering that electrodes all around T3 are more activity is present exclusively under FP1. The
electronegative and also more active. activity may be present under A1 or under both FP1
Now consider the explanation (2) above. If we are and A1.
dealing with an electropositive spike arising close to
Localization and Polarity 17
3. In studying any cerebral activity, one should first sharp wave focus, say in left central (C3) with the
try to determine its location and then identify its potential field as shown in lower figure (FigD).
polarity The recording is made with the left sided scalp
electrodes connected to the left ear and the sensitivity
The application of referential technique to is set at 10µV/mm.
localization of cerebral potentials can be best explained
by taking an example of a surface negative spike or
Fig-D
In this example the left ear(A1)being quite farther

from the area of maximum activity(C3), picks up the 3- The distribution of the potential field can be judged
spike activity only very minimally, so that all the scalp by the relative magnitude of pen deflections in the
electrodes are more active than the left ear. This is an channels exploring the activity under different
ideal situation where the reference electrode is electrodes around the focus. In the above example
"contaminated" minimally or not at all by the cortical of 8 channel recording, one can say that the left
activity under study. One should note three points in central spike though spreads to FP1, F3, P3, O1,
the recording: T3, T5, and F7,but its spread is maximum antero-
posteriorly because F3 and P3 are more active than
1- In all channels, the spike is upgoing,i.e. the pens are T3.
deflecting in one direction. This is because at the
time of spike activity the Grid 1 of all channels The above ideal situation in which the reference
become more negative with respect to Grid 2(A1). electrode is least active is not always obtainable. No
2- The electrodes under which the spike is highest in matter where the surface electrode is placed, it may
amplitude is easily determined by the channel appreciably pickup the activity in question. Far
which shows the maximum pen deflection. reference electrodes may therefore pickup very
significant cerebral activity arising from the temporal
lobe thereby complicating the interpretation of a
recording using this ear as the reference. This can be
seen, if we move the hypothetical spike focus to say T3
region as shown in (Fig-E)and record again using A1
as the reference.
Fig-E
In this example the left ear electrode being close The situation may become even more complicated
to the T3 spike focus picks up very significant spike if the spike focus lies somewhat below the T3 electrode
activity. One notes that the pen deflection is not in the so that A1 is as active as T3 as shown in (Fig-F). Note
same direction in all channels. T3-A1 channel shows that there is a downward deflection in all channels at
upward deflection because T3 being at the peak of the the time of the spike discharge except in T3-A1
focus is more negative than A1. The channel F7-A1 do channel, which shows no pen deflection. There are
not show any pen deflection during spike activity,not obviously two possible interpretations of this situation:
because F7 and T5 are not active but because they are a. There, there is a spike discharge diffusely over left
equipotential with respect to A1. In the channels FP1- hemispherc leads but not at left midtemporal, and
A1, F3-A1, C3-A1, P3-A1 and O1-A1, the pens move that it is surface positive.
downward during spike activity because A1 connected b. That the spike focus is close to left temporal
to the Grid 2 of these channels is more active and more electrode and that A1 and T3 are equipotential and
electronegative with respect to the electrodes in Grid 1. that the spike is surface negative.
One should not interpret this situation saying that there These two interpretation are entirely opposite to each
is positive spike at FP1, F3, C3, P3 and O1 , negative other. The first interpretation though theoretically
spike at T3 and no spike at F7 and T5. The spike in all possible, is not likely because it will be difficult to
channels is negative in polarity irrespective of pen conceive of a potential field which would extend all
movement. By making a referential recording using over left hemisphere but would spare T3 area.
A2(which will be least contaminated by left Therefore the second possibility will be most likely and
hemisphere spike activity) as the reference, the above this could be proved by changing the reference to A2
facts can be easily varified. or CZ as shown in the same diagram.
Fig-F
From the above example, the following facts can but also with a temporal focus of slow activity
be summarized regarding a common referential when ipsilatertal ear is used as a reference. In the
recording: latter instance, apparently generalized slow
I. Where the common reference electrode picks up activity over one hemispheric derivations may
only minimal activity of interest, the situation is really be focal arising in the temporal region.
very ideal. Channels showing pen deflection will IV. In referential recording complete cancellation of
deflect in one direction. The channels receiving abnormality can occur over the temporal region if
from the electrode overlying the potential peak the ear close to the focal disturbance is used as a
will show largest pen deflection and the height of reference.
deflection in other channels will be proportional If above limitations and cautions are properly
to the magnitude of activity under the active understood one can derive very useful information
electrodes. Under these circumstances the polarity and avoid pitfalls in localization using common
is very easy to determine, if pen moves up, the referential recording.
activity is surface negative and vice versa.
II. During a common referential recording of a
transient or paroxysmal activity, if the pen 2-Localization in bipolar technique:
deflection in some channels are upward and in
others downward, one should be highly suspicious
In bipolar technique, the principles of localization are
of a "contaminated" or "hot" reference electrode.
outlined by five principles. These principles or rules
III. An activity seen in all channels in a common
are illustrated in the diagrams of (Fig-G) through (Fig-
referential recording may not necessarily be
M). In these diagrams, F(focus) is the point of
generalized activity, it may be on the other hand
abnormal negative electrical activity.
extremely focal arising at or close to the reference
electrode. This is particularly so if the waveform
Rule 1: If one of a pair of electrodes is at F, the
of the activity is very similar in all the channels.
amplitude of the recorded potential will increase as the
This is not only true with a temporal spike focus
distance between this electrode and the second
electrode of the pair increases. Thus in (Fig-G), the

distance FB is greater than FA; therefore, the Rule 4: If three electrodes are connected so that one is
amplitude of the voltage recorded between F and B is at F and is common to two recording channels, being
greater than the amplitude recorded between F and A. the grid 2 input of the first channel and the grid 1 of
In short, widely spaced electrodes record larger the second, the pen deflections in the two channels will
voltages than closely spaced electrodes. be in opposite directions. (Fig-J) shows this set of
conditions. The outputs of the two channels illustrate
what is meant by the term "phase reversal". Note that
the reversal results from the fact that the shared
electrode goes to opposing inputs and hence causes the
opposing deflections to occur. A phase reversal
identifies the electrode that is nearest to the point of
maximum voltage, or the focus.
Fig-G
Rule 2: Given two pairs of electrodes having equal

interelectrode distances, the potential recorded from
the pair having one electrode at F will be greater than
the potential recorded from the pair having neither
electrode at F. In Fig-H, the interelectrode distances
FA and AB are equal. The voltage recorded is greater
in channel 1 than channel 2 because one of the channel
1 inputs is connected to F. Fig-J
Rule 5: If two electrodes are equidistant from F, the

focus, no voltage will be recorded between them.
In FigK-(a) , B and C are equidistant from F and no
voltage is recorded from the "equipotential zone"
surrounding these two electrodes, which are the inputs
to channel 2. This outcome is an example of
cancellation.
Fig-H
An interesting, practical application of rule 5
Rule 3: The farther away the dipole is from the surface occurs in the case of the so-called "active ear", in
of the scalp, the smaller will be the potential observed which a focus is situated in the temporal area adjacent
at the surface and the smaller the voltage recorded to the ear. This is illustrated in FigK(b), where
between pairs of electrodes, interelectrode distances electrodes are placed in a coronal chain across the top
being constant. This rule is illustrated by two examples of the head, from left to right, starting with the
in (Fig-I). Note that the dipole in case 1 is nearer the electrode on the left earlobe. With the focus located
surface than it is in case 2 so that the voltage recorded midway between the earlobe and the midtemporal
by electrodes at F and A is greater in case 1 than in electrode , an equipotential zone is created about
case 2. electrodes P and Q so that no voltage is recorded
between the inputs of the channel 1 amplifier. The
deflection observed in channel 2 is larger than that in
channel 3 because Q is closer to the focus than R—a
corollary of rule 2.
Fig-I
Fig-K
FigL(a) shows a special case of rule 5. In this instance Fig-L

the focus F is not on the line joining electrodes A, B, C
and D but instead is to one side. Nevertheless, F is Another special case of rule 5 occurs when F is
equidistant from B and C so that the rule still holds. between two electrodes, but nearer to one than the
However, the exact position of F along the other. In such a case a voltage will be recorded
perpendicular from the midpoint of the line joining B between these two electrodes, but the voltage will be
and C cannot be determined using the configuration of less than it is when one of the electrodes is directly
electrodes shown in FigL(a). To locate the focus in this over F.
dimension, a chain of electrodes perpendicular to the
ABCD chain at the midpoint between B and C is
applied. This configuration is shown in FigL(b), where
the electrode at R happens to be directly over the focus
F. Note that there is a phase reversal at electrode R,
which by rule 4, localizes the focus to this electrode.
Fig-M
Chapter 4
Normal Adult EEG
The normal adult human EEG is comprised of patterns Neurophysiology (IFSECN) proposed the following
and wave forms that vary in frequency, amplitude, and definition of alpha rhythm:
location or distribution. EEG patterns may change with Rhythm at 8-13 Hz occurring during wakefulness over the
age, or with alterations in an individual's state of posterior regions of the head, generally with higher voltage
consciousness, for example, the transition from over the occipital areas. Amplitude is variable but is mostly
wakefulness to sleep. Extensive study of the human below 50 microV in adults. Best seen with eyes closed and
under conditions of physical relaxation and relative mental
EEG beginning in the early twentieth century has
inactivity. Blocked or attenuated by attention , especially
resulted in the discovery of numerous brain wave visual, and mental effeort(IFSECN,1974).
patterns present in normal adults, children, and
neonates. This chapter will discuss normal patterns of
wakefulness found in the adult EEG. Frequency
The story on EEG maturation shows the gradual

frequency increase of a posterior basic rhythm that is
Normal adult EEG detectable around the age of 4 months with a
frequency of approximately 4/sec. This posterior basic
Before recording, patient should be in resting rhythm shows a progressive frequency increase with
condition. Resting condition denotes that the person average values of around 6/sec at age 12 months and
has not been fasting and that he or she has not 8/sec at age 3years. At that time, the alpha frequency
consumed stimulants like coffee,tea,,or soft drinks band is reached, and there is justification for the use of
before the time the EEG is taken. It is the responsibility the term alpha rhythm. The frequency reaches a mean
of the technician to inform the patient of this at the of about 10/sec at age 10 years. This is essentially the
time the appointment is made for the EEG. mean alpha frequency of adulthood; in other words, the
Features of the awake EEG in adults progressive alpha rhythm acceleration usually ends
Electroencephalography (EEG) waveforms generally around the age of 10 years, but the second decade of
are classified according to their frequency, amplitude, life(and to some degree also the third decade) features
and shape, as well as the sites on the scalp at which a constant decline of intermixed posterior slow activity
they are recorded. The most familiar classification uses that is usually present in considerable quantity at age
EEG waveform frequency (e.g; alpha, beta, theta). 10. The frequency of the alpha rhythm tends to
decline in elderly individuals.
Alpha rhythm:
First described by BERGER in 1929 who named it

alpha. It is the most prominent feature of the normal
mature EEG. The international federation of societies
for Electroencephalography and clinical
moment to moment. Therefore, we should look for

stretches of optimal alpha output. A referential
montage to the ipsilateral ear is usually most suitable
for the determination of the alpha rhythm amplitude,
but the interelectrode distances must always be
considered. The maximum alpha voltage is usually
over the occipital region as such, but a bipolar montage
with a parasagittal array may obscure rather than reveal
Amplitude the true alpha maximum.
Alpha rhythm amplitudes vary considerably from

individual to individual and, in a given person, from
Fig- 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.
Generally Alpha rhythm amplitude vary from 20- Location

100µV; values above 100µV are uncommon in the
adult. There is good evidence of a mild to moderate The alpha rhythm is mainly located in the posterior
alpha amplitude asymmetry with higher voltage on the half of the head and is usually found over occipital,
right. The alpha amplitudes tend to show constant parietal, and posterior temporal regions.
waxing and waning.
Normal Adult EEG 25
Reactivity
with voltage reduction. Alpha attenuation due to other
The poterior alpha rhythm is temporarily blocked by an
stimuli (auditory, tactile, other somatosensory stimuli
influx of light(eye opening), other afferent stimuli, and
and mental activity) is usually less pronouced than the
mental activities. The degree of reactivity varies; it
blocking effect with eye opening.
may be completely blocked, suppressed, or attenuated
Reactivity of alpha rhythm to eye opening
Reactivity of alpha rhythm with eye

opening and closing
Alpha reactivity- increased alpha on eye closure
Alpha Variants: in the theta range. Differentiation from slow

background can be made by the notched appearance
Alpha squeak was first recognized and described by which is a clue to the faster native background. In
Storm van Leeuwan and Bekkering in 1958. The addition, the slow alpha variant is attenuated with eye
normal phenomenon can occur momentarily after eye opening. The usual posterior dominant rhythm
closing and is a brief acceleration of the patient's frequency or the transition between that faster
normal alpha rhythm. It can be facilitated by visual frequency and the slow alpha variant can sometimes be
attention before eye closure but does not occur every seen elsewhere in the recording. Also, central and
time the eyes are closed. anterior activity is of normal frequency composition,
whereas most patients with a theta activity background
Slow alpha variant The posterior dominant rhythm in would have abnormal slow activity in these forward
most adults is 8.5-11 Hz. In some patients, there can be regions.
a sub-harmonic of the posterior rhythm at 4-5 Hz. The
slower frequency is typically notched. The sub- Slow alpha variant can be misinterpreted as slow
harmonic can be misinterpreted as a slow background background associated with encephalopathy, but some
guidelines for differentiation are:
1-Notched appearance of the rhythm

2-Stereotypic appearance of the background of the slow alpha variant as opposed to polymorphic appearance of
pathologic slow activity of encephalopathy
3-Normal frontal and cerebral activity with slow alpha variant as opposed to slowing associated with
encephalopathy.
Normal Adult EEG 27
Slow alpha variant
Slow alpha variant

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."
Fast-alpha variant harmonic of the native rhythm, appearing at twice the

Fast-alpha variant is characterized by an otherwise- native frequency (16-20 Hz), appearing in the beta
normal posterior dominant rhythm which appears as a range.
The fast alpha variant is easy to interpret as normal, since there is not the slowing which is more typical of pathology
Normal Adult EEG 29
• Paradoxical alpha response is the reverse of alpha Alpha rhythm in brief:

reactivity in a fully alert individual. Upon eye
opening in the normal alert adult, alpha rhythms • FREQUENCY: 8-13Hz(alpha rhythm of most
are attenuated. Patients, however, alerted from a adults ranges between 9.5-10.5 Hz)
drowsy state can produce an accentuated alpha • LOCATION: posterior dominant but may
rhythm with eyes open. Since this is contradictory extending to central and temporal
behavior for alpha rhythm, the term paradoxical is regions.Occasionally may be widespread.
used. • MORPHOLOGY: Rhythmic, regular, and waxing
In young adults, alpha rhythm can spread into and waning
the mid and posterior temporal head regions. This so
called temporal alpha behaves just like alpha rhythm • AMPLITUDE: Generally 20-100µv. The alpha
in the occipital head regions and is symmetrical as well rhythm is often of slightly higher voltage over the
as reactive to eye opening. right hemisphere. There should be little (less than 1
Hz) or no difference in the frequency of the alpha
rhythm between the left and right hemispheres.
• REACTIVITY: Best seen with eyes closed,
attenuates with eye opening.
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.
Although any activity that is 8-13hz is called its location and reactivity are different. Mu rhythm will
alpha but if is not attenuates with eye opening it is not be discussed in more detail in this chapter.
alpha rhythm (reactivity to eye opening is typically
used as evidence).Alpha rhythm attenuates due to Beta rhythm:
auditory,tactile,and other somatosensory stimuli or
heightened mental activity (such as solving The term "beta rhythm" was first used to describe
arithmetical problems) but these stimulants are usually frequencies faster than alpha rhythm by Hans Berger in
less pronounced than the blocking effect with eye 1930. Beta rhythm is usually low voltage (less than 30
opening. µvolts) in adults. Often, during the awake EEG, beta is
Other EEG patterns may fall within the 8-13 Hz present in the anterior head area, but may be obscured
range. They are described as being within the alpha by muscle artifact (EMG) and eye movement potentials
frequency, but not called the alpha rhythm. Mu rhythm, from the frontal electrodes . Beta rhythm is a normal
for example, is within the alpha frequency range, but
finding in the adult awake EEG and can sometimes be 1. frontal beta: fairly common, may be very fast, no
better seen when the patient's eyes are open. relationship to physiological rhythm.
Any rhythmical EEG activity above 13/sec may 2. central beta: partly but not generally the basis of
be regarded as beta rhythm. Rhythmical beta activity is rolandic mu rhythm often mixed with mu rhythm.
encountered chiefly over the frontal and central 3. posterior beta: often a fast alpha equivalent,
regions; it usually does not exceed 35/sec. The reactive like alpha rhythm.
amplitude of beta activity seldom exceeds 30µV. 4. diffuse beta: no linkage with any special
The physiological beta frequencies may be broken physiological rhythm
down as follows:
This is the normal amount of beta, frontally predominant, with waxing and waning amplitude
Normal Adult EEG 31
Diffuse beta activity
A sample of awake EEG showing the normal or often seen amount of beta activity.As shown here, beta activity
is often easier to identify during relaxed wakefulness or early drowsiness.
Beta rhythm in brief: comb rhythm and somatosensory alpha rhythm. Mu is

a distinct, surface-negative or arch-like or comb like
Normal beta activity has the following characteristics: rhythm of a frequency approximately 7-11 Hz. It can
be as high in amplitude as 80 µvolts and is seen, not in
• FREQUENCY: Greater than 13Hz , Common 18-
the posterior head regions, but in the central head
25Hz ,less common 14-16Hz,and rare 35-40Hz
regions with eyes closed or open. It can appear
• LOCATION: Mostly frontocentral but somewhat unilaterally, bilaterally or independently in either
variable,some describe various types according to hemisphere. It can be continuous or appear
location and reactivity:generalized, precentral,and intermittently throughout an EEG recording. When
posterior. identified on the recording, it is important to
• AMPLITUDE: Usually range 5-20µv distinguish this rhythm from alpha. Mu is attenuated by
• Can be mildly different (<35%) in amplitude real or imagined contralateral motor activity. Eye
between the two hemispheres,which may be caused opening which attenuates the alpha, combined with
by differences in skull thickness. Definit clenching of the contralateral fist or movement of the
focal,regional, or hemispheric differences(at least contralateral thumb, which blocks the mu, helps verify
50%)in amplitude may be significant and may the pattern. Often just thinking about contralateral
suggest either skull defect(side with higher movement (or the technologist touching this limb) will
amplitude)or a structural lesion (side with lower attenuate this activity. The potentials are most
amplitude). prominent at C3 and C4. Mu is very often
• MORPHOLOGY: Usually rhythmic,waxing and asymmetrical or unilateral. The absence of mu activity
waning,and symmetric. on one side is not abnormal, unless there is very
frequent mu activity on one side and none on the other
• REACTIVITY: beta activity enhanced during side. The key to identification of Mu rhythm is
stage1 and 2 sleep and tends to decrease during blocking by movement of the contralateral arm. Even
deeper sleep stages. contemplating movement can produce this change.This
• Amount and voltage of beta activity is enhanced by rhythm is observed in 17-19% of young adults.An
commonly used sedative medications increase association between mu rhythm and a variety
(benzodiazepines and barbiturates). dysfunctions such as migrain,bronchial asthema, peptic
ulcer,eczema,tinnitus,arterial HTN, and hyperthyroid
states is described.At the other hand,Mu rhythm is
Mu rhythm: common in patients with mild to moderate psychiatric
disorders such as anxiety,aggressiveness,emotional
This rhythm first described by Gastaut in 1952. Other instability,and psychosomatic disorders.
terms are wicket rhythm, central alpha, arcade rhythm,
Mu rhythm
Normal Adult EEG 33
Excessive mu activity
Reactivity of mu rhythm to wiggle fingers not to eye opening
Bilateral mu activity in an adult

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
Mu rhythm in brief: • When detected in an EEG,it should be verified by

testing its reactivity.
• CHARACTERISTIC:
– AMPLITUDE:Like alpha rhythm
– FREQUENCY:7-11hz (in range of alpha – REACTIVITY:Most characteristic featuring defining
frequency) the mu rhythm;mu rhythm attenuates with
– LOCATION:Centroparietal region(c3,c4,cz) contralateral extremity movement,the thought of a
– MORPHOLOGY:Arch like or comblike shape or movement,or tactile stimulation;contrary to the alpha
like an "m"symmetric or asymmetric between the rhythm,does not react to eye opening and closing
2 sides and may be unilateral.
• In cases of strictly unilateral mu rhythm ,a
careful search for bone defects and/or local Theta rhythm
pathology is indicated.
• Very high voltage mu activity may be recorded
According to the international nomenclature, the theta
in the central regions over skull defects and
band is the “frequency band from 4 to under 8 Hz” and
may become sharp in configuration,and thus
the theta rhythm is the “rhythm with a frequency of 4 to
can be mistaken for epileptiform discharges.
under 8 Hz”.
Normal Adult EEG 35
Theta activity in the waking adult represent an evoked response to visual stimuli
produced by the rapid shifts of images across the
The normal adult waking record contains but a small retina. Lambda waves occur when reading and
amount of theta frequencies and no organized theta occasionally when watching TV. Its amplitude is
rhythm. Theta frequencies and theta rhythms, however, usually below 20µV and may exceed 50µV in some
play an important role in infancy and childhood, as persons.
well as in states of drowsiness and sleep. Their form has been described as triangular or
sawtooth shaped and may spread to parietal or
posterotemporal areas. They may be symmetric or
Lambda wave asymmetric.Lambda waves are best found in brightly
laboratories and can not be elicited in darkness.The
Lambda activity is found in the occipital regions in the lambda waves may be mistaken for occipital spikes,
normal waking EEG. It is a surface-positive event and however, their positive polarity and blocking with eye
has a configuration like the Greek letter lambda (λ), for closure make this clearly not epileptiform.
which it is named. Lambda activity is seen with eyes Morphologically, they are similar to positive occipital
open and can be elicited by saccadic eye movement, sharp transients of sleep(POSTS) both in form and in
which would occur if you asked your subject to view or occipital distribution.
scan a complex image. Lambda, which occurs in
65% of the population, is normal and appears to
Lambda wave
Lambda wave
Breach rhythm absence allows the electrodes to record more voltage

or amplitude from the underlying cortex. Frequently,
Breach rhythm is a sharply focal 6-11 Hz pattern if found over the central motor cortex, the breach
associated with a defect in the skull, resulting from rhythm will be reactive to contralateral fist clenching
surgery or an accident . This rhythm is of higher or movement as mu rhythm is. Breach rhythm
amplitude than alpha rhythm, (generally exceeding appears normally with skull defects and can be
80 µvolts) and often has a spike-like appearance, differentiated from a slow alpha rhythm or mu
particularly when beta frequencies are riding atop of rhythm by this particular characteristic.
it. The human skull is a natural insulator and its
Breach rhythm ,Note: increased voltages recorded on right side where there is a skull defect
Breach rhythm over the left midtemporal region following a left temporal lobectomy in a 50-year-old man
Normal Adult EEG 37
Chapter 5
EEG artifacts
Artifacts are waves or groups of waves which are causes. EMG artifact consists of short needle-like
produced by technical or other disturbances which are spikes which may occur in such frequency that they
not due to brain activity i,e is not of cerebral origin. A become confluent and give an appearance that
good rule to remember is that if the activity in question resembles epileptic spikes.
is limited to a single channel or electrode, it must be Some guidelines for differentiating EMG from
assumed to be artifactual in origin until proved epileptiform spikes are a follows:
otherwise.
• EMG is very fast, much faster than spikes.
Artifacts divided into two groups: Activity recorded at the scalp that is shorter than
20 msec is highly unlikely to be epileptiform
1-Physiologic: A group of waves that are generated activity.
from patient(sources other than the brain). • EMG spikes are not followed by a slow wave.
2-Nonphysiologic: A group of waves that arises from • EMG is prominent in the waking state, and
outside of the body(ie,equipment,environment). disappears with sleep
• EMG spikes recur at a rate which is much faster
than would be seen with repetitive spikes.
Variety of physiologic artifacts: • EMG is attenuated by asking the patient to relax
the jaw, open the mouth, or other maneuver
1-EMG artifact: It is the most common artifacts.
EMG activity frequently contaminates EEG recordings, Other causes of EMG artifacts are some
and this is prominent when patients are tense, seizing, movement disorder such as essential tremor, parkinson
or have other reasons for increased tone of scalp disease and hemifacial spasms.
muscles.Frontalis and temporalis muscles are common
Diffuse EMG artifact
EMG (muscle) artifact. These waveforms represent motor unit potentials as typically seen on needle electrode
examination during EMG, with a frequency of 20-100 Hz. Distribution varies, and in this case it is more prominent
on the left side.
Occasionally, muscle artifact is more restricted, noted, particularly in the midtemporal region.
and may even arise from a single motor unit can be
EEG artifacts 41
Most EMG artifacts can be reduced or eliminated with the use of relaxation techniques, such as reassuring the patient,
comforting the patient, or simply massaging the muscle groups . The use of high-frequency filters to eliminate the
artifact should be avoided, because these filters rarely eliminate the high frequency; rather, they alter its appearance
from a sharp or spike wave to a more sinusoidal frequency that may look more like cerebral beta activity.
The top segment has a high frequency filter setting of 70 Hz, whereas the lower segment has a high
frequency setting of 15 Hz. Without looking at the unfiltered EEG the muscle activity may be
misinterpreted as beta activity.
The photomyogenic or photomyoclonic response occur in normal subjects and are time locked to photic
is a special type of EMG artifacts that occurs during stimulation, occur at the same frequency of photic
intermittent photic stimulaion due to contraction of the stimulation and begin and end with the onset and
frontalis and orbicularis muscles.These contractions cessation of photic stimulation. The main problem with
occur 50-60msec after each flash,disappear after eye the photomyoclonic response is in differentiation of
opening,are located mostly frontally,and have no this from photoparoxysmal response.
concomitant EEG changes. These responses may
2- Glossokinetic artifact: In addition to muscle • Glossokinetic artifact is associated with activities

