Review of Clinical EEG

Review Of Clinical

Electroencephalography

G.R.Shamsaei Assistant Professor of Neurology Jundishapour University of Medical Sciences

Foreword

Thanks God helped me to gather this collection in a book. In fact this book contains a series of electroencephalography teaching classes for neurology residents. Of course ,it is gathered from many references and many lectures about EEG, which some of them are mentioned at the end of the book. It is necessary to acknowledge all those ones who encouranged me, special my dear professor Dr. pakdaman for his emotional support. This book is written primarily for clinicians who interpret

electroencephalo-graphy as well as neurology residents. It is hoped that this book contains sufficient encyclopedic and practical information on electroencephalo-graphy so that my colleages will find it an invaluable companion.

G.R Shamsaei

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Introduction

Electroencephalography is the neurophysiologic measurement of the electrical activity of the brain by recording from electrodes placed on the scalp, or in the special cases on the cortex. The resulting traces are known as an electroencephalogram (EEG) and represent so-called brainwaves. This device is used to assess brain damage, epilepsy, sleep disorders and other problems. In some jurisdictions it is used to assess brain death. Some investigators claim that the EEG can be used to predict abnormal development and aid in the evaluation of nonspecific symptoms such as behavioral disorders, anxiety, or learning disabilities. On the other hand, by the addition of the averaging computer,electrical potential recording has been extended to the whole class of evoked or eventrelated potentials,thus improving the clinician,s ability to diagnose multiple sclerosis and lesions located in the optic nerve, brain stem, cerebellopontine angle, and spinal cord. Finally, EEG can also be used in conjunction with other types of brain imaging.

Many technical advances have been made in recording the electrical activity of the brain. Extended tracings lasting hours or days are now possible. Radiotelemetry allows the patient to move about in a restricted area while his brain activity is being recorded. The use of television has improved the encephalographer,s ability to compare the patient,s clinical condition with his or her EEG activity. The use of cortical and depth electrodes has made it possible to define epileptic foci not seen on conventional tracings. It has always been clear to electroencephalographers that the EEG is a physiological recording that is related to the functioning of large groups of neurons, the interpretation of which is directly related to the clinical history. The development of radiologic techniques, such as CT or MRI , has served to emphasize the limitations of the EEG as an instrument for anatomic localization.

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Physiologial basis of the EEG

Electroencephalographic signals are generated by the cerebral cortex. Spontaneous electroencephalographic activity is a reflection of currents flowing in the extracellular space. These currents are generated by the summation of excitatory and inhibitory synaptic potentials occurring on thousands or even millions of cortical neurons. Individual action potentials do not contribute directly to electroencephalographic activity. Conventional EEG is a continuous graph of the spatial distribution of changing voltage fields at the scalp surface recorded over time that result from ongoing synaptic activity in the underlying cortex. In addition to reflecting the spontaneous intrinsic activities of cortical neurons, EEG depends on important afferent inputs from subcortical structures, including the thalamus and brainstem reticular formation. For example, thalamic afferents probably are responsible for entraining cortical neurons to produce the rhythmic oscillations that characterize such normal patterns as the alpha rhythm and sleep spindles. Similarly, an electroencephalographic abnormality may result

directly from disruption of cortical neural networks or indirectly from modification of subcortical inputs onto cortical neurons. EEG is not the same as electrocorticography because not all potentials recorded at the cortical surface are detectable at the scalp. In the case of epileptiform activity, it has been estimated that 20-70% of cortical spikes do not appear on the electroencephalogram, depending on the region of cortex involved. This is largely because of the pronounced voltage attenuation that occurs in overlying cerebrospinal fluid and dura. Large areas of cortex must be involved in similar activity for a discharge to appear on the electroencephalogram. Furthermore, potentials involving surfaces of gyri are recorded more readily than are potentials arising in the walls and depths of sulci. Activity generated over the lateral convexities of the hemispheres is recorded more accurately than is activity coming from interhemispheric, mesial, or basal areas.

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History of Electroencephalography

discovery basic to the use of evoked potentials in today,s clinical neurology.

Historical background •

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From the time of the ancients to 18th century, electricity was regarded as a strange invisible power. Gradually the role of electricity in relation to the nervous system was to emerge,first from observation of the effect of applying it to the body,and eventually from the discovery that many tissues such as muscle and nerve could themselves be sources of this power. Luigi galvani, an italian physiologist(1780), was the first one who showed that the contraction of the frog,s leg was caused by electricity originating in the animal tissues themselves. Du bois-reymond(a German physiologist) in 1848 showed normal electrical potentials recorded from surface of a muscle on contraction.It was what we now know as the action potential of nerve and is the basis of electroneurography. With Du boisReymond,s demonstration of this in man, electromyography was born. When, in 1850, Helmholtz designed an instrument for measuring the conduction velocity of nerve. Richard Caton(1874) in England concluded that in the brain also this phenomenon should be occurred. He not only detected these electrical potentials but noticed that when both of his electrodes lay on the cortical surface there was a continuous waxing and waning of potential. This oscillation of the baseline was present in the unstimulated animal brain and Caton proved it to be unrelated to respiratory or cardiac rhythms. He also proved these fluctuations to be biologic in origin by showing them to be vulnerable to anoxia and to anesthesia and to be abolished by the death of the animal. He also had found the cerebral potential change evoked by sensory stimulation, a

Fig-1 Richard Caton

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But the first one who showed the electrical activity of brain in human was a German psychiatrist as named Hans Berger. He named this activity as electro-enkephalogram. He had found not only the EEG but also described various waves of brain. He also described different patterns of EEG in various pathology such as epilepsy,trauma and tumors.

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Fig-2 Hans Berger

Among many research interests in neurology, Berger studied brain circulation,and psychophysiology. However his main contribution to medicine and neurology was the systematic study of the electrical activity of human brain and the development of electroencephalography (EEG), following the pioneering work done by Richard Caton (1842-1926) in England with animals. In 1924, Berger made the first EEG recording in man. Using the EEG he was 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 alterations in brain diseases such as epilepsy and 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

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attached to the head by a rubber bandage. As a recording device he first used the Lippmann capillary electrometer, but results were disappointing. He then switched to the string galvanometer and later to a double-coil Siemens recording galvanometer, which allowed him to record electrical voltages as small as one ten thousandth of a volt. The resulting output, up to three seconds in duration, was then photographed by an assistant.

Fig-3 The first EEG recording, obtained by Hans Berger in 1929

CONTENTS

Introduction

Chapter 7

Physiological basis of the EEG................................vii History of electroencephalography...........................ix

Activation procedures................................................75

Chapter 1

Part Two

Principles in recording of EEG...................................1

Abnormal EEG patterns…..........................................83

Chapter 2 Techniques of EEG recording....................................5 Special electrodes……………..……………………..9 Derivations………………………………………..…10 Montages ……...……………………….…………....10 Polarity conventions…………………...................…11 Methods of derivation…………………..…………..13

Chapter 8 Epileptic discharges....................................................85

Chapter 9 Chapter 3

Electroencephalography in common epileptic syndromes...................................................................97

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

Chapter 10 Epileptiform normal variants....................................125

Chapter 4 Normal adult EEG.......................................................23

Chapter 11 Chapter 5 EEG artifacts..............................................................39

Chapter 6 Normal sleep EEG......................................................59

Nonepileptic abnormalities.......................................139 Abnormalities of the background rhythms............139 Abnormal sleep patterns..........................................145 Focal or generalized slow activity.........................147 Abnormal periodic patterns.....................................166

Chapter 12 Reading and reporting EEG...................................179

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Chapter 1

Principles in Recording of EEG

Before describtion of normal EEG some basic principles of recording of an EEG should be noticed: 1. First it should be emphasized that a cooperative and relaxed patient is essential for an ideal EEG study. An intelligent and trained technician can often obtain maximum cooperation and relaxation even from difficult patient such as children or subjects who are emotionally disturbed. During electrode placement, the technician should converse with the patient in a friendly manner, asking questions about his symptoms and assuring him about the painless nature of the test.The actual recording should be carried out with the subject in the supine position. A bed or a soft easy chair may be used for this purpose. 2. EEG paper : In EEG paper the horizontal axis is time and vertical axis is amplitude. This paper is divided by some darker and some lighter lines. The distance between two darker lines is 30mm. This vertical distance is further subdivided into five equal parts(6mm each)by four lighter lines, each subdivision therefore representing 0.2second or 200millisecond.

Instrument settings Each electroencephalograph has some main controls which are: a) Sensitivity: sensitivity of system is the magnitude of input voltage required to produce a unit pen deflection. It is usually denoted as microvolts (µV) per mm. Common values of sensitivity used in routine EEG is 7µV/mm in adults and 10µV/mm in children. This means that an input voltage of

7µV/mm will produce a pen deflection of 1mm or an input voltage of 70µV/mm, a pen deflection of 10mm or 1cm. If high amplitude potentials appear during recording so that the pens are overloaded(making a square top), the sensitivity is reduced to 10 or 15 so that the wave form of the activity can be recognized or vise versa. It should be kept in mind, that a sensitivity of 2 or 5µV/mm is higher than 7. For example, a 20µV/mm EEG potential will have a pen deflection of less than 3mm on 7µV/mm setting but 10mm on 2µV/mm setting. Some situations that we have a very high voltage potentials are: i) Infant who have frequent myoclonic jerks may have very high amplitude irregularly mixed slow and sharp activity in the EEG, often called hypsarrhythmia pattern. ii) Patients in "petit mal status"(absence status)may show almost continuous high voltage 3cps spikewave activity in the EEG. iii) patients with altered mental state due to encephalitis or various encephalopathies may show almost continuous high voltage very slow(delta) activity. Rarely high amplitude activity may appear in periodic bursts,typically seen in subacute sclerosing panencephalitis. In this condition high amplitude slow wave complexes occur every 4-15 seconds throughout most of the recording, synchronous with body jerks. Using higher sensitivities will be necessary to study the low voltage activity, such as the EEG study for determination of cerebral death or electrocerebral silence. It cannot be overemphasized that any change in the sensitivity setting should be noted on the record.

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Review Of Clinical Electroencephalography

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

Fig-(continued)The same EEG with lower sensitivity(15µV/mm) Note decrease in amplitude in lower sensitivity

Principles in Recording of EEG

b) Paper speed: Most EEG instruments have at least three paper speeds, 15,30 and 60mm/second. EEG records are conventionally run on a chart speed of 30mm/sec. At this speed a distance of 3cm or 30mm, which exists between two successful dark vertical lines on the EEG paper represents 1 second. This vertical distance is further subdivided into five equal parts(6mm each)by four lighter lines, each subdivision therefore representing 0.2second or 200millisecond. Higher speed than usual (60) and lower speed(15) is used in special situation, such as use of high speed in paroxymal activity for distinction between primary or secondary activity, and low speed in situation such as periodic phenomena or low amplitude and intermittent slow activity. Any deviation from the normal paper speed should be noted on the record at the time the change is made.

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perfectly aligned. This is of utmost importance if the phase relationship of an activity(e.g spike)in two different areas has to be meaningful. III. The space between the channels should be exactly equal. If one pen is closer to another (above or below), the mechanical baseline zero for this pen will have to be adjusted so that all the pens should be equidistant from the adjoining ones. At the end of the record, calibration should be performed again at each of the instrument settings of the amplification and frequency filters used during the recording.

c) Calibration : In the onset of every EEG study a calibration signal is recorded a few times simultaneously in all channels. Calibration consists of recording the response of the EEG to a known value of square-wave signal. The value of the calibration signal should be according to the sensitivity. The calibration signal should usually produce a pen deflection of 5-10mm. Because we commonly use sensitivity of 7 or 10µV/mm , a 50µV/mm calibration signal may be used which should produce a pen deflection of 7.1mm or 5mm respectively. It is important that after the calibration knob has been released to discontinue the calibration signal, the knob should be pushed in again to record another calibration signal only after the pens have returned to baseline. Too rapid on-off-on would overload the pens and the calibration could be inaccurate.After calibration signal has been recorded on all channels,the following should be carried out: I.

II.

Measure the pen deflection for the calibration signal for each channel and make adjustment so that each channel responds equally and appropriately to the signal. In channels showing less or more deflection, the sensitivity of the amplifier may have to be adjusted to obtain same pen deflection in all channels. The time axis alignment of all pens should be equal. If one or more pens lead or lag behind the others on the time axis, an adjustment of these pens have to be carried out so that all the pens are

Fig- Calibration deflections in response to three signals but with a constant sensitivity. Only the center calibration has a deflection in a range where the pen is not exceeding its limit but is large enough for easy and accurate measurement.

d) EEG filtering: Because sensitivity of the recording in EEG instrument are very high, so we have a large series of unwanted waves such as electricity from scalp muscles, heart , and eye muscles. At the other hand, we have many nonphysiologic waves that originate from media and electrical instruments. In general,the aims of using of these filtering in EEG instrument are attenuate certain frequency component of a signal leaving other frequencies unaffected. There are two main filtering, depending on whether the low or high frequencies are affected, the low frequency filter(L.F.F) and high frequency filter(H.F.F). Low frequency filter(L.F.F): these filters, control the response of the instrument to lower frequencies while the response to higher frequencies remains unaffected. High frequency filter(H.F.F): these filters attenuate the very high frequencies while the lower frequencies remain unaffected.

