Electroencephalography
G.R.Shamsaei
Assistant Professor of Neurology
Jundishapour University of Medical Sciences
Foreword
iii
Introduction
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
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 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
Chapter 6 Chapter 12
Normal sleep EEG......................................................59 Reading and reporting EEG...................................179
xi
Chapter 1
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.
Fig-(continued)The same EEG with lower sensitivity(15µV/mm) Note decrease in amplitude in lower sensitivity
Principles in Recording of EEG 3
c) Calibration :
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
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
6 Review Of Clinical Electroencephalography
Fig-International 10-20 system placement. Odd number on the left, even on the right, and Z or zero in the midline.
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
8 Review Of Clinical Electroencephalography
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.
Techniques of EEG recording: Electrode placements 9
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
Montages
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
12 Review Of Clinical Electroencephalography
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
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
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
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.
Localization and Polarity 19
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
20 Review Of Clinical Electroencephalography
Fig-G
Fig-I
Localization and Polarity 21
Fig-K
Fig-M
Chapter 4
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
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.
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
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."
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
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
30 Review Of Clinical Electroencephalography
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
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.
32 Review Of Clinical Electroencephalography
Mu rhythm
Normal Adult EEG 33
Excessive mu activity
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
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
36 Review Of Clinical Electroencephalography
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
40 Review Of Clinical Electroencephalography
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
42 Review Of Clinical Electroencephalography
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.
44 Review Of Clinical Electroencephalography
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.
46 Review Of Clinical Electroencephalography
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
48 Review Of Clinical Electroencephalography
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
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.
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).
50 Review Of Clinical Electroencephalography
ECG atrifact
EEG artifacts 51
ECG artifact
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.
Electrode artifact at O1. The morphology is very unusual for any cerebral waveform, and the distribution is limited to a
single electrode
54 Review Of Clinical Electroencephalography
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.
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
56 Review Of Clinical Electroencephalography
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
IV artifact: Note regularity and distribution of the artifact, which allows for easier recognition of it
Chapter 6
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
60 Review Of Clinical Electroencephalography
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.
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
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
64 Review Of Clinical Electroencephalography
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,
66 Review Of Clinical Electroencephalography
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)
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
70 Review Of Clinical Electroencephalography
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
Stage 3 sleep
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.
74 Review Of Clinical Electroencephalography
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
76 Review Of Clinical Electroencephalography
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
78 Review Of Clinical Electroencephalography
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
80 Review Of Clinical Electroencephalography
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
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.
86 Review Of Clinical Electroencephalography
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.
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.
88 Review Of Clinical Electroencephalography
Spike, generalized. Note the high amplitude, and the aftergoing background suppression and slow wave.
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.
90 Review Of Clinical Electroencephalography
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.
Epileptic discharges 91
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.
Polyspike, generalized.
Note the aftergoing slow
wave. This is associated
with the “primary” or
idiopathic generalized
epilepsies, most typically
Juvenile Myoclonic
Epilepsy.
92 Review Of Clinical Electroencephalography
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).
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.
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.
Epileptic discharges 95
Generalized atypical spike and wave in an adult patient with a mixed seizure disorder that includes atypical absence
seizures.
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
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
98 Review Of Clinical Electroencephalography
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.
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
Electroencephalgraphy in common epileptic syndromes 101
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
102 Review Of Clinical Electroencephalography
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.
Electroencephalgraphy in common epileptic syndromes 105
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.
106 Review Of Clinical Electroencephalography
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
Electroencephalgraphy in common epileptic syndromes 107
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
108 Review Of Clinical Electroencephalography
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.
Electroencephalgraphy in common epileptic syndromes 109
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.
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
Electroencephalgraphy in common epileptic syndromes 111
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.
112 Review Of Clinical Electroencephalography
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
Electroencephalgraphy in common epileptic syndromes 113
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
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.
Electroencephalgraphy in common epileptic syndromes 115
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)
Electroencephalgraphy in common epileptic syndromes 117
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).
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
120 Review Of Clinical Electroencephalography
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
Electroencephalgraphy in common epileptic syndromes 121
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.
122 Review Of Clinical Electroencephalography
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.
Electroencephalgraphy in common epileptic syndromes 123
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.
124 Review Of Clinical Electroencephalography
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.
Electroencephalgraphy in common epileptic syndromes 125
(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 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)
Small sharp spikes or BETs. Note that these waveforms do not correspond to ECG see bottom trace.
Wickets
Wicket Spikes
Epileptiform Normal Variants 131
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
132 Review Of Clinical Electroencephalography
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
Epileptiform Normal Variants 133
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.
EEG of a 26-year-old patient, showing 6 Hz spike wave paroxysms (phantom spike wave)
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
136 Review Of Clinical Electroencephalography
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
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
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
140 Review Of Clinical Electroencephalography
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
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.
Nonepileptic Abnormalities 143
Focal attenuation of posterior alpha rhythm on the right side after a seizure
Excess beta activity. This patient has been treated with clonazepam
Generalized suppression background with intermittent bursts in a 76 year-old man with anoxic encephalopathy
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.
146 Review Of Clinical Electroencephalography
Asymmetric reduced sleep spindle in left hemisphere in a 29 year old man with TLE
Nonepileptic Abnormalities 147
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.
Nonepileptic Abnormalities 149
OIRDA during hyperventilation in a 13 year old boy- this is a normal finding in this patient
Bursts of high-voltage bilaterally synchronous frontal intermittent rhythmic delta activity in a 41-year-old lethargic
patient with uremic encephalopathy.
152 Review Of Clinical Electroencephalography
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.
Nonepileptic Abnormalities 153
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).
154 Review Of Clinical Electroencephalography
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
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.
156 Review Of Clinical Electroencephalography
(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.
Nonepileptic Abnormalities 157
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.
158 Review Of Clinical Electroencephalography
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.
Alpha coma: The EEG is dominated by alpha activity, which is non-reactive in a patient in coma of unknown nature
160 Review Of Clinical Electroencephalography
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. 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
162 Review Of Clinical Electroencephalography
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.
Nonepileptic Abnormalities 163
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.
164 Review Of Clinical Electroencephalography
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.
166 Review Of Clinical Electroencephalography
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
Nonepileptic Abnormalities 167
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.
168 Review Of Clinical Electroencephalography
Typical generalized periodic discharges in a child with SSPE. The interval between periodic complexes is 5-7 seconds
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
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.
Nonepileptic Abnormalities 171
Burst-suppression pattern. Suppression periods are characterized by activity less than 10 mV.
172 Review Of Clinical Electroencephalography
Burst-suppression pattern recorded in the EEG of a 70- year-old man after a cardiac arrest from which he was resuscitated.
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
174 Review Of Clinical Electroencephalography
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.
176 Review Of Clinical Electroencephalography
Right temporal PLEDs in a patient with herpes encephalitis and nonconvulsive SE recorded in the ICU.
Nonepileptic Abnormalities 177
Left temporal PLEDs in a patient with left temporal lobe epilepsy immediately following serial complex partial seizure.
BiPLEDs in a 36-year-old man with severe diffuse anoxic encephalopathy after cardiovascular arrest.
Chapter 12
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,
180 Review Of Clinical Electroencephalography
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
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
188 Review Of Clinical Electroencephalography
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