activity, the tongue (like the eyeball) functions as a such as speaking, chewing, swallowing.
dipole, with the tip negative with respect to the base. In • Glossokinetic artifact is often concurrent with EMG
this case, the tip of the tongue is the most important artifact of the frontalis and temporalis muscles
part because it is more mobile., although it is less steep
than that produced by eye movement artifacts. If there is still doubt about identification, then
Movement of the tongue is common in the waking electrodes can be placed below the eyes or on the
state, and can occasionally be mistaken for pathologic submental muscle of the lower jaw. The patient is
frontal slow activity. This is potentially more asked to make lingual movements such as “la la la” and
problematic in a comatose patient who is having the potentials observed. Cerebral activity will be higher
tongue movements and also observed in patients with in voltage in the frontopolar electrodes. Identification
dementia or those who are uncooperative. of glossokinetic artifact is much better if the technician
recognizes the problem and is able to perform these
Glossokinetic artifact can be differentiated from
maneuvers. Combinations of muscle and glossokinetic
slow activity in the following ways:
artifact produce very characteristic patterns.
• Glossokinetic artifact usually disappears in
drowsiness and light sleep.
Glossokinetic artifact
EEG artifacts 43
Chewing artifact: The high voltage muscle potentials are related to temporalis muscle contraction. The slow
potentials are glossokinetic, related to tongue movement.
EMG artifact recorded while the patient is eating lunch in a monitoring unit.
Glossokinetic artifact generated by tongue movement as the patient is instructed to say "la, la, la."This is
monitored by an electrode placed on the submental muscle and in this case referred to a PZ reference.
3-Eye movements: Eye movements are observed on Vertical eye movements typically are observed with
all EEGs and are useful in identifying sleep stages. The blinks (ie, Bell phenomenon). A blink causes the
eyeball acts as a dipole with a positive pole oriented positive pole (ie, cornea) to move closer to frontopolar
anteriorly (cornea) and a negative pole oriented (Fp1-Fp2) electrodes, producing symmetric downward
posteriorly (retina). When the globe rotates about its deflections. During downward eye movement the
axis, it generates a large-amplitude alternate current positive pole (ie, cornea) of the globe moves away
field, which is detectable by any electrodes near the from frontopolar electrodes, producing an upward
eye( i,e Fp1 , Fp2, F7, and F8). Other source of deflection.
artifacts comes from EMG potentials from muscles in
and around the orbit.
EEG artifacts 45
Eye closures: Eye closure results in Bell’s phenomenon, an upward deviation of the eyes. This will be
associated with a positive deflection in the frontopolar electrodes.
Eye blink: An eye blink causes the same positive potential in the frontopolar regions.
Eye blink can be more repetitive and have the appearance of frontal slow or sharp activity
Eye flutter can produce artifact which is even faster than normal eye blink and can be mistaken for epileptiform
activity or for fast frontal beta activity. Below is an example of eye flutter which occurs after the patient opens eyes,
in the middle of the recording epoch.
EEG artifacts 47
Eye flutter
Eye opening: Eye opening results in a negative this phenomenon along with other patient movements.
potential in the frontopolar electrodes plus alteration in Eye closure results in restoration of the posterior
the posterior rhythm. The attenuation of the posterior rhythm. The posterior dominant frequency may be
rhythm with eye opening and reappearance with eye slightly faster immediately after closure. Therefore that
closing are good clues to the presence of vertical eye should be measured a few seconds after eye closure.
movements, although the technician should indicate
Lateral eye movements: Lateral eye movements most electrode F7 and maximum negativity in electrode F8 is
affect lateral frontal electrodes F7 and F8 . During a recorded. With right lateral eye movement, the opposite
left lateral eye movement, the positive pole of the occurs. In these instances, so-called lateral rectus EMG
globe moves toward F7 and away from F8. Using a artifact may be present in electrode F7 or F8.
bipolar longitudinal montage, maximum positivity in
Eye movement artifact
Lateral eye movements such as these are usually seen in frontal electrodes and not further posteriorly then mid
temporal. The phase reversals at F7 and F8 are of opposite polarity, indicating lateral eye movements. Because the
cornea is positively charged, and the retina negative, the side of the positivity indicates the direction of the eye
movement.
Eye rolling movement

EEG artifacts 49
Lateral eye movement artifact
Asymmetric eye movements can occur for several 4- ECG artifact: Some individual variations in the
reasons . The first problem to be looked for is amount and persistence of ECG artifact are related to
asymmetrical placement of the electrodes.A small the field of the heart potentials over the surface of the
deviation from the standard placement can lead to scalp. Generally, people with short and wide necks,
slight asymmetries in the recording. The next most obese patient and babies have the largest ECG artifacts
obvious cause for this type of artifact is unilateral on their EEGs. artifact is observed best in referential
enucleation and a prosthetic eye replacement. Patients montages using earlobe electrodes A1 and A2.
with a third cranial nerve palsy or external Increased inter-electrode distance predisposes to ECG
ophthalmoplegia will be unable to produce conjugate artifact. Differentiation from electrocerebral artifact is
upward gaze and will have an asymmetrical eye blink most obvious if a special ECG channel is recorded, but
with decreased amplitude, (a smaller deflection) on the even in the absence of this, the regular nature of the
side of the paralysis. Asymmetry of eye movement QRS complex and the distribution of the sharp activity
may also be due to a skull defect, usually a craniotomy makes the source evident.
(breach effect).
ECG atrifact
EEG artifacts 51
ECG artifact
5-Pulse artifact: 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.
The relationship between ECG and Pulse artifact
Pulse artifact can be differentiated from
pathological slow activity by the following features:
Initial inspection could mistake pulse artifact with
• The artifact localizes over one electrode. polymorphic delta activity, but in this situation the
• The artifact is time-locked to the ECG but with a background is usually abnormal, with slowing and
delay. disorganization. If there is still doubt, examination of
• The background is otherwise normal the scalp by the technician can be revealing.
6-skin artifacts: Biological processes such as sweats

may alter impedance and cause artifacts. Sodium
chloride and lactic acid from sweating reacting with
metals of the electrodes may produce huge slow
baseline sways. On the other hand, 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.
Sweat artifact. This is characterized by very low frequency (here 0.25 to 0.5 Hz) oscillations. The distribution here
(electrodes T3 and O1) suggests sweat on the left side. Note that morphology and frequency is also consistent with
slow rolling eye movements, but distribution is not.
NON-PHYSIOLOGICAL Movement of the electrode results in changes in the

junction potential. The discharge of the junction
ARTIFACTS potential results in a potential which can be mistaken
for a spike discharge. The appearance is of a brief
Non-physiological artifacts are generated externally or spike followed by a gradual decay to baseline. The
in the environment and come from a vast variety of most common electrode artifact is the electrode
sources. Many of these originate within the equipment popping. Electrode artifact identified easily by its
used to record the EEG. Others are generated by the characteristic appearance (i.e, abrupt vertical transient
actual recording electrodes and environmental sources. that does not modify the background activity) and its
usual distribution, which is limited to a single
1-Electrodes and leads: Electrode leads can be a electrode.
source of artifact especially if there is instability in
fixation of the electrode and high impedance.
EEG artifacts 53
Electrode artifact at O1. The morphology is very unusual for any cerebral waveform, and the distribution is limited to a
single electrode
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.
Single electrode artifact at T5

EEG artifacts 55
Electrode (impedance) artifact at P3. There is initially a slow artifact followed by a more abrupt one at the 7th second. This is
commonly referred to as an “electrode pop.” Note again the unusual morphology of the sharp component, and the fact that it is
at a single electrode. Also note an eye blink In the 3rd second, and slight EMG artifact in the frontal regions in the first 2
seconds.
2- Alternating current (60-Hz) artifact : situation, the ground becomes an active electrode that,
Adequate grounding on the patient has almost depending on its location, produces the 60-Hz artifact .
eliminated this type of artifact from power lines. The The artifact presents at exact frequency (60 Hz, as its
problem arises when the impedance of one of the name indicates). A better identification can be made by
active electrodes becomes significantly large between increasing the paper speed (ie, sweep time) to 60 mm/s
the electrodes and the ground of the amplifier. In this and counting it (1 cycle per millimeter).
60-Hz artifact
3- Movement artifact: Movement artifact is due to compared to most electrical circuits, there is resistance
disturbance of the electrodes and/or leads. Electrode gel is of the leads and capacitance between the leads.
a malleable extension of the electrode, and minor head Movement of the leads results in disturbance of the
movement produces little effect on the electrode-gel-scalp capacitance. The built-up charge can dissipate with loss
attachment. However, movement sufficient to disturb the of the capacitance, and this too is recorded as EEG.
connection results in charge movement between the
electrode and gel and scalp, which is recorded as EEG.
Differential amplification does not remove this artifact
because the lead artifact is individual.
Movement artifact is also produced by movement
of the leads. A small amount of current flows through
the electrode leads, and while this current is miniscule
Movement artifact related to head motion with hyperventilation

EEG artifacts 57
Movement artifact
4-intravenous artifact: This artifact is seen

commonly in ICU recordings.The 'drip' artifact or IV
artifact is periodic and small in amplitude and easily
recognized. Morphologically it appears as spike
transient potentials at fixed intervals that coincide with
drops of the infusion. IV artifact
IV artifact: Note regularity and distribution of the artifact, which allows for easier recognition of it
Chapter 6
NORMAL SLEEP EEG
This chapter discusses the EEG activity of sleeping fact that,in some cases of TLE, the anterior temporal
healthy adults. This section is limited to sleep spikes focus becomes most active in stage 3 or 4.
recordings obtained in the regular EEG laboratory. The In the clinical EEG laboratory,most sleepers reach
purpose of these EEG sleep studies is to search for only stage 2. Stage 3 is occasionally,and stage 4
abnormalities that may be hidden in the waking state. seldom,reached unless unusually long sleep recording
There is no doubt that the overall information derived time is alloted or in cases of profound tiredness after
from a wakefulness record is greater and hence sleep loss.REM stages are seldom seen in the clinical
clinically more significant.There are,however, a laboratory except in infants,young children,and adults
number of conditions, especially in domain of epileptic with sleep loss.
seizure disorders,in which sleep provides essential
information.(this excludes the sleep disorders
themselves, which should be evaluated in a specialized Normal sleep EEG patterns
sleep laboratory)
The drowsy state and light sleep(stage 2)are Loomis provided the earliest detailed description of
usually the most informative phases; for this reason, various stages of sleep in the mid-1930s, and in the
the sleep-onset portion with a length of 5 to 30 minutes early 1950s Aserinsky and Kleitman identified rapid
in stage 2 sleep may be sufficient. In infants and eye movement (REM) sleep.
children , a sleep(nap) recording is almost a necessity, Sleep generally is divided in two broad types:
not simply because of easier management of the nonrapid eye movement (NREM) sleep and REM
sleeping child but also because of the needed sleep. On the basis of EEG changes, NREM is divided
information. further into 4 stages (stage I, stage II, stage III, stage
Generally, Sleep without medication is IV). NREM and REM occur in alternating cycles, each
undoubtedly preferable to sedated sleep.Whenever a lasting approximately 90-100 minutes, with a total of
sleep recording can not be obtained naturally,sedated 4-6 cycles. In general, in the healthy young adult
sleep is dictated by necessity. In these NREM sleep accounts for 75-90% of sleep time (3-5%
circumstances,the patient must not be over powered by stage I, 50-60% stage II, and 10-20% stages III and
strong and rapidly sedatives because the highly IV). REM sleep accounts for 10-25% of sleep time.
informative stages of sleep(stage1,2) are quickly
passed and the ensuing deep sleep will yield little
information in most cases.Enormous amounts of fast Stage 1 sleep or drowsiness
activity may also obscure important The transition from the awake to the drowsy state or
details.Therefore,the IV and IM routes must be stage 1 sleep is marked by some profound changes in
avoided.Orally and rectally administered sedatives act the background activity of the EEG. These changes in
more gently and slowly. The ensuing sleep contains brief are:
many or most features of spontaneous sleep.In special
cases of TLE, there is still a place for the IV route and • Slow rolling eye movements (SEMs)
deep sleep.The effectiveness of these drugs lies in the • Attenuation (drop out) of the alpha rhythm
• Central or frontocentral theta activity Slow rolling eye movements (SEMs)

• Enhanced beta activity SEMs are usually the first evidence of drowsiness seen
• Positive occipital sharp transients of sleep (POSTS) on the EEG. SEMs of drowsiness most often are
• Vertex sharp transients horizontal but can be vertical or oblique, and their
• Hypnagogic hypersynchrony distribution is similar to eye movements in general .
However, they are slow (ie, typically 0.25-0.5 Hz).
SEMs disappear in stage II and deeper sleep stages.
Alpha dropout the alpha rhythm gone, the background becomes

Drop out of alpha activity typically occurs together dominated by theta activity, which occurs in
with or nearby SEMs. The alpha rhythm gradually generalized distribution but is commonly most
becomes slower, less prominent, and fragmented. With prominent in central or frontocentral regions.
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
Normal Sleep EEG 61
Enhanced beta activity by age 50 years. POSTS are seen very commonly on
EEG and have been said to be more common during
Another change in the background activity that occurs daytime naps than during nocturnal sleep. Most
in the transition from the awake to the drowsy state characteristics of POSTS are contained in their name.
concerns the beta activity. Beta activity in the range of They have a positive maximum at the occiput, are
18-25 Hz usually, but not always, increase in amplitude contoured sharply, and occur in early sleep (stages I
with drowsiness. When sedatives are administered to and II). Their morphology classically is described as
promote sleep during the EEG, beta activity may "reverse check mark," and their amplitude is 50-100
become widespread and quite prominent, sometimes µV. They typically occur in runs of 4-5 Hz and are
attaining amplitudes in excess of 50 µV. bisynchronous, although they may be asymmetric.
They persist in stage II sleep but usually disappear in
subsequent stages.POSTS are very similar to occipital
Positive occipital sharp transients of sleep lambda waves and the term “lambdoid” activity of
(POSTS) drowsiness and sleep was used but are present only in
sleep, whereas lambda waves are only seen in the
POSTS start to occur in healthy people at age 4 years, waking state with the eyes open. POSTS are not seen
become fairly common by age 15 years, remain in patients who are blind or who are severely visually
common through age 35 years, and start to disappear impaired.
Positive Occipital Sharp Transients of Sleep, (POSTS)

Stage I sleep. POSTS are seen in both occipital regions, with their typical characteristics contained in their name:
Positive Occipital Sharp Transients of Sleep. They also have the morphology classically described as comparable
to a reverse check mark, and often occur in consecutive runs of several seconds, as shown here.
POSTS
Vertex waves biphasic, with an initial negative phase followed by a

smaller, positive phase.Although they often are
Also called vertex sharp transients or V waves, these grouped together with K complexes, strictly speaking,
transients are almost universal. V waves are usually vertex waves are distinct from K complexes. Like K
Normal Sleep EEG 63
complexes, vertex waves are maximum at the vertex discharges. V waves occur synchronously over both
(Cz), so that, depending on the montage, they may be hemisphaes, usually with a phase reversal at the
seen on both sides, usually symmetrically. They appear midline. It is normal for V waves to be higher in
in late Stage I and into Stage II sleep. Their amplitude amplitude on one side, and then shift to the other
is 50-150 µV. They can be contoured sharply and hemisphere, as long as they are not consistently
occur in repetitive runs, especially in children. They decreased on one side. As mentioned later in this
persist in stage II sleep but usually disappear in chapter,V waves may be followed by a sleep spindle.V
subsequent stages. Unlike K complexes, vertex waves waves may become small and inconspicucous in aged
are narrower and more focal and by themselves do not individuals and are often poorly demonstrable in such
define stage II. The morphology of V waves varies in persons.
sleeping individuals. In some cases they are sharply
contoured, and can look very much like epileptiform
Stage I sleep. 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 stages I and II sleep.
Stage I sleep. On this transverse montage, there are typical vertex sharp transients. By contrast toK-complexes,
these are narrow (brief) and more focal, with a maximum negativity at the midline(Cz and to a lesser degree Fz).
These are seen in stages I and II sleep.
Normal Sleep EEG 65
Hypnagogic hypersynchrony that brake after the cerebral activity amplitude drops
during drowsiness. When intermixed with fast activity
Hypnagogic hypersynchrony (first described by Gibbs that may be present at the same time, these paroxysmal
and Gibbs, 1950) is a well-recognized normal variant bursts may falsely give the impression of spike and
of drowsiness in children aged 3 months to 13 years. wave discharges. Despite their ominous appearance,
This is described as paroxysmal bursts (3-5 Hz) of these waves are a normal feature of the EEG in
high-voltage (as high as 350 µV) sinusoidal waves, childhood.
maximally expressed in the prefrontal-central areas,
infants aged 6-8 weeks and are bilaterally

Stage 2 sleep asynchronous. These become well-formed spindles and
Stage II is the predominant sleep stage during a normal bilaterally synchronous by the time the individual is
night's sleep. The distinct and principal EEG criterion aged 2 years. Sleep spindles are bursts of sinusoidal
to establish stage II sleep is the appearance of sleep 12-14 Hz activity, tapered at both ends. They are
spindles or K complexes. The presence of sleep seen over the frontocentral head regions, most often
spindles is necessary and sufficient to define stage II with a maximum over the central midline. Sleep
sleep. Another characteristic finding of stage II sleep is spindles last from less than one second to 2 seconds.
the appearance of K complexes, but since K complexes They can occur alone, or in combination with vertex
typically are associated with a spindle, spindles are the waves and K complexes. In some individuals, sleep
defining features of stage II sleep. Except for slow spindles are maximum in the frontal electrodes. The
rolling eye movements, all patterns described under amplitude of sleep spindles usually is 20-100µV. Sleep
stage I persist in stage II sleep. Delta begins to appear spindles may or may not be synchronous, but they
at this stage. should be symmetric and bilateral. Sleep spindles are
also present in Stage III sleep.
Sleep spindles
Sleep spindles, or sigma waves, indicate the onset of
Stage II sleep . Sleep spindles normally first appear in
Sleep spindle (12-14 Hz)

Normal Sleep EEG 67
Stage II sleep. There is a mixture of POSTS (positive occipital sharp transients of sleep),and spindles (fronto-
central short-lived rhythmic 14 Hz bursts)
K complexes slow wave portion of the K complex can exceed 1000

K complexes usually appear in Stage II sleep, and may milliseconds in duration. The amplitude may exceed
also seen in Stages III and IV sleep. They are high 400 microvolts. K complexes appear spontaneously, or
voltage transients with similarities to V waves in they can be elicited by an auditory stimulus. Calling
amplitude and location. Location is frontocentral, with a the patient's name, clapping, or tapping a pencil on a
typical maximum at the midline (central midline placement hard surface are good ways to elicit K complexes
of electrodes [Cz] or frontal midline placement of electrodes during EEG recordings. K complexes should be of
[Fz]). The K complex consists of a small sharp equal voltage over both hemispheres. K complexes are
component followed by a high voltage slow wave, largest in children and early adolesence,with advancing
often with sleep spindles superimposed upon it . The age,the K complexes shows a decline of voltage.
Normal Sleep EEG 69
Stage II sleep. On this transverse montage, there is a K-complex in the fifth second, with its typical broad duration
(>500 ms), diphasic morphology, and overriding spindle. There are also abundant spindles before and after
K complexes and sleep spindle in stage II sleep
Stage II sleep. 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).
Normal Sleep EEG 71
sleep progresses, the frequencies seen are slower and

Stage 3 sleep the number of sleep spindles decreases. In Stage III
sleep the slow waves make up less than 50% of the
Stage III sleep is characterized by an increase in higher
total record.
voltage slow waves in the theta and delta range. Sleep
spindles and K complexes may be present. As Stage III
Stage 3 sleep
differentiated from seizures. These "slow wave sleep

Stage 4 sleep parasomnias" include confusional arousals, night
terrors (pavor nocturnus), and sleepwalking
Stage IV sleep begins about 30 minutes after sleep
(somnambulism).
onset. By definition, the tracing must display more
than 50% delta activity to be called Stage IV sleep.
Sleep spindles are no longer present, and the EEG
consists of generalized, high voltage, irregularly REM sleep
shaped slow waves. Stage IV sleep is seldom seen in
routine EEG recordings unless the patient is sleep REM sleep normally is not seen on routine EEGs,
deprived and the recording period is lengthened. because the normal latency to REM sleep (100 min) is
Stages III and IV usually are grouped together as well beyond the duration of routine EEG recordings
“slow wave sleep” or “delta sleep.” Slow wave sleep (approximately 20-30 min). The appearance of REM
(SWS) usually is not seen during routine EEG, which sleep during a routine EEG is referred to as sleep-onset
is too brief a recording. However, it is seen during REM period (SOREMP) and is considered an
prolonged (>24 h) EEG monitoring. One important abnormality. While not observed on routine EEG,
clinical aspect of SWS is that certain parasomnias REM sleep commonly is seen during prolonged (>24h)
occur specifically out of this stage and must be EEG monitoring.
Normal Sleep EEG 73
Stage 4 sleep
By strict sleep staging criteria on • Rapid eye movements: These are saccadic,
polysomnography, REM sleep is defined by (1) rapid predominantly horizontal, and occur in repetitive
eye movements; (2) muscle atonia; and (3) EEG bursts.
“desynchronization” (compared to stage 3 and 4 sleep). • Muscle atonia:means no muscle artifacts
Thus, 2 of the 3 defining characteristics are not • Saw tooth waves:a special type of central theta
cerebral waves and theoretically require monitoring of activity that has a notched morphology resembling
eye movements (electrooculogram [EOG]) and muscle the blade of a saw.
tone (electromyelogram [EMG]). Fortunately, muscle
activity and eye movements can be evaluated on EEG, Despite the lack of a dedicated EMG channel, the
thus REM sleep is usually not difficult to identify. In muscle atonia that characterizes REM sleep is usually
addition to the 3 features already named, “saw tooth” apparent as a general sense of “quiet” muscle artifacts
waves also are seen in REM sleep. compared to wakefulness. The duration of REM sleep
• EEG desynchronization: The EEG background increases progressively with each cycle and tends to
activity changes from that seen in slow wave sleep predominate late in the sleep period into early morning.
(stage III or IV) to faster and lower voltage activity The occurrence of REM too soon after sleep onset,
(theta and beta), resembling wakefulness. Saw tooth referred to as SOREMP, is considered pathological.
waves are a special type of central theta activity that However, newborns and infants enter REM more
has a notched morphology resembling the blade of a rapidly and spend a higher proportion of sleep in
saw and usually occurs close to rapid eye REM.Sleep onset REM period is seen in patients with
movements (ie, phasic REM). They are only rarely narcolepsy cataplexy,dilirium tremens and in sedative
clearly identifiable. withdrawal.
REM sleep. There are rapid (saccadic eye movements). While muscle “atonia” cannot be proven without a dedicated
EMG channel, there is certainly absence of any EMG artifact with a “quiet” recording. There is also no alpha rhythm
that would suggest wakefulness.
REM sleep. A good example of saw-tooth waves and they “notched” morphology, best seen here in the Cz-Pz (last)
channel.
Chapter 7
Activation Procedures
A met hod used to bring out abnormalities in the EEG, hyperventilation. The effect of hyperventilation on the
such as hyperventilation, photic stimulation and sleep. EEG begins earlier in children than adults and is
These procedures are known to activate or stimulate apparent in 50% of cases within the first minute and
abnormalities in some patients. For example, 90% within the first 2 minutes.
Hyperventilation and photic stimulation are most As recommended by the American Clinical
useful for activating epileptiform abnormalities, Neurophysiology Society, hyperventilation should not
whereas drowsiness and sleep are useful for activating be performed in certain clinical settings, including
all forms of EEG abnormalities as well as normal acute stroke, recent intracranial hemorrhage, large-
epileptiform patterns (so-called pseudoepileptiform vessel severe stenosis and associated TIA , documented
patterns). moyamoya disease, severe cardiopulmonary disease,
and sickle cell disease or trait.
Hyperventilation
Hyperventilation is perhaps the most widely used Normal and abnormal responses
activation procedure in EEG laboratories. The procedure,
The normal response to hyperventilation consists of
which is simple and relatively safe, consists of three to
the occurrence of symmetrical slow activity on both
five minutes of deep breathing. It is, however, difficult to
sides. The absence of any change in the EEG is also
perform in patients who are uncooperative, mentally
normal. Although this slow activity may be diffuse
retarded, or below the age of 4 or 5 years, and it is
theta activity, a more characteristic finding is the
preferable to avoid in patients with recent myocardial
occurrence of intermittent or continuous 3 to 4 Hz high
infarction, chronic obstructive pulmonary disease, and
amplitude activity that is frontally or occipitally
other conditions causing difficulty in breathing. Although
dominant. If the activity is continuous, it may build up
hyperventilation has become a common procedure during
gradually to amplitudes in excess of 250µV. The slow
routine EEG recording, it is of special importance in the
activity may persist for up to a minute after
case of patients suspected of having seizure disorders,
hyperventilation ceases, and the EEG may not return to
particularly absence seizures.
its prehyperventilation state for two to three minutes.
The amplitude and frequency of the slow activity are of
no clinical importance unless there is consistent
Procedure asymmetry between the two hemispheres. The side that
The standard procedure is to have the patient take deep shows a slower frequency and/or a lower amplitude is
breaths at the rate of about 20 per minute for three to usually considered to be the abnormal side.
five minutes. The first is to explain the procedure in On the other hand, the hyperventilation response
detail to the patient. Tell the patient to relax, keep the often includes frontal intermittent rhythmic delta
eyes closed and mouth open, and to breath deeply in activity (FIRDA) or, particularly in children, occipital
and out at a regular pace until told to stop. A minimum intermittent rhythmic delta activity (OIRDA).
1 minute baseline recording is made before starting Although spontaneously occurring FIRDA or OIRDA
indicates the presence of a diffuse cerebral for the blood vessels of the brain is carbon dioxide.
dysfunction,their isolated appearance in The higher the carbon dioxide content, the greater the
hyperventilation is considered normal. vasodilatation. So when there is hypocarbia, the
The most striking EEG abnormality seen during reverse occurs, namely, vasoconstriction. This
hyperventilation is 3 Hz spike and wave discharges often presumably alters the metabolic rate of the neurons and
brought on in patients with absence seizures. These leads to the slow activity.
discharges usually are frontally dominant and may occur The effect of hyperventilation on the EEG is
in brief epochs, or they may persist for several seconds much more marked in children than in adults, with
during which time an episode of unresponsiveness may children,s EEGs sometimes showing an enormous
be documented. Sometimes, other types of epileptiform buildup of slow activity. Blood sugar level also appears
abnormalities, such as generalized spike discharges or to influence the response to hyperventilation. The
even focal spikes, may be brought on by lower the blood sugar, the more marked the
hyperventilation. hyperventilation-induced slow activity. When an adult
How does hyperventilation bring about such EEG shows marked and prolonged slowing as a result
dramatic changes in the EEG? The major biochemical of hyperventilation, one should consider the possibility
finding during hyperventilation is a drop in carbon of hypoglycemia and should repeat the procedure 15 to
dioxide content of the blood(hypocarbia). It is well 30 minutes after giving a drink containing gloucose.
known that the most important vasodilatory stimulus
Posterior delta activity produced by hyperventilation in a 6-year-old boy. Older adolescents and adults
typically show anterior-dominant slowing in response to hyperventilation.
Activation Procedures 77
response:(1)visual evoked response (2) photic driving,