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

Fig- Another example of filtering EEG

Duration of recording: the chance of detecting a specific abnormality is directly proportional to the total recording time. This is especially true of paroxysmal disorders such as epilepsy. Not less than 15-20 minutes 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

sample in time from a patient,s life- a very short sample indeed. Considering this serious limitation, the high percentage of epileptiform abnormalities seen in epileptics makes the procedure amazingly valuable

Chapter 2

Techniques of EEG recording: Electrode placements

When EEG was first carried out on human by Berger, electrodes were placed on the front and back of the head and used to record over a number of years; Berger viewed much of what he saw as a measure of global cortical activity. It was soon discovered by others that, in fact, EEG activity varied in different locations on the head. In 1930,s, as the number of laboratories investigating EEG increased, there was a rapid proliferation of techniques and interpretations of the activity recorded and multiple channels allowed investigators to record simultaneously from multiple scalp areas. These observations were in turn followed by increased attempts to place electrodes at points where they might particularly enhance the observation of one or another type of activity that occurred. The observation that simultaneous different types of activity was occuring in turn encouraged the use of more electrodes for more channels of 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

different patients could be compared to each other. There was very wide diversity from place to place in established methods and standard placements. A committee of the international federation of societies for electroencephalography and clinical neurophysiology recommended a specific system of electrode placment for use in all laboratories under standard conditions. Their recommendation was the system now known as the international 10-20 system. Specific measurments from bony landmarks are used to determine the placement of electrodes. Many of the systems had done this earlier, but they generally used a specific standard interelectrode distance on every patient. The breakdown of such a system is apparent if the application of electrodes to a microcephalic patient is compared to application to a hydrocephalic patient using the same number of centimeters from landmark locations or between electrodes.

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Fig-International 10-20 system placement. Odd number on the left, even on the right, and Z or zero in the midline.

In 1958 the 10-20 system of electrode placement was established by electroencephalographers wanting a standard format and common terminology for electrode locations on the scalp. The establishment of the International 10-20 System made it possible for electroencephalographers to not only compare their patients' serial EEG tracings but allowed for comparisons between labs in different hospitals, in different cities and even in different countries. The initial recommendation was made at the International Congress of Electroencephalography and Clinical Neurophysiology in London in 1947


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

Fig- Relationship of 10-20 system electrode positions to the lobes of the brain.

The international 10-20 system of electrode placement is already standard in all EEG laboratories worldwide. It is supported by anatomic studies. Although the actual distance between electrodes varies with the size and shape of the skull, these electrodes

reflect the electrical activity over similar brain areas in different patients.

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Alphabetical and Numerical Nomenclature to identify electrodes The 10-20 System assigns an alphabetical abbreviation to identify the location of the electrode with a particular lobe or area of the brain under the electrode placement. The alphabetical abbreviations are as follows: Fp = Frontal Polar F = Frontal T = Temporal C = Central P = Parietal O = Occipital A = Auricular (ear lobes) M = Mastoid (sometimes used as a substitute for ear lobes, as a reference electrode) Pg = Nasopharyngeal (These are optional electrodes for recording from the medial aspect of temporal lobe. Placed through the nostril, the tip resting at the roof of the nasopharynx the tip of the electrode is near the anterior mesial surface of the temporal lobe and is thought to record from that area).

Technique The 10-20 system is so named because it divides each of three lines connecting skull landmarks into segments the length of which is 10% and 20% of the whole line. The baselines are the sagittal distance from nasion to inion, the horizontal distance from the frontal polar midline(Fpz)to the occipital midline(Oz), and the transverse distance from the left to the right preauricular depression. Electrodes are located along each line at intervals of 10% and 20% of the entire

length of the line, giving a total of 21 positions. Each position is named; it is given both an abbreviation, such as(Fp) for frontal polar, and a subscript number, such as Fp1(left frontal polar). Odd numbers designate electrodes placed over the left hemisphere, and even numbers those placed over the right hemisphere. The subscript Z indicates a midline position, for example Fz(frontal midline). The left and right ears are respectively labeled A1 and A2(auricular).

Fig- The term 10-20 is used because the electrodes are placed either 10% or 20% of the total distance between a given pair of skull landmarks.


Numerical System to further specify location Brain Area Frontal Pole Frontal Inferior Frontal Anterior Temporal Mid-Temporal Posterior Temporal Central Parietal Occipital

Left Fp1 F3 F7 T1 or F9 T3 T5 C3 P3 O1

Midline Fpz Fz

Cz Pz (Oz)

Right Fp2 F4 F8 T2 or F10 T4 T6 C4 P4 O2

The 10-20 System assigns a number to further specify the location in the left or right hemisphere. The "z" is used to indicate that the location of the electrode is in the midline or "zero" meaning that it is neither left hemisphere or right hemisphere. * The electrode placed at Cz is said to be the "Vertex" meaning that it is the Mid Central or at the top of the head. * Fpz and Oz are not standard placements but are used in achieving the other measurements and can be used as additional electrode placements for localization of activity. Fpz is sometimes used as the location of the COM (common) or ground electrode placement.

Special electrodes The electrical activity of certain portions of the cerebral cortex, notably the basomedial parts of the temporal lobe and the orbital and medial parts of the frontal lobe, is not accessible to the electrodes taken up thus far. This sometimes leads to problems in accurately locating seizure foci, particularly in patients who are being considered for temporal lobectomy. To overcome such problems, a number of special electrodes may be used.

T1 and T2 electrodes The most commonly used additions to the 21 standard derivations are the T1 and T2 electrodes. These are located by first finding the point that is one third of the way from the external auditory meatus to the outer canthus of the eye, and locating a point 1cm directly above. T1 and T2 are closer to the anterior part of the temporal lobes than F7 and F8, which are actually located over the inferior frontal area.

Fig- Placement of T1 and T2 electrodes. As you see, From this surface electrode, electrical activity from the anterior inferior tip of the temporal lobe can be recorded. Patients with symptoms of temporal lobe seizures should have these additional electrode placements applied for routine EEG recordings.

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Zygomatic electrodes These are located over the easily palpated zygomatic arch, below and anterior to the T1 and T2 electrodes. Zygomatic electrodes are useful for picking up activity from the tips of the temporal lobes.

Nasopharyngeal (NPG) electrodes The tips of these electrodes are placed in contact with the roof of the nasopharynx, so that activity from the uncus, hippocampus, and orbitofrontal cortex may be picked up.

Because two connections are needed to complete an electrical circuit, two electrodes have to be connected to each channel (amplifier)of the machine. A particular pair of electrodes connected to a single amplifier is referred to as a derivation. Experince has shown that a machine that displays at least eight derivations simultaneously is necessary to adequately study the spatial characteristics of the brain,s electrical activity. However, the larger machines and more derivations are capable of gathering more data in the same amount of time as well as providing better resolution of the spatial characteristics of the brain,s electrical activity. With the use of 21 electrodes, one can have a total of 210 different derivations. But in actual practice, all possible combinations of electrodes are seldom used. There is an important reason for this. Since interpretation of the EEG ultimately involves comparison of different derivations, it is essential to use derivations having comparable interelectrode distances. Indeed, most routine EEG only use a few derivations.

Montages

Fig- Basal view of the brain showing the approximate locations of special electrodes

Derivations With a total of 21 electrodes to work with, how should the electrodes be arranged to best display the brain,s electrical activity? In other words, what combinations of electrodes should be connected to the various channels of the EEG machine?

The particular arrangements whereby a number of different derivations is displayed simultanously in an EEG record is termed a montage. A large number of different montages can be disgned. The main reason for using different montages is to make EEG interpretation as easy and accurate as possible. For this purpose, certain guidelines have to be followed, and the american EEG society has given some recommendations in this regard. First of all, a montage should be simple and easy to comprehend. Montages should follow some kind of anatomical order or pattern. For example, channels representing the more anterior electrodes should be arranged on the recording chart above those from the more posterior regions. Derivations from the left side should be located on the chart above derivations from the right side. This may be accomplished either by alternating the derivations,i.e; left,right,left,right, and so, or by placing derivations from the different sides in blocks,e.g; left,left,left,left; right,right,right,right. It is advantageous for a laboratory to use a few common or standard montages so that records from different laboratories can be compared with ease.


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Fig- montages for routine EEG

The American Electroencephalographic Society Guidelines in EEG, Evoked Potentials, and Polysomnography (1994) have made basic recommendations for montages as well as other technical aspects of performing routine EEG. These will be called the Guidelines, for the rest of this text. The guidelines recommend the following:

1-Record at least 8 channels. 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 transverse bipolar. 4-Label each montage in the recording.

5-Use simple montages that allow for easy visualization of the spatial orientation of the waveforms - for example, bipolar montages should be in straight lines with equal inter-electrode distances. 6-Have the anterior and left-sided channels above the posterior and right-sided channels. 7-Use at least some montages that are commonly used in other laboratories.

Polarity conventions The EEG study is essentially an attempt to record the distribution of electric potentials on the scalp as they

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fluctuate with time. It would have been a very simple procedure if an area of zero electric potential was available on the body or elsewhere so that the electric potential at different electrodes on the scalp could have been easily measured with respect to this indifferent electrode. Because such an ideal in different electrode having zero potential does not exist, all EEG measurements essentially indicate potential differences between pairs of electrodes, rather than an absolute electrical potential at any electrode position. Essentially each EEG amplifier is connected to two electrodes on the scalp and it measures the potential differences between these two inputs. In other word, it has two sources of input, one connected to the first grid

or input1 (G1) and the other connected to the second grid or input2(G2). Conventionally , the EEG amplifiers are so designed that whenever the G1 input of a channel is relatively negative to G2, the pen of that channel deflects upward. With the same token, when G1 is relatively positive to G2 the pen moves downward. This concept is extremely important for the understanding of localization and polarity of a normal or an abnormal cerebral activity. A few example are shown in the accompanying diagram (see below fig A,B,C) showing the direction and amplitude of pen deflection with varying inputs of grid 1 and grid 2.

Fig- Symbol for the differential amplifier

Fig- symbol for the differential amplifier


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Fig- Some examples of pen deflection with varing inputs One should note that the pen deflection upwards of the same magnitude occurs in th first two examples even though the activity is electronegative in the first and electropositive in the second example. In the first example G1 is 80µV more negative than G2 whereas in the second example G2 is 80µV more positive than G1(or G1, 80µV less positive than G2), both producing similar pen deflections.

Summarizing 1. If pen moves upwards in a channel. One of the two possibilities exist: G1 more negative than G2(example 1) or G2 more positive than G1(example 2) 2. If pen moves downward in a channel, one of the two possibilities exist: G2 more negative than G1(example 3) or G1 more positive than G2(example 4)

3. If there is no deflection of the pen, again two possibilities exist: No activity at G1 and G2 or Equal activity at G1 and G2 (G1 and G2 equipotential, Example 5 ,6) More details on polarity and localization are described in next chapter.

Fig- According to the standard polarity convention, an upward signal deflection results if input1(G1) is more negative than input2(G2) or if input2(G2) is more positive than input1(G1). Conversely, a downward signal deflection results if input1(G1) is more positive than input2(G2) or if input2(G2) is more negative than input1(G1).

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Methods of derivation There are essentially two methods of recording the potential fields on the scalp. These are commonly known as monopolar(or referential) and bipolar derivations. In monopolar (referential) technique, one reference electrode is selected and the potential under other electrodes on the scalp is measured with respect to this common reference electrode. Usually the scalp electrodes are connected to G1 and the reference electrode connected to G2 of the channels. The term monopolar is misleading because it may imply that in this technique one is measuring the absolute potential under different scalp electrodes, but this is not true at

all because each channel is measuring the potential difference between the scalp electrode (G1) and the reference electrode (G2). The latter electrode though often called "inactive" or "indifferent" may have appreciable normal or abnormal cerebral activity. In other words there is no true monopolar measuring device, all measurments are bipolar. Because of this the best term for this technique is referential recording In the bipolar technique, there is no common reference electrode for G2 of all channels. One measures the potential difference between each pair of neighboring electrodes going serially in an anterior-posterior or transverse planes.

Fig- Examples of referential montages

Fig- Examples of bipolar montages

Chapter 3

Localization and Polarity

1-Referential or monopolar technique As mentioned in the previous chapter, the referential recording involves the measuring of potentials under different scalp electrodes as against one or two reference electrodes which are usually so placed that they are least contaminated with cerebral activity. The scalp electrodes which are often referred to as "active" electrodes are connected to Grid 1 of the input of each channel and the common reference often called "inactive" or "indifferent " electrode is connected to Grid 2. The referential recording therefore attempts to measure more or less local activity under different scalp electrodes in a fairly "absolute" manner. Various reference points have been used, the common being left and right ear lobules, midcentral(Cz), nose,chin,mastoid,neck,etc. One should bear in mind that whatever reference point is used, it can not and never should be regarded as an "indifferent" or "inactive" point because it will be affected by cerebral activity to a variable extent. Noncephalic electrodes like the one placed on the neck is markedly "noisy" in terms of EKG activity. Again, in spite of their distance from the brain these noncephalic electrodes may pick up appreciable activity arising from base of the brain. In the following discussion, it will become obvious that any one reference is not ideal for all cases. Use of montages employing either simultaneously two or more different references give more clarification regarding localization than obtained by the use of a single reference. First let us study a few theoretical examples to explain how one may determine localization and polarity of an activity in referential technique. In the following example, there is a spike recorded in the first channel where FP1 is connected to grid 1

and A1 is connected to Grid 2. Remaining 3 channels do not show any pen deflection(fig.A).