Photic stimulation (3) the photomyogenic (formerly referred to as
photomyoclonic) response, and (4) the
Visual stimuli are perhaps one of the most effective
photoepileptiform response (PER) (also referred to as
means of stimulating the brain. The ready availability
the photoparoxysmal response [PPR]).
of user friendly stroboscopes has resulted in the routine
use of intermittent photic stimulation(IPS) as an
activation procedure during EEG. The method is most Visual evoked response
valuable in documenting photosensitivity, which has a
The visual evoked response is the same potential which
high clinical correlation with primary generalized
is recorded during evoked potentials. The difference in
epilepsy.
appearance is because of the method of data display
and the absence of averaging. The VER is seen with
Technique low flash frequencies, usually most prominent at and
below 5/sec.
The device used is called a stroboscope or photic
stimulator. It is capable of delivering single or
Photic evoked potential: Flash at 5/sec produces an
continuous bright flashes of light at frequencies
evoked potential in the fourth channel, due to activity
ranging from 1 to 50 flashes per second.
in the occcipital lead. The upgoing potential in this
The test begins by explaining the procedure to the
bipolar montage indicates positivity at the O1
patient. Tell the patient he or she will be seeing very
electrode. The positivity is delayed from the stimulus
bright flashes of light(bright even with the eyes closed)
by about 100 msec, indicating that this is an evoked
and to keep the eyes closed or open as instructed
potential rather than a photic response.
during the course of the test. The flash lamp is
The absence of a VER is not abnormal unless
positioned approximately 30cm in front of the eyes.
unilateral. Such asymmetry suggests abnormality in
Start with one or two flashes per second and increase
projections from one lateral geniculate to the cortex, or
the rate gradually up to 30 flashes per second. Each
the calcarine cortex, itself.
flash rate is presented for a duration of about 10
seconds, and the eyes are kept closed in the first 5
Photic Driving Response
seconds and open in the next 5 seconds. If a
The driving response appears as the flash frequency
photoparoxysmal response (explained later) is elicited,
accelerates beyond 7/sec, and the next evoked potential
the IPS should be stopped to avoid precipitating a
starts before the last evoked potential has ended. It is
seizure. If the response occurs only during a brief part
created by the visual evoked responses merging into
of the stimulation, the technician needs to confirm that
each other.
it is indeed a photoparoxysmal response by cautiously
repeating the stimulation at the same flash rate.
The photic driving response consists of rhythmic,
occipital-dominant waveforms that either show a one-
Responses to photic stimulation to-one relationship with each flash or appear as a
harmonic (an integer multiple) or subharmonic (an
It was found that diffuse light stimulation produces
integer dividend) of the flash frequency.
four main categories of electrographic
Photic driving response: Photic driving response is time-locked to the stimulus and appears at faster frequencies
than the photic evoked response
Just as POSTS or lambda waves may be strikingly usually associated with a similar asymmetry of the
asymmetrical in normal individuals, an asymmetrical driving response Cortical epileptogenic lesions or skull
driving response is considered normal unless defects can enhance the amplitude of the photic driving
accompanied by other EEG abnormalities . In normal response ipsilaterally, whereas destructive lesions can
individuals, asymmetrical POSTS or lambda waves are attenuate it ipsilaterally.
Photic driving
Photomyogenic Response or Photomyoclonic

Response
The photomyoclonic response is not cerebral in origin, leads. There is a delay of 50-60 msec between the flash
but rather is electrical activity in the frontal scalp and the EMG activity.
muscles which is induced by the flash stimulus in The main problem with the photomyoclonic response
susceptible individuals. Repeated contraction of these is in differentiation of this from photoepileptiform
muscles produces EMG activity which is time-locked response. Some general guidelines are discussed in the
to the stimulus, and recorded from the frontal next table.
Differentiation of photomyogenic from photoepileptiform responses
Feature Photomyogenic Photoepileptiform

Spatial distribution Anterior Posterior or generalized
Termination End of the stimulus May stop before the end of the stimulus
or outlast the stimulus.
Rise time of the spike Fast (EMG) spikes Slower, spike-and-wave complexes most
common.
Frequency Sale frequency as the flash Frequency is independent of the flash
frequency, usually slower.
Photomyogenic (photomyoclonic) response to 14-Hz

photic stimulation. Prominent frontalis and temporalis
myogenic potentials time locked to the flash stimulus
end with a whole-body jerk.
Photoepileptiform or Photoparoxysmal with partial epilepsy (occipital lobe epilepsy, and even
Responses less commonly temporal lobe epilepsy). While some
patients will have already noticed that there is photic
The photoepileptiform response is characterized by trigger of their seizures, this is not always the case.
spike-wave complexes during photic stimulation. The Some patients with photosensitivity have never had a
discharge is usually activated only by a few specific spontaneous seizure. The correlation of a
flash frequencies. This response is a marker for seizure photoparoxysmal discharge with seizures is greatest if
tendency, and most often noted with generalized the discharge continues after the end of the flash train.
epilepsies. Less commonly, photosensitivity is noted
Photoparoxysmal response to 8-Hz photic stimulation

in a 6-year-old girl. Note the irregular spike-and-wave
complexes and greater amplitudes in more anterior
derivations
Photoparoxysmal response to 15-Hz

photic stimulation with initial fast activity
evolving into a typical generalized 3-Hz
spike-and-wave pattern. Eye fluttering
typical of a myoclonic absence seizure
was observed.
Photoparoxysmal response
SLEEP ACTIVATION be counseled about restricting their activities until the

effect of sedation has worn off.
Activation during Sleep Epilepsy syndromes that commonly show activation
Sleep is a highly effective method for eliciting both with sleep are listed below:
generalized and focal interictal epileptiform discharges
(IEDs). In as many as onethird of patients with 1. Benign occipital epilepsy in infancy
complex partial epilepsy, IEDs may not be present 2. Generalized tonic seizures in chronic childhood
during wakefulness but appear only during sleep . epileptic encephalopathies (e.g., Lennox-Gastaut
Epileptiform discharges are also often more easily syndrome)
detected during sleep. Recordings during wakefulness 3. benign rolandic epilepsy
are often obscured by muscle and movement artifacts, 4. Benign juvenile myoclonic epilepsy (i.e., on
especially in children and adults who are unable to awakening)
cooperate or relax during the recording. Nearly all 5. Frontal lobe epilepsy
patients with IEDs during daytime nap recording have
their first discharge within 15-30 minutes of sleep Activation by Sleep Deprivation
onset . Thus outpatient EEGs in patients with suspected
Sleep deprivation increases the possibility of seeing
seizures should always include sleep, but the actual
epileptiform activity in some patients, and also
sleep recording generally does not have to exceed 30
increases the chance of obtaining sleep. Sleep
minutes in duration. When a sleep EEG recording is
deprivation increases the yield of epileptiform
clinically indicated and the patient is unable to fall
discharges beyond that expected from sleep alone, and
asleep, a short-acting sedative can be used to help
therefore is considered a separate physiologic
induce sleep. Short-acting barbiturates and chloral
activation method. It is often used for patients in whom
hydrate are two agents that have been used for this
routine EEG has not been able to identify interictal
purpose. Chloral hydrate is generally preferred
epileptiform activity. Sleep deprivation may be a
because, unlike barbiturates, it does not induce beta-
particularly potent activation method in patients with
frequency activity in the background EEG. Every
juvenile myoclonic epilepsy. In these patients, the
patient considered for sedation should be medically
highest yield is in recording most of the EEG after
assessed for the risk of sedation. Patients should also
arousal from a brief nap following sleep deprivation.
Part two
Abnormal EEG Patterns
The term abnormal EEG patterns refers to patterns Like most neurophysiologic tests, EEG is a test of
of activity that are judged to be outside the normal cerebral function; hence for the most part it will be
range. In defining normal EEG ,we need to take into nonspecific as to etiology. Although at one time
account the age and state of the patient to correctly authors discussed the application of EEG in
interpret a particular EEG pattern.Thus, for example, a differentiating various types of lesions, this clearly has
pattern that is normal for a drowsy patient may be not been clinically useful in the modern era. The
considered abnormal if the patient is fully exercise of describing EEG abnormalities by pathology
awake.Similarly, a pattern that is normal for a child (eg, stroke, abscess, tumor, even various types of
may be quite abnormal for an adult.These example tumors!), which was common in old EEG texts, is
underscore the importance of the technologist,s therefore not followed here. Instead, the different
notations regarding age and state of the patient on the patterns of abnormal EEG and their clinical
EEG tracing.Without such information,EEG significance are reviewed. So, for the convenience we
interpretation and judgments of normality or divide the EEG abnormalities into two main groups:
abnormality may be of doubtful clinical value. 1. Epileptic abnormalities
2. Non epileptic abnormalities
Chapter 8
Epileptic discharges
Although no longer used for identification and regarding the sensitivity and specificity of interictal EEG.
localization of gross structural brain lesions, Clinicians may encounter any of the following
electroencephalography (EEG) remains the primary abnormalities when evaluating a patient with possible
diagnostic test of brain function. Unlike relatively new seizures: interictal epileptiform discharges (IEDs), focal
functional imaging procedures, such as functional MRI slowing, periodic lateralized epileptiform
(fMRI), single-photon emission computed tomography discharges(PLEDs), generalized periodic epileptiform
(SPECT), and positron emission tomography (PET), discharges (GPEDs), diffuse slowing, and several
EEG provides a continuous measure of cortical nonspecific paroxysmal abnormalities (e.g., frontal
function with excellent time resolution and is relatively intermittent rhythmic delta activity). Among all of these,
inexpensive. EEG is especially valuable in only IEDs and perhaps PLEDs are associated with
investigation of patients with known or suspected epilepsy at rates sufficiently high to be clinically useful.
seizures. The remaining patterns are much less useful in supporting
Seizures are infrequent events in the majority of the diagnosis of epilepsy, although they may provide very
patients, making recording of ictal EEG both time- important information regarding the underlying
consuming and expensive. The mainstay of diagnosis, conditions associated with seizures or epilepsy.
therefore, remains detection of interictal (ie, between In this chapter, we first describe interictal
seizures) epileptiform discharges. Continuous video- epileptiform discharges(IDEs) and then in next chapter
EEG monitoring, developed over the last 20 years to more common epileptic syndromes.
facilitate recording of ictal events, also greatly
increases the time available to detect interictal
epileptiform discharges (IEDs). In the diagnosis of Interictal epileptiform discharges
epilepsy and localization of seizure onset, these can be The International Federation of Societies for
as useful as ictal recordings. Electroencephalography and Clinical Neurophysiology
(IFSECN) describes interictal discharges as a
Electroencephalography in the subcategory of "epileptiform pattern," in turn defined
as "distinctive waves or complexes, distinguished from
diagnosis Of Epilepsy background activity, and resembling those recorded in
Epilepsy can have protean clinical manifestations, and a proportion of human subjects suffering from epileptic
some of these can be easily confused with those of disorders…." This somewhat circular definition makes
other medical conditions. Thus, the first question the clear that criteria must be verified empirically.
physician must address is whether the patient's Interictal discharges may be divided
symptoms represent epileptic seizures or some other morphologically into:
disorder. Although the diagnosis of epilepsy remains a 1. Spike discharges
clinical judgment, EEG findings, interpreted in the 2. Sharp wave discharges
context of other clinical data, are often pivotal in 3. Polyspikes or multiple spikes
reaching an answer. However, it is important to 4. Spike and wave or sharp and wave complexes
recognize that different EEG findings have different
degrees of association with epilepsy. This basic IEDs may occur in isolation or in brief bursts;
observation explains, in part, much of the confusion bursts longer than a few seconds are likely to represent
electrographic seizures rather than interictal discharges.
Spike discharges Positive spikes like 6-14Hz bursts and lambdoid

activity(POST) have little clinical significance.
A spike discharge is defined as a transient that is Spikes represent the basic element of paroxysmal
clearly distinguished from the background activity, has activity in the EEG. A Unitarian view that all spikes
a pointed peak at a paper speed of 30mm/s, and has a mean a hidden or overt paroxysmal event would be
duration of 20-70msec(Potentials of less than 20 ms erroneous. The fine semiology of spikes is extremely
duration are usually not of cerebral origin, being either important and the EEG interpreter should consider the
muscle or electrical artifact); the main component is following question:
generally negative. Amplitude is variable and may be 1. What is the precise wave morphology?
followed by slow wave. Ordinarily, a spike stands out 2. Where do the spikes occur?
from the background activity because of its distinct 3. What is the patient,s age?
appearance and/or size; but when the amplitude is 4. What is the state of awareness?
small, it may be difficult to identify, especially when 5. Is there any possibility of an artifact of similar
there is a considerable amount of beta activity in the appearance?
background. This is one reason why it is better to avoid 6. Is there any possibility of a physiological potential
using medications for promoting sleep when taking an of similar appearance?
EEG, as most such drugs cause diffuse beta activity.
As mentioned earlier in this book, we should be
cautious in use of high frequency filter, for example
use of the 15Hz high frequency filter should be
avoided because the sharp-pointed character of a spike
is lost and its amplitude becomes markedly attenuated.
When this happens, a spike may be indistinguishable
from beta activity or muscle artifacts.
Polarity of a spike may provide clues as to its potential
for epileptogenicity(negative spikes are more
significant from the point of view of epileptogenicity). A spike discharge
Wave morphology Age

The largest and most pronounced spikes are not The significance of the age factor is enormous. From
necessarily associated with more serious epileptic the spikes of an epileptic newborn to a seizure focus of
seizure disorders. For example, rolandic spikes in a an old age, age-determined varieties of spikes can be
child age 4 to 10 years are very prominent; however, distinguished.
the seizure disorder is usually quite benign or there
may be no clinical seizures at all. Distinction from similar physiological patterns
This differentiation is particularly important in the case of
Spatial distribution vertex sharp waves during deep drowsiness and stage 2 of
In childhood, occipital spikes are , in general, the most light non-REM sleep. In childhood (after age 4), these
benign spike discharges, with less than 50% having waves may have a particularly spiky appearance and may
clinical seizures; rolandic central-midtemporal-parietal be misinterpreted as paroxysmal spikes.
spikes are also quite benign, whereas frontal or anterior
temporal spikes or multifocal spikes are more Distinction from artifacts of similar appearance
epileptogenic. This distinction depends on the electroencephalographer,s
experience and is usually an easy one. The interpretation
of the clinical significance of spikes can be extremely
difficult and depends on the electroencephalographer,s
Epileptic discharges 87
difficult and depends on the electroencephalographer,s Extensive personal laboratory experience is just as
experience in the art of reading the EEG tracing and also essential as scientific knowledge in interpreting the EEG.
on the clinical understanding of epileptological problems.
Schematic of an interictal epileptiform discharge (IED), upper tracing, vs nonspecific sharp

transient, lower tracing. Note interruption of the background, asymmetric contour with
descending limb falling below the baseline, and aftercoming slow wave associated with the
IED; sharpness of the peak does not distinguish the 2 waveforms
Left temporal spike Spike, regional left frontal. 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.
Spike, regional left frontal. 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.
Spike, generalized. Note the high amplitude, and the aftergoing background suppression and slow wave.
Abnormal anterior midtemporal spike (F7-T3)with focal background abnormalities
Sharp wave discharges

msec; amplitude is variable and like spikes, sharp waves
A sharp wave is defined as a transient that clearly stands usually are surface negative. Since there is little
out from the background activity, has a pointed peak at a distinction between spikes and sharp waves from the
paper speed of 30mm/sec, and has a duration of 70 to 200 standpoint of their potential for epileptogenicity; the
terms are used interchangeably.
A sharp wave
Sharp waves, regional right temporo-occipital. The sharp waves are, as 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.
Sharp waves, regional left temporal. The maximum (phase reversal) is consistently at T3. Note the associated slow
activity and background attenuation.
Left temporal sharp wave in a 35 year old woman with epilepsy and left hippocampal sclerosis
Sharp waves, regional left temporal. The maximum (phase reversal) is at T3.
Sharp waves, multifocal. Sharp waves are seen at T4, T6, T5 and F3 on this 9 sec segment.With other findings, this is
often seen in the symptomatic/ cryptogenic epilepsies of theLennox-Gastaut type.
Polyspikes or multiple spikes waves.Polyspikes and polyspike wave complexes are

Polyspikes or multiple spikes are two or more sometimes associated with myoclonus for example in
spikes(monophasic or biphasic) that comprise a single lennox Gastaut syndrome.
waveform. As with spike discharges, multispike
discharges may also be accompanied by slow
Polyspikes or multiple spikes
Polyspike, generalized.
Note the aftergoing slow
wave. This is associated
with the “primary” or
idiopathic generalized
epilepsies, most typically
Juvenile Myoclonic
Epilepsy.
Generalized polyspikes in a patient with intractable epilepsy
Left temporal polyspikes
Spike and wave or sharp and wave Generally, SWC can be divided into 2 specific
types:
complexes (swc) 1. 3-Hz SWC : characterized by a frequency of 2.5-
4Hz and a monomorphic (regular) morphology. It
Spike or sharp and wave complexes(SWC) are repetitive occurs in discrete bursts,and between bursts the
occurrence of a spike or sharp followed by a slow EEG is normal (typically seen in absence).
wave,usually of the same polarity. Since any significant 2. Slow (<2.5Hz) SWC: this pattern is not only slower
spike or sharp wave usually is followed by a slow wave but also more irregular(less monomorphic)than 3Hz
,a run of 3 seconds is required to classify a record as SWC.Bursts are less discrete and other
SWC. abnormalities are seen.(typically in lennox Gastaut
syndrome).
sharp-and-slow-wave complexes spike-and-wave complexes

Spike, generalized. Significant spikes are usually followed by a slow wave,as shown here.This example also illustrates
that generalized spikes are typically maximum frontally.This is typical of the primary (idiopathic,genetic) epilepsies. If
the burst lasted 3 seconds or more, it could be classified as spike-wave complexes.
Spike and wave complexes

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 (i.e., genetic) generalized epilepsies,
such as absence epilepsy. The 3 Hz SWC is often faster (4-5 Hz) at onset, as shown here.
Slow spike-wave complexes. In addition to being slower, this is also less monomorphic than the 3 Hz SWC. With
other findings, this is often seen in the symptomatic/ cryptogenic epilepsies of the Lennox-Gastaut type.
Generalized atypical spike and wave in an adult patient with a mixed seizure disorder that includes atypical absence
seizures.
Use of IEDs in medical treatment

decision
Detection of IEDs after a transient neurological event and would tend to favor treatment. EEG also can
greatly increases the likelihood that a seizure was contribute to answering the reverse question, ie, whether
responsible; in most cases, IEDs can be classified as medications should be stopped after a 2-year or longer
generalized or focal, providing valuable information period of seizure freedom after the diagnosis of epilepsy
with respect to syndrome classification and treatment. is established. For patients with idiopathic generalized
In the case of a single unprovoked seizure, the risk of epilepsy, EEGs tend to "normalize" when complete
recurrence is approximately 20-80% depending on seizure control is attained, and lack of IEDs suggests a
whether the cause is cryptogenic or symptomatic. This decreased risk of relapse when medications are
risk is increased by a history of previous neurological withdrawn. However, the type of idiopathic epilepsy
insult, especially if accompanied by an acute syndrome is most important in predicting the chance for
symptomatic seizure and by detection of IEDs. In some remission (eg, good for childhood absence and poor for
studies, particularly those of children, focal IEDs juvenile myoclonic epilepsy). For patients with partial
suggest an increased recurrence risk as well, epilepsy, or in whom IEDs were not seen before
treatment, the value of a negative study is less clear.
Chapter 9
Electroencephalgraphy in common epileptic

syndromes
EEG is an essential component in the evaluation of guidelines help focus initial clinical impressions and
epilepsy.In fact after the medical history,EEG findings prompt a search for the more specific EEG findings
provide the most important information necessary for associated with the particular epilepsy syndromes.
syndromic diagnosis. Identifying the type of epilepsy
or "epilepsy syndrome" is important for optimal
management and for advising patients and families Specific Epilepsy Syndromes
about prognosis, guides selection of antiepileptic
medication, and suggests when to discontinue
medication.
Childhood and Juvenile Absence Epilepsy
The International Classification of Epilepsy Syndromes
distinguishes between childhood and juvenile onset
Characteristics of the Major Categories of forms of absence epilepsy. Childhood absence epilepsy
Epilepsy Syndromes (CAE) manifests between the ages of 3 to 5 years and
remits between 10 to 12. Absence seizures are
The Classification of Epilepsy Syndromes is based on frequent, often occurring in clusters. In contrast,
two distinctions: first, between localization-related and generalized tonic-clonic seizures are infrequent, and
generalized epilepsies and, second, between idiopathic remission by late adolescence is the rule . Juvenile
and symptomatic epilepsies. EEG findings assist in absence epilepsy (JAE) manifests at the ages of 10 to
making these distinctions. Focal IEDs are seen in 12 years (or later). Absence seizures are less frequent,
localization-related epilepsies, whereas generalized and generalized tonic-clonic seizures more frequent,
IEDs indicate one of the generalized epilepsies. In the than in CAE. Remission is less likely to occur, and
localization-related epilepsies, the location of IEDs seizures often persist into adulthood. Such distinctions,
usually corresponds approximately to the area of although generally applicable to large numbers of
seizure onset, but there are exceptions(described later). patients, are not always clear in individual patients. In
Normal or near-normal background activity is most addition, the clinical features of JAE overlap with
characteristic of idiopathic epilepsy syndromes; focal, those of two other syndromes: tonic clonic seizures
multi focal, or diffuse abnormalities of background upon awakening and juvenile myoclonic epilepsy. EEG
activity are most suggestive of the symptomatic features of CAE and JAE are also broadly similar.
epilepsies. Persistent focal voltage attenuation, Minor differences, however, can sometimes be
especially of faster frequencies, or polymorphic delta diagnostically useful.
activity is correlated strongly with a structural lesion as
the cause of symptomatic epilepsy. These general
EEG findings children. High-voltage OIRDA is a frequent interictal

finding, occurring in 15% to 38% of all patients with
absence epilepsy. However, the occurrence of OIRDA
EEG shows a normal background for age and
is strongly age related: it is found in more than 70% of
3-Hz generalized spike and wave discharges .
children between 6 and 10 years of age, and it is rare in
Frequency of the spike-wave complexes is usually
persons older than 15 years . It is also rare in children
4 Hz at the onset of the absence seizures and may slow
with atypical absence seizures . Thus, OIRDA is more
to 2.5 Hz at the end of a seizure. The repetition rate of
strongly associated with CAE than with JAE. OIRDA
generalized spike-wave bursts is faster at onset in JAE
is predictive of activation of generalized spike-wave
than in CAE, and polyspikes are seen more often in
activity by hyperventilation.Hyperventilation increases
JAE. Typically, an initial positive component is
3-Hz spike-wave bursts in 50% to 80% of patients with
followed by one or more negative components and then
CAE, especially if occipital intermittent rhythmic delta
a negative slow wave. They are frontally dominant.
activity (OIRDA) is present . Photic stimulation
Duration of discharges is typically 3-25 seconds.
increases spike-wave bursts in about 18% of cases.
Discharges are not truly bisynchronous; usually a
Generalized discharges are ictal in nature. They
millisecond difference is noted between left and right
may be so brief that no obvious clinical movements are
cerebral hemispheres. Eye opening does not alter the
seen, although typically minor eyelid fluttering or
discharges. However, discharges are state dependent.
subtle rhythmic contractions of the mouth are seen.
Their frequency increases with non-REM sleep,
These minor motor accompaniments occur in 85% of
although the duration of the discharges is reduced.
patients with absence epilepsy.
During REM sleep, the frequency of discharges
Absence should be differentiated from atypical
resembles that seen in wakefulness. Some patients
absence seizures, which usually are seen in patients
display occipital intermittent rhythmic delta discharges
with LGS. EEG in atypical absence seizures shows a
(OIRDA), which is thought to be a favorable
less abrupt onset and offset than in typical absence
prognostic indicator.
seizures. Furthermore, EEG background is slow, and
Interictal background activity is usually normal in
duration of discharges is shorter.
both CAE and JAE, although minor degrees of slowing
have been reported in heterogeneous groups of
Electroencephalgraphy in common epileptic syndromes 99
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 absence epilepsy. The 3 Hz SWC is often faster (4-5 Hz)
at onset, as shown here.
Typical absence epilepsy with maximum voltage anteriorly

EEG of a 9-year-old girl with childhood absence epilepsy. The EEG shows runs of 3-Hz bilateral synchronous occipital
intermittent rhythmic delta activity (OIRDA)
Typical absence attack in a 10-year old boy following hyperventilation. Note the occipital delta activity (OIRDA)
before the 3-Hz spike and wave
Atypical absence attack in a 20-year old woman. Note the polyspike component before slow wave
Absence epilepsy - Anteriorly dominant, typical 3-Hz spike and wave discharges
Benign Childhood Epilepsy EEG findings

The interictal EEG demonstrates the characteristic
Two benign partial epilepsy syndromes of childhood centralmidtemporal epileptiform discharges . These are
have been well defined: (1) benign rolandic epilepsy stereotyped, diphasic or sometimes triphasic sharp
(BRE), also called benign partial epilepsy of childhood waves, usually followed by an aftergoing slow wave.
with centrotemporal spikes and (2) benign partial The sharp waves average 100 to 300 µV in voltage. In
epilepsy of childhood with occipital paroxysms bipolar recordings, the discharges most often show
(BPEOP). Other less well-defined syndromes include maximal voltage in the central (C3-C4) and
frontal and parietal partial epilepsy syndromes. midtemporal (T3- T4) areas. On occasion, the maximal
voltage is displaced posteriorly, to P3-P4 or T4- T6.
Discharges are usually seen simultaneously in both
1-Benign Epilepsy of Childhood with central and temporal regions, although they may be of
Centrotemporal Spikes (BECTS) or higher voltage in one or the other of these. On
occasion, they are confined to either the central or the
Benign Rolandic Epilepsy (BRE) temporal area. They occur bilaterally and
independently in homologous areas of both
Benign epilepsy of childhood with centrotemporal
hemispheres, but in a single recording, they may
spikes (BECTS) is an idiopathic, localization-related
predominate on one side . The sharp waves occur either
epilepsy syndrome . It is also commonly referred to as
as isolated discharges or as runs of repetitive spikes.
benign rolandic epilepsy. It is one of the most
The latter is especially common during sleep.
common forms of childhood epilepsy, occurring in
Discharges may be bilateral in 30% of patients;
16% to 24% of children with epilepsy . BECTS is
when they occur bilaterally, the discharges are
characterized by two defining features, one clinical and
independent and asynchronous,however,Unilateral
one electrographic:
discharges are more common. Activating procedures
1. Stereotyped partial seizures consisting of unilateral
such as hyperventilation or photic stimulation or eye
paresthesias of the tongue, lips, inner cheeks, and
opening does not block the discharges. Sleep, however,
gums, accompanied by unilateral tonic or clonic
has a prominent activation on the epileptiform
activity of the facial and pharyngeal/laryngeal
discharges. Non-REM sleep, in particular, may show a
muscles, speech arrest (anarthria), and excessive
400-500% increase in the spike-wave index.
salivation. Nocturnal secondarily generalized
The frequency of spiking does not correlate with
seizures are common and are often the first
the frequency or severity of seizures. The EEG
manifestation of the disorder. Seizures remit
abnormality typically persists for some time after
spontaneously during adolescence.
remission of clinical seizures. The EEG discharge also
2. Interictal EEG demonstrating central-midtemporal
eventually disappears, almost always by late
spikes and otherwise normal background activity.
adolescence(at around age 15 years). On the other
hand, in patients with BRE, there is an increased
Onset of seizures usually occurs between the ages
incidence of generalized spike-and-wave discharges. In
of 4 and 10 years, although the syndrome can occur as
fact, in some patients, there may even be typical
early as the age of 2 years and, rarely, begin as late as
absence seizures. In such instances, it may be
13 years. In the majority of patients, nearly 80% in
somewhat difficult to identify the specific clinical
some series, seizures occur exclusively during sleep. In
syndrome, as to whether it is benign rolandic epilepsy
about 20%, seizures occur during both sleep and
or childhood absence epilepsy.
wakefulness. Seizures that occur solely during the
BRE appears to be a dominantly inherited
waking state are least common. Early onset seems to be
condition with variable penetrance. The reader should
predictive of a longer active phase of seizures before
keep in mind that BRE is a syndromic diagnosis with
remission . Partial status epilepticus is rare.
the EEG forming an important component of the
diagnosis. Epileptiform discharges in the rolandic
region do not necessarily mean that the patient has
BRE. The occurrence of central-midtemporal spikes in
neurologically normal patients without epilepsy is well
recognized.
Central right mid-temporal spikes in a child with BRE
Benign rolandic epilepsy associated with typical left centrotemporal spikes

Benign epileptiform discharges of childhood, left central and right temporocentral
EEG of a 9-year-old boy with BRE. In this child, the discharges are predominantly left-sided and mainly temporal in
their distribution. Note: the K complexes and sleep spindles.
EEG of a 5-year-old boy with BECTS. There are independent left and right discharges localized to C3 and C4 without
significant involvement of temporal electrodes.
Generalized spike-and-wave discharge in a patient with benign rolandic epilepsy. The first segment to the left shows
typical discharges of benign rolandic epilepsy, with bifrontal positivity. A generalized epileptiform discharge (like 3
Hz spike and wave)is seen to the right in the same patient.
Left central spike in a child with rolandic epilepsy(BRE)
Another example of generalized discharges in a child with a BECTS;such bilateral discharges are observed especially
during drowsiness but , contrary to idiopathic generalized epilepsies, they are not activated by sleep such as the next
example
Stage 2 nREM sleep ( note spindles over the anterior regions) in a child with a BECTS
2-Benign Partial Epilepsy of Childhood with has not been elucidated. A family history of epilepsy is
Occipital Paroxysms (BPEOP) evident in 37% to 44% of cases , and occipital spikes
have been reported in 26% of nonepileptic relatives.
Gastaut described a partial epilepsy that was analogous In the late-onset BPEOP variant, seizures begin
to BRE, although the 2 syndromes have important between the ages of 15 months and 17 years; the peak
differences. age at onset is between 7 and 9 years . Seizures nearly
Since publication of the initial description, it has always begin with visual symptoms (amaurosis,
become evident that BPEOP encompasses a phosphenes, illusions, or hallucinations) and are
heterogeneous group of patients whose disease is one typically brief, lasting only seconds, without alteration
of two subtypes: an early-onset variant, and a late- in consciousness . In the immediate postictal period,
onset variant that corresponds to the syndrome initially about one-third of patients develop a severe diffuse
described by Gastaut. headache, often with associated nausea and vomiting.
Although there are no epidemiological studies of Seizures tend to occur frequently, but response to
the incidence of BPEOP, several case series indicate medication is usually good. Although details of
that it is two to three times less common that BECTS . prognosis remain unresolved, the long-term outcome of
The early-onset variant accounts for most cases. the late-onset variant BPEOP is generally less
In addition to the EEG findings , the two variants favorable than that of BECTS.
of BPEOP share several features. Children are In the early-onset variant, the peak age at onset is
neurologically normal and have normal computed between 3 and 5 years. In contrast to the late-onset
tomographic and magnetic resonance imaging scans. variant, seizures lack the characteristic visual
Boys and girls are equally affected in both early- and phenomena. Rather, stereotyped seizures consist of
late-onset variants. As in BECTS, genetic factors are lateral gaze deviation and ictal vomiting, with a
clearly involved, although the pattern of inheritance varying degree of alteration in consciousness . Seizures
are exclusively nocturnal in about two-thirds of cases duration longer than 70 milliseconds. In a similar
and are typically prolonged (5 to 10 minutes or longer percentage of discharges, spikes occur without
in duration). Partial status epilepticus occurs in nearly aftergoing slow waves. Discharges occur in runs with a
half the patients. Despite the long duration of seizures degree of rhythmicity and a frequency of 1-3 Hz.
and the high incidence of status epilepticus, prognosis Typically, they are blocked or prominently attenuated
in the early-onset variant is universally excellent. Up to with eye opening. They may be unilateral or bilateral
30% of patients experience only a single seizure, and in and may occur independently on each side.
the remainder, seizures occur infrequently. Duration Hyperventilation usually has no effect on epileptiform
of the disease is typically 1 to 2 years, and nearly all activity , although a few authors have reported
patients become seizure free by age 12. activation. Similarly, in most patients, photic
stimulation has no effect on epileptiform activity . In a
EEG findings few, however, photic stimulation can either activate
EEG findings are indistinguishable in the two BPEOP epileptiform discharges or inhibit them. The inhibition
variants. The interictal EEG demonstrates normal effect seems to occur mainly with high flash rates.
background activity and occipital epileptiform Occipital discharges are activated by NREM sleep and
discharges that are morphologically stereotyped . The inhibited by REM sleep . In a minority of cases,
characteristic discharge consists of a diphasic spike or occipital discharges may be evident only during sleep.
sharp wave with a high-voltage (200- to 300-µV) In many patients-more than half in one series ,interictal
surface-negative peak, followed by a low-voltage epileptiform discharges persist after clinical remission
surface-positive peak and an aftergoing surface- of seizures, sometimes for several years. As in BECTS,
negative slow wave . Although maximal in the some patients have other epileptiform abnormalities
occipital derivations, the discharges at times extend such as generalized spike-wave or centralmidtemporal
into the posterior temporal areas . In about 20% of discharges and frontal discharges.
discharges, the principal sharp component has a
EEG of a 10-year-old girl with childhood epilepsy with occipital paroxysms. Her seizures consisted of lateral gaze
deviation and vomiting with subtle impairment in awareness.The EEG shows normal background activity and high-
amplitude occipital (T6/02) spikes that have a stereotyped waveform.
EEG of a 11-year old girl with type 2 BPEOP. Posterior bilateral spike-waves, very ample over temporal electrodes.
The changes react to eye opening. Note the presence of a mu rhythm, more obvious with open eyes.
Cryptogenic or Symptomatic Focal and the post-ictal period is characterized by temporal

and spatial disorientation and language deficit if the
Epilepsies dominant side is involved. The patient resumes normal
contact progressively and is amnesic of the seizure.
Medial temporal lobe epilepsy Seizures occurs mainly during waking and particularly
at awakening. The most common etiology is
This is the most common of focal epilepsies, and it hippocampal sclerosis, but other causes may be found:
typically associates a history of complicated febrile dysplasias, tumors(ganglioglioma, low grade tumors),
seizures followed by a period of latency before onset AVM, and a history of meningitis or encephalitis.
of epilepsy in the peri-pubertal period, and Some cases are cryptogenic. These epilepsies are
hippocampal sclerosis. Seizures may be simple, simple typically drug-resistant but may respond to surgical
followed by complex, or complex from onset. treatment.
Secondary generalization is usually observed before
treatment, or during withdrawal, and mostly occurs
during sleep. Impairment of consciousness may be EEG findings
preceded by an aura with a rising epigastric feeling, The interictal EEG shows spikes and spike-waves over
nausea, déjà-vu or jamis-vu. It is followed by staring, the anterior and middle temporal leads, especially over
oral automatisms(chewing, lip smacking…), vocal and the lower anterior temporal leads. There may also be
verbal automatisms, simple gestural automatisms, in a theta activity and even slower waves in the same
patient with more or less complete loss of contact. One region. The changes are enhanced in nREM sleep, all
may also find autonomic signs(pallor, flushing, the more if they are rare or even absent during waking.
tachycardia, breathing irregularities, mydriasis, In nREM sleep , the changes tend to diffuse over
bleching). The seizure lasts 30 seconds to 2 minutes, adjacent regions and even contralaterally. In REM
sleep, the changes become more focal. The frequency during waking but also during sleep, the latter being
and morphology of the abnormalities is determined by more common than in mesial temporal seizures.
the etiology. In cases with hippocampal sclerosis,
spikes and spike-waves often occur in pairs or triplets,
EEG findings
but they are not necessarily frequent. In other lesional
cases, slow elements may predominante, with slow
Since the epileptogenic zone is external temporal,
waves, theta waves, and slow spikes, and the
interictal changes are easily recorded by surface EEG
abnormalities may occur more frequently.
over middle and posterior temporal leads. They are
The ictal EEG shows a precise organization with
often frequent and high-voltage. According to the
flattening over the anterior and middle temporal region
etiology, the changes include spikes, spike-waves, slow
followed by rhythmic slow spikes at 6-7 Hz. The
spikes, polyspikes, polyspike-waves, fast rhythms and
spikes become progressively less rhythmical and fade
theta activities. The changes are enhanced and become
into slow wave over the same territory. The ictal
more diffuse during nREM sleep. In REM sleep, they
activity may diffuse to adjacent regions contralaterally
become more lateralized again.
after a variable delay. The surface EEG shows an
The ictal EEG shows a flattening followed by fast
apparent seizure onset that is delayed with respect to
recruiting rhythms over the middle and posterior
the onset of the aura.
temporal region, with rapid diffusion. This is followed
by rhythmic slow waves that may be faster, slower or
Lateral temporal lobe epilepsy similar(6-7Hz) to those found in mesial temporal
Seizure originating in the external temporal cortex may seizures.
or may not propagate to the limbic structures. The
seizures are simple or complex and rarely generalized.
They include simple auditory hallucinations, complex Frontal Lobe Epilepsy
auditory hallucinations or illusions, but also an
Although neither the incidence nor prevalence of
auditory dreamy state and language deficits if the
frontal lobe epilepsy (FLE) is known with certainty,
dominant temporal lobe is involved. Complex seizures
large surgical series indicate that it is the second most
without aura are associated with behavioral arrest and
common localization-related epilepsy, accounting for
non-oral automatisms, in contrast to internal temporal
about 20% of patients undergoing epilepsy surgery.
seizures. This may be followed by elements of
Unlike temporal lobe epilepsy, seizure symptoms are
propagation towards other structures. Seizures are seen
Left temporal spikes in a 39 year old woman with TLE. Note asymmetrical alpha background rhythms between
two hemisphere
heterogeneous, reflecting both the large size of the Furthermore, functional networks permit rapid
frontal lobe with its many functional and anatomical propagation within and outside the frontal lobes, which
divisions, as well as the different pathways of results in the appearance of diffuse (secondary bilateral
propagation from different areas of the frontal lobe. As synchrony), multi focal, or falsely localizing
a result, several syndromes have been described as epileptiform abnormalities .In contrast to temporal lobe
types of FLE referable to specific anatomical areas of epilepsy, the placement of additional, closely spaced
presumed seizure onset within the frontal lobe. scalp electrodes does not usually improve the
Although the ictal manifestations of frontal lobe localizing value of scalp EEG in FLE . lnterictal EEGs
seizures suggest particular localizations, no features are in FLE can demonstrate one of several patterns:
definitive for any. Recognizing significant overlap
among the regions, the ILAE Commission classified 1. For the reasons just listed, epileptiform discharges
the frontal lobe epilepsies by anatomical areas that are not identified on scalp EEG recordings in up to
produce relatively characteristic seizure symptoms: one-third of patients. This is most commonly seen in
supplementary motor, cingulate, anterior frontopolar, patients with medial frontal epilepsy.
orbitofrontal, dorsolateral, opercular, and motor cortex. 2. Secondary bilaterally synchronous discharges may
All frontal lobe seizures share a number of features: (a) be seen in up to two thirds of patients with FLE;
early and prominent motor manifestations, including these discharges are especially frequent with medial
clonic activity, asymmetrical tonic posturing, or frontal foci. The term secondary bilateral synchrony
complex semipurposeful, repetitive movements that is used in describing the bilateral discharges seen in
often involve the legs (e.g., bicycling); (b) short patients with parasagittal epileptogenic lesions.
duration with minimal or no postictal confusion; (c) 3. Focal epileptiform discharges occurring over one
occurrence in clusters; (d) frequent secondary frontal lobe are seen in 42% to 63% of cases of FLE
generalization; and (e) predilection for occurring at . When these arise from epileptogenic cortex in the
night. Three manifestations are especially correlated medial frontal lobe, the discharges are of highest
with frontal lobe epilepsy: voltage at or adjacent to the vertex.
4. High-voltage (up to 300µV), sharply contoured slow
1. Supplementary motor area seizures manifested by waves that are broadly distributed over the frontal
sudden asymmetrical tonic posturing of the limbs, regions but maximal at F3-F4 and Fp1-Fp2 are
usually with one arm extended upward, and characteristic of orbital frontal foci. These
contralateral head and eye deviation; consciousness discharges are almost always seen bilaterally to
may or may not be impaired. some extent, but they show voltage andf ield
2. Complex partial seizures with prominent motor asymmetries that accurately indicate the
activity, such as vigorous rocking, bicycling, epileptogenic hemisphere.
circling, or vocalization; minimal or no impairment
in consciousness; and no postictal confusion. Ictal EEG: The ictal EEG is nonlocalizing in
Because of their frequently bizarre manifestations, more than half the patients with FLE . Often, there is
nonepileptic psychogenic seizures are often first no electrographic correlate to be seen in scalp
suspected. Although such seizures are typical of the electrodes. Equally problematic, however, is that the
medial frontal or orbital frontal areas, they may arise early and prominent motor activity of many frontal
anywhere within the frontal lobe. lobe seizures produces large amounts of muscle and
3. Simple partial motor clonic seizures, arising from movement artifact that obscures EEG activity. False
regions within or adjacent to the primary motor localization, particularly to the temporal lobe, also
cortex. occurs as a result of frontal-limbic connections.
Although supplementary motor area seizures can be
associated with a focal rhythmic discharge localized or
EEG findings adjacent to the vertex , most other seizures of medial
frontal origin are not accompanied by a lateralized
Intericlal EEG: Diagnosis of FLE rests largely on discharge; EEGs sometimes show only diffuse,
clinical features, in as much as the EEG is often normal bilateral frontal voltage attenuation followed by
or non diagnostic. This is largely because much of the bilateral frontal or diffuse rhythmic theta or delta
frontal lobe, including the orbital-frontal cortex, activity. Although diffuse, bilateral frontal voltage
interhemispheric convexity and cingulum, and the attenuation is frequently correlated with onset of
sulcal depths are relatively inaccessible to scalp EEG orbital frontal seizures, focal rhythmic alpha or beta
recording. Consequently, small epileptogenic foci may frequency activity is sometimes seen in the frontopolar
be missed entirely; conversely, epileptiform electrodes. Seizures of dorsolateral frontal origin are
abnormalities may appear widespread because of the usually associated with a localizing ictal discharge.
often large distances and intervening cortex between
the epileptogenic area and scalp electrodes.
Juvenile myoclonic epilepsy (JME) EEG Findings
JME is a common idiopathic generalised epileptic As in other idiopathic generalized epilepsy syndromes,
syndrome . It is an inherited disorder (positive family the interictal EEG in JME is characterized by two main
history in 40% of cases). It is responsible for about 5- features:
11% of the adult epileptic population with an equal 1. Normal or near-normal background activity, with a
distribution between sexes. It appears around puberty. well-modulated alpha rhythm .
Eighty percent of first seizures occur between ages 12 2. Spontaneous bursts of generalized, bisynchronous
and 18 with a mean age of onset of 14.6 years; onset epileptiform discharges.
may, however, vary between 8 and 30 years. JME is
frequently under-diagnosed and under-appreciated. Polyspikes and polyspike-wave discharges are
Many patients do not mention that they are having characteristic of JME, although they are not
myoclonic seizures until asked specifically about body pathognomonic, Such discharges are also common in
jerks. Typically,myoclonic jerks appear 2-3 yrs before other idiopathic generalized epilepsies. However, when
the first generalized T-C seizure,although it is almost polyspikes are abundant and are the predominant form
always the latter that brings the patient to medical of epileptiform activity, it is more likely that the patient
attention. has JME than another idiopathic generalized syndrome.
JME is characterised by multiple seizure types; The epileptiform discharge consists of a burst of
myoclonic seizures with short, bilateral, single or generalized bisynchronous, symmetrical multiple
repetitive arrhythmic, irregular jerks, predominantly in spikes (polyspikes) that are of maximal voltage in the
the shoulders and arms, it mostly occurs after frontal and central regions, followed by high-voltage,
awakening from sleep. Myoclonic jerks are seen in irregular 2- to 5-Hz slow waves with intermixed
100% of JME cases and are the sine qua non of spikes. The polyspike component is often evident only
diagnosis. They occur as the only seizure type in at the beginning of the epileptiform paroxysm. The
about 3%–5% of JME patients. The amplitude and number of repetitive spikes may be as high as 20; two
force of the jerks vary. They may cause some patients to four spikes are more usual . Epileptiform activity
to suddenly fall. Some jerks occur unilaterally. can occur either as isolated polyspike-wave bursts or as
Sometimes myoclonic seizures of JME are perceived prolonged paroxysms lasting up to 20 seconds . Spike-
only as a subjective electric shock sensation inside the wave complexes and polyspikes without associated
body. Patients are sometimes reluctant, to volunteer slow waves are also frequent and may sometimes be
information about their myoclonus unless specifically the only epileptiform abnormality. The spike-wave and
asked. Sometimes, the myoclonus is noticed only by polyspike-wave discharges seen in JME are usually
the patient’s family. Myoclonus is especially marked "fast"; that is, the repetition rate is higher than the 3-Hz
in the setting of fatigue and sleep deprivation. GTCS spike-wave pattern seen in childhood absence epilepsy.
occur in 90%–95% of patients with JME. GTCS are The most common frequencies are 3.5 to 6 Hz, and the
often preceded by a few minutes of generalised mild to range is between 2 and 10 Hz . "Typical," stereotyped
moderate myoclonus of increasing frequency and 2.5- to 3-Hz spike-wave discharges, indistinguishable
intensity. They occur predominantly after awakening from those seen in childhood absence epilepsy, are
and are often precipitated by sleep deprivation. present in up to 25% of patients.
Absence seizures feature in 30-40% of patients. These Hyperventilation generally activates epileptiform
seizures are relatively infrequent, brief, and not activity , although there have been no quantitative
associated with automatisms. They may occur several studies of this effect. In a minority of patients,
times a day. Sometimes, they may be the first epileptiform activity is seen only during
manifestation of the disorder, even preceding the hyperventilation.
development of myoclonic jerks . Absence seizures in A relatively high percentage of patients,
JME are typically less frequent and less intrusive than demonstrate photosensitivity. Photosensitivity is two to
those seen in childhood absence epilepsy and three times more common among girls with JME than
frequently go unnoticed. among boys with JME. Photic stimulation, commonly
JME is the epilepsy syndrome which is most at a frequency of 10-20 Hz, will elicit a
commonly associated with photosensitivity with a photoparoxysmal response that often may outlast the
reported prevalence of 25–42% and with a female duration of the photic stimulation or even induce a
predominance. Photosensitivity is defined by the seizure
occurrence of generalised spikes, spike and wave or Ictal EEG: Myoclonic seizures are always
polyspike and wave in response to intermittent light associated with polyspike or polyspike-wave bursts
stimulation (ILS). An earlier onset is seen in that are generally indistinguishable from those that are
photosensitive patients. not accompanied by clinically detectable jerks.
Sometimes the number of multiple spikes is higher (10
to 16 Hz) with ictal discharges, and the voltage may may last as long as 4 seconds. Absence seizures in
increase from the first spike to the last. The intensity of JME are associated with generalized, somewhat
the myoclonic jerks correlates with a higher number of irregular 2.5- to 4-Hz spike and polyspike-waves that
repetitive spikes . The polyspikes are of medium to last several seconds and may be interrupted with
high voltage, maximally expressed over the frontal discontinuities lasting 1 second or less. The repetition
regions, and followed by high-voltage, 1- to 3-Hz rate of the spike-wave and polyspike-wave discharges
rhythmic slow waves . While the jerk itself is can range from 2 to 7 Hz. A classical 3-Hz spike-wave
extremely brief ("lightning-like"), the associated EEG pattern is uncommon.
discharge is typically 1 to 2 seconds in duration and
Polyspike and wave discharges seen in juvenile myoclonic epilepsy
Spike and wave discharges in a patient with JME