Fig-A

What can we say about the origin of this spike and its polarity? Because the spike is seen from the channel recording from FP1 and A1, the spike must arise at or close to either FP1 or A1. By looking to this channel alone, one cannot automatically say that the spike is definitely arising from FP1, it might very well originate from an area close to A1 electrode. However the fact that the lower three channels also having input from A1 do not record the spike would strongly favour FP1 as the site of origin of the spike seen in channel 1. There is also another possibility that spike might be arising close to A1 but it is not recorded in the last 3 channels because spike potential in C3, T3 and O1 is equipotential with A1. This , however, is an extremely remote possibility. The study of the activity simultaneously in 4 channels therefore suggests that spike is most probably originating under FP1 electrode. The next question is what is the polarity of the spike

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potential. Once the location is known the polarity usually poses no problem. Because the spike potential is arising under FP1, which is connected to Grid 1 and because the pen moves up, the spike potential is surface negative. It is therefore obvious from this example, that in the study of any type of cerebral activity one has to first detrermine the localization of the activity before correct conclusions can be drawn about its polarity. This working rule will be more clear in the next example shown in fig(B).

A1, the downward deflection in channel T3-A1 would suggest that T3 is more positive and more active than A1. In other words the area of maximum electropositivity is under the T3 electrode. It is then conceivable that the A1 electrode being quite close to T3 is picking up the activity quite appreciably. In the first 3 channels(FP1-A1, C3-A1, and O1-A1), there is upward deflection of the pen because the relatively electropositive A1 electrode is connected to Grid 2 of these 3 channels. The most logical and the correct interpretation of the events in fig(B) can be summarized by stating that there is a spike potential arising from left midtemporal(T3) region, that it is surface positive in polarity and that the potential fields spread to A1 therefore more positive than other electrodes on the left side such as FP1, C3 and O1. Fig(C) shows a very similar situation but in this instant the spike is negative in polarity and originates again in left midtemporal(T3) region.

Fig-B

Here the first three channels show upward deflection of pens at the time of spike potential, but the 4th channel shows downward pen movement. One may interpret that there is a negative spike of widespread distribution on the left side seen under FP1, C3 and O1 but a posiotive spike at left temporal(T3) region. By looking at the first 3 channels, in which there is upgoing spike, two interpretations are possible: I. That spike is arising in fairly diffuse manner over left hemisphere, seen under FP1,C3, and O1, electrodes and that it is an electronegative spike and that A1 electrode is relatively less active. II. That the spike is arising close to A1 which is the most active electrode in these three channels and that it is an electropositive spike. Now study the fourth channel which records between T3 and A1 and shows a downgoing spike. If the explanation (1) was correct that we are dealing with an electronegative spike then downward deflection in T3-A1 channel would suggest that T3 is less negative than A1. In otherwords of the five electrodes FP1,C3,O1, T3and A1 the least negative(and least active) in T3 which would be difficult to conceive considering that electrodes all around T3 are more electronegative and also more active. Now consider the explanation (2) above. If we are dealing with an electropositive spike arising close to

Fig-C

The first 3 channels show downward deflection because it is the A1 in Grid 2 of these 3 channels which is most active and is relatively more negative. In the 4th channel the spike deflects upward because T3 is more active (and more negative)than A1. Again it is the negative spike recorded in all 4 channels though it deflects downward in the first 3 and upwards in the last channel. In summary therefore , one should clearly remember that: 1. upward deflection in a recording channel such as FP1-A1, doesnot automatically mean that it is an activity of negative polarity and similarly a downward deflection doesnot always mean a positive activity. 2. if an activity is seen in a recording channel such as FP1-A1, it cannot be simply assumed that the activity is present exclusively under FP1. The activity may be present under A1 or under both FP1 and A1.


3. In studying any cerebral activity, one should first try to determine its location and then identify its polarity The application of referential technique to localization of cerebral potentials can be best explained by taking an example of a surface negative spike or

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sharp wave focus, say in left central (C3) with the potential field as shown in lower figure (FigD). The recording is made with the left sided scalp electrodes connected to the left ear and the sensitivity is set at 10µV/mm.

Fig-D In this example the left ear(A1)being quite farther from the area of maximum activity(C3), picks up the spike activity only very minimally, so that all the scalp electrodes are more active than the left ear. This is an ideal situation where the reference electrode is "contaminated" minimally or not at all by the cortical activity under study. One should note three points in the recording: 1- In all channels, the spike is upgoing,i.e. the pens are deflecting in one direction. This is because at the time of spike activity the Grid 1 of all channels become more negative with respect to Grid 2(A1). 2- The electrodes under which the spike is highest in amplitude is easily determined by the channel which shows the maximum pen deflection.

3- The distribution of the potential field can be judged by the relative magnitude of pen deflections in the channels exploring the activity under different electrodes around the focus. In the above example of 8 channel recording, one can say that the left central spike though spreads to FP1, F3, P3, O1, T3, T5, and F7,but its spread is maximum anteroposteriorly because F3 and P3 are more active than T3. The above ideal situation in which the reference electrode is least active is not always obtainable. No matter where the surface electrode is placed, it may appreciably pickup the activity in question. Far reference electrodes may therefore pickup very significant cerebral activity arising from the temporal lobe thereby complicating the interpretation of a recording using this ear as the reference. This can be seen, if we move the hypothetical spike focus to say T3 region as shown in (Fig-E)and record again using A1 as the reference.

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Fig-E In this example the left ear electrode being close to the T3 spike focus picks up very significant spike activity. One notes that the pen deflection is not in the same direction in all channels. T3-A1 channel shows upward deflection because T3 being at the peak of the focus is more negative than A1. The channel F7-A1 do not show any pen deflection during spike activity,not because F7 and T5 are not active but because they are equipotential with respect to A1. In the channels FP1A1, F3-A1, C3-A1, P3-A1 and O1-A1, the pens move downward during spike activity because A1 connected to the Grid 2 of these channels is more active and more electronegative with respect to the electrodes in Grid 1. One should not interpret this situation saying that there is positive spike at FP1, F3, C3, P3 and O1 , negative spike at T3 and no spike at F7 and T5. The spike in all channels is negative in polarity irrespective of pen movement. By making a referential recording using A2(which will be least contaminated by left hemisphere spike activity) as the reference, the above facts can be easily varified.

The situation may become even more complicated if the spike focus lies somewhat below the T3 electrode so that A1 is as active as T3 as shown in (Fig-F). Note that there is a downward deflection in all channels at the time of the spike discharge except in T3-A1 channel, which shows no pen deflection. There are obviously two possible interpretations of this situation: a. There, there is a spike discharge diffusely over left hemispherc leads but not at left midtemporal, and that it is surface positive. b. That the spike focus is close to left temporal electrode and that A1 and T3 are equipotential and that the spike is surface negative. These two interpretation are entirely opposite to each other. The first interpretation though theoretically possible, is not likely because it will be difficult to conceive of a potential field which would extend all over left hemisphere but would spare T3 area. Therefore the second possibility will be most likely and this could be proved by changing the reference to A2 or CZ as shown in the same diagram.


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Fig-F From the above example, the following facts can be summarized regarding a common referential recording: I. Where the common reference electrode picks up only minimal activity of interest, the situation is very ideal. Channels showing pen deflection will deflect in one direction. The channels receiving from the electrode overlying the potential peak will show largest pen deflection and the height of deflection in other channels will be proportional to the magnitude of activity under the active electrodes. Under these circumstances the polarity is very easy to determine, if pen moves up, the activity is surface negative and vice versa. II. During a common referential recording of a transient or paroxysmal activity, if the pen deflection in some channels are upward and in others downward, one should be highly suspicious of a "contaminated" or "hot" reference electrode. III. An activity seen in all channels in a common referential recording may not necessarily be generalized activity, it may be on the other hand extremely focal arising at or close to the reference electrode. This is particularly so if the waveform of the activity is very similar in all the channels. This is not only true with a temporal spike focus

but also with a temporal focus of slow activity when ipsilatertal ear is used as a reference. In the latter instance, apparently generalized slow activity over one hemispheric derivations may really be focal arising in the temporal region. IV. In referential recording complete cancellation of abnormality can occur over the temporal region if the ear close to the focal disturbance is used as a reference. If above limitations and cautions are properly understood one can derive very useful information and avoid pitfalls in localization using common referential recording.

2-Localization in bipolar technique: In bipolar technique, the principles of localization are outlined by five principles. These principles or rules are illustrated in the diagrams of (Fig-G) through (FigM). In these diagrams, F(focus) is the point of abnormal negative electrical activity. Rule 1: If one of a pair of electrodes is at F, the amplitude of the recorded potential will increase as the distance between this electrode and the second

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electrode of the pair increases. Thus in (Fig-G), the distance FB is greater than FA; therefore, the amplitude of the voltage recorded between F and B is greater than the amplitude recorded between F and A. In short, widely spaced electrodes record larger voltages than closely spaced electrodes.

Rule 4: If three electrodes are connected so that one is at F and is common to two recording channels, being the grid 2 input of the first channel and the grid 1 of the second, the pen deflections in the two channels will be in opposite directions. (Fig-J) shows this set of conditions. The outputs of the two channels illustrate what is meant by the term "phase reversal". Note that the reversal results from the fact that the shared electrode goes to opposing inputs and hence causes the opposing deflections to occur. A phase reversal identifies the electrode that is nearest to the point of maximum voltage, or the focus.

Fig-G

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

Fig-J

Rule 5: If two electrodes are equidistant from F, the focus, no voltage will be recorded between them. In FigK-(a) , B and C are equidistant from F and no voltage is recorded from the "equipotential zone" surrounding these two electrodes, which are the inputs to channel 2. This outcome is an example of cancellation. Fig-H

Rule 3: The farther away the dipole is from the surface of the scalp, the smaller will be the potential observed at the surface and the smaller the voltage recorded between pairs of electrodes, interelectrode distances being constant. This rule is illustrated by two examples in (Fig-I). Note that the dipole in case 1 is nearer the surface than it is in case 2 so that the voltage recorded by electrodes at F and A is greater in case 1 than in case 2.

Fig-I

An interesting, practical application of rule 5 occurs in the case of the so-called "active ear", in which a focus is situated in the temporal area adjacent to the ear. This is illustrated in FigK(b), where electrodes are placed in a coronal chain across the top of the head, from left to right, starting with the electrode on the left earlobe. With the focus located midway between the earlobe and the midtemporal electrode , an equipotential zone is created about electrodes P and Q so that no voltage is recorded between the inputs of the channel 1 amplifier. The deflection observed in channel 2 is larger than that in channel 3 because Q is closer to the focus than R—a corollary of rule 2.


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Fig-K

FigL(a) shows a special case of rule 5. In this instance the focus F is not on the line joining electrodes A, B, C and D but instead is to one side. Nevertheless, F is equidistant from B and C so that the rule still holds. However, the exact position of F along the perpendicular from the midpoint of the line joining B and C cannot be determined using the configuration of electrodes shown in FigL(a). To locate the focus in this dimension, a chain of electrodes perpendicular to the ABCD chain at the midpoint between B and C is applied. This configuration is shown in FigL(b), where the electrode at R happens to be directly over the focus F. Note that there is a phase reversal at electrode R, which by rule 4, localizes the focus to this electrode.

Fig-L

Another special case of rule 5 occurs when F is between two electrodes, but nearer to one than the other. In such a case a voltage will be recorded between these two electrodes, but the voltage will be less than it is when one of the electrodes is directly over F.

Fig-M

Chapter 4

Normal Adult EEG

The normal adult human EEG is comprised of patterns and wave forms that vary in frequency, amplitude, and location or distribution. EEG patterns may change with age, or with alterations in an individual's state of consciousness, for example, the transition from wakefulness to sleep. Extensive study of the human EEG beginning in the early twentieth century has resulted in the discovery of numerous brain wave patterns present in normal adults, children, and neonates. This chapter will discuss normal patterns of wakefulness found in the adult EEG.

Normal adult EEG Before recording, patient should be in resting condition. Resting condition denotes that the person has not been fasting and that he or she has not consumed stimulants like coffee,tea,,or soft drinks before the time the EEG is taken. It is the responsibility of the technician to inform the patient of this at the time the appointment is made for the EEG.

Features of the awake EEG in adults Electroencephalography (EEG) waveforms generally are classified according to their frequency, amplitude, and shape, as well as the sites on the scalp at which they are recorded. The most familiar classification uses EEG waveform frequency (e.g; alpha, beta, theta). Alpha rhythm: First described by BERGER in 1929 who named it alpha. It is the most prominent feature of the normal mature EEG. The international federation of societies for Electroencephalography and clinical

Neurophysiology (IFSECN) proposed the following definition of alpha rhythm: Rhythm at 8-13 Hz occurring during wakefulness over the posterior regions of the head, generally with higher voltage over the occipital areas. Amplitude is variable but is mostly below 50 microV in adults. Best seen with eyes closed and under conditions of physical relaxation and relative mental inactivity. Blocked or attenuated by attention , especially visual, and mental effeort(IFSECN,1974).

Frequency The story on EEG maturation shows the gradual frequency increase of a posterior basic rhythm that is detectable around the age of 4 months with a frequency of approximately 4/sec. This posterior basic rhythm shows a progressive frequency increase with average values of around 6/sec at age 12 months and 8/sec at age 3years. At that time, the alpha frequency band is reached, and there is justification for the use of the term alpha rhythm. The frequency reaches a mean of about 10/sec at age 10 years. This is essentially the mean alpha frequency of adulthood; in other words, the progressive alpha rhythm acceleration usually ends around the age of 10 years, but the second decade of life(and to some degree also the third decade) features a constant decline of intermixed posterior slow activity that is usually present in considerable quantity at age 10. The frequency of the alpha rhythm tends to decline in elderly individuals.