EEG of an 18-year-old woman with juvenile myoclonic epilepsy (JME). The interictal EEG demonstrates generalized
spike-wave and polyspike-wave discharges.
EEG of an 18-year-old patient with juvenile myoclonic epilepsy (JME). A myoclonic jerk of the arms accompanies this
burst of bilateral synchronous polyspikes.
Photoparoxysmal response in JME
Multispike and wave in JME

Two discharges of fast, irregular spike-and polyspike-waves, both associated with myoclonic jerks(recorded on EMG
leads over the deltoid muscles)
ILS in a patient with JME. Note the three photoparoxysmal responses, the first of which is associated with a myoclonic
jerk(deltoid muscle surface EMG)
Epilepsy with Generalized Tonic-Clonic always be sought, as these constitute an important

element for etiological diagnosis and prognosis.
Seizures on Awakening Specific etiologies can be found in half of the cases,
mainly a neurocutaneous syndrome(tuberous sclerosis),
The concept of awakening epilepsy was first developed
malformations, pre-, peri-, or postnatal
by Janz. This type of idiopathic generalized epilepsy is
encephalopathies, as well as metabolic, degenerative,
less common than JME. Onset is generally in the
or chromosomal diseases, or prenatal infections.
second decade but earlier or later onset is possible
Prognosis is in part related to the etiology. It has poor
(range: 5-25 years). There is a slight male
prognosis in most cases, often evolving into another
predominance . A family history of epilepsy is
epileptic encephalopathy, such as the lennox- Gastaut
frequent. Generalized tonic-clonic seizures occur
syndrome, or into another severe type of epilepsy
within one hour of spontaneous morning awakening at
associated with major mental retardation.
the end of the nocturnal sleep period(90%), or during
spontaneous or provoked intermediate awakenings. A
lesser peak of occurrence is found during the evening
relaxation period. Seizures are rare and are often
EEG findings
elicited by sleep deprivation or excessive consumption
The interictal EEG often shows typical
of alcohol on the previous evening. Some patients may
"hypsarrhythmia". Hypsarrhythmia is seen in 75% of
experience rare myoclonic jerks or absences. Prognosis
patients with West syndrome. Background is
is usually good, as seizures remain rare spontaneously
disorganized, with high-voltage, asynchronous and
and treatment is effective.
arrhythmic slow waves, in association with asymmetric
and multifocal spikes and polyspikes. It is often
necessary to lower the amplitude to have a better look
EEG Findgs at the EEG tracings. Hypsarrhythmia is mostly present
at onset and can precede the occurrence of spasms. It is
Background is normal. There are rare generalized
seen in waking and is fragmented during sleep. It can
spike-waves and rare fast polyspike-waves(2-4Hz).
occur selectively during somnolence. In light nREM
Changes are activated at spontaneous or provoked
sleep,it becomes discontinuous. Spikes become more
awakening or during transitions between sleep stages.
frequent and tend to be more diffuse and
In some patients, interictal changes will never be
synchronouos. Irregular bursts of polyspike waves are
recorded.
separated by apparently fairly normal segments that
may include sleep transients like spindles. Duration of
REM sleep is shortened.
West,s Syndrome Clinical spasms are associated with a marked
suppression of the background that lasts for the
duration of the spasm. This characteristic response is
The west syndrome is one of the most frequent called the "electrodecremental response”. Spasms are
epileptic syndrome in infants, with an incidence of 2.9- associated with a brief tonic muscular contraction
4.9 per 100,000. This encephalopathy is characterized evidenced by surface EMG, that is symmetric or not
by a triad: 1.Infantile spasms 2.developmental according to the etiology. Serial spasms may occur at
retardation 3.hypsarrhythmia on EEG. Onset nearly awakening, with or without interictal hypsarrhythmia.
always occurs in the first year of life, usually between The presence of hypsarrhythmia between spasms may
the ages of 4 and 7 months . Nearly 90% of cases are be characteristic of idiopathic cases and of a better
associated with neurological abnormalities arising from prognosis. Focal seizures can initiate the series of
a diverse array of structural, metabolic, and genetic spasms, occur during the series, or occur
disorders. Only 10% to 15% of cases are independently. EEG is useful in judging successful
cryptogenic/idiopathic. treatment of West syndrome. Typically, shortly after
Spasms are brief, symmetric, bilateral tonic treatment with adrenocorticotropic hormone (ACTH)
contractions of muscles of trunk, neck and limbs(flexor or vigabatrin is initiated, the spasms stop and
spasms). Contractions are often followed by crying. hypsarrhythmia disappears.
Less frequently, there are extensor spasms with a
sudden extension of trunk and neck with abduction and
extension of the arms. Spasms can also be mixed
(flexor-extensor), asymmetric or unilateral, and in the
two latter cases often contralateral to a brain lesion.
Spasms occur in series, often at awakening or at sleep
onset, less commonly during nREM sleep and never
during REM sleep. Associated focal seizures should
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 (infantile spasms).
Electrodecremental episode associated with infantile spasms (EEG during a spasm)

Typical hypsarrhythmia in an awake 5-month-old infant. The background activity is disorganized and replaced
by a high-voltage activity with spikes, polyspikes and slow waves.
Hypsarrhythmia in a 5-month old child with a suprasellar hypothalamic hamartoma and tonic seizure
Flexor spasms in an infant with west syndrome. At the 6th second, there is a burst of fast rhythms on all leads,
followed by desynchronisation with low voltage activity. Clinically, the child has a flexor spasm.
Lennox-Gastaut syndrome
1. High seizure frequency; tonic, atonic, and atypical
The Lennox-Gastaut syndrome (LGS) encompasses a absence seizures are the most common. Myoclonic,
characteristic triad of severe generalized epilepsy, generalized tonic-clonic, and partial seizures may
mental retardation,and an EEG pattern of slow-spike- also be present. As a rule, patients with LGS have
and-wave discharges. Age at onset is usually between 1 multiple seizure types, and at least one episode of
and 8 years; most cases begin between the ages of 2 status epilepticus occurs in the majority .
and 5 years. Onset after 10 years of age is rare. The 2. Mental retardation, in general. More recently, some
ILAE Classification of Epilepsies and Epileptic authors have argued that behavioral disorders, not
Syndromes includes LGS among the generalized accompanied by cognitive impairment, should be
cryptogenic or symptomatic epilepsies. It is defined by sufficient for diagnosis.
the following criteria: 3. EEG demonstrating abnormal background activity
with diffuse sharp slow waves that have a repetition
rate of less than 3 Hz. There are often multifocal however, and in some patients, the discharges may
spikes or sharp waves and, during sleep, frequent actually decrease in both NREM and REM sleep .
bursts of 10Hz and faster frequencies. On occasion, SSW discharges are prominent during
sleep even when they are infrequent during
LGS accounts for about 10% of all childhood wakefulness, which underscores the importance of
epilepsies , although the actual prevalence may be obtaining an adequate sleep recording .
much lower if rigorous criteria are used. Tonic, atonic, Polyspikewave discharges may emerge during sleep.
and myoclonic seizures can all result in the In a minority of patients, sleep causes fragmentation
characteristic "drop attacks" seen in LGS, and of SSW bursts and a pseudoperiodic or burst-
differentiating among these on the basis of clinical suppression appearance, with 2- to 3-second
features alone is often difficult. Moreover, there is paroxysms of SSW alternating with diffuse voltage
significant overlap among the ictal patterns. Despite attenuation of background activity.
the consistent electroclinical triad, LGS cannot be
attributed to a single cause or common pathological 2-Paroxymal fast activity(PFA)or polyspike
substrate. Diverse prenatal, perinatal, and postnatal discharges: the second defining electrographic
disorders have been implicated. About two-thirds of feature of LGS, is present mainly or exclusively
cases are considered symptomatic, because a during sleep in nearly all patients . PFA consists of
preexisting neurological condition can be identified. diffuse, bilaterally synchronous bursts of 15- to 20Hz
One-third of cases are classified as cryptogenic. activity that last several seconds. It is of highest
voltage in the frontal areas . The frequency of PFA
can vary from 7 to 30 Hz, and the voltage may vary
EEG findings from 25 to 250 µV The duration of PFA bursts
ranges from 2 to 12 seconds . Bursts of PFA occur
EEG features of LGS may be divided into interictal up to hundreds of times each night, but only in
and ictal. Interictal EEG features include: NREM sleep; they are absent during REM .
Although indistinguishable from the ictal pattern
1-Slow spike and wave pattern(SSW) that are associated with tonic seizures , the majority of PFA
bilateral,symmetrical and highest voltage in fronto- discharges are not accompanied by any visually
central with frequency of 1.5-2.5 Hz . SSW discernible clinical changes. Autonomic changes,
discharges can vary, both between and within including tachycardia and apnea, can occur in
individual bursts, in morphological appearance, association with PFA, even when motor
distribution,voltage, and frequency. The repetition manifestations are absent . Thus, it can be argued
rate of SSW discharges can be quite erratic, with that PFA is not, strictly speaking, an interictal
frequencies ranging from I to 4 Hz. The extended finding, although the ictal manifestations may be
runs of SSW discharges commonly lack discrete subtle and not visually detectable.
onsets or terminations; sometimes they are nearly
continuous during the greater part of an entire 3-Background slowing: Diffuse abnormalities of
recording. Most SSW discharges are not background activity occur in up to 90% of patients
accompanied by obvious clinical manifestations. with LGS . In two-thirds of cases, background
Although usually symmetrical, SSW complexes slowing is moderate to severe and is generally
sometimes show shifting asymmetries. Persistent correlated with the degree of cognitive impairment.
focal or lateralized asymmetries of SSW discharges
usually occur in symptomatic cases with focal Ictal EEG features: Electrographic accompaniment
neurological abnormalities. NREM sleep varies with the seizure type.However, there is
dramatically enhances SSW discharges in the great significant overlap among the ictal patterns between
majority of patients . This effect is not universal, the various type of seizures.
Eleven-year-old boy with moderately severe mental retardation and intractable generalized tonic, atonic,
myoclonic,and atypical absence seizures since age 4 years. Awake EEG showed generalized sharp- and slow-wave
complexes.
EEG of a 29-year-old woman who had Lennox-Gastaut syndrome (LGS) since early childhood. Interictal EEG
recording demonstrating diffuse background delta frequency slowing and nearly continuous 1.5- to 2.0-Hz bilateral
synchronous slow-spike-and-wave (SSW) discharges. During this time, the patient was attentive and interactive.
Atypical absence seizure in a patient with LGS. Clinically characterized by decreased responsiveness and gaze
deviation to the right. Although very similar to the interictal recording shown in previos recordind, the SSW
discharges appear more organized and sustained at a consistent 2-Hz frequency.
Sleep EEG of a patient with Lennox-Gastaut syndrome (LGS). There are frequent bursts of diffuse 16- to 20-Hz
paroxysmal fast activity (PFA) without any visually detectable clinical changes.
Generalized paroxysmal fast activity and electrodecrement. This pattern is characteristic of the the symptomatic/
cryptogenic epilepsies of the Lennox-Gastaut type, and may be subclinical or associated with tonic or atonic seizures.
Tonic seizure in Lennox-Gastaut syndrome (LGS). During sleep, the child exhibited abrupt onset of arm and neck
stiffening, which lasted several seconds. The EEG shows an 8-second run of bilateral synchronous 16- to 20-Hz
activity, which is the ictal discharge.
The Syndrome of Continuous Spike and The Syndrome of Acquired Epileptic

Wave Discharges During Slow Sleep Aphasia (Landau-Kleffner syndrome)
(CSWS)[electrical status epilepticus
This syndrome, first described by Landau and
during slow sleep] Kleffner(LKS) , is characterized by acquired aphasia
This syndrome was first described by Patry et al as associated with epileptiform activity on EEG
"subclinical electrical status epilepticus induced by ("epileptic aphasia"). Although the nature of this
sleep." It was later renamed because of the lack of syndrome is controversial, it is probably not
typical clinical features associated with status fundamentally an epileptic disorder. It occurs in
epilepticus. The syndrome of CSWS is a rare previously healthy children between the ages of 3- 9
condition, accounting for fewer than 0.5% of cases of years (peak incidence, 5 to 7 years), and never after
childhood epilepsies . Age at onset ranges from 1 to 12 age 12. Boys are affected twice as often.The first
years, but onset peaks between the ages of 5 and 7 indication of aphasia is verbal auditory agnosia , but
years. In primary school-age children, there is a more language function continues to deteriorate. Some
or less pronounced cognitive regression, psychomotor children become mute and do not respond even to
impairment, and epilepsy of varied severity, with focal nonverbal sounds. Hyperactivity and personality
or generalized seizures including atypical absences and changes appear as the aphasia worsens . Seizures occur
falls. Boys are more concerned (63%). More than 1/3 in about 70% of patients; they tend to be relatively
of patients have abnormal neuroimaging, e.g; infrequent, although status epilepticus has been
polymicrogyria, unilateral or diffuse cortical atrophy, reported. Partial motor, atypical absence, generalized
or porencephalia. CSWS disappears in all cases after 1 tonic-clonic, and atonic seizures have all been reported
to 5 years. In nearly all patients, seizures appear 1 to 2 . More subtle seizures, such as eyelid myoclonia,ocular
years before the EEG abnormality of this syndrome . deviation, and head drops also occur. Type and
Simple partial motor and generalized tonic-clonic frequency of seizures are not correlated with outcome .
seizures predominate. Later, with appearance of the Similarly, treatment with antiseizure drugs does not
syndrome of CSWS, other seizure types emerge, clearly affect aphasia, EEG findings, or prognosis.
including atypical absence seizures associated with About two-thirds of children have residual language
atonia and falls. Most patients have frequent seizures, impairment; cognitive and behavioral abnormalities are
often multiple times in a week or even in a single day . less frequent consequences.
Tonic seizures do not occur . With development of the Total return to normal is possible in 10-20% of
syndrome, nearly all patients have a significant decline cases. In its typical forms, the landau-kleffner
in IQ with deterioration in language, temporospatial syndrome is cryptogenic.
disorientation, impaired memory, and reduced attention
span. Behavioral changes such as aggressiveness or,
rarely, psychosis also occur. EEG findings
A paroxysmal EEG is one of the defining features of
LKS, and epileptiform discharges are thus invariably
EEG findings present. Epileptiform activity is extremely variable in
both location and amount. High-voltage multi focal
At seizure onset, around age 4-5, EEG changes are spikes and spike-wave discharges occur both singly
non-specific. CSWS appear at around age 5 to 7. and repetitively . Discharges occur over the posterior
During the period of CSWS, the children will exhibit temporal regions preferentially but are not limited to
bursts of diffuse spike-waves at 2-3Hz, which can be these areas . Epileptiform activity can be unilateral or
associated with absences, during waking. CSWS bilateral. When bilateral, the discharges can be diffuse
appear as soon as the child falls asleep, and persist and bisynchronous and either symmetrical or
throughout the stages of nREM sleep, during which asymmetrical. In the early stages of the disorder,
they occupy more than 85% of the total duration. epileptiform activity may be limited to sleep. The EEG
However, a lesser proportion is accepted by some abnormalities vary considerably over time, so that the
authors. Discharges can be asymmetric. During REM distribution, abundance, and topography may change
sleep, there is a fragmentation of spike-wave from one tracing to the next . NREM sleep activates
discharges and the percentage falls below 25%. The epileptiform activity, often to a marked degree.
discharges can ever disappear, and focal, frontally Epileptiform discharges exhibit larger fields, tend to
predominant changes can be discerned. In REM sleep, become generalized, and occur repetitively at
subclinical frontal seizures can also be recorded and frequencies of 1.5 to 3 Hz . During REM sleep, the slow
are a characteristic element of the syndrome. The EEG spike-wave pattern fragments and focal or multi focal
becomes progressively normal after remission of discharges appear in a pattern similar to that seen in the
epilepsy. waking state . Sometimes there is continuous
(occupying more than 85% of sleep time) spike-wave degree of language dysfunction persists in the majority.
activity that is similar to that seen in the syndrome of Most patients show improvement, but the degree of
CSWS . Seizure remit and the EEG normalizes in recovery is variable and unpredictable; some patients
nearly all patients by the end of adolescence , but some remain profoundly impaired.
A
EEG of a 6-year-old boy with Landau-Kleffner syndrome (LKS). He had been neurologically normal until 9 months
previously, when he developed rapidly progressive loss of language skills. He had only three seizures, all generalized
convulsions. Results of brain imaging, cerebrospinal fluid studies, and metabolic evaluation were normal. A: EEG in the
waking state demonstrates mild slowing of background activity and infrequent right midtemporal spikes.
B
B: EEG during non-rapid-eye-movement sleep shows nearly continuous spike-and wave discharges. Although
broadly distributed bilaterally, they are maximal over the right temporal region
Chapter 10
Epileptiform Normal Variants
Epileptiform normal variants are EEG patterns that SSSs have a single aftercoming slow-wave component
resemble epileptogenic abnormalities. Most of these or may be associated with an aftercoming dip in the
patterns initially were thought to be associated with background; however, they do not have the prominent
epilepsy or other neurological conditions but aftercoming slow wave that temporal spikes have, and
subsequently were demonstrated to have no such they do not occur in repetitive trains. The main features
significance. They now are considered normal variants of SSSs are in their name: duration is short, amplitude
of no clinical significance. Their recognition is is small, and an easy guideline states that SSSs
important to avoid overinterpretation or generally should be less than 50 µV and less than 50
misinterpretation with regard to their significance. This milliseconds. Rarely seen in children, they are seen
chapter reviews the following such patterns: small most often in adults and the elderly. They can occur in
sharp spikes (SSS), wicket spikes, 14- and 6-Hz epileptic patients but often are seen in healthy
positive spikes, phantom spike and waves, individuals. They may occur in patients with CVA,
psychomotor variants, subclinical rhythmic EEG syncopal attacks,and psychiatric problems(manic-
discharges of adults (SREDA), and midline theta. depressive). SSSs are generally easy to distinguish
from spikes because of their short duration and small
amplitude.
Small Sharp Spikes(SSSs)
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 or frontotemporal ,
either unilateral or bilaterally independent, and with a
broad field of distribution. Morphology is typically
monophasic, occasionally diphasic or polyphasic, and
the decline after the first negative peak is very steep.
Small sharp spikes or BETs. Note that these waveforms do not correspond to ECG see bottom trace.
Small sharp spikes

Epileptiform Normal Variants 129
Left temporal small sharp spike. Note low amplitude

(<50mA)and short duration (<50msec)
Wicket spikes wicket spikes especially when wicket spikes occur

singly. Although wicket spikes are seen mainly during
First described by Reiher and Lebel in 1977, Wicket drowsiness and light sleep, but may be present during
spikes are trains of arch shaped or a single spike-like the awake recording and are often masked by other
waveform that resembles a Mu rhythm. Wickets have background rhythms and usually emerge or become
a frequency of 6 to 11 Hz and range from 60 to 200 apparent during drowsiness, when the alpha and other
microvolts in amplitude. Wicket spikes occur awake patterns disappear.
bilaterally or independently over the temporal regions
and there is usually no slow wave seen after the spike-
like waveform. Wickets are best seen in drowsiness
and light sleep when the alpha rhythm drops out. They
occur perdominantly in adults older than 30 years . It
can be difficult to differentiate temporal spikes from
Wickets
Wicket Spikes
Wicket spikes in the left temporal region
14- and 6-Hz positive spikes asynchronously or independently over the two sides
but may preferentially involve one side; they may also
These bursts occur predominantly during drowsiness shift from side to side in predominance. In a normal
and light sleep and consist of short trains of arch- population, 14- and 6-Hz positive bursts begin to
shaped waveforms with alternating positive spiky appear in children between 3 and 4 years old, are
components and a negative, smooth, rounded maximally expressed in the adolescent age group (with
waveform that resembles a sleep spindle with a sharp a peak at age 13-14 years), and then progressively
positive phase. The bursts occur at a rate of 14 Hz or 6- decrease in incidence with increasing age.
7 Hz and last from 0.5 to 1 second. Usually, the faster Sleep spindles - 12 to 14 hertz bursts of rhythmic
frequency is the more prevalent, but the slower rate can waves which often increase and decrease in voltage
occur either independently or in association with a train and are maximal in the central midline head region.
of 14-Hz positive bursts. The waveform is best
displayed on a long-distance or referential montage to 14 and 6 hertz positive spikes - surface-positive spikes
the ear. It usually has maximal amplitude over the most prominent in the posteriortemporal regions
posterior temporal region. The bursts can occur occurring at 14 Hz, 6 Hz, or a mixture of 14 Hz and 6 Hz
14 and 6Hz positive spikes
14 and 6Hz positive spikes in the 6th and 7th second, seen in posterior temporal, temporal and central regions on
this contralateral referential montage
Phantom spike and waves been called the "phantom spike and wave" because of
the evanescent nature of the spike, which is usually
(6Hz spike and wave) very brief and small in amplitude, in contrast to the
more prominent slow-wave component, which has a
The 6-Hz spike-and-wave discharges have a repetition higher amplitude and a more widespread distribution.
rate of 6 Hz, with a range of 5-7 Hz. The bursts are The 6-Hz spike-and-wave pattern is seen in both
usually brief, lasting 1 or 2 seconds, although rarely adolescents and adults. It generally occurs during
they persist for 3 or 4 seconds. The pattern has also relaxed wakefulness and stage I sleep and disappears
during deeper levels of sleep. Location is usually Phantom spike and wave may be difficult to distinguish
diffuse, bisynchronous, and relatively symmetric. This from the definitive clinically significant spike and
pattern may predominate in the anterior and posterior wave complexes.A helpful way to distinguish them is
head regions. Morphology is a typically small (<30 µV by the tendency of benign phantom spike and waves to
and <30 ms), evanescent diphasic spike followed by a disappear during sleep while epileptic discharges(spike
higher (50-100 µV) slow wave component. Thus, at and wave complexes)tend to persist or become more
times the spike component may be difficult to see. prominent with deeper levels of sleep.
Six-Hertz spike-and-wave bursts in a 39-year-old woman

EEG of a 26-year-old patient, showing 6 Hz spike wave paroxysms (phantom spike wave)
psychomotor variants (Rhythmic seizures. Amplitude is medium to high. Psychomotor

variant differs from a seizure discharge because it is
Midtemporal Theta of Drowsiness) usually a monomorphic or monorhythmic pattern that
does not evolve into other frequencies or waveforms as
A more useful and descriptive term is rhythmic
usually occurs during seizures.
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. It is an unusual form that occurs as
asymmetrical runs of theta or delta activity primarily in
the temporal regions, lasting for a few seconds or as
long as 30-45 and thus resemble temporal lobe
RTMD
Subclinical rhythmic EEG discharges of contoured waveform of 5 - 6 hertz. Once developed, the
pattern sustains its rhythmic fashion until gradually
adults (SREDA) dissolving into the background activity. SREDA may last
from a brief 4 seconds to a prolonged 80 seconds in either
This uncommon pattern is seen mainly in people older than the parietal and/or temporal head regions bilaterally. Once
50 years. SREDA may occur at rest or during drowsiness, you have identified SREDA, you must distinguish it from
and occasionally occurs mainly during hyperventilation. epileptiform activity by having the patient perform various
This 40 to 100 microvolt discharge is a repetitive sharply mental or physical activities during the discharge period to
define the patients level of consciousness. Use such discharges and bear no clinical motor manifestations or
techniques as eye opening and closing, mental arithmetic, complaint of sensory symptoms, as might be found during a
reading, answering questions, and hyperventilation. All partial seizure.
patients with SREDA are fully responsive during the
SREDA
Another sample of SERDA

drowsiness, and is usually reactive to eye opening or limb

Midline Theta movement. Although initially described in association with
temporal lobe epilepsy, it probably represents a normal
This is a focal rhythm maximal at the midline, most variant. Midline theta rhythm does not have any clinical
prominently at Cz, which occasionally may spread to significance and appears to represent a nonspecific variant of
adjacent electrodes. It has a frequency of 5-7 Hz and theta activity.
typically has an arciform, spiky, mulike appearance. It
waxes and wanes, can appear during wakefulness or
Midline theta rhythm