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Amplitude

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

Alpha rhythm amplitudes vary considerably from individual to individual and, in a given person, from

Fig- A 10-second segment showing a well-formed and well-regulated alpha rhythm at 9 Hz. Note that it is very regular, rhythmic, waxing and waning, and posterior dominant. The contrast between the first and second halves of the page illustrates the reactivity of a normal alpha rhythm, with attenuation upon eye opening.

Generally Alpha rhythm amplitude vary from 20100µV; values above 100µV are uncommon in the adult. There is good evidence of a mild to moderate alpha amplitude asymmetry with higher voltage on the right. The alpha amplitudes tend to show constant waxing and waning.

Location The alpha rhythm is mainly located in the posterior half of the head and is usually found over occipital, parietal, and posterior temporal regions.

Normal Adult EEG

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Reactivity The poterior alpha rhythm is temporarily blocked by an influx of light(eye opening), other afferent stimuli, and mental activities. The degree of reactivity varies; it may be completely blocked, suppressed, or attenuated

with voltage reduction. Alpha attenuation due to other stimuli (auditory, tactile, other somatosensory stimuli and mental activity) is usually less pronouced than the blocking effect with eye opening.

Reactivity of alpha rhythm to eye opening

Reactivity of alpha rhythm with eye opening and closing

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Alpha reactivity- increased alpha on eye closure

Alpha Variants:

Alpha squeak was first recognized and described by Storm van Leeuwan and Bekkering in 1958. The normal phenomenon can occur momentarily after eye closing and is a brief acceleration of the patient's normal alpha rhythm. It can be facilitated by visual attention before eye closure but does not occur every time the eyes are closed. Slow alpha variant The posterior dominant rhythm in most adults is 8.5-11 Hz. In some patients, there can be a sub-harmonic of the posterior rhythm at 4-5 Hz. The slower frequency is typically notched. The subharmonic can be misinterpreted as a slow background

in the theta range. Differentiation from slow background can be made by the notched appearance which is a clue to the faster native background. In addition, the slow alpha variant is attenuated with eye opening. The usual posterior dominant rhythm frequency or the transition between that faster frequency and the slow alpha variant can sometimes be seen elsewhere in the recording. Also, central and anterior activity is of normal frequency composition, whereas most patients with a theta activity background would have abnormal slow activity in these forward regions. Slow alpha variant can be misinterpreted as slow background associated with encephalopathy, but some guidelines for differentiation are:

1-Notched appearance of the rhythm 2-Stereotypic appearance of the background of the slow alpha variant as opposed to polymorphic appearance of pathologic slow activity of encephalopathy 3-Normal frontal and cerebral activity with slow alpha variant as opposed to slowing associated with encephalopathy.

Normal Adult EEG

Slow alpha variant

Slow alpha variant

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This is an example of "slow alpha variant." The patient's alpha rhythm at 12 Hz is seen in the second half of the sample. The first half shows a subharmonic at half that frequency, and this is the "slow alpha variant."

Fast-alpha variant Fast-alpha variant is characterized by an otherwisenormal posterior dominant rhythm which appears as a

harmonic of the native rhythm, appearing at twice the native frequency (16-20 Hz), appearing in the beta range.

The fast alpha variant is easy to interpret as normal, since there is not the slowing which is more typical of pathology

Normal Adult EEG •

Paradoxical alpha response is the reverse of alpha reactivity in a fully alert individual. Upon eye opening in the normal alert adult, alpha rhythms are attenuated. Patients, however, alerted from a drowsy state can produce an accentuated alpha rhythm with eyes open. Since this is contradictory behavior for alpha rhythm, the term paradoxical is used. In young adults, alpha rhythm can spread into the mid and posterior temporal head regions. This so called temporal alpha behaves just like alpha rhythm in the occipital head regions and is symmetrical as well as reactive to eye opening.

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Alpha rhythm in brief: • FREQUENCY: 8-13Hz(alpha rhythm of most adults ranges between 9.5-10.5 Hz) • LOCATION: posterior dominant but may extending to central and temporal regions.Occasionally may be widespread. • MORPHOLOGY: Rhythmic, regular, and waxing and waning • AMPLITUDE: Generally 20-100µv. The alpha rhythm is often of slightly higher voltage over the right hemisphere. There should be little (less than 1 Hz) or no difference in the frequency of the alpha rhythm between the left and right hemispheres. • REACTIVITY: Best seen with eyes closed, attenuates with eye opening.

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

Although any activity that is 8-13hz is called alpha but if is not attenuates with eye opening it is not alpha rhythm (reactivity to eye opening is typically used as evidence).Alpha rhythm attenuates due to auditory,tactile,and other somatosensory stimuli or heightened mental activity (such as solving arithmetical problems) but these stimulants are usually less pronounced than the blocking effect with eye opening. Other EEG patterns may fall within the 8-13 Hz range. They are described as being within the alpha frequency, but not called the alpha rhythm. Mu rhythm, for example, is within the alpha frequency range, but

its location and reactivity are different. Mu rhythm will be discussed in more detail in this chapter.

Beta rhythm: The term "beta rhythm" was first used to describe frequencies faster than alpha rhythm by Hans Berger in 1930. Beta rhythm is usually low voltage (less than 30 µvolts) in adults. Often, during the awake EEG, beta is present in the anterior head area, but may be obscured by muscle artifact (EMG) and eye movement potentials from the frontal electrodes . Beta rhythm is a normal

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finding in the adult awake EEG and can sometimes be better seen when the patient's eyes are open. Any rhythmical EEG activity above 13/sec may be regarded as beta rhythm. Rhythmical beta activity is encountered chiefly over the frontal and central regions; it usually does not exceed 35/sec. The amplitude of beta activity seldom exceeds 30µV. The physiological beta frequencies may be broken down as follows:

1. 2. 3. 4.

frontal beta: fairly common, may be very fast, no relationship to physiological rhythm. central beta: partly but not generally the basis of rolandic mu rhythm often mixed with mu rhythm. posterior beta: often a fast alpha equivalent, reactive like alpha rhythm. diffuse beta: no linkage with any special physiological rhythm

This is the normal amount of beta, frontally predominant, with waxing and waning amplitude

Normal Adult EEG

Diffuse beta activity

A sample of awake EEG showing the normal or often seen amount of beta activity.As shown here, beta activity is often easier to identify during relaxed wakefulness or early drowsiness.

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Beta rhythm in brief: Normal beta activity has the following characteristics: • FREQUENCY: Greater than 13Hz , Common 1825Hz ,less common 14-16Hz,and rare 35-40Hz • LOCATION: Mostly frontocentral but somewhat variable,some describe various types according to location and reactivity:generalized, precentral,and posterior. • AMPLITUDE: Usually range 5-20µv • Can be mildly different (<35%) in amplitude between the two hemispheres,which may be caused by differences in skull thickness. Definit focal,regional, or hemispheric differences(at least 50%)in amplitude may be significant and may suggest either skull defect(side with higher amplitude)or a structural lesion (side with lower amplitude). • MORPHOLOGY: Usually rhythmic,waxing and waning,and symmetric. • REACTIVITY: beta activity enhanced during stage1 and 2 sleep and tends to decrease during deeper sleep stages. • Amount and voltage of beta activity is enhanced by commonly used sedative medications (benzodiazepines and barbiturates).

Mu rhythm: This rhythm first described by Gastaut in 1952. Other terms are wicket rhythm, central alpha, arcade rhythm,

comb rhythm and somatosensory alpha rhythm. Mu is a distinct, surface-negative or arch-like or comb like rhythm of a frequency approximately 7-11 Hz. It can be as high in amplitude as 80 µvolts and is seen, not in the posterior head regions, but in the central head regions with eyes closed or open. It can appear unilaterally, bilaterally or independently in either hemisphere. It can be continuous or appear intermittently throughout an EEG recording. When identified on the recording, it is important to distinguish this rhythm from alpha. Mu is attenuated by real or imagined contralateral motor activity. Eye opening which attenuates the alpha, combined with clenching of the contralateral fist or movement of the contralateral thumb, which blocks the mu, helps verify the pattern. Often just thinking about contralateral movement (or the technologist touching this limb) will attenuate this activity. The potentials are most prominent at C3 and C4. Mu is very often asymmetrical or unilateral. The absence of mu activity on one side is not abnormal, unless there is very frequent mu activity on one side and none on the other side. The key to identification of Mu rhythm is blocking by movement of the contralateral arm. Even contemplating movement can produce this change.This rhythm is observed in 17-19% of young adults.An increase association between mu rhythm and a variety dysfunctions such as migrain,bronchial asthema, peptic ulcer,eczema,tinnitus,arterial HTN, and hyperthyroid states is described.At the other hand,Mu rhythm is common in patients with mild to moderate psychiatric disorders such as anxiety,aggressiveness,emotional instability,and psychosomatic disorders.

Mu rhythm

Normal Adult EEG

Excessive mu activity

Reactivity of mu rhythm to wiggle fingers not to eye opening

Bilateral mu activity in an adult

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

Mu rhythm in brief: •

CHARACTERISTIC:

– FREQUENCY:7-11hz (in range of alpha frequency) – LOCATION:Centroparietal region(c3,c4,cz) – MORPHOLOGY:Arch like or comblike shape or like an "m"symmetric or asymmetric between the 2 sides and may be unilateral. • In cases of strictly unilateral mu rhythm ,a careful search for bone defects and/or local pathology is indicated. • Very high voltage mu activity may be recorded in the central regions over skull defects and may become sharp in configuration,and thus can be mistaken for epileptiform discharges.

• When detected in an EEG,it should be verified by testing its reactivity. – AMPLITUDE:Like alpha rhythm – REACTIVITY:Most characteristic featuring defining the mu rhythm;mu rhythm attenuates with contralateral extremity movement,the thought of a movement,or tactile stimulation;contrary to the alpha rhythm,does not react to eye opening and closing

Theta rhythm According to the international nomenclature, the theta band is the “frequency band from 4 to under 8 Hz” and the theta rhythm is the “rhythm with a frequency of 4 to under 8 Hz”.

Normal Adult EEG

Theta activity in the waking adult The normal adult waking record contains but a small amount of theta frequencies and no organized theta rhythm. Theta frequencies and theta rhythms, however, play an important role in infancy and childhood, as well as in states of drowsiness and sleep.

Lambda wave Lambda activity is found in the occipital regions in the normal waking EEG. It is a surface-positive event and has a configuration like the Greek letter lambda (λ), for which it is named. Lambda activity is seen with eyes open and can be elicited by saccadic eye movement, which would occur if you asked your subject to view or scan a complex image. Lambda, which occurs in 65% of the population, is normal and appears to

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represent an evoked response to visual stimuli produced by the rapid shifts of images across the retina. Lambda waves occur when reading and occasionally when watching TV. Its amplitude is usually below 20µV and may exceed 50µV in some persons. Their form has been described as triangular or sawtooth shaped and may spread to parietal or posterotemporal areas. They may be symmetric or asymmetric.Lambda waves are best found in brightly laboratories and can not be elicited in darkness.The lambda waves may be mistaken for occipital spikes, however, their positive polarity and blocking with eye closure make this clearly not epileptiform. Morphologically, they are similar to positive occipital sharp transients of sleep(POSTS) both in form and in occipital distribution.

Lambda wave

Lambda wave

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Breach rhythm Breach rhythm is a sharply focal 6-11 Hz pattern associated with a defect in the skull, resulting from surgery or an accident . This rhythm is of higher amplitude than alpha rhythm, (generally exceeding 80 µvolts) and often has a spike-like appearance, particularly when beta frequencies are riding atop of it. The human skull is a natural insulator and its

absence allows the electrodes to record more voltage or amplitude from the underlying cortex. Frequently, if found over the central motor cortex, the breach rhythm will be reactive to contralateral fist clenching or movement as mu rhythm is. Breach rhythm appears normally with skull defects and can be differentiated from a slow alpha rhythm or mu rhythm by this particular characteristic.

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

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Chapter 5

EEG artifacts

Artifacts are waves or groups of waves which are produced by technical or other disturbances which are not due to brain activity i,e is not of cerebral origin. A good rule to remember is that if the activity in question is limited to a single channel or electrode, it must be assumed to be artifactual in origin until proved otherwise.

causes. EMG artifact consists of short needle-like spikes which may occur in such frequency that they become confluent and give an appearance that resembles epileptic spikes. Some guidelines for differentiating EMG from epileptiform spikes are a follows: •

Artifacts divided into two groups: 1-Physiologic: A group of waves that are generated from patient(sources other than the brain). 2-Nonphysiologic: A group of waves that arises from outside of the body(ie,equipment,environment).

• •

Variety of physiologic artifacts:

•

1-EMG artifact: It is the most common artifacts. EMG activity frequently contaminates EEG recordings, and this is prominent when patients are tense, seizing, or have other reasons for increased tone of scalp muscles.Frontalis and temporalis muscles are common

•

EMG is very fast, much faster than spikes. Activity recorded at the scalp that is shorter than 20 msec is highly unlikely to be epileptiform activity. EMG spikes are not followed by a slow wave. EMG is prominent in the waking state, and disappears with sleep EMG spikes recur at a rate which is much faster than would be seen with repetitive spikes. EMG is attenuated by asking the patient to relax the jaw, open the mouth, or other maneuver

Other causes of EMG artifacts are some movement disorder such as essential tremor, parkinson disease and hemifacial spasms.

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Diffuse EMG artifact

EMG (muscle) artifact. These waveforms represent motor unit potentials as typically seen on needle electrode examination during EMG, with a frequency of 20-100 Hz. Distribution varies, and in this case it is more prominent on the left side.

Occasionally, muscle artifact is more restricted, and may even arise from a single motor unit can be

noted, particularly in the midtemporal region.