Chapter 11
Nonepileptic Abnormalities
It is an obvious but important fact that the differentiating various types of lesions, this clearly has
electroencephalogram (EEG) evaluates brain function, not been clinically useful in the modern era. The
not structure. Although many different pathological exercise of describing EEG abnormalities by pathology
processes disturb brain function, the repertoire of which is common in EEG texts, is therefore not
resulting EEG abnormalities is limited. As with other followed here. Instead, the different patterns of
physiological tests, EEG abnormalities, although abnormal EEG and their clinical significance are
reliable indicators of brain dysfunction, cannot, except reviewed.
in rare instances, distinguish etiology or pathology. The abnormal nonepileptic EEG abnormalities
Advances in neuroimaging have fortunately reduced may be broadly divided into four catrgories:
dependence on the EEG for information that it cannot
reliably provide, while new methods of data processing 1. Abnormalities of the background rhythms
have led to further development of its usefulness in 2. Abnormal sleep patterns
examining brain physiology.Although at one time 3. Focal or generalized abnormal slow activity
authors discussed the application of EEG in 4. Abnormal periodic patterns
1. Abnormalities of the background rhythms
Alterations in rate, rhythm, distribution, symmetry, In the awake adult an alpha rhythm of less than
amplitude, or reactivity of the background activity may 8Hz is abnormal. Since a number of clinical conditions
occur during various CNS disorders. The alterations can produce slowing of the alpha rhythm, the slowing
may involve one or more of the physiological rhythms, is considered a nonspecific abnormality. Thus, bilateral
namely, the alpha, beta, or mu rhythms. slowing of the alpha rhythm may be seen in metabolic,
toxic, and infectious encephalopathies of diverse
etiology. It is also a consistent finding in patient with
Alpha rhythm dementia irrespective of the underlying cause. The
degree of slowing often parallels alterations in the
Generally, absent or scanty posterior alpha rhythm may mental status of the patient. It should also be noted
be due eye opening, attention, anxiety, or that the alpha rhythm slows down in patients with
drowsiness.Some asymptomatic individuals normally hypothyroidism and can become normal when a
have little or no alpha rhythm,perhaps on a genetic euthyroid state results from adequate treatment.
basis. Asymmetrical slowing of the alpha rhythm with a
consistent difference of greater than 1.5Hz between
the two sides is abnormal and should suggest the cardiac arrest. In the case of alpha coma resulting from
possibility of a lesion on the slower side. However, lower brain stem lesions, there may be some degree of
such a finding does not necessarily indicate the reactivity. This contrasts with findings in psychogenic
presence of a lesion in the occipital lobe itself; unresponsiveness where reactivity to eye opening is
asymmetrical slowing of the alpha rhythm is known to normal.
occur even with lesions that are more anteriorly A focal increase in amplitude and or frequency of
located. the alpha rhythm is known to occur in patients with
A difference in amplitude of the alpha rhythm structural lesions, particularly tumors; but this is quite
between the two sides is considered significant if it an uncommon finding. Remember that a localized
exceeds 50%. Since the alpha rhythm in most normal increase in amplitude may also be seen over a skull
persons is of higher amplitude on the right side, even a defect.
35% decrease on the right side may be significant.
Lesions that involve the cerebral cortex, especially in
the posterior regions or that cause accumulation of the Unilateral failure of alpha blocking on eye opening:
fluid between the brain and the recording electrode, as
in the case of subdural or scalp edema, may lead to often referred to as bancaud,s phenomenon, occurs
attenuation of alpha rhythm ipsilaterally. with lesions of the parietal and temporal lobe on the
Markedly diminished background amplitude on side which fails to block.
one side of the EEG, compared to homologous
channels of the contralateral hemisphere, is found with
abnormalities of cortical gray matter, or with excess Bilateral failure of alpha blocking:
fluid between the cortex and recording electrodes. This
finding is characteristic of ischemic stroke with gray Normal subjects show great variability of alpha
matter involvement or subdural hematoma. In patients blocking and may have only very brief reductions of
with gray matter involvement, concurrent white matter alpha amplitude in response to eye opening and
involvement causing delta activity is typical. alerting.
Decreased background amplitude also may occur with Unilateral cerebral lesions located in the frontal
congenital lesions, such as porencephalic cysts, or with or temporal lobes that abolish the blocking of alpha
Sturge-Weber syndrome. Transient background activity are usually associated with an impairment of
attenuation also is characteristic of the postictal EEG of consciousness, prominent neurological deficits, or
patients with focal-onset seizures. Focal suppression both. In contrast, lesions located in the parietal or
will usually involve multiple electrodes. Focal occipital lobes that abolish blocking of the alpha
suppression which is confined to one electrode is more rhythm are often not associated with impaired
likely to be due to smear of electrode paste, or some consciousness or severe deficits.
other artifact which affects the recording system. Less Binocular blindness, when acquired after the
commonly, increased amplitude of background development of alpha, leads to a loss of the reactivity
waveforms (alpha rhythm, sleep spindles, beta activity, of alpha rhythm to eye opening. The alpha rhythm in
or mu rhythm) can be seen ipsilateral to cerebral this condition may have a central or unusually wide
lesions. distribution. Like congenitally blind persons, persons
Abnormalities may also occur in the distribution with acquired blindness may have no alpha rhythm and
of the alpha rhythm. Normally, it is distributed in the may develop occipital spikes even in the absence of
occipital, parietal, and, to some extent, posterior occipital lesions.
temporal areas; however, activity may occur over Monocular blindness or loss of discrimiminative
widespread areas, including the frontal regions. Such vision can cause failure of alpha blocking in both
an alpha patterns is abnormal and is seen in alpha hemisphere when the blind eye is opened; opening of
coma, which may result from a number of conditions the seeing eye produces normal bilateral alpha
such as brain stem infarct or cerebral anoxia, or it may blocking.
be a drug effect. In this context, it is worth restating
that an alpha rhythm may appear spuriously in the
frontal areas when using an average potential reference Beta activity
, and this should not be mistaken for an alpha coma
pattern. Beta activity in normal controls may be up to 35%
Lack of reactivity to eye opening is a significant lower on one side, but a greater asymmetry, especially
finding, particularly if consistently demonstrated on if combined with other abnormalities, is a sensitive
one side. This may be an early finding in occipital lobe indicator of cortical injury underlying the region of
lesions. A total lack of reactivity of the alpha rhythm lower amplitude.
is a feature that may be seen in alpha coma, Both attenuation and accentuation of beta activity
particularly in cases of diffuse cerebral anoxia due to may be abnormal. Beta attenuation is often seen in
Nonepileptic Abnormalities 141
Epilepsy with Generalized Tonic-Clonic always be sought, as these constitute an important

element for etiological diagnosis and prognosis.
Seizures on Awakening Specific etiologies can be found in half of the cases,
mainly a neurocutaneous syndrome(tuberous sclerosis),
The concept of awakening epilepsy was first developed
malformations, pre-, peri-, or postnatal
by Janz. This type of idiopathic generalized epilepsy is
encephalopathies, as well as metabolic, degenerative,
less common than JME. Onset is generally in the
or chromosomal diseases, or prenatal infections.
second decade but earlier or later onset is possible
Prognosis is in part related to the etiology. It has poor
(range: 5-25 years). There is a slight male
prognosis in most cases, often evolving into another
predominance . A family history of epilepsy is
epileptic encephalopathy, such as the lennox- Gastaut
frequent. Generalized tonic-clonic seizures occur
syndrome, or into another severe type of epilepsy
within one hour of spontaneous morning awakening at
associated with major mental retardation.
the end of the nocturnal sleep period(90%), or during
spontaneous or provoked intermediate awakenings. A
lesser peak of occurrence is found during the evening
relaxation period. Seizures are rare and are often
EEG findings
elicited by sleep deprivation or excessive consumption
The interictal EEG often shows typical
of alcohol on the previous evening. Some patients may
"hypsarrhythmia". Hypsarrhythmia is seen in 75% of
experience rare myoclonic jerks or absences. Prognosis
patients with West syndrome. Background is
is usually good, as seizures remain rare spontaneously
disorganized, with high-voltage, asynchronous and
and treatment is effective.
arrhythmic slow waves, in association with asymmetric
and multifocal spikes and polyspikes. It is often
necessary to lower the amplitude to have a better look
EEG Findgs at the EEG tracings. Hypsarrhythmia is mostly present
at onset and can precede the occurrence of spasms. It is
Background is normal. There are rare generalized
seen in waking and is fragmented during sleep. It can
spike-waves and rare fast polyspike-waves(2-4Hz).
occur selectively during somnolence. In light nREM
Changes are activated at spontaneous or provoked
sleep,it becomes discontinuous. Spikes become more
awakening or during transitions between sleep stages.
frequent and tend to be more diffuse and
In some patients, interictal changes will never be
synchronouos. Irregular bursts of polyspike waves are
recorded.
separated by apparently fairly normal segments that
may include sleep transients like spindles. Duration of
REM sleep is shortened.
West,s Syndrome Clinical spasms are associated with a marked
suppression of the background that lasts for the
duration of the spasm. This characteristic response is
The west syndrome is one of the most frequent called the "electrodecremental response”. Spasms are
epileptic syndrome in infants, with an incidence of 2.9- associated with a brief tonic muscular contraction
4.9 per 100,000. This encephalopathy is characterized evidenced by surface EMG, that is symmetric or not
by a triad: 1.Infantile spasms 2.developmental according to the etiology. Serial spasms may occur at
retardation 3.hypsarrhythmia on EEG. Onset nearly awakening, with or without interictal hypsarrhythmia.
always occurs in the first year of life, usually between The presence of hypsarrhythmia between spasms may
the ages of 4 and 7 months . Nearly 90% of cases are be characteristic of idiopathic cases and of a better
associated with neurological abnormalities arising from prognosis. Focal seizures can initiate the series of
a diverse array of structural, metabolic, and genetic spasms, occur during the series, or occur
disorders. Only 10% to 15% of cases are independently. EEG is useful in judging successful
cryptogenic/idiopathic. treatment of West syndrome. Typically, shortly after
Spasms are brief, symmetric, bilateral tonic treatment with adrenocorticotropic hormone (ACTH)
contractions of muscles of trunk, neck and limbs(flexor or vigabatrin is initiated, the spasms stop and
spasms). Contractions are often followed by crying. hypsarrhythmia disappears.
Less frequently, there are extensor spasms with a
sudden extension of trunk and neck with abduction and
extension of the arms. Spasms can also be mixed
(flexor-extensor), asymmetric or unilateral, and in the
two latter cases often contralateral to a brain lesion.
Spasms occur in series, often at awakening or at sleep
onset, less commonly during nREM sleep and never
during REM sleep. Associated focal seizures should
Focal EEG waveform abnormalities. This EEG of a 62-year-old patient with a right parietal glioblastoma . As you
see it demonstrates decrease in amplitude of the ongoing background activity on right side, indicating that an
abnormality of cortical gray matter is present as well.
Left background suppression in 7y-old boy with a large left frontotemporal porencephalic cyst. Note a well developed alpha
rhythm is seen occipitally in both sides.
Focal attenuation of posterior alpha rhythm on the right side after a seizure
Increased beta activity over a right frontal skull defect(breach effect)

Excess beta activity. This patient has been treated with clonazepam
Excessive beta activity in a comatose patient

Generalized suppression background with intermittent bursts in a 76 year-old man with anoxic encephalopathy
2. Abnormal sleep patterns
Amplitude asymmetry of sleep spindles is suggestive Another group of sleep- pattern abnormalities
of a lesion on the side with the lower amplitude. This includes disorders of sleep architecture. A person
may happen both in structural lesions and also when normally goes through stage 1 and 2 sleep before the
there is abnormal collection of fluid between the brain first phase of REM sleep occurs,usually 90 minutes
and the recording electrode, as in subdural hematoma. after the onset of sleep. But the REM phase can occur
By contrast, sleep spindles may appear with higher at the onset of sleep,and this abnormality is a feature of
amplitude over a skull defect. narcolepsy. Polysomnographic studies are needed to
The V waves may also be asymmetrical in evaluate such sleep disorders.
amplitude. The presence of consistently asymmetrical
V waves indicates a structural lesion,a subdural
hematoma or effusion on the side of a skull defect.
Asymmetry of sleep spindles in a 36-year-old patient with a right thalamic glioma.
Asymmetric reduced sleep spindle in left hemisphere in a 29 year old man with TLE
3. Focal or generalized abnormal slow activity
One of the commonest abnormalities in EEG is the A. Generalized intermittent slow

occurrence of abnormal slow activity. It must be
understood that certain forms of slow activity are activity
entirely normal. These include the delta activity that This is a common and easily identified abnormal EEG
occurs in stages 3 and 4 sleep,the theta activity that is pattern. It consists of intermittent rhythmic, usually
present in the background activity of children during monomorphic, slow activity most commonly occurring
wakefulness,and also the theta or delta activity that in the delta frequency band. The acronym IRDA
may be seen during hyperventilation. The distinction (intermittent rhythmic delta activity) is often used for
between normality and abnormality is less precise in this pattern. The activity is characteristically bilateral
the case of theta than delta activity. With theta activity, and synchronous, showing frontal (FIRDA) or occipital
asymmetries in amplitude and frequency may be more dominance(OIRDA); rarely, it may be most prominent
significant than the mere presence of the activity. This over the temporal areas. The dominance seems to be
is due to the variable occurrence of theta activity in age related, OIRDA being more common in children.
drowsiness and in the waking state of normal young Intermittent rhythmic delta activity is usually of high
and very old persons. amplitude; it stands out from the background and often
Slow activity may occur intermittent or has a frequency of 2to 3 Hz. These patterns attenuate
persistent. It can be generalized, focal, or regional. with alerting or eye opening. On the other hand,eye
It may be rhythmic (means monomorphic and closure, drowsiness, and hyperventilation accentuate
regular) or arrhythmic (means polymorphic and IRDA. Although IRDA disappears in stage 2 and
irregular). deeper non–rapid eye movement (NREM) sleep, it may
Arrhythmic or polymorphic delta activity consists reappear in REM sleep.
of delta waves that are irregular in shape and have a IRDA is not specific for a single etiology and can
variable duration and frequency without a stable occur in response to systemic toxic or metabolic
predominant frequency. Rhythmic delta activity disturbances as well as to diffuse or focal intracranial
consists of delta waves that are regular in shape and diseases. This may be due to diverse etiologies, such as
have a fairly constant duration and stable predominant infectious, inflammatory, degenerative, traumatic,
frequency. vascular, or neoplastic disorders. IRDA is also the
Focal slowing is most commonly seen with nonspecific type of slowing that occurs in normal
structural lesions. Generalized slowing is most individuals in response to hyperventilation. In such
commonly seen with encephalopathy. cases, it should not be interpreted as an abnormality,
Regional slowing is uncommon, and usually but rather as the response of a normal CNS to the stress
manifest as intermittent rhythmic delta activity. of an acutely changing Pco2.
Although this might be considered focal, it is Because IRDA may occur in response to systemic
bihemispheric, so should be considered regional. toxic or metabolic disturbances, diffuse intracranial
pathology, or focal intracranial pathology, its localizing
For convenience , the discussion of slowing is value obviously is limited. Even when it is due to a
divided into these sections: focal expanding lesion, the peak localization of the
IRDA tends to be age-dependent[maximal frontal in
A. Generalized intermittent slow activity adults and maximal posterior in children]. It is
B. Focal and regional intermittent slow activity independent of the localization of the lesion, which
C. Persistent slow activity may be at some distance, either in the supra- or
D. Encephalophatic patterns (theta coma, alpha infratentorial space, from the maximum expression of
coma, beta coma, spindle coma, triphasic waves) the IRDA. The recognition that IRDA is a non-
localizing rhythm, even when associated with an
intracranial lesion, led to its earlier designation as a
“projected” or “distant” rhythm.
Although frequently bilateral, IRDA may occur lesions, the mechanisms may be sufficient distortion of
predominantly unilaterally. Even when it occurs the brain to produce secondary disturbances at both
unilaterally in association with a lateralized the subcortical and cortical levels. With primary
supratentorial lesion, the lateralization of the IRDA, intracranial encephalopathies, it appears to be due to
although usually ipsilateral, may even be contralateral widespread involvement of the gray matter at
to the focal lesion . Therefore, when IRDA is present, subcortical and cortical levels.
determining whether it is due to a focal lesion (and if
so, the location of the focal lesion) is the best based on
persistent localizing signs, and not on the morphology B. Focal and regional intermittent
or even the laterality of IRDA.
TIRDA(temporal intermittent rhythmic delta activity) slow Activity
is an important epileptogenic abnormality., highly
pathognomonic for temporal lobe epilepsy. These These abnormalities have the same features as
rhythmical unilateral delta trains indicate a focal lesion. generalized intermittent delta activity except that they
Thus, TIRDA markedly differs from FIRDA and are limited to one area or to one side of the brain. Focal
OIRDA(and their mainly global significance). slow activity usually indicates a focal subcortical
In summary, IRDA is nonspecific in that it can be structural lesion. The slow activity typically has an
seen in association with a wide variety of pathological irregular, polymorphic appearance, hence the name
processes varying from systemic toxic or metabolic polymorphic delta activity (PDA). In general, the area
disturbances to focal intracranial lesions. Even when of the slow activity is overlying the location of the
associated with a focal lesion, IRDA by itself is structural lesion, but the anatomic correlation is not
nonlocalizing. The common denominator in the wide always exact.
variety of pathological processes producing IRDA is The differential diagnosis of focal irregular slow
that, when such an abnormality appears, it is likely to activity is large, with some of the possibilities
be associated with the development of widespread including:
brain dysfunction ; the earliest clinical correlates are
fluctuating levels of alertness and attention. With focal
• Tumor
• Stroke - ischemic or hemorrhagic
• Infection - abscess or encephalitis
• Trauma - contusion or hematoma
• Epileptic focus – irregular slow activity may be associated with an epileptic focus in the absence of
structural lesion
• Transient focal abnormality as may be seen in migraine, ischemia, postictal dysfunction after a focal
seizure
Unfortunately, one cannot usually be definite As previously pointed out one form of focal slow
about the etiology of the slow activity from the activity, temporal intermittent rhythmic delta activity
appearance. While additional historical information (TIRDA), has a strong association with seizure
may help the analysis, the diagnosis of focal structural activity.
lesions rests largely with imaging studies.
Frontal intermittent rhythmic delta activity (FIRDA).
Frontal intermittent delta activity (FIRDA)

OIRDA during hyperventilation in a 13 year old boy- this is a normal finding in this patient
Frontal intermittent delta activity

Frontal intermittent delta activity
Bursts of high-voltage bilaterally synchronous frontal intermittent rhythmic delta activity in a 41-year-old lethargic
patient with uremic encephalopathy.
Frontal intermittent rhythmic delta activity recorded in the EEC of a 14-yearold boy with obstructive hydrocephalus
Intermittent slow activity in left temporal in a 20 year old patient with TLE.
A 75-year-old patient with an acute left frontal ischemic infarct. Note the left regional polymorphic delta that affects
the entire hemisphere
A 64-year-old s/p right hemisphere infarct. Over the right hemisphere, a well-formed alpha rhythm is not present
(it is well formed on the left) and is replaced by polymorphic slow waves (2 to 4 Hz).
EEC of a 52-year old man who had a right parietal glioma. Note the polymorphic slow-wave focus in the right central
region and the diffusely slowed background.
Intermittent slow activity, left temporal in a 20-yaer old patient with TLE
C. Persistent slow activity other and maintain a somewhat constant frequency. On

the other hand, the polymorphic delta activity (PDA)
usually has a frequency of 0.5 to 3 Hz, and the
Persistent slow activity is usually in the delta frequency waveforms change in frequency, amplitude, and
band. It may occur as monomorphic, rhythmic waves morphology in a continuous fashion. In other words, no
or as polymorphic, arrhythmic waves. It may be two succeeding waves appear to be quite alike.
generalized, lateralized, or focal. In the case of the Polymorphic delta activity (PDA) tends to show no
rhythmic delta activity, the waveforms resemble each reactivity to stimulation and persists both during
wakefulness and sleep. Even hyperventilation may not destructive lesion may be of such low amplitude that it
have much effect on PDA. appears to be flat, whereas the surrounding areas show
Continuous PDA, especially when it is focal, is large amplitude PDA.
indicative of an underlying structural lesion unless It is now believed that deafferentation of the
proved otherwise. The finding often correlates well cortex by a lesion that interrupts that thalamocortical
with other tests like the CT scan and MRI, but there are afferents is the underlying mechanism in the genesis of
certain situations where the neuroimaging may be PDA. Polymorphic delta activity is most likely to be
negative as, for example, in recent infarct or contusion. associated with acute destructive lesions, but it gives
For the exact localization of the lesion, the frequency no clues as to the specific etiology of the lesion.
of the waveform is a better indicator than the Sometimes PDA and rhythmic delta activity may
amplitude; thus, the area showing the slowing activity coexist in the same tracing. This may conceivably
is the most likely site of the lesion. The amplitude is depend on different degrees of involvement of the
often higher in the immediately surrounding areas. cortical and subcortical areas by the lesion.
Sometimes the tracing from the area overlying a
Diffuse background slow activity in a 47 year old man with hepatic encephalopathy. Note EMG artifacts
throughout the recording.
(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.
There is a brief 2-sec burst of polymorphic delta activity in the posterior temporal-parietal region of the left
hemisphere in a 55-year-old patient with a left subcortical white matter lacunar infarction.
Focal delta in a 28-year-old patient with right temporal polymorphic delta due to a anterior temporal ganglioglioma.
Note the anterior–mid-temporal localization with loss of intermixed faster frequencies.
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.
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.
D. Encephalopathic patterns (alpha

Alpha coma: Unremitting 8- to 13-Hz EEG activity
coma, theta coma, beta coma, that is unresponsive to eye opening or other stimulation
spindle coma, triphasic waves) has been termed alpha coma. This activity differs in
appearance from alpha rhythm (normal background
activity) in its lack of reactivity and its spatial
The terms alpha coma,theta coma, alpha-theta coma
distribution. It is monorhythmic or diffuse, or it may
ana beta coma patterns are often used to denote
have anterior or posterior accentuation. Only minor
patterns of rhythmical waves which have theta, alpha
fluctuations in amplitude occur, and minimal to no
or beta frequency but differ from normal rhythms in
reactivity to external stimulation can be elicited.
that they occur in isolation without other
Two kinds of alpha coma patterns have been
accompanying waveforms in comatose patients. In
distinguished which loosely correspond with different
addition, they usually do not demonstrate spontaneous
anatomical distributions of pathological involvement.
variability or reactivity to sensory stimulation. Their
topography(distribution over the head) is usually
a) The posterior dominant alpha coma pattern shows
abnormal in that neither the alpha nor theta activities
either no reaction or, rarely, a variable attenuation
have a posterior dominant amplitude gradient and beta
or increase in amplitude following altering
patterns are widespread. These waves show little
maneuvers. This patterns is usually encountered in
variation in frequency and are either the only activity
patients with brain stem lesions, particularly
present or are clearly the dominant activity. Variants of
pontine infarction. It is important to attempt to
these coma patterns occurs with less stable dominant
differentiate patients with similarly located lesions
frequency and with intermixed generalized slow
who are in the so-called ‘locked-in syndrome’
waves.
from those who are comatose. A posterior
The beta coma patterns usually indicates a high
dominant alpha background activity that attenuates
likelihood of recovery from coma whereas the other
with alerting in patients with little other evidence
coma patterns are more often associated with poor
of response to stimulation(or in some cases only
outcome.
vertical eye movements)is indicative of the
Regardless the dominant frequency of the pattern
‘locked-in syndrome’. Such patients may have
seen, in the absence of general anesthesia, hypotension,
nearly complete awareness, but are immobilized
or hypothermia, non-reactivity and lack of spontaneous
by an interruption of corticospinal motor
variability are the most important predictors of poor
pathways.
outcome.
b) Generalized or predominantly frontal alpha cases of anoxic encephalopathy. However,

activity without reaction to altering stimuli can be complete recovery has been reported to occur
seen in patients with widespread cerebral damage, frequently in cases of electrical injury and sedative
especially that following cardiac or respiratory intoxication uncomplicated by anoxia. Alpha coma
arrest, prolonged hypoglycemia or bilateral patterns in patients who have overdose with
destruction of midline thalamic nuclei. Variants sedative medications usually contain asynchronous
present with intermixed focal or generalized slow and bisynchronous delta activity. As noted above,
waves or amplitude abnormalities. This alpha an alpha coma pattern without spontaneous
pattern is usually seen for up to 5 days after the variability or reactivity suggests a much worse
insult and is then replaced by other abnormalities. prognosis than a reactive alpha pattern or a record
The prognosis for complete recovery or survival is with spontaneously changing patterns.
generally considered to be poor, particularly in
Alpha coma.This 29-year-old man

sustained a closed head injury in an
automobile accident. The patient
was on a respirator, was deeply
comatose, and responded to painful
stimulation with decerebrate
posturing. Later, he "improved" to a
neurovegetative state. He could
open his eyes and could breathe
without the respirator, but he could
not follow commands and made no
purposeful movements.The EEG at
one week contains high-voltage
frontally predominant relentless
alpha activity that was minimally
responsive when stimulated. In this
patient, reactivity did not suggest a
good prognosis.
Alpha coma: The EEG is dominated by alpha activity, which is non-reactive in a patient in coma of unknown nature
Alpha coma in a 33 year old man

with severe diffuse anoxic
encephalopathy following
cardiovascular arrest
Theta coma: The theta coma patterns is characterized predicting a poor outcome as the absence of reactivity
by generalized monorhythmic activity in the theta and spotaneous variability.
frequency range that shows little or no evidence of Beta coma: The beta coma patterns consists of a
either spontaneous variability or reactivity to noxious generalized, sometimes frontal dominant, pattern of
stimulation. The clinical correlates of the theta coma mainly rhythmic beta waveforms. It usually occurs in
patterns are similar to those of the generalized or coma caused by or complicated by barbiturate or
frontal dominant alpha coma pattern. Interestingly, it is benzodiazepine intoxication. Unlike the alpha and theta
not unusual for the alpha coma pattern to be replaced coma patterns, the beta coma pattern is usually associated
by the theta coma pattern. Such transitions indicate a with a favorable outcome, because in most cases it is a
poor prognosis for normal recovery or survival. As demonstration of the ability of cortical structures to
with the alpha coma pattern, the theta coma or mixed generate a ‘normal’ response to pharmacological
alpha-theta coma patterns are not as reliable for stimulation. It may also occur in acute brainstem lesions .
Beta coma in a 69-year old comatose