EEG artifacts

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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 is a special type of EMG artifacts that occurs during intermittent photic stimulaion due to contraction of the frontalis and orbicularis muscles.These contractions occur 50-60msec after each flash,disappear after eye opening,are located mostly frontally,and have no concomitant EEG changes. These responses may

occur in normal subjects and are time locked to photic stimulation, occur at the same frequency of photic stimulation and begin and end with the onset and cessation of photic stimulation. The main problem with the photomyoclonic response is in differentiation of this from photoparoxysmal response.

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2- Glossokinetic artifact: In addition to muscle activity, the tongue (like the eyeball) functions as a dipole, with the tip negative with respect to the base. In this case, the tip of the tongue is the most important part because it is more mobile., although it is less steep than that produced by eye movement artifacts. Movement of the tongue is common in the waking state, and can occasionally be mistaken for pathologic frontal slow activity. This is potentially more problematic in a comatose patient who is having tongue movements and also observed in patients with dementia or those who are uncooperative. Glossokinetic artifact can be differentiated from slow activity in the following ways: • Glossokinetic artifact usually disappears in drowsiness and light sleep.

• •

Glossokinetic artifact is associated with activities such as speaking, chewing, swallowing. Glossokinetic artifact is often concurrent with EMG artifact of the frontalis and temporalis muscles

If there is still doubt about identification, then electrodes can be placed below the eyes or on the submental muscle of the lower jaw. The patient is asked to make lingual movements such as “la la la” and the potentials observed. Cerebral activity will be higher in voltage in the frontopolar electrodes. Identification of glossokinetic artifact is much better if the technician recognizes the problem and is able to perform these maneuvers. Combinations of muscle and glossokinetic artifact produce very characteristic patterns.

Glossokinetic artifact

EEG artifacts

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.

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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 all EEGs and are useful in identifying sleep stages. The eyeball acts as a dipole with a positive pole oriented anteriorly (cornea) and a negative pole oriented posteriorly (retina). When the globe rotates about its axis, it generates a large-amplitude alternate current field, which is detectable by any electrodes near the eye( i,e Fp1 , Fp2, F7, and F8). Other source of artifacts comes from EMG potentials from muscles in and around the orbit.

Vertical eye movements typically are observed with blinks (ie, Bell phenomenon). A blink causes the positive pole (ie, cornea) to move closer to frontopolar (Fp1-Fp2) electrodes, producing symmetric downward deflections. During downward eye movement the positive pole (ie, cornea) of the globe moves away from frontopolar electrodes, producing an upward deflection.

EEG artifacts

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.

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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

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Eye flutter

Eye opening: Eye opening results in a negative potential in the frontopolar electrodes plus alteration in the posterior rhythm. The attenuation of the posterior rhythm with eye opening and reappearance with eye closing are good clues to the presence of vertical eye movements, although the technician should indicate

this phenomenon along with other patient movements. Eye closure results in restoration of the posterior rhythm. The posterior dominant frequency may be slightly faster immediately after closure. Therefore that should be measured a few seconds after eye closure.

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Lateral eye movements: Lateral eye movements most affect lateral frontal electrodes F7 and F8 . During a left lateral eye movement, the positive pole of the globe moves toward F7 and away from F8. Using a bipolar longitudinal montage, maximum positivity in

electrode F7 and maximum negativity in electrode F8 is recorded. With right lateral eye movement, the opposite occurs. In these instances, so-called lateral rectus EMG artifact may be present in electrode F7 or F8.

Eye movement artifact

Lateral eye movements such as these are usually seen in frontal electrodes and not further posteriorly then mid temporal. The phase reversals at F7 and F8 are of opposite polarity, indicating lateral eye movements. Because the cornea is positively charged, and the retina negative, the side of the positivity indicates the direction of the eye movement.

Eye rolling movement

EEG artifacts

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Lateral eye movement artifact

Asymmetric eye movements can occur for several reasons . The first problem to be looked for is asymmetrical placement of the electrodes.A small deviation from the standard placement can lead to slight asymmetries in the recording. The next most obvious cause for this type of artifact is unilateral enucleation and a prosthetic eye replacement. Patients with a third cranial nerve palsy or external ophthalmoplegia will be unable to produce conjugate upward gaze and will have an asymmetrical eye blink with decreased amplitude, (a smaller deflection) on the side of the paralysis. Asymmetry of eye movement may also be due to a skull defect, usually a craniotomy (breach effect).

4- ECG artifact: Some individual variations in the amount and persistence of ECG artifact are related to the field of the heart potentials over the surface of the scalp. Generally, people with short and wide necks, obese patient and babies have the largest ECG artifacts on their EEGs. artifact is observed best in referential montages using earlobe electrodes A1 and A2. Increased inter-electrode distance predisposes to ECG artifact. Differentiation from electrocerebral artifact is most obvious if a special ECG channel is recorded, but even in the absence of this, the regular nature of the QRS complex and the distribution of the sharp activity makes the source evident.

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ECG atrifact

EEG artifacts

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ECG artifact

5-Pulse artifact: Pulse artifact occurs when an EEG electrode is placed over a pulsating vessel. The pulsation can cause slow waves that may simulate EEG activity. A direct relationship exists between ECG and the pulse waves. The QRS complex (ie, electrical component of the heart contraction) happens slightly ahead of the pulse waves. The relationship between ECG and Pulse artifact

Pulse artifact can be differentiated from pathological slow activity by the following features: • • •

The artifact localizes over one electrode. The artifact is time-locked to the ECG but with a delay. The background is otherwise normal

Initial inspection could mistake pulse artifact with polymorphic delta activity, but in this situation the background is usually abnormal, with slowing and disorganization. If there is still doubt, examination of the scalp by the technician can be revealing.

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6-skin artifacts: Biological processes such as sweats may alter impedance and cause artifacts. Sodium chloride and lactic acid from sweating reacting with metals of the electrodes may produce huge slow baseline sways. On the other hand, Significant asymmetry also can be observed when a collection (eg, subgaleal hematoma) is under or in the skin. In this last example, the amplitude of the background rhythm is reduced in derivations from electrodes overlying the hematoma.

Sweat artifact. This is characterized by very low frequency (here 0.25 to 0.5 Hz) oscillations. The distribution here (electrodes T3 and O1) suggests sweat on the left side. Note that morphology and frequency is also consistent with slow rolling eye movements, but distribution is not.

NON-PHYSIOLOGICAL ARTIFACTS Non-physiological artifacts are generated externally or in the environment and come from a vast variety of sources. Many of these originate within the equipment used to record the EEG. Others are generated by the actual recording electrodes and environmental sources.

1-Electrodes and leads: Electrode leads can be a source of artifact especially if there is instability in fixation of the electrode and high impedance.

Movement of the electrode results in changes in the junction potential. The discharge of the junction potential results in a potential which can be mistaken for a spike discharge. The appearance is of a brief spike followed by a gradual decay to baseline. The most common electrode artifact is the electrode popping. Electrode artifact identified easily by its characteristic appearance (i.e, abrupt vertical transient that does not modify the background activity) and its usual distribution, which is limited to a single electrode.

EEG artifacts

Electrode artifact at O1. The morphology is very unusual for any cerebral waveform, and the distribution is limited to a single electrode

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

Single electrode artifact at T5

EEG artifacts

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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 : Adequate grounding on the patient has almost eliminated this type of artifact from power lines. The problem arises when the impedance of one of the active electrodes becomes significantly large between the electrodes and the ground of the amplifier. In this

situation, the ground becomes an active electrode that, depending on its location, produces the 60-Hz artifact . The artifact presents at exact frequency (60 Hz, as its name indicates). A better identification can be made by increasing the paper speed (ie, sweep time) to 60 mm/s and counting it (1 cycle per millimeter).

60-Hz artifact

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3- Movement artifact: Movement artifact is due to disturbance of the electrodes and/or leads. Electrode gel is a malleable extension of the electrode, and minor head movement produces little effect on the electrode-gel-scalp attachment. However, movement sufficient to disturb the 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

compared to most electrical circuits, there is resistance of the leads and capacitance between the leads. Movement of the leads results in disturbance of the capacitance. The built-up charge can dissipate with loss of the capacitance, and this too is recorded as EEG.

Movement artifact related to head motion with hyperventilation

EEG artifacts

Movement artifact

4-intravenous artifact: This artifact is seen commonly in ICU recordings.The 'drip' artifact or IV artifact is periodic and small in amplitude and easily recognized. Morphologically it appears as spike transient potentials at fixed intervals that coincide with drops of the infusion.

IV artifact

IV artifact: Note regularity and distribution of the artifact, which allows for easier recognition of it

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Chapter 6

NORMAL SLEEP EEG

This chapter discusses the EEG activity of sleeping healthy adults. This section is limited to sleep recordings obtained in the regular EEG laboratory. The purpose of these EEG sleep studies is to search for abnormalities that may be hidden in the waking state. There is no doubt that the overall information derived from a wakefulness record is greater and hence clinically more significant.There are,however, a number of conditions, especially in domain of epileptic seizure disorders,in which sleep provides essential information.(this excludes the sleep disorders themselves, which should be evaluated in a specialized sleep laboratory) The drowsy state and light sleep(stage 2)are usually the most informative phases; for this reason, the sleep-onset portion with a length of 5 to 30 minutes in stage 2 sleep may be sufficient. In infants and children , a sleep(nap) recording is almost a necessity, not simply because of easier management of the sleeping child but also because of the needed information. Generally, Sleep without medication is undoubtedly preferable to sedated sleep.Whenever a sleep recording can not be obtained naturally,sedated sleep is dictated by necessity. In these circumstances,the patient must not be over powered by strong and rapidly sedatives because the highly 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 activity may also obscure important details.Therefore,the IV and IM routes must be avoided.Orally and rectally administered sedatives act more gently and slowly. The ensuing sleep contains many or most features of spontaneous sleep.In special cases of TLE, there is still a place for the IV route and deep sleep.The effectiveness of these drugs lies in the

fact that,in some cases of TLE, the anterior temporal spikes focus becomes most active in stage 3 or 4. In the clinical EEG laboratory,most sleepers reach only stage 2. Stage 3 is occasionally,and stage 4 seldom,reached unless unusually long sleep recording time is alloted or in cases of profound tiredness after sleep loss.REM stages are seldom seen in the clinical laboratory except in infants,young children,and adults with sleep loss.

Normal sleep EEG patterns Loomis provided the earliest detailed description of various stages of sleep in the mid-1930s, and in the early 1950s Aserinsky and Kleitman identified rapid eye movement (REM) sleep. Sleep generally is divided in two broad types: nonrapid eye movement (NREM) sleep and REM sleep. On the basis of EEG changes, NREM is divided further into 4 stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles, each lasting approximately 90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult NREM sleep accounts for 75-90% of sleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV). REM sleep accounts for 10-25% of sleep time.

Stage 1 sleep or drowsiness The transition from the awake to the drowsy state or stage 1 sleep is marked by some profound changes in the background activity of the EEG. These changes in brief are: • Slow rolling eye movements (SEMs) • Attenuation (drop out) of the alpha rhythm

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Central or frontocentral theta activity Enhanced beta activity Positive occipital sharp transients of sleep (POSTS) Vertex sharp transients Hypnagogic hypersynchrony

Slow rolling eye movements (SEMs) SEMs are usually the first evidence of drowsiness seen on the EEG. SEMs of drowsiness most often are horizontal but can be vertical or oblique, and their distribution is similar to eye movements in general . However, they are slow (ie, typically 0.25-0.5 Hz). SEMs disappear in stage II and deeper sleep stages.

Alpha dropout Drop out of alpha activity typically occurs together with or nearby SEMs. The alpha rhythm gradually becomes slower, less prominent, and fragmented. With

the alpha rhythm gone, the background becomes dominated by theta activity, which occurs in generalized distribution but is commonly most prominent in central or frontocentral regions.

Stage I. The earliest indication of transition from wakefulness to stage I sleep (drowsiness) is shown here and usually consists of a combination of 1) drop out of alpha activity and 2) slow rolling eye movements

Normal Sleep EEG

Enhanced beta activity Another change in the background activity that occurs in the transition from the awake to the drowsy state concerns the beta activity. Beta activity in the range of 18-25 Hz usually, but not always, increase in amplitude with drowsiness. When sedatives are administered to promote sleep during the EEG, beta activity may become widespread and quite prominent, sometimes attaining amplitudes in excess of 50 µV.

Positive occipital sharp transients of sleep (POSTS) POSTS start to occur in healthy people at age 4 years, become fairly common by age 15 years, remain common through age 35 years, and start to disappear

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by age 50 years. POSTS are seen very commonly on EEG and have been said to be more common during daytime naps than during nocturnal sleep. Most characteristics of POSTS are contained in their name. They have a positive maximum at the occiput, are contoured sharply, and occur in early sleep (stages I and II). Their morphology classically is described as "reverse check mark," and their amplitude is 50-100 µV. They typically occur in runs of 4-5 Hz and are bisynchronous, although they may be asymmetric. They persist in stage II sleep but usually disappear in subsequent stages.POSTS are very similar to occipital lambda waves and the term “lambdoid” activity of drowsiness and sleep was used but are present only in sleep, whereas lambda waves are only seen in the waking state with the eyes open. POSTS are not seen in patients who are blind or who are severely visually impaired.

Positive Occipital Sharp Transients of Sleep, (POSTS)

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

POSTS

Vertex waves Also called vertex sharp transients or V waves, these transients are almost universal. V waves are usually

biphasic, with an initial negative phase followed by a smaller, positive phase.Although they often are grouped together with K complexes, strictly speaking, vertex waves are distinct from K complexes. Like K

Normal Sleep EEG

complexes, vertex waves are maximum at the vertex (Cz), so that, depending on the montage, they may be seen on both sides, usually symmetrically. They appear in late Stage I and into Stage II sleep. Their amplitude is 50-150 µV. They can be contoured sharply and occur in repetitive runs, especially in children. They persist in stage II sleep but usually disappear in subsequent stages. Unlike K complexes, vertex waves are narrower and more focal and by themselves do not define stage II. The morphology of V waves varies in sleeping individuals. In some cases they are sharply contoured, and can look very much like epileptiform

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discharges. V waves occur synchronously over both hemisphaes, usually with a phase reversal at the midline. It is normal for V waves to be higher in amplitude on one side, and then shift to the other hemisphere, as long as they are not consistently decreased on one side. As mentioned later in this chapter,V waves may be followed by a sleep spindle.V waves may become small and inconspicucous in aged individuals and are often poorly demonstrable in such persons.

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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-CzPz). 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

Hypnagogic hypersynchrony Hypnagogic hypersynchrony (first described by Gibbs and Gibbs, 1950) is a well-recognized normal variant of drowsiness in children aged 3 months to 13 years. This is described as paroxysmal bursts (3-5 Hz) of high-voltage (as high as 350 µV) sinusoidal waves, maximally expressed in the prefrontal-central areas,

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that brake after the cerebral activity amplitude drops during drowsiness. When intermixed with fast activity that may be present at the same time, these paroxysmal bursts may falsely give the impression of spike and wave discharges. Despite their ominous appearance, these waves are a normal feature of the EEG in childhood.

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Stage 2 sleep Stage II is the predominant sleep stage during a normal night's sleep. The distinct and principal EEG criterion to establish stage II sleep is the appearance of sleep spindles or K complexes. The presence of sleep spindles is necessary and sufficient to define stage II sleep. Another characteristic finding of stage II sleep is the appearance of K complexes, but since K complexes typically are associated with a spindle, spindles are the defining features of stage II sleep. Except for slow rolling eye movements, all patterns described under stage I persist in stage II sleep. Delta begins to appear at this stage.

infants aged 6-8 weeks and are bilaterally asynchronous. These become well-formed spindles and bilaterally synchronous by the time the individual is aged 2 years. Sleep spindles are bursts of sinusoidal 12-14 Hz activity, tapered at both ends. They are seen over the frontocentral head regions, most often with a maximum over the central midline. Sleep spindles last from less than one second to 2 seconds. They can occur alone, or in combination with vertex waves and K complexes. In some individuals, sleep spindles are maximum in the frontal electrodes. The amplitude of sleep spindles usually is 20-100µV. Sleep spindles may or may not be synchronous, but they should be symmetric and bilateral. Sleep spindles are also present in Stage III sleep.

Sleep spindles Sleep spindles, or sigma waves, indicate the onset of Stage II sleep . Sleep spindles normally first appear in

Sleep spindle (12-14 Hz)

Normal Sleep EEG

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Stage II sleep. There is a mixture of POSTS (positive occipital sharp transients of sleep),and spindles (frontocentral short-lived rhythmic 14 Hz bursts)

K complexes K complexes usually appear in Stage II sleep, and may also seen in Stages III and IV sleep. They are high voltage transients with similarities to V waves in amplitude and location. Location is frontocentral, with a typical maximum at the midline (central midline placement of electrodes [Cz] or frontal midline placement of electrodes [Fz]). The K complex consists of a small sharp

component followed by a high voltage slow wave, often with sleep spindles superimposed upon it . The

slow wave portion of the K complex can exceed 1000 milliseconds in duration. The amplitude may exceed 400 microvolts. K complexes appear spontaneously, or they can be elicited by an auditory stimulus. Calling the patient's name, clapping, or tapping a pencil on a hard surface are good ways to elicit K complexes during EEG recordings. K complexes should be of equal voltage over both hemispheres. K complexes are largest in children and early adolesence,with advancing age,the K complexes shows a decline of voltage.

Normal Sleep EEG

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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

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K complexes and sleep spindle in stage II sleep

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

Normal Sleep EEG

Stage 3 sleep Stage III sleep is characterized by an increase in higher voltage slow waves in the theta and delta range. Sleep spindles and K complexes may be present. As Stage III

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sleep progresses, the frequencies seen are slower and the number of sleep spindles decreases. In Stage III sleep the slow waves make up less than 50% of the total record.

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Stage 3 sleep

Stage 4 sleep Stage IV sleep begins about 30 minutes after sleep onset. By definition, the tracing must display more than 50% delta activity to be called Stage IV sleep. Sleep spindles are no longer present, and the EEG consists of generalized, high voltage, irregularly shaped slow waves. Stage IV sleep is seldom seen in routine EEG recordings unless the patient is sleep deprived and the recording period is lengthened. Stages III and IV usually are grouped together as “slow wave sleep” or “delta sleep.” Slow wave sleep (SWS) usually is not seen during routine EEG, which is too brief a recording. However, it is seen during prolonged (>24 h) EEG monitoring. One important clinical aspect of SWS is that certain parasomnias occur specifically out of this stage and must be

differentiated from seizures. These "slow wave sleep parasomnias" include confusional arousals, night terrors (pavor nocturnus), and sleepwalking (somnambulism).

REM sleep REM sleep normally is not seen on routine EEGs, because the normal latency to REM sleep (100 min) is well beyond the duration of routine EEG recordings (approximately 20-30 min). The appearance of REM sleep during a routine EEG is referred to as sleep-onset REM period (SOREMP) and is considered an abnormality. While not observed on routine EEG, REM sleep commonly is seen during prolonged (>24h) EEG monitoring.

Normal Sleep EEG

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Stage 4 sleep

By strict sleep staging criteria on polysomnography, REM sleep is defined by (1) rapid eye movements; (2) muscle atonia; and (3) EEG “desynchronization” (compared to stage 3 and 4 sleep). Thus, 2 of the 3 defining characteristics are not cerebral waves and theoretically require monitoring of eye movements (electrooculogram [EOG]) and muscle tone (electromyelogram [EMG]). Fortunately, muscle activity and eye movements can be evaluated on EEG, thus REM sleep is usually not difficult to identify. In addition to the 3 features already named, “saw tooth” waves also are seen in REM sleep. • EEG desynchronization: The EEG background activity changes from that seen in slow wave sleep (stage III or IV) to faster and lower voltage activity (theta and beta), resembling wakefulness. Saw tooth waves are a special type of central theta activity that has a notched morphology resembling the blade of a saw and usually occurs close to rapid eye movements (ie, phasic REM). They are only rarely clearly identifiable.

• Rapid

eye movements: These are saccadic, predominantly horizontal, and occur in repetitive bursts. • Muscle atonia:means no muscle artifacts • Saw tooth waves:a special type of central theta activity that has a notched morphology resembling the blade of a saw. Despite the lack of a dedicated EMG channel, the muscle atonia that characterizes REM sleep is usually apparent as a general sense of “quiet” muscle artifacts compared to wakefulness. The duration of REM sleep increases progressively with each cycle and tends to predominate late in the sleep period into early morning. The occurrence of REM too soon after sleep onset, referred to as SOREMP, is considered pathological. However, newborns and infants enter REM more rapidly and spend a higher proportion of sleep in REM.Sleep onset REM period is seen in patients with narcolepsy cataplexy,dilirium tremens and in sedative withdrawal.

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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, such as hyperventilation, photic stimulation and sleep. These procedures are known to activate or stimulate abnormalities in some patients. For example, Hyperventilation and photic stimulation are most useful for activating epileptiform abnormalities, whereas drowsiness and sleep are useful for activating all forms of EEG abnormalities as well as normal epileptiform patterns (so-called pseudoepileptiform patterns).

hyperventilation. The effect of hyperventilation on the EEG begins earlier in children than adults and is apparent in 50% of cases within the first minute and 90% within the first 2 minutes. As recommended by the American Clinical Neurophysiology Society, hyperventilation should not be performed in certain clinical settings, including acute stroke, recent intracranial hemorrhage, largevessel severe stenosis and associated TIA , documented moyamoya disease, severe cardiopulmonary disease, and sickle cell disease or trait.

Hyperventilation Hyperventilation is perhaps the most widely used activation procedure in EEG laboratories. The procedure, which is simple and relatively safe, consists of three to five minutes of deep breathing. It is, however, difficult to perform in patients who are uncooperative, mentally retarded, or below the age of 4 or 5 years, and it is preferable to avoid in patients with recent myocardial infarction, chronic obstructive pulmonary disease, and other conditions causing difficulty in breathing. Although hyperventilation has become a common procedure during routine EEG recording, it is of special importance in the case of patients suspected of having seizure disorders, particularly absence seizures.

Procedure The standard procedure is to have the patient take deep breaths at the rate of about 20 per minute for three to five minutes. The first is to explain the procedure in detail to the patient. Tell the patient to relax, keep the eyes closed and mouth open, and to breath deeply in and out at a regular pace until told to stop. A minimum 1 minute baseline recording is made before starting

Normal and abnormal responses The normal response to hyperventilation consists of the occurrence of symmetrical slow activity on both sides. The absence of any change in the EEG is also normal. Although this slow activity may be diffuse theta activity, a more characteristic finding is the occurrence of intermittent or continuous 3 to 4 Hz high amplitude activity that is frontally or occipitally dominant. If the activity is continuous, it may build up gradually to amplitudes in excess of 250µV. The slow activity may persist for up to a minute after hyperventilation ceases, and the EEG may not return to 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 asymmetry between the two hemispheres. The side that shows a slower frequency and/or a lower amplitude is usually considered to be the abnormal side. On the other hand, the hyperventilation response often includes frontal intermittent rhythmic delta activity (FIRDA) or, particularly in children, occipital intermittent rhythmic delta activity (OIRDA). Although spontaneously occurring FIRDA or OIRDA

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indicates the presence of a diffuse cerebral dysfunction,their isolated appearance in hyperventilation is considered normal. The most striking EEG abnormality seen during hyperventilation is 3 Hz spike and wave discharges often brought on in patients with absence seizures. These discharges usually are frontally dominant and may occur in brief epochs, or they may persist for several seconds during which time an episode of unresponsiveness may be documented. Sometimes, other types of epileptiform abnormalities, such as generalized spike discharges or even focal spikes, may be brought on by hyperventilation. How does hyperventilation bring about such dramatic changes in the EEG? The major biochemical finding during hyperventilation is a drop in carbon dioxide content of the blood(hypocarbia). It is well known that the most important vasodilatory stimulus

for the blood vessels of the brain is carbon dioxide. The higher the carbon dioxide content, the greater the vasodilatation. So when there is hypocarbia, the reverse occurs, namely, vasoconstriction. This presumably alters the metabolic rate of the neurons and leads to the slow activity. The effect of hyperventilation on the EEG is much more marked in children than in adults, with children,s EEGs sometimes showing an enormous buildup of slow activity. Blood sugar level also appears to influence the response to hyperventilation. The lower the blood sugar, the more marked the hyperventilation-induced slow activity. When an adult EEG shows marked and prolonged slowing as a result of hyperventilation, one should consider the possibility of hypoglycemia and should repeat the procedure 15 to 30 minutes after giving a drink containing gloucose.

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.


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Photic stimulation Visual stimuli are perhaps one of the most effective means of stimulating the brain. The ready availability of user friendly stroboscopes has resulted in the routine use of intermittent photic stimulation(IPS) as an activation procedure during EEG. The method is most valuable in documenting photosensitivity, which has a high clinical correlation with primary generalized epilepsy.

Technique The device used is called a stroboscope or photic stimulator. It is capable of delivering single or continuous bright flashes of light at frequencies ranging from 1 to 50 flashes per second. The test begins by explaining the procedure to the patient. Tell the patient he or she will be seeing very bright flashes of light(bright even with the eyes closed) and to keep the eyes closed or open as instructed during the course of the test. The flash lamp is positioned approximately 30cm in front of the eyes. Start with one or two flashes per second and increase the rate gradually up to 30 flashes per second. Each flash rate is presented for a duration of about 10 seconds, and the eyes are kept closed in the first 5 seconds and open in the next 5 seconds. If a photoparoxysmal response (explained later) is elicited, the IPS should be stopped to avoid precipitating a seizure. If the response occurs only during a brief part of the stimulation, the technician needs to confirm that it is indeed a photoparoxysmal response by cautiously repeating the stimulation at the same flash rate.

Responses to photic stimulation It was found that diffuse light stimulation produces four main categories of electrographic

response:(1)visual evoked response (2) photic driving, (3) the photomyogenic (formerly referred to as photomyoclonic) response, and (4) the photoepileptiform response (PER) (also referred to as the photoparoxysmal response [PPR]). Visual evoked response The visual evoked response is the same potential which is recorded during evoked potentials. The difference in appearance is because of the method of data display and the absence of averaging. The VER is seen with low flash frequencies, usually most prominent at and below 5/sec. Photic evoked potential: Flash at 5/sec produces an evoked potential in the fourth channel, due to activity in the occcipital lead. The upgoing potential in this bipolar montage indicates positivity at the O1 electrode. The positivity is delayed from the stimulus by about 100 msec, indicating that this is an evoked potential rather than a photic response. The absence of a VER is not abnormal unless unilateral. Such asymmetry suggests abnormality in projections from one lateral geniculate to the cortex, or the calcarine cortex, itself. Photic Driving Response The driving response appears as the flash frequency accelerates beyond 7/sec, and the next evoked potential starts before the last evoked potential has ended. It is created by the visual evoked responses merging into each other. The photic driving response consists of rhythmic, occipital-dominant waveforms that either show a oneto-one relationship with each flash or appear as a harmonic (an integer multiple) or subharmonic (an integer dividend) of the flash frequency.