man who has received high doses of
sedative medication
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.
Spindle coma: Spindle coma is a term used when arousal. As pointed out, it is usually associated with a
diurnal EEG activity in comatose patients contain favorable outcome, but is not as good an electrographic
features of stage 2 sleep, including prominent spindle- prognostic sign as a reactive beta coma pattern. It is
like activity. This EEG pattern usually carries a good often seen following head trauma but has also been
prognosis. It is often accompanied by other sleep observed in patients recovering from anoxic
patterns such as vertex waves or K complexes and encephalopathy or encephalitis.
appears to represent a sleep stage with impaired
Spindle coma
Spindle coma.This 14-year-old male patient suffered a closed head injury. At the time of the EEG (3 d after the
injury) the patient was comatose, but respirations were spontaneous and he responded appropriately to painful
stimulation. There is a generalized high-voltage delta activity with "sleep spindles" superimposed. The
"spindles" are more widespread than normal sleep spindles, although they are of similar morphology. The patient
gradually improved to normal neurologic function.
Spindle coma. Note the prominent spindlelike activity at 13-16 Hz. Typically, spindlelike activity assocziated with
coma is even more continuous than shown here, and unreactive. The term "spindle coma" is reserved for patients
known to be comatose.
Spindle coma: The EEG in a comatose patient shows spindle like activity.
Spindle coma, including spindles, and K complexes in response to auditory and noxious stimuli. Twelve
hours after head injury, this 17-year old girl was stuporous and demonstrated anisocoria, left pupil
larger than right, and left Babinski's sign. Noxious stimulation elicited inconstant withdrawal
movements and agitation. The patient recovered with slight left upper extremity paresis.
Triphasic waves: Triphasic waves are frontally and occur in bursts of repetitive waves at 1-3 Hz. The
positive sharp transients, usually of greater than 70 total duration of each triphasic wave complex varies
microvolts amplitude. They consist of waveforms with between approximately 0.25 and 0.5 s. The second
3 phases, each succeeding phase with longer duration phase is positive in polarity and usually has the
than the one before, that clearly stand out from the greatest amplitude of the 3 phases. Occasionally a
background and other slow waves. They are bilateral relatively low amplitude positive phase can be seen
consistently proceeding the subsequent 3 phases.
Triphasic waves may appear sporadically or generation is enhanced by biochemical and

periodically at 0.5-1s intervals. Although the amplitude ultrastructural changes associated with aging; well
distribution of triphasic waves varies in individual developed triphasic wave patterns rarely occur in
cases between either anterior or posterior individuals less than 20 years of age, are infrequent
dominance(with some individuals showing both before age 30, and increase in incidence thereafter.
simultaneously or at different times in the same Clinical conditions associated with the triphasic
record), in most cases triphasic waves are maximal wave pattern are mainly metabolic / toxic disturbances
over the anterior head regions. In instances in which with the most common being hepatic failure, renal
maximal amplitudes occur at FP1 and FP2, triphasic failure and anoxia. Sporadic triphasic waves are also
waves may closely resemble vertical eye movement not uncommon in elderly individuals with clinically
artifact. In longitudinal bipolar recordings triphasic advanced dementing disorders. The triphasic wave
wave phase reversals may occur over the anterior or pattern has also been associated with other disorders
posterior head regions. including: hypo- or hypernatremia, hypercalcemia,
In many cases there is an apparent phase lag(time hypoglycemia, stroke, hypertensive encephalopathy,
delay) of the second phase when comparing the cerebral abscess, encephalitis, congestive heart failure,
anterior and posterior derivations of longitudinal septic shock, lithium intoxication and postictal state.
bipolar montages. This delay can occur in either the The prognosis for patients with triphasic waves is
anterior to posterior or posterior to anterior direction mainly dependent on the degree of background
and may last more than 100 ms. In ear referential slowing, suppression or reduced reactivity, not the
montage the time lag is usually not present. presence or absence of triphasic waves.
The pathophysiology of triphasic waves is poorly Many other patterns can have a triphasic
understood. As with other bisynchronous patterns, morphology. Triphasic waves often are observed in the
thalamic pacing probably plays an important role. context of nonconvulsive status epilepticus. Often the
Unilateral lesions that attenuate thalamically generated decision whether to consider triphasic waves ictal must
rhythms such as sleep spindles may also attenuate rely on the clinical information or the response to
triphasic waves. It appears that triphasic wave anticonvulsant treatment.
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.
Triphasic waves in a 58-year –old woman with hepatic encephalopathy. Note the anteropoterior delay typical of
triphasic waves recorded in a bipolar longitudinal derivation.
EEG in a patient with postanoxic generalized nonconvulsive SE that followed convulsive SE.
4. Abnormal periodic patterns
These are defined as stereotyped recurrences of shape of the complexes varies in different patients and
paroxysmal complexes at relatively fixed intervals. can change in the same patient at different stages of the
They should be present throughout the entire tracing or disease process. Although the complexes are usually
a major portion of it. The discharges should stand out symmetric and synchronous, they may be asymmetric
from the background. They may be composed of slow with a time lag between hemispheres or lobes. The
waves, sharp waves, or sharp and slow wave EEG background is slow and progressively more
complexes. Although they may appear to be disorganized as the disease advances. The stages of
epileptiform , they are not necessarily associated with a sleep eventually become difficult to distinguish.
chronic seizure disorder. They often indicate severe A prominent feature of SSPE is the stereotyped motor
encephalopathy and may or may not be associated with jerks or spasms occurring with the periodic complexes.
clinical seizures. Some of these patterns may suggest a The movements are often described as myoclonic
specific diagnosis when taken in conjunction with the jerks; however, they do not have the momentary
clinical picture, and for this reason it is important to lightning-quick nature of true myoclonus; instead, the
recognize them. The discharges may be generalized, movements consist of an initial “shock-like
lateralized, or even focal. Generalized periodic abruptness” followed by a momentary arrest of the
paroxysmal patterns are seen classically in subacute movement, and then a gradual melting away to the
sclerosing panencephalitis(SSPE), jakob-Creutzfeldt position of the rest.
disease (JKD), and herpes simplex encephalitis(HSE). Abnormal movements, cognitive deterioration, and the
Electroencephalographic tracings with a burst- diagnostic EEG characterize the clinical disease.
suppression pattern may also appear periodic, Stereotypic jerking or other movement abnormalities
especially when the bursts occur at regular intervals. occur with the periodic complexes. Rarely, the periodic
Lateralized and focal periodic paroxysmal patterns are complexes become apparent before the movements
seen in acute destructive lesions involving one manifest. The movements often disappear in sleep,
hemisphere. These particular patterns are taken up in even though the complexes persist.
turn. This disease is a long-latency infection caused by
a prion. The characteristic EEG shows biphasic or
triphasic discharges that are initially sporadic and may
Generalized Periodic Paroxysmal even be asymmetric. As the disease advances, the
pattern becomes generalized and synchronous with
Patterns continuous periodic stereotypic 200- to 400-
millisecond sharp waves occurring at intervals of 0.5-
1.0 seconds. Myoclonic jerks often occur in association
I. Subacute sclerosing panencephalitis with the sharp waveforms, but the relationship is not
(SSPE) constant. Late in the illness and during sleep,
myoclonic jerks disappear, despite the persistence of
Subacute sclerosing panencephalitis (SSPE) is an the periodic EEG. The sharp waves typically react to
inflammatory disease of children and adolescents external stimuli. Early in the disease, alerting the
caused by chronic infection with the measles virus. The patient may elicit the periodic pattern; later, when the
characteristic EEG pattern, initially described by periodic pattern is readily apparent, rhythmic photic or
Radermecker and Cobb and Hill, consists of high- other stimuli can "drive" the periodic frequency.
voltage (300-1500 µV), repetitive, polyphasic sharp Benzodiazepines or barbiturates can temporarily
and slow wave complexes of 0.5- to 2-second duration eliminate both myoclonic jerks and periodic patterns.
that recur every 4-15 seconds. Rarely, the complexes As the disease progresses, there may be a
can occur at intervals of 1-5 minutes. The interval shortening in the interval between the complexes. In
between complexes may shorten as the disease the late stages of the disease, there is often a reduction
progresses. in amplitude and abundance of the
The periodic complexes may be present at any electroencephalographic activity, and the recording
stage of the disease, but they usually are seen during may become almost isoelectric. In some instances,
the intermediate stages. Although the form and however, alpha activity may still be present shortly
appearance of the periodic complexes are fairly before death.
constant and stereotyped in a single recording, the
SSPE (early) in a patient presenting with encephalopathy and periodic episodes of atonia.
Subacute sclerosing panencephalitis. This is a 7-year-old boy who is comatose and having myoclonic jerks. The onset of the
illness began 14 months ago with deterioration of intellectual function and he has become progressively unresponsive. This
EEG shows stereotyped high-voltage (300-400 mV) bursts of activity every 4-6 seconds.
Typical generalized periodic discharges in a child with SSPE. The interval between periodic complexes is 5-7 seconds
Another example of typical generalized periodic discharges(SSPE)
II. Creutzfeldt-jacob disease(CJD) stereotyped sharp waves, recurring at intervals of 0.5-1

second and having a duration of 200-400 msec. A
majority of patients with CJD develops the
CJD is one of the other prion diseases causing a characteristic EEG pattern by 12 weeks of the disease
diffuse disorder of the CNS that is characterized by process. On a few occasions the discharges appear as
progressive dementia, motor dysfunction, myoclonus, periodic lateralized epileptiform discharges (PLEDs)
and a characteristic periodic EEG pattern. The earliest before evolving into a bilateral pattern. Myoclonic
EEG changes consist of a disorganization and decrease jerks often occur in association with the periodic sharp
of normal background activity and the development of waves; however, there is not always a constant
progressive slow-wave abnormalities. The slow-wave relationship between the myoclonic jerks and periodic
abnormalities are usually generalized, but at times sharp waves; one can occur without the other. This is
they occur in a more focal or lateralized fashion. As the particularly true during sleep or late in the course of the
disease progresses, diphasic or triphasic slow-wave disease, when the myoclonic jerks decrease or
discharges appear. Initially, these discharges occur in a disappear, but the periodic sharp waves persist.
sporadic or intermittent fashion and may be One characteristric feature of the periodic
asymmetric or predominant over region, but eventually discharges in CJD is the reactivity of the sharp waves
they evolve into the characteristric pattern, consisting to alerting or afferent stimuli. Prior to the time when
of generalized and bisynchronous continuous periodic the periodic pattern has been established or when the
sharp waves occur in a more intermittent or sporadic complexes over the posterior head regions. Some
fashion, alerting the patient or arousing the patient out lateralization of the abnormalities may occur in the
of sleep may bring out the periodic pattern. Loud early stages, but the abnormalities usually become
noises and certain types of drugs such as diazepam and bilateral as the disease progresses. The periodic
the barbiturates, can temporarily abolish the periodic complexes may become more widespread with a
sharp waves and myoclonic jerks. maximal amplitude over the posterior head regions.
As the disease progresses, the interburst interval On occasion CJD may progress rapidly, and the
increases and the amplitude of the periodic sharp typical EEG abnormalities may evolve over a period
waves decreases. In the late stages of the disease, the of 1-3 weeks, and serial EEGs are helpful in making or
EEG becomes almost isoelectric, with intermittent confirming the diagnosis. One should be aware,
bursts of sharp or slow waveforms that finally however, that some patients with CJD may not show
disappear in the terminal stages of the disease. the typical pattern of periodic sharp waves.
In Heidenhain,s variant of the disease, where The “mad cow” variant of CJD has been described
there is a predominant involvement of the occipital as occurring at a younger age of onset than is typical
head regions, the EEG often shows more focal for CJD and without the typical EEG changes of CJD.
abnormalities consisting of slowing and periodic
CJD in a patient with encephalopathy and myoclonic jerks
Sporadic CJD in a 69-year-old.

Periodic pattern in an 81-year old man with CJD.

Note the EMG artifacts in anterior leads
The periodic discharges

in a patient with CJD
Creutzfeldt-Jakob disease.This
is a 56-year-old female
professor who became more
withdrawn and increasingly
forgetful. Over the next 4
months she deteriorated rapidly
and became mute, bedridden,
and unable to eat with
myoclonic jerks of her arms.
The EEG done 6 months into
her illness shows a
pseudoperiodic, well-organized
1- to 2-Hz biphasic and triphasic
waves and very little other
activity. In this clinical setting,
this EEG is virtually
pathognomonic of Creutzfeldt-
Jakob disease and is regarded as
a manifestation of severe gray
matter disease involving the
cortex and deep nuclei.
refractory status epilepticus.The duration of the

III. Burst-suppression pattern intervals between the bursts is often fairly regular in a
given recording and ranges from 5 to 10s depending
The burst-suppression pattern is sometimes called the on the severity of the cerebral dysfunction.
suppression-burst pattern when the duration of the The duration increases as the patient,s condition
suppression is greater than the duration of the burst. worsens. Before death or with deepening anesthesia,
This may be considered as a periodic pattern, since it bursts become shorter, simpler and of lower
consists of periodic bursts of activity with intervals amplitude; periods of suppression become longer until
between in which the background activity is markedly complete eletrocerebral silence supervenes. The
attenuated. complexes are not responsive to stimuli.
This subtype of periodic pattern consists of bursts Seizure manifestations associated with this pattern
of activity (mixture of sharp and slow waves) are limited to myoclonus. However, a variety of
periodically interrupted by episodes of suppression behaviours have been associated with the bursts of
(activity <10 µV). Typically, the episodes of activity, including chewing and tonic posturing.
suppression are longer (typically 5-10 s) than the bursts Clinical conditions causing burst-suppression
of activity (typically 1-3 s). Background suppression is patterns include a variety of severe disorders of
a "nearly flat" EEG, with very low voltage activity cerebral structure or function. Structural lesions
(<10 µV) and no reactivity, but the activity is still too include acute strokes, postanoxic encephalopathy, head
large to meet criteria for electrocerebral inactivity injury and encephalitis. Local burst-suppression
(ECI). patterns can be seen over abnormal cortical areas
They are usually widespread and bisynchronous, during surgical anesthesia. Commonly reversible
but they may be limited to one hemisphere or part of it. disorders causing this pattern include deep anesthesia
As previously mentioned, bursts last 1-3s and are and coma due to barbiturates and other CNS depressant
separated from each other by low amplitude delta drugs, hypothermia, and Reye,s syndrome. The
waves or by periods of no activity recognizable at association of myoclonus, burst-suppression patterns
regular gain. Successive bursts may vary in shape. The and postanoxic coma suggests a very poor prognosis
bursts usually have a polymorphic appearance, but may for survival.
contain high voltage epileptiform activity in some
patients who are placed in barbiturate coma because of
Burst-suppression pattern. Suppression periods are characterized by activity less than 10 mV.
Burst-suppression pattern recorded in the EEG of a 70- year-old man after a cardiac arrest from which he was resuscitated.
Burst suppression, in a 3-year-old boy with severe diffuse anoxic encephalopathy

Burst suppression from anoxic encephalopathy. This 54-year-old patient was seen 5 days after a coronary artery
bypass complicated by a prolonged hypotension causing diffuse cerebral anoxia. The patient is deeply comatose
and unresponsive to any stimulation. He has occasional episodes of rapid eye blinking. The EEG has high-voltage
bursts of spikes and polyspikes lasting for less than 1 sec followed by low-voltage epochs. This type of
abnormality is usually associated with anoxic encephalopathy. It carries a very poor prognosis
Burst suppression pattern in right hemisphere in a 5y old patient with refractory epilepsy
Burst-suppression pattern after anoxic injury in a 76 year old man.
IV. Periodic Lateralized Epileptiform such as epilepsia partialis continua or transient

confusional states, may be associated with PLEDs. For
Discharges (PLEDs) clinical purposes the PLED pattern is generally
regarded as a highly epileptogenic interictal pattern.
There are case reports of PLED patterns persisting for
Periodic lateralized epileptiform discharges (PLEDs) years. Approximately 1% of all ischemic hemispheric
are EEG abnormalities consisting of repetitive spike or non-lacunar infarctions are accompanied by PLEDs.
sharp wave discharges, which are focal or lateralized More recently, PLEDs have been reported in
over one hemisphere, recur at intervals of 0.5-5 mitochondrial encephalopathies(MERRF, MELAS)
seconds, and continue through most of the duration of and in Jakob-Creutzfeldt disease.
the EEG study. They are seen most frequently in the Bilateral independent PLEDs (BIPLEDs) are
setting of acute unilateral lesions such as cerebral periodic complexes over both hemispheres. BIPLEDS
infarctions. They also may occur in other cerebral are not synchronous and may differ in morphology and
diseases, such as encephalitis or tumors(or in the site of maximal expression on each side. This is an
setting of chronic lesions or long-standing epileptic uncommon EEG finding. In a series of 18 patients, the
disorders. most common etiologies were anoxic brain injury
PLEDs are usually self-limited and resolve after (28%) and CNS infection (28%). While BIPLEDs have
the acute phase of a cerebral insult. Rarely, they may been associated with herpes simplex encephalitis, the
persist on a chronic basis. Seizures often occur when pattern can occur in other CNS infections as well. The
PLEDs are seen on the EEG, but clinical and clinical correlates of BIPLEDs differ somewhat from
electrographic seizure manifestations typically differ those of PLEDs. With BIPLEDs, incidence of coma is
from the baseline (PLEDs) condition. The seizures higher compared to PLEDs (72% vs 24%), mortality
were either partial or generalized and the partial rate is higher (61% vs 29%), and likelihood of focal
seizures were always contralateral to the seizures or focal neurological deficits is lower.
PLEDs.Certain paroxysmal neurological symptoms,
Focal EEG waveform

abnormalities. This EEG
demonstrates periodic lateralized
epileptiform discharges (PLEDs)
in the left hemisphere in a 54-
year-old patient with a history of
left temporal ischemic stroke.
Examples of PLEDs seen from the left hemisphere. There is a slight reflection of PLEDs in the right hemisphere,
which is not unusual. The patient developed confusion, aphasia, and witnessed focal motor seizure activity of the
right arm and face, 10 days after a left carotid endarterectomy and was found to have a hyperperfusion syndrome.
PLEDs pattern in right hemisphere
Right temporal PLEDs in a patient with herpes encephalitis and nonconvulsive SE recorded in the ICU.
Left temporal PLEDs in a patient with left temporal lobe epilepsy immediately following serial complex partial seizure.
Left temporal PLEDs in a patient with an acute occipital ischemic infarction.

PLED in right hemisphere in a patient with Alzheimer,s disease
BiPLEDs in a 36-year-old man with severe diffuse anoxic encephalopathy after cardiovascular arrest.
Chapter 12
Reading and Reporting EEGs
To read a new language , needles to say, one needs first and the technique of recording, it is impossible to learn
to learn the alphabet. The alphabet of the EEG consists to read EEGs properly. One needs to know what
of the various frequencies and waveforms that calibration means, hoe the various frequency filters
comprise the tracing. Just as the letters of the alphabet work, how various artifacts are identified, and how
are combined in different permutations and neurologic disorders produce alterations in electrical
combinations to form words and then sentences, so the activity of the brain.
EEG tracings are made up of combinations of
waveforms of different frequencies and morphology. Description of the EEG
To carry the analogy further, it is not enough to be able The report should describe the essential normal and
just to read the words and sentences; one needs to abnormal patterns appearing under the various
understand quickly the meaning of what is written. In recording conditions so that a person with some
the same way, EEG reading involves analyzing the knowledge of EEG can imagine the findings on which
waveforms and deducing their significance. With diagnosis and interpretation are based. Sufficient detail
experience, one uses a speed reading technique in should be given to enable the reader of a later EEG to
which a whole page is rapidly scanned for evidence of estimate whether the major features of the two
normal and abnormal phenomena. How successfully recordings are similar or different. The report should
this is done depends to a large extent on developing not be exhaustive in describing normal detail but
pattern-recognition skills. should include those rare or unusual features in the
record which may have clinical significance. As far as
possible, the report should use the terms defined in the
Learning to Read glossary of the International Federation of Societies for
EEG and Clinical Neurophysiology. Judgments like
How does one learn to read EEG? Like any other ‘good’ and ‘ poor’ should be used only sparingly and
branch of medicine this involves a continuous process only to characterize the overall composition of a
of learning for many months or sometimes even years. record, but not to rate individual rhythm: persons not
Often the intial learning is accomplished through familiar with the EEG can not know that ‘poor’
observing an experienced electroencephalographer read driving has no different clinical significance than has
EEGs. The next step involves reading under ‘good’ or even ‘excellent’ driving.
supervision; having seen how an experienced On the other hand, patterns should be described by
electroencephalographer interprets a record, and having indicating the frequency, amplitude, and distribution of
gathered essential information regarding normal and the component waves. Wave shape, rhythmicity,
abnormal patterns, the trainee interprets records in the symmetry, synchrony, persistence, reactivity, and
precence of his or her instructor. Ideally, the instructor periodicity, may be important for the description of
should regularly quiz the trainee on the various abnormal patterns. Because the frequency of a rhythm
waveforms and artifacts in the tracings, and the trainee often varies, it is usually indicated in terms of a
should complement this by seeking answers to the frequency range or band of a few hertz in width rather
questions. Without at least an elementary knowledge of than in terms of a single frequency. In most instances,
the basic principles of electricity, neurophysiology, it is not sufficient to use only the wide bands of delta,
theta, alpha, and beta frequency to describe the association with behavioral seizure manifestations.
frequencies of waves in a record; the frequency of Slow waves are described in terms of frequency,
alpha and beta rhythms and of theta and delta waves amplitude, shape, rhythmicity, regularity,
observed in a recording should be specified in narrower persistence, distribution, symmetry, synchrony,
bands. Amplitude may be reported in absolute or and any other parameter of clinical importance. If
relative measurements, preferably with the montage more than one type of slow wave is present, the
specified. Absolute units must be used in the diagnosis specifications for each type must be given.
of electrocerebral silence in which no cerebral activity Abnormal generalized asynchronous slow waves
of over 2µV should be present. Even if activity of very must be distinguished by amplitude, frequency,
low amplitude over 2µV is found in these cases, the distribution and persistence from the range of
amplitude should be specified to indicate the severity asynchronous slow waves normally seen at the age
of the abnormality and to provide a basis for of the patient.
comparison with subsequent recordings. In most other
instances, it is sufficient to characterize amplitude as Asymmetries and generalized changes of
low, medium, or high. To avoid omitting important amplitude are usually noted when describing the
features in the report, one should adhere to a standard normal background.
sequence of reporting.
Although many electroencephalographers do not Deviations from normal must be described by
include a summary of the clinical history, it is indicating the specific features which make a
advisable to briefly state the referring complaint and pattern abnormal, for instance the appearance of
any other information that is immediately relevant to alpha activity which has a frontal maximum, lacks
the interpretation of the recording under a separate reactivity and is associated with coma.
heading such as "history". This provides the referring
physician with feedback as to the Hyperventilation. Normal responses can be
electroencephalographers, understaning of the referring described in one short sentence, for example
complaint, facilitates future review of the EEG report, ‘Hyperventilation produced no change’ or
and helps in the interpretations of subsequent EEGs. It ‘Hyperventilation did not elicit any abnormalities.’
is also an important exercise for those who are training The performance of the patient may be mentioned.
to become electroencephalographers. Symptoms induced by hyperventilation should be
The general level of consciousness of the patient, reported, particularly if the symptoms resemble
other behavioral abnormalities(such as lack of episodic symptoms for which the patient is
cooperation, or persistent movement causing excessive examined. Changes in the patient,s behavior such
artifact), the equipment used(e.g., digital or analog), as jerking movements or loss of responsiveness,
the recording environment( e.g., outpatient, bedside, must be reported. Abnormal responses such as an
ICU, patient ventilator dependent), and whether or not asymmetrical buildup, enhancement of
sedation was given(e.g., chloral hydrate) should either abnormalities of the resting record and induction of
be stated under a separate heading, such as "conditions new abnormalities must be described in detail.
of the recording" , or in the opening of the general
body of the descriptive report. Photic stimulation. Normal responses can be
described briefly by stating ‘Photic stimulation did
The resting record not elicit a driving response’ or ‘Photic stimulation
elicited a symmetric driving response.’ Abnormal
1. Description of normal background. Alpha, beta, responses such as significant asymmetries and
mu and other rhythms and patterns, if present, are photoparoxymal responses should be described.
described in terms of their frequency range,
relative amplitude and distribution. Wave shape, Sleep. It is helpful to either briefly describe the
rhythmicity, symmetry, distribution, persistence major EEG findings during sleep or simply list the
and reactivity should be mentioned if they are deepest stage of sleep that occurred. If the patient
abnormal. Excessive beta activity and unilateral referred for the evaluation of a possible seizure
blocking of the alpha rhythm must be reported. disorder and epileptiform activity did not occur,
then the depth and duration of sleep will be of
2. Description of abnormal patterns. Epileptiform particular importance. The report should also
activity is characterized by its shape, amplitude, indicate whether sleep was induced with a sedative
repetition rate, persistence, distribution, synchrony, or occurred spontaneously. Abnormalities during
symmetry, relationship between focal and sleep should be described in detail. Most important
generalized discharges and any other feature of is the appearance of epileptiform activity.
possible clinical significance including the
Reading and Reporting EEGs 181
The report of an EEG symmetry or asymmetry, and rhythmicity or lack of it