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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 asymmetrical in normal individuals, an asymmetrical driving response is considered normal unless accompanied by other EEG abnormalities . In normal individuals, asymmetrical POSTS or lambda waves are

usually associated with a similar asymmetry of the driving response Cortical epileptogenic lesions or skull defects can enhance the amplitude of the photic driving response ipsilaterally, whereas destructive lesions can attenuate it ipsilaterally.

Photic driving

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Photomyogenic Response or Photomyoclonic Response The photomyoclonic response is not cerebral in origin, but rather is electrical activity in the frontal scalp muscles which is induced by the flash stimulus in susceptible individuals. Repeated contraction of these muscles produces EMG activity which is time-locked to the stimulus, and recorded from the frontal

leads. There is a delay of 50-60 msec between the flash and the EMG activity. The main problem with the photomyoclonic response is in differentiation of this from photoepileptiform response. Some general guidelines are discussed in the next table.

Differentiation of photomyogenic from photoepileptiform responses Feature Spatial distribution Termination

Photomyogenic Anterior End of the stimulus

Rise time of the spike

Fast (EMG) spikes

Frequency

Sale frequency as the flash

Photoepileptiform Posterior or generalized May stop before the end of the stimulus or outlast the stimulus. Slower, spike-and-wave complexes most common. Frequency is independent of the flash frequency, usually slower.

Photomyogenic (photomyoclonic) response to 14-Hz photic stimulation. Prominent frontalis and temporalis myogenic potentials time locked to the flash stimulus end with a whole-body jerk.


Photoepileptiform or Photoparoxysmal Responses The photoepileptiform response is characterized by spike-wave complexes during photic stimulation. The discharge is usually activated only by a few specific flash frequencies. This response is a marker for seizure tendency, and most often noted with generalized epilepsies. Less commonly, photosensitivity is noted

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with partial epilepsy (occipital lobe epilepsy, and even less commonly temporal lobe epilepsy). While some patients will have already noticed that there is photic trigger of their seizures, this is not always the case. Some patients with photosensitivity have never had a spontaneous seizure. The correlation of a photoparoxysmal discharge with seizures is greatest if the discharge continues after the end of the flash train.

Photoparoxysmal response to 8-Hz photic stimulation in a 6-year-old girl. Note the irregular spike-and-wave complexes and greater amplitudes in more anterior derivations

Photoparoxysmal response to 15-Hz photic stimulation with initial fast activity evolving into a typical generalized 3-Hz spike-and-wave pattern. Eye fluttering typical of a myoclonic absence seizure was observed.

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Photoparoxysmal response

SLEEP ACTIVATION Activation during Sleep Sleep is a highly effective method for eliciting both generalized and focal interictal epileptiform discharges (IEDs). In as many as onethird of patients with complex partial epilepsy, IEDs may not be present during wakefulness but appear only during sleep . Epileptiform discharges are also often more easily detected during sleep. Recordings during wakefulness are often obscured by muscle and movement artifacts, especially in children and adults who are unable to cooperate or relax during the recording. Nearly all patients with IEDs during daytime nap recording have their first discharge within 15-30 minutes of sleep onset . Thus outpatient EEGs in patients with suspected seizures should always include sleep, but the actual sleep recording generally does not have to exceed 30 minutes in duration. When a sleep EEG recording is clinically indicated and the patient is unable to fall asleep, a short-acting sedative can be used to help induce sleep. Short-acting barbiturates and chloral hydrate are two agents that have been used for this purpose. Chloral hydrate is generally preferred because, unlike barbiturates, it does not induce betafrequency activity in the background EEG. Every patient considered for sedation should be medically assessed for the risk of sedation. Patients should also

be counseled about restricting their activities until the effect of sedation has worn off. Epilepsy syndromes that commonly show activation with sleep are listed below: 1. 2.

3. 4. 5.

Benign occipital epilepsy in infancy Generalized tonic seizures in chronic childhood epileptic encephalopathies (e.g., Lennox-Gastaut syndrome) benign rolandic epilepsy Benign juvenile myoclonic epilepsy (i.e., on awakening) Frontal lobe epilepsy

Activation by Sleep Deprivation Sleep deprivation increases the possibility of seeing epileptiform activity in some patients, and also increases the chance of obtaining sleep. Sleep deprivation increases the yield of epileptiform discharges beyond that expected from sleep alone, and therefore is considered a separate physiologic activation method. It is often used for patients in whom routine EEG has not been able to identify interictal epileptiform activity. Sleep deprivation may be a particularly potent activation method in patients with juvenile myoclonic epilepsy. In these patients, the highest yield is in recording most of the EEG after arousal from a brief nap following sleep deprivation.


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Part two Abnormal EEG Patterns

The term abnormal EEG patterns refers to patterns of activity that are judged to be outside the normal range. In defining normal EEG ,we need to take into account the age and state of the patient to correctly interpret a particular EEG pattern.Thus, for example, a pattern that is normal for a drowsy patient may be considered abnormal if the patient is fully awake.Similarly, a pattern that is normal for a child may be quite abnormal for an adult.These example underscore the importance of the technologist,s notations regarding age and state of the patient on the EEG tracing.Without such information,EEG interpretation and judgments of normality or abnormality may be of doubtful clinical value.

Like most neurophysiologic tests, EEG is a test of cerebral function; hence for the most part it will be nonspecific as to etiology. Although at one time authors discussed the application of EEG in differentiating various types of lesions, this clearly has not been clinically useful in the modern era. The exercise of describing EEG abnormalities by pathology (eg, stroke, abscess, tumor, even various types of tumors!), which was common in old EEG texts, is therefore not followed here. Instead, the different patterns of abnormal EEG and their clinical significance are reviewed. So, for the convenience we divide the EEG abnormalities into two main groups: 1. Epileptic abnormalities 2. Non epileptic abnormalities

Chapter 8

Epileptic discharges

Although no longer used for identification and localization of gross structural brain lesions, electroencephalography (EEG) remains the primary diagnostic test of brain function. Unlike relatively new functional imaging procedures, such as functional MRI (fMRI), single-photon emission computed tomography (SPECT), and positron emission tomography (PET), EEG provides a continuous measure of cortical function with excellent time resolution and is relatively inexpensive. EEG is especially valuable in investigation of patients with known or suspected seizures. Seizures are infrequent events in the majority of patients, making recording of ictal EEG both timeconsuming and expensive. The mainstay of diagnosis, therefore, remains detection of interictal (ie, between seizures) epileptiform discharges. Continuous videoEEG monitoring, developed over the last 20 years to facilitate recording of ictal events, also greatly increases the time available to detect interictal epileptiform discharges (IEDs). In the diagnosis of epilepsy and localization of seizure onset, these can be as useful as ictal recordings.

Electroencephalography in the diagnosis Of Epilepsy Epilepsy can have protean clinical manifestations, and some of these can be easily confused with those of other medical conditions. Thus, the first question the physician must address is whether the patient's symptoms represent epileptic seizures or some other disorder. Although the diagnosis of epilepsy remains a clinical judgment, EEG findings, interpreted in the context of other clinical data, are often pivotal in reaching an answer. However, it is important to recognize that different EEG findings have different degrees of association with epilepsy. This basic observation explains, in part, much of the confusion

regarding the sensitivity and specificity of interictal EEG. Clinicians may encounter any of the following abnormalities when evaluating a patient with possible seizures: interictal epileptiform discharges (IEDs), focal slowing, periodic lateralized epileptiform discharges(PLEDs), generalized periodic epileptiform discharges (GPEDs), diffuse slowing, and several nonspecific paroxysmal abnormalities (e.g., frontal intermittent rhythmic delta activity). Among all of these, only IEDs and perhaps PLEDs are associated with epilepsy at rates sufficiently high to be clinically useful. The remaining patterns are much less useful in supporting the diagnosis of epilepsy, although they may provide very important information regarding the underlying conditions associated with seizures or epilepsy. In this chapter, we first describe interictal epileptiform discharges(IDEs) and then in next chapter more common epileptic syndromes.

Interictal epileptiform discharges The International Federation of Societies for Electroencephalography and Clinical Neurophysiology (IFSECN) describes interictal discharges as a subcategory of "epileptiform pattern," in turn defined as "distinctive waves or complexes, distinguished from background activity, and resembling those recorded in a proportion of human subjects suffering from epileptic disorders…." This somewhat circular definition makes clear that criteria must be verified empirically. Interictal discharges may be divided morphologically into: 1. Spike discharges 2. Sharp wave discharges 3. Polyspikes or multiple spikes 4. Spike and wave or sharp and wave complexes IEDs may occur in isolation or in brief bursts; bursts longer than a few seconds are likely to represent electrographic seizures rather than interictal discharges.

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Spike discharges A spike discharge is defined as a transient that is clearly distinguished from the background activity, has a pointed peak at a paper speed of 30mm/s, and has a duration of 20-70msec(Potentials of less than 20 ms duration are usually not of cerebral origin, being either muscle or electrical artifact); the main component is generally negative. Amplitude is variable and may be followed by slow wave. Ordinarily, a spike stands out from the background activity because of its distinct appearance and/or size; but when the amplitude is small, it may be difficult to identify, especially when there is a considerable amount of beta activity in the background. This is one reason why it is better to avoid using medications for promoting sleep when taking an EEG, as most such drugs cause diffuse beta activity. As mentioned earlier in this book, we should be cautious in use of high frequency filter, for example use of the 15Hz high frequency filter should be avoided because the sharp-pointed character of a spike is lost and its amplitude becomes markedly attenuated. When this happens, a spike may be indistinguishable from beta activity or muscle artifacts. Polarity of a spike may provide clues as to its potential for epileptogenicity(negative spikes are more significant from the point of view of epileptogenicity).

Wave morphology The largest and most pronounced spikes are not necessarily associated with more serious epileptic seizure disorders. For example, rolandic spikes in a child age 4 to 10 years are very prominent; however, the seizure disorder is usually quite benign or there may be no clinical seizures at all. Spatial distribution In childhood, occipital spikes are , in general, the most benign spike discharges, with less than 50% having clinical seizures; rolandic central-midtemporal-parietal spikes are also quite benign, whereas frontal or anterior temporal spikes or multifocal spikes are more epileptogenic.

Positive spikes like 6-14Hz bursts and lambdoid activity(POST) have little clinical significance. Spikes represent the basic element of paroxysmal activity in the EEG. A Unitarian view that all spikes mean a hidden or overt paroxysmal event would be erroneous. The fine semiology of spikes is extremely important and the EEG interpreter should consider the following question: 1. What is the precise wave morphology? 2. Where do the spikes occur? 3. What is the patient,s age? 4. What is the state of awareness? 5. Is there any possibility of an artifact of similar appearance? 6. Is there any possibility of a physiological potential of similar appearance?

A spike discharge

Age The significance of the age factor is enormous. From the spikes of an epileptic newborn to a seizure focus of an old age, age-determined varieties of spikes can be distinguished. Distinction from similar physiological patterns This differentiation is particularly important in the case of vertex sharp waves during deep drowsiness and stage 2 of light non-REM sleep. In childhood (after age 4), these waves may have a particularly spiky appearance and may be misinterpreted as paroxysmal spikes. Distinction from artifacts of similar appearance This distinction depends on the electroencephalographer,s experience and is usually an easy one. The interpretation of the clinical significance of spikes can be extremely difficult and depends on the electroencephalographer,s


difficult and depends on the electroencephalographer,s experience in the art of reading the EEG tracing and also on the clinical understanding of epileptological problems.

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Extensive personal laboratory experience is just as essential as scientific knowledge in interpreting the EEG.

Schematic of an interictal epileptiform discharge (IED), upper tracing, vs nonspecific sharp transient, lower tracing. Note interruption of the background, asymmetric contour with descending limb falling below the baseline, and aftercoming slow wave associated with the IED; sharpness of the peak does not distinguish the 2 waveforms

Left temporal spike Spike, regional left frontal. Note the typical aftergoing slow wave. The referential montage (right panel) shows that the maximum is at Fp1 and F7 about equally, followed by F3.

Spike, regional left frontal. Note the typical aftergoing slow wave. The referential montage (right panel) shows that the maximum is at Fp1 and F7 about equally, followed by F3.

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Spike, generalized. Note the high amplitude, and the aftergoing background suppression and slow wave.

Abnormal anterior midtemporal spike (F7-T3)with focal background abnormalities

Sharp wave discharges A sharp wave is defined as a transient that clearly stands out from the background activity, has a pointed peak at a paper speed of 30mm/sec, and has a duration of 70 to 200

msec; amplitude is variable and like spikes, sharp waves usually are surface negative. Since there is little distinction between spikes and sharp waves from the standpoint of their potential for epileptogenicity; the terms are used interchangeably.


A sharp wave

Sharp waves, regional right temporo-occipital. The sharp waves are, as any significant epileptiform discharges, followed by slowing and “disruption” of the background. The referential montage (right panel) confirms that the maximum is at T6, closely followed by O2.

Sharp waves, regional left temporal. The maximum (phase reversal) is consistently at T3. Note the associated slow activity and background attenuation.

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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.


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Sharp waves, multifocal. Sharp waves are seen at T4, T6, T5 and F3 on this 9 sec segment.With other findings, this is often seen in the symptomatic/ cryptogenic epilepsies of theLennox-Gastaut type.

Polyspikes or multiple spikes Polyspikes or multiple spikes are two or more spikes(monophasic or biphasic) that comprise a single waveform. As with spike discharges, multispike discharges may also be accompanied by slow

Polyspikes or multiple spikes

Polyspike, generalized. Note the aftergoing slow wave. This is associated with the “primary” or idiopathic generalized epilepsies, most typically Juvenile Myoclonic Epilepsy.

waves.Polyspikes and polyspike wave complexes are sometimes associated with myoclonus for example in lennox Gastaut syndrome.

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Generalized polyspikes in a patient with intractable epilepsy

Left temporal polyspikes

Spike and wave or sharp and wave complexes (swc) Spike or sharp and wave complexes(SWC) are repetitive occurrence of a spike or sharp followed by a slow wave,usually of the same polarity. Since any significant spike or sharp wave usually is followed by a slow wave ,a run of 3 seconds is required to classify a record as SWC.

sharp-and-slow-wave complexes

Generally, SWC can be divided into 2 specific types: 1. 3-Hz SWC : characterized by a frequency of 2.54Hz and a monomorphic (regular) morphology. It occurs in discrete bursts,and between bursts the EEG is normal (typically seen in absence). 2. Slow (<2.5Hz) SWC: this pattern is not only slower but also more irregular(less monomorphic)than 3Hz SWC.Bursts are less discrete and other abnormalities are seen.(typically in lennox Gastaut syndrome).

spike-and-wave complexes


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

Spike and wave complexes

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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.


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Generalized atypical spike and wave in an adult patient with a mixed seizure disorder that includes atypical absence seizures.

Use of IEDs in medical treatment decision Detection of IEDs after a transient neurological event greatly increases the likelihood that a seizure was responsible; in most cases, IEDs can be classified as generalized or focal, providing valuable information with respect to syndrome classification and treatment. In the case of a single unprovoked seizure, the risk of recurrence is approximately 20-80% depending on whether the cause is cryptogenic or symptomatic. This risk is increased by a history of previous neurological insult, especially if accompanied by an acute symptomatic seizure and by detection of IEDs. In some studies, particularly those of children, focal IEDs suggest an increased recurrence risk as well,

and would tend to favor treatment. EEG also can contribute to answering the reverse question, ie, whether medications should be stopped after a 2-year or longer period of seizure freedom after the diagnosis of epilepsy is established. For patients with idiopathic generalized epilepsy, EEGs tend to "normalize" when complete seizure control is attained, and lack of IEDs suggests a decreased risk of relapse when medications are withdrawn. However, the type of idiopathic epilepsy syndrome is most important in predicting the chance for remission (eg, good for childhood absence and poor for juvenile myoclonic epilepsy). For patients with partial epilepsy, or in whom IEDs were not seen before treatment, the value of a negative study is less clear.

Chapter 9

Electroencephalgraphy in common epileptic syndromes

EEG is an essential component in the evaluation of epilepsy.In fact after the medical history,EEG findings provide the most important information necessary for syndromic diagnosis. Identifying the type of epilepsy or "epilepsy syndrome" is important for optimal management and for advising patients and families about prognosis, guides selection of antiepileptic medication, and suggests when to discontinue medication.

Characteristics of the Major Categories of Epilepsy Syndromes The Classification of Epilepsy Syndromes is based on two distinctions: first, between localization-related and generalized epilepsies and, second, between idiopathic and symptomatic epilepsies. EEG findings assist in making these distinctions. Focal IEDs are seen in localization-related epilepsies, whereas generalized IEDs indicate one of the generalized epilepsies. In the localization-related epilepsies, the location of IEDs usually corresponds approximately to the area of seizure onset, but there are exceptions(described later). Normal or near-normal background activity is most characteristic of idiopathic epilepsy syndromes; focal, multi focal, or diffuse abnormalities of background activity are most suggestive of the symptomatic epilepsies. Persistent focal voltage attenuation, especially of faster frequencies, or polymorphic delta activity is correlated strongly with a structural lesion as the cause of symptomatic epilepsy. These general

guidelines help focus initial clinical impressions and prompt a search for the more specific EEG findings associated with the particular epilepsy syndromes.

Specific Epilepsy Syndromes Childhood and Juvenile Absence Epilepsy The International Classification of Epilepsy Syndromes distinguishes between childhood and juvenile onset forms of absence epilepsy. Childhood absence epilepsy (CAE) manifests between the ages of 3 to 5 years and remits between 10 to 12. Absence seizures are frequent, often occurring in clusters. In contrast, generalized tonic-clonic seizures are infrequent, and remission by late adolescence is the rule . Juvenile absence epilepsy (JAE) manifests at the ages of 10 to 12 years (or later). Absence seizures are less frequent, and generalized tonic-clonic seizures more frequent, than in CAE. Remission is less likely to occur, and seizures often persist into adulthood. Such distinctions, although generally applicable to large numbers of patients, are not always clear in individual patients. In addition, the clinical features of JAE overlap with those of two other syndromes: tonic clonic seizures upon awakening and juvenile myoclonic epilepsy. EEG features of CAE and JAE are also broadly similar. Minor differences, however, can sometimes be diagnostically useful.

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EEG findings EEG shows a normal background for age and 3-Hz generalized spike and wave discharges . Frequency of the spike-wave complexes is usually 4 Hz at the onset of the absence seizures and may slow to 2.5 Hz at the end of a seizure. The repetition rate of generalized spike-wave bursts is faster at onset in JAE than in CAE, and polyspikes are seen more often in JAE. Typically, an initial positive component is followed by one or more negative components and then a negative slow wave. They are frontally dominant. Duration of discharges is typically 3-25 seconds. Discharges are not truly bisynchronous; usually a millisecond difference is noted between left and right cerebral hemispheres. Eye opening does not alter the discharges. However, discharges are state dependent. Their frequency increases with non-REM sleep, although the duration of the discharges is reduced. During REM sleep, the frequency of discharges resembles that seen in wakefulness. Some patients display occipital intermittent rhythmic delta discharges (OIRDA), which is thought to be a favorable prognostic indicator. Interictal background activity is usually normal in both CAE and JAE, although minor degrees of slowing have been reported in heterogeneous groups of

children. High-voltage OIRDA is a frequent interictal finding, occurring in 15% to 38% of all patients with absence epilepsy. However, the occurrence of OIRDA is strongly age related: it is found in more than 70% of children between 6 and 10 years of age, and it is rare in persons older than 15 years . It is also rare in children with atypical absence seizures . Thus, OIRDA is more strongly associated with CAE than with JAE. OIRDA is predictive of activation of generalized spike-wave activity by hyperventilation.Hyperventilation increases 3-Hz spike-wave bursts in 50% to 80% of patients with CAE, especially if occipital intermittent rhythmic delta activity (OIRDA) is present . Photic stimulation increases spike-wave bursts in about 18% of cases. Generalized discharges are ictal in nature. They may be so brief that no obvious clinical movements are seen, although typically minor eyelid fluttering or subtle rhythmic contractions of the mouth are seen. These minor motor accompaniments occur in 85% of patients with absence epilepsy. Absence should be differentiated from atypical absence seizures, which usually are seen in patients with LGS. EEG in atypical absence seizures shows a less abrupt onset and offset than in typical absence seizures. Furthermore, EEG background is slow, and duration of discharges is shorter.


3 Hz spike-wave complexes (SWC), generalized.This pattern is very monomorphic, with a maximum (shown here by a phase reversal) frontally, typically at F3/F4. This is typical of absence epilepsy. The 3 Hz SWC is often faster (4-5 Hz) at onset, as shown here.

Typical absence epilepsy with maximum voltage anteriorly

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EEG of a 9-year-old girl with childhood absence epilepsy. The EEG shows runs of 3-Hz bilateral synchronous occipital intermittent rhythmic delta activity (OIRDA)

Typical absence attack in a 10-year old boy following hyperventilation. Note the occipital delta activity (OIRDA) before the 3-Hz spike and wave


Atypical absence attack in a 20-year old woman. Note the polyspike component before slow wave

Absence epilepsy - Anteriorly dominant, typical 3-Hz spike and wave discharges

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Benign Childhood Epilepsy Two benign partial epilepsy syndromes of childhood have been well defined: (1) benign rolandic epilepsy (BRE), also called benign partial epilepsy of childhood with centrotemporal spikes and (2) benign partial epilepsy of childhood with occipital paroxysms (BPEOP). Other less well-defined syndromes include frontal and parietal partial epilepsy syndromes.

1-Benign Epilepsy of Childhood with Centrotemporal Spikes (BECTS) or Benign Rolandic Epilepsy (BRE) Benign epilepsy of childhood with centrotemporal spikes (BECTS) is an idiopathic, localization-related epilepsy syndrome . It is also commonly referred to as benign rolandic epilepsy. It is one of the most common forms of childhood epilepsy, occurring in 16% to 24% of children with epilepsy . BECTS is characterized by two defining features, one clinical and one electrographic: 1. Stereotyped partial seizures consisting of unilateral paresthesias of the tongue, lips, inner cheeks, and gums, accompanied by unilateral tonic or clonic activity of the facial and pharyngeal/laryngeal muscles, speech arrest (anarthria), and excessive salivation. Nocturnal secondarily generalized seizures are common and are often the first manifestation of the disorder. Seizures remit spontaneously during adolescence. 2. Interictal EEG demonstrating central-midtemporal spikes and otherwise normal background activity. Onset of seizures usually occurs between the ages of 4 and 10 years, although the syndrome can occur as early as the age of 2 years and, rarely, begin as late as 13 years. In the majority of patients, nearly 80% in some series, seizures occur exclusively during sleep. In about 20%, seizures occur during both sleep and wakefulness. Seizures that occur solely during the waking state are least common. Early onset seems to be predictive of a longer active phase of seizures before remission . Partial status epilepticus is rare.

EEG findings The interictal EEG demonstrates the characteristic centralmidtemporal epileptiform discharges . These are stereotyped, diphasic or sometimes triphasic sharp waves, usually followed by an aftergoing slow wave. The sharp waves average 100 to 300 µV in voltage. In bipolar recordings, the discharges most often show maximal voltage in the central (C3-C4) and midtemporal (T3- T4) areas. On occasion, the maximal voltage is displaced posteriorly, to P3-P4 or T4- T6. Discharges are usually seen simultaneously in both central and temporal regions, although they may be of higher voltage in one or the other of these. On occasion, they are confined to either the central or the temporal area. They occur bilaterally and independently in homologous areas of both hemispheres, but in a single recording, they may predominate on one side . The sharp waves occur either as isolated discharges or as runs of repetitive spikes. The latter is especially common during sleep. Discharges may be bilateral in 30% of patients; when they occur bilaterally, the discharges are independent and asynchronous,however,Unilateral discharges are more common. Activating procedures such as hyperventilation or photic stimulation or eye opening does not block the discharges. Sleep, however, has a prominent activation on the epileptiform discharges. Non-REM sleep, in particular, may show a 400-500% increase in the spike-wave index. The frequency of spiking does not correlate with the frequency or severity of seizures. The EEG abnormality typically persists for some time after remission of clinical seizures. The EEG discharge also eventually disappears, almost always by late adolescence(at around age 15 years). On the other hand, in patients with BRE, there is an increased incidence of generalized spike-and-wave discharges. In fact, in some patients, there may even be typical absence seizures. In such instances, it may be somewhat difficult to identify the specific clinical syndrome, as to whether it is benign rolandic epilepsy or childhood absence epilepsy. BRE appears to be a dominantly inherited condition with variable penetrance. The reader should keep in mind that BRE is a syndromic diagnosis with the EEG forming an important component of the diagnosis. Epileptiform discharges in the rolandic region do not necessarily mean that the patient has BRE. The occurrence of central-midtemporal spikes in neurologically normal patients without epilepsy is well recognized.


Central right mid-temporal spikes in a child with BRE

Benign rolandic epilepsy associated with typical left centrotemporal spikes

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Benign epileptiform discharges of childhood, left central and right temporocentral

EEG of a 9-year-old boy with BRE. In this child, the discharges are predominantly left-sided and mainly temporal in their distribution. Note: the K complexes and sleep spindles.


EEG of a 5-year-old boy with BECTS. There are independent left and right discharges localized to C3 and C4 without significant involvement of temporal electrodes.

Generalized spike-and-wave discharge in a patient with benign rolandic epilepsy. The first segment to the left shows typical discharges of benign rolandic epilepsy, with bifrontal positivity. A generalized epileptiform discharge (like 3 Hz spike and wave)is seen to the right in the same patient.

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Left central spike in a child with rolandic epilepsy(BRE)

Another example of generalized discharges in a child with a BECTS;such bilateral discharges are observed especially during drowsiness but , contrary to idiopathic generalized epilepsies, they are not activated by sleep such as the next example


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Stage 2 nREM sleep ( note spindles over the anterior regions) in a child with a BECTS

2-Benign Partial Epilepsy of Childhood with Occipital Paroxysms (BPEOP) Gastaut described a partial epilepsy that was analogous to BRE, although the 2 syndromes have important differences. Since publication of the initial description, it has become evident that BPEOP encompasses a heterogeneous group of patients whose disease is one of two subtypes: an early-onset variant, and a lateonset variant that corresponds to the syndrome initially described by Gastaut. Although there are no epidemiological studies of the incidence of BPEOP, several case series indicate that it is two to three times less common that BECTS . The early-onset variant accounts for most cases. In addition to the EEG findings , the two variants of BPEOP share several features. Children are neurologically normal and have normal computed tomographic and magnetic resonance imaging scans. Boys and girls are equally affected in both early- and late-onset variants. As in BECTS, genetic factors are clearly involved, although the pattern of inheritance

has not been elucidated. A family history of epilepsy is evident in 37% to 44% of cases , and occipital spikes have been reported in 26% of nonepileptic relatives. In the