should follow, using the same units as for the dominant
frequency. Responses to opening and closing eyes as
The report of an EEG should consist of three principal parts:
well as to purposeful movement of the extremities when
A. Introduction
appropriate, should then be described. The responses
B. Description of the record, and
should be described as symmetric or asymmetric,
C. Interpretation, including (a) impression
complete or incomplete , sustained or unsustained.
regarding its normality or degree of
Abnormal records, infants records, or recordes limited to
abnormality and (b) correlation of the EEG
sleep may not have clearly dominant frequencies. In
findings with the clinical picture.
those cases, the different activities with their amplitude,
frequency, etc., should be described, in any order. When
A . Introduction. The introduction should start with
the record shows a marked interhemispheric asymmetry,
a statement of the kind of preparation the patient had,
the characteristics of each hemisphere should be
if any, for the recording session. The initial sentence
described separately(i.e., dominant, nondominant
should state whether the patient received any
frequency, etc., of one hemisphere first, followed by
medication or other preparation, such as sleep
those of the other). The description of the background
deprivation, as well as the patient,s state of
activity should be followed by description of the
consciousness at the onset of the record. If the patient
abnormalities that do not form part of this background
was fasting, this should be stated.
activity. This should include a description of the type(
If the printed form used for the report does not provide
spikes, sharp waves, slow waves), distribution (diffuse
a space for the regular medication the patient is
or focal), topography or location, symmetry, synchrony
receiving , as distinguished from medication given
(intra- and interhemispheric), amplitude, timing
specifically for the recording, any medication that
(continuous, intermittent, episodic, or paroxysmal), and
could influence the EEG should be included in the
quantity of the abnormal patterns. Quantity has to be
electroencephalographer,s report. If the number of
expressed in a subjective fashion, since in clinical,
electrodes used is not the standard 21 of the 10-20
unaided interpretation of the EEG , no exact quantities
system or if monitoring of other physiologic
or ratios can be given. When the abnormality is
parameters is used, this should be stated in the
episodic, attention should be given to the presence or
introduction.
absence of periodicity between episodes and to the
rhythmicity or irregularity of the pattern within each
B. Description. The description of the EEG should
episode. The range of duration of the episodes should
include all the characteristic of the record, both
be given. In the description of activation procedures, a
normal and abnormal, presented in an objective way,
statement should be included pertaining to their quality(
avoiding, as much as possible, judgment about their
e.g., good, fair, or poor hyperventilation, duration of
significance. The aim is to produce a complete and
sleep, and stage attained). The type of photic stimulation
objective report that would allow another
used(i.e., stepwise) should be stated and the range of
electroencephalographer to arrive at a conclusion
frequencies given. Effects of hyperventilation and photic
concerning the normality or degree of abnormality of
stimulation should be described, including normal and
the record from the written report, without the benefit
abnormal responses. If hyperventilation or photic
of looking at the EEG. This conclusion could
stimulation are not done, the reason for this omission
conceivably be different from that of the original
should be given. If referring clinicians know that these
interpreter, since it is by necessity a subjective one.
procedures are used routinely, they may expect results
The description should start with the background
even if they have not been specifically requested. There
activity, beginning with the dominant activity, its
is no point in including in the description the absence of
frequency, quantity(persistent, intermittent), location,
certain characteristics, except for the lack of normal
amplitude, symmetry or asymmetry, and whether it is
features, such as low- voltage fast frequencies, sleep
rhythmic or irregular. The frequency should be given
spindles, etc. Phrases such as ‘no focal abnormality’ or ‘
preferably in hertz or cycles per second. For the
no epileptiform abnormality’ have a place in the
purpose of standardizing the report, while recognizing
impression when the clinician has asked for it either
that any decision on this point must be arbitrary, it is
explicitly or implicitly in the request form. They have
recommended that the amplitude of this activity be
no place in the description. Artifacts should be
determined in derivations employing adjacent scalp
mentioned only when they are questionable and could
electrodes placed according to the 10-20 system. It is
represent cerebral activity, when they are unusual or
desirable but not mandatory that the estimated mean
excessive (eye movements, muscle) and interfere with
amplitude be given in micrivolts. This will obviate the
the interpretation of the record, or when they may
need for defining terms such as ‘low’, ‘medium’, and
provide valuable diagnostic information(e.g.,
high. Enumeration of nondominant activities with
myokymia, nystagmus, etc).
their frequency, quantity, amplitude, location,
C. Interpretation. suspicion of the presence of a given condition, it may

be stated that the EEG finding is consistent with or
(a) Impression. The impression is the supportive of the diagnosis. In EEG reports, the term
interpreter,s subjective statement about the normality "compatible with" is frequently found. Strictly
or abnormality of the record. The description of the speaking, any EEG is compatible with practically any
record is directed primarily to the clinical picture. Therefore, the term is not helpful and
electroencephalographer who writes it for review at a should not be used.
later date, or to another expert, and should be detailed In cases in which the EEG is strongly suggestive
and objective. The impression, on the other hand, is of a certain condition that is not mentioned in the
primarily written for the referring clinician and should , clinical history, it is prudent to mention the fact that
therefore, be as succinct as possible. Most clinicians such EEG abnormalities are frequently found in
know that their information will not significantly association with the clinical condition but are not
increase by reading the detailed description and hence necessarily indicative of it. An EEG can be said to be
limit themselves to reading the impression. diagnostic of a certain condition only in the rare cases
If this is too long and seemingly irrelevant to the in which there is a clinical manifestation present at the
clinical picture, the clinician will lose interest and the time of the recording of an EEG and the record shows
report of the record becomes less useful. If the record an electrical abnormality known to the generally
is considered abnormal, it is desirable to grade the associated with the specific clinical manifestation.
abnormality in order to facilitate comparison between Such a case would be one in which a patient presents a
successive records for the person who receives the typical absence concomitant with a bilaterally
report. Since this part of the report is largely synchronous 3/s spike-and-wave burst.
subjective, the grading will vary from laboratory to In situations in which the diagnostic clinical
laboratory, but the different grades should be properly impression seems at odds with the EEG findings, some
defined and the definitions consistently adhered to in possible reasons for the apparent discrepancy should be
any given laboratory. After the statement regarding offered in the EEG report. These reasons should be
normality or degree of abnormality of the record, the presented cautiously, trying to avoid any impression of
reasons upon which the conclusion is based should be criticism of the clinical diagnosis, or to appear
briefly listed. When dealing with several types of apologetic for an apparent failure of the EEG as a
abnormal features, the list should be limited to the two supplemental diagnostic test.
or three main ones; the most characteristic of the If an EEG is abnormal, but the abnormal features
record. If all the abnormalities are enumerated again in could be produced, at least in part by medication or
the impression, the more important ones become other therapeutic interventions such as recent
diluted and emphasis is lost. If previous EEGs are electroconvulsive treatment, it should be so stated.
available , comparison with previous tracings should be Under no circumstances should the
included. electroencephalographer suggest changes in medication
or other clinical approaches. However, the clinical
(b) Clinical correlation. The clinical correlation correlation statement could be followed by a
should be an attempt to explain how the EEG findings recommendation pertaining to further EEGs with
fit(or do not fit)the total clinical picture. This different added procedures, e.g., "in view of the
explanation should vary , depending on whom it is clinical picture a sleep record could be useful", or "
addressed to. More careful wording is necessary if the since the record was taken shortly after a clinical
recipient is not versed in EEG or neurology. seizure, a follow-up EEG may be helpful in
If an EEG is abnormal it is indicative of cerebral determining whether the slow wave focus present in
dysfunction, since EEG is a manifestation of cerebral this record is of permanent or of only transitory
function. However, the phrase "cerebral dysfunction" nature".
may sound too strong to some and it should be used A normal record does not, in general, require
only when the abnormality is more than mild and when further explanation. However, when the clinical
enough clinical information is available to make the information suggests a serious question between two
statement realistic within the clinical context. conditions, such as hysteria and epilepsy, a statement
Otherwise , a sentence like, "the record indicates should be added that might prevent the clinician from
minor irregularities in cerebral dysfunction, " may be jumping to a wrong conclusion. Such a statement
appropriate. could be: " a normal record does not rule out a
Certain types of EEG patterns are suggestive of convulsive disorder. If the clinical picture warrants , a
more or less specific clinical entities, a delta focus may recording with (some type of activation) may be
suggest a structural lesion in the proper clinical helpful".
context; certain types of spikes or sharp waves suggest
potential epileptogenesis. If the EEG abnormality fits
the clinical information containing the diagnosis or the
References
1. Tatum, William.O: Handbook of EEG 6. Karl E Misulis, Thomas C. Head: Essentials of

interpretation, Demos inc, USA, 2008 clinical neurophysiology, Butterworth Heinemann,
2. Neidermyer E, Lopes da Silva: USA,2002
Electroencephalography, basic principles,clinical 7. John S. Ebersole, Timothy A. pedley: current
applications and related fields, 3th edition, U&S practice of clinical electroencephalography, 3th
inc, 1999 edition, Lippincott Williams & Wilkins, USA, 2003
3. Bassel Abou-Khalil, Karl E, Misulis: Atlas of EEG 8. Hans O. luders, Soheyl Noachtar: Atlas and
and seizure semiology, Elsevier inc,2006 classification of electroencephalography,
4. Aminoff, Michael J: Electrodiagnosis in clinical W.B.Saunders, 2001
neurology, 4th edition, Churchill livingstone, USA, 9. F.H.Duffy, V.G.Iyer, W.W Surwillo, Clinical
1999 electroencephalography and Topographic brain
5. Wyllie, Elaine: The treatment of epilepsy, 4th mapping, springer-verlag,USA, 1989
edition, Lippincott Williams & Wilkins, USA, 2006 10. Selim R Benbadis, EEG atlas, www.emedicine.com,
2006
INDEX
A EMG artifact, 39-41, 39f-41f

photomyogenic response, 41
- Abnormal EEG patterns, 83-178 eye movement, 44-49, 44f-49f
- Abnormal sleep patterns, 145-146f bell's phenomen, 44, 45f
sleep spindle asymmetry, 145-146f glossokinetic artifact, 42, 42f-43f
V wave asymmetry, 145 chewing artifact, 43f
- Absence Epilepsy, 97-101, 99f- 101f pulse artifact, 51, 51f
photic stimulation, 41, 75, 78, 81, 98, 102, 108, 112, 180 skin artifact, 52, 52f
-Acquired Epileptic Aphasia, 125-126, 126f sweat artifact, 52, 52f
clinical feature of, 125
EEG finding in, 125-126, 126f
- Activation during sleep, 82 B
- Activation procedures in the EEG, 75-82, 76f-82f
hyperventilation, 75-78, 76f-77f - Bects, see benign epilepsy of childhood
abnormal response, 75 with central-midtemporal spike, 102
photic stimulation, 75 - Benign epilepsy of childhood with centrotemporal
response to, 78, 78f-82f spike (Bects),
photic driving response, 78-79, 79f clinical feature of, 102
photic evoked potential, 78 EEG finding in, 102, 103f-107f
photoepileptiform response, 81 - Benign epileptiform transient of sleep (Bets), 127,
photomyogenic response, 79-80, 79f-80f 127f-129f
photomyoclonic response, 79-80, 79f-80f - Benign partial epilepsy of childhood with occipital
photoparoxysmal response, 81-82, 81f-82f paroxysm (Bpeop),
Visual evoked response, 78 activation during sleep, 82
sleep, 82 clinical feature of, 107-108
- Alpha coma, 158-159, 159f-160f EEG finding in, 108, 108f-109f
- Alpha dropout, 58-60, 60f familial occurrence of, 107
- Alpha rhythm (alpha activation), 23-29, 24f-29f - Beta coma, 160, 160f-161f
abnormal, 139-140, 142f-143f - Beta rhythm (Beta activity), 29-34, 30f-34f, 140-141
characteristics of, 29 Excess Beta activity, 31, 31f
in breif, 29 focal attenuation of, 140
reactivity of, 140 focal enhancement of, 141, 143f
- Alpha variant pattern, 26-29, 26f-29f in brief, 32
alpha squeak, 26 - Breach rhythm, 36-37, 36f-37f
fast alpha variant, 28, 28f - Burst suppression pattern, 171, 145f, 171f-174f
paradoxical alpha response, 29
slow alpha variant, 26-27, 26f-27f
temporal alpha, 29 C
- Artifacts, 39-58, 39f-57f
non physiologic artifact, 52-57, 52f-57f
alternating current artifacts (60 Hz), 55, 55f - Chewing artifact, 43f
electrodes and leads, 52-55, 52f-55f - Childhood absence epilepsy, 97-101
electrode pop artifact, 53, 53f clinical feature of, 97
interavenous artifact, 57, 57f EEG finding, 98, 99f-101f
movement artifact, 56, 56f OIRDA, 98
physiologic artifacts, 39-52, 39f- 52f
ECG artifact, 51f, 49-51
- Complex partial seizure, benign partial epilepsy of childhood with occiprtal

activation during sleep, 82 paroxysm(BPEOP), 107-109, 108f-109f
- Continous spike and wave discharge during slow sleep, 125 childhood absence epilepsy, 97-101, 99f-101f
- Craniotomy EEG of, 36-37 electrical status epilepticus during slow sleep, 125
- Creutzfeldt- Jakob disease, 168-169, 169f-170f epilepsy with generalized tonic-clonic seizure on
awaking, 117
juvenile absence epilepsy, 97-101, 99f-101f
juvenile myoclonic epilepsy, 112-116, 113f-116f
D landau-kleffner syndrome, 125-126, 126f
lennox-gastaut syndrome,120-124, 122f-124f
- Delta activity, symptomatic focal epilepsy, 109-111, 110f
polymorphic, 148, 154-155, 154f-150f, 156f-158f west syndrome, 117-120, 118f-120f
rhythmic, intermittent, 147 - Epilepsy with generalized tonic-clonic seizure on
- Derivations of EEG, 10 awaking, 117
- Excess Beta activity, 31, 86 - Epileptic discharge, 85-95
- Drip artifact of EEG, 57, 57f - Epileptiform normal variant, 127-138
mid line theta rhythm, 138
psychomotor variants, 134-135
rhythmic mid temporal theta of drowsiness, 134-135
small sharp spike, 127-129
E subclinical rhythmic EEG discharge of adults
(SREDA), 135-137
- ECG artifact, 49-51, 51f wicket spike, 129-131
- EEG, see under electroencephalogram 6HZ spike and wave, 132, 134
- EEG, 14-and6-HZ positive bursts, 132-134
activation procedures of, 75-82, 76f-82f - Eye movement artifact, 44-49, 44f-49f
artifacts, 39-58, 39f-57f eye blink, 45f
brain maps, 6-10, 6f-10f eye closure, 45, 45f
derivation in, 10 eye flutter, 46f-47f
method of derivation, 13-14, 14f eye opening, 47, 47f
electrode placement in, 3-11, 4f-11f lateral eye movement, 48, 48f-49f
filters in, 3-4, 4f
montage in, 14, 14f
- Normal in adults, 23-39, 24f-39f
physiological basis of, vii F
polarity conventions in, 11
- Principles in recording of, 1-4 - FIRDA, see also frontal intermittent rhythmic delta
instrument setting, 1 activity (FIRDA)
calibration, 3, 3f -FIRDA, 147, 149f-152f, 75
EEG filtering, 3, 4f - Focal epilepsy, 109-111, 110f
paper speed, 3 - Frontal lobe epilepsy, 110
sensitivity, 1 clinical feature of, 110-111
- Reading and report of, 179-182 EEG finding in, 111
- Techniques of EEG recording, 5-14, 6f-14f
-Electrical status epilepticus during slow sleep, 125
- Electrode placements, 5-11, 6f-11f
special electrodes, 9-10, 10f
- Electrode popping, 53m 53f
G
- EMG artifact, 39-41, 39f-41f
- Encephalopathic pattern, 158-165 - Generalize periodic pattern, 166-170
alpha coma, 158-159, 159f-160f SSPE, 166, 167f-168f
beta coma, 160, 160f-161f CJD, 168-169, 169f-170f
spindle coma, 161, 161f-163f - Glossokinetic artifact, 42, 42f-43f
theta coma, 160
triphasic waves, 163-164, 164f-165f, 141
- Enhancement beta activity, 61
- Epilepsy, 85, 115 H
medication stop, 95
recurrence risk, 95 - Hypnagogic hypersynchrony, 65, 65f
- Epilepsy syndrome, - Hyperventilation, 75-78, 76f-77f
benign epilepsy of childhood with centrotemporal - Hypsarrhythmia, 117, 118f-120f
spiked, 102-107, 103f-107f
index 187
I M
- IED, see under interictal epileptiform discharges, 82 -Medial temporal lobe epilepsy (MTLE), 109-110
-Impedance artifact, 55 - Methods of derivation, 10
-Interictal epileptiform discharges, 85-94, 82 - Midline theta rhythm, 138
multiple spikes, 91, 91f-92f - Montages of EEG, 14, 14f
poly spikes, 91, 91f-92f - Multiple spike, 91, 91f-92f
sharp wave, 88, 89f-91f - Mu rhythm, 32-34, 32f-34f
sharp and wave complex(swc), 92, 92f characteristics of, 34
spike and wave complex(swc), 92, 92f-95f in brief, 34
spike discharges, 86-88, 86f-88f
- Intermittent rhythmic delta activity(IRDA), 147-154
FIRDA, 147, 149f-152f
OIRDA, 148, 150f N
TIRDA, 148, 152f, 154f
- Intermittent slow activity, focal, 148, 152f-154f - Non physiologic artifacts, 52-57, 52f-57f
- Intermitten slow activity,Generalize, 147-148, 149f-152f - Normal EEG in adult, 23-39, 24f-39f
- International 10-20 system placement, 6-8, 6f-8f - Normal sleep EEG, 58-74, 59f-74f
- Isoelectvic EEG, 141 - Non REM, 58
- IV artifact, 57, 57f
O
J
- OIRDA, see under occipital intermitten rhythmic delta
activity,
- Juvenile absence epilepsy, 97-101
-OIRDA, 148, 150f
clinical feature of, 97
EEG finding, 98, 99f-101f
- Juvenile myoclonic epilepsy, 112-116
activation during sleep, 82
clinical feature of, 112 P
EEG finding in, 112-113, 113f-116f
ictal, 112 - Periodic patterern, 166-178
interictal, 112 burst-suppression pattern, 121,145f, 171f-174f
generalize periodic pattern, 166-170
SSPE, 166, 167f-168f
K CJD, 168-169, 169-170f
- Periodic lateralized epileptiform discharge
- K complex, 68-70, 68f-70f (PLEDS), 174, 175f-178f
- Persistent slow activity, 154-155, 155f-158f
- Phantom spike and wave, 132-133, 133f-134f
- Photic stimulation, 78-82, 78f-82f
photic driving response, 78-79, 79f
L
photoepileptiform response, 81
photo myogenic response, 79-80, 79f-80f
- Lambda wave, 35, 35f photo paroxysmal response, 80-81, 80f-81f
- Landau-kleffner syndrome, 125-126 visual evoked potential, 78
clinical feacture of, 125 visual evoked response, 78
EEG finding in, 125-126, 126f technique, 78
- Lateral eye movement artifact, 49f - Photomyoclonic response, 79-80, 79f-80f
- Lateral rectus spike, 49f - Physiologic artifact, 39-52, 39f-52f
- Lateral temporal lobe epilepsy, 110 , 110f - Physiologic basis of EEG, vii
- Lennox- Gastaut syndrome, 120-124 - Polarity convetions of EEG, 11
clinical feature of, 120-121 - Polymorphic delta activity, 148, 154-155, 153f-158f
EEG findin in, 121, 122f-124f - Polyspike, 91-91f-92f
inter ictal EEG, 121 - Positive occipital sharp transients of sleep, 61-62, 61f-62f
ictal EEG, 121 - POST, 61-62, 61f-62f
- Principles in recording of EEG, 1-4
- Psychomotor variant pattern, 134, 134f-135f
- Pulse artifact, 51, 51f
R T
- Reading and report EEG, 179-182 - Technique of EEG recording, 5-14, 6f-14f
description of, 179-180 - Temporal intermittent rhythmic delta activity
report, 181-182 (TIRDA), 148, 152f, 154f
- Referential technique, 14, 14f - Temporal lobe epilepsy, 109-110, 110f
-REM sleep, 72-74, 74f - TIRDA, see under temporal intermittent rhythmic
- Rhythmic mid temporal theta of drowsiness, 134-135 delta activity, 72
- Rolandic epilepsy, 102-107 - Theta coma, 160
clinical feature of, 102 - Theta rhythm, 34-35, 34f
EEG finding in, 102, 103f-107f - Triphasic waves, 163-164, 164f-165f
S V
- Saccadic eye movements, 74 - Vertex waves(V waves), 62-64, 62f-64f

- Sharp wave, 88, 89f-91f - Visual evoked response, 78
- Sharp and wave complex (SWC), 92, 92f
- Skin artifact, 52, 52f
- Sleep activation, 82
epilepsy syndromes with, 82 W
- Sleep EEG,
normal sleep patterns, 58-74, 59f-74f - West syndrome
REM sleep, 72-74, 74f clinical feature of, 117
stage I sleep (Drowsines), 58-66, 59f-66f EEG finding in, 117, 118f-120f
alpha drop out, 58-60, 60f - Wicket rhythm, 32
enhanced beta activity, 61 - Wicket spike, 129, 129f-131f
hypnagogic hyper synchrony, 65, 65f
positive occipital sharp transients of sleep, 61-62,
61f-62f
SEM (slow rolling eye movement), 58
vertex waves, 62-64, 62f-64f Z
stage II sleep patterns, 66-71, 66f-71f
K complex, 68-70, 68f-70f - Zygomatic electrode, 10
sleep spindles (sigma waves), 66-68, 66f-68f - 6 HZ spike and wave, 132-133, 133f-134f
stage III sleep patterns, 71-72, 71f-72f -14-and 6 HZ positive bursts, 131, 131f-132f
stage IV sleep patterns, 72-73, 73f
- Slow wave activity
encephalopathic pattern, 158-165
focal intermittent, 148, 152f-154f
generalize intermittent, 147-148, 149f-152f
normal variant, 147
periodic pattern, 154-158
persistent slow activity, 127, 127f-129f
- Small sharp spike, 127, 127f-129f
- SOREM, (sleep onset REM), 72
- Special electrodes, 9-10, 10f
- Spike and wave complex (SWC), 92, 92f-95f
- Spike discharge, 86-88, 86f-88f
- Spindle coma, 161, 161f-163f
- SSPE, see under subacute sclerosing panencephalitis
- Sub clinical rhythmic EEG discharge of adult,
(SREDA), 135-136, 136f-137f
- Subacute sclerosing panencephalitis, 166-167f-168f
- Sweet artifact, 52, 52f
- Symptomatic focal epilepsy, 109-111
Frontal lobe epilepsy, 110-111
lateral temporal lobe epilepsy, 110, 110f
medial temporal lobe epilepsy, 109-110

Review of Clinical EEG

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Review of Clinical EEG

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Review Of Clinical

Thanks God helped me to gather this collection in a electroencephalo-graphy as well as neurology

Electroencephalography is the neurophysiologic Many technical advances have been made in

Historical background discovery basic to the use of evoked potentials in

Chapter 1 Part Two

Localization and polarity............................................15

Principles in Recording of EEG

Rarely high amplitude activity may appear in

Fig- EEG with high sensitivity(7µV/mm)

perfectly aligned. This is of utmost importance if

In the onset of every EEG study a calibration signal is

Fig- Note the effect of (H.F.F) on EEG

Fig- Another example of filtering EEG

Techniques of EEG recording:

In 1958 the 10-20 system of electrode placement

The International 10-20 System of Electrode Placement is

Fig- Relationship of 10-20 system electrode positions to

Alphabetical and Numerical Nomenclature to identify electrodes

Numerical System to further specify location

Brain Area Left Midline Right

The most commonly used additions to the 21 standard

Zygomatic electrodes Because two connections are needed to complete

The particular arrangements whereby a number of

Fig- montages for routine EEG

Fig- Symbol for the differential amplifier

Fig- symbol for the differential

Fig- Some examples of pen deflection with varing inputs

Summarizing 3. If there is no deflection of the pen, again two

Fig- According to the standard polarity convention, an

Methods of derivation all because each channel is measuring the potential

Fig- Examples of referential montages

Fig- Examples of bipolar montages

Localization and Polarity

1-Referential or monopolar technique and A1 is connected to Grid 2. Remaining 3 channels

Here the first three channels show upward deflection of

In this example the left ear(A1)being quite farther

electrode of the pair increases. Thus in (Fig-G), the

Rule 2: Given two pairs of electrodes having equal

Rule 5: If two electrodes are equidistant from F, the

FigL(a) shows a special case of rule 5. In this instance Fig-L

Normal Adult EEG

The story on EEG maturation shows the gradual

First described by BERGER in 1929 who named it

moment to moment. Therefore, we should look for

Alpha rhythm amplitudes vary considerably from

Generally Alpha rhythm amplitude vary from 20- Location

Reactivity of alpha rhythm to eye opening

Reactivity of alpha rhythm with eye

Alpha reactivity- increased alpha on eye closure

Alpha Variants: in the theta range. Differentiation from slow

1-Notched appearance of the rhythm

Slow alpha variant

Slow alpha variant

Fast-alpha variant harmonic of the native rhythm, appearing at twice the

• Paradoxical alpha response is the reverse of alpha Alpha rhythm in brief:

Diffuse beta activity

Beta rhythm in brief: comb rhythm and somatosensory alpha rhythm. Mu is

Reactivity of mu rhythm to wiggle fingers not to eye opening

Bilateral mu activity in an adult

Mu rhythm in brief: • When detected in an EEG,it should be verified by

Breach rhythm absence allows the electrodes to record more voltage

Diffuse EMG artifact

2- Glossokinetic artifact: In addition to muscle • Glossokinetic artifact is associated with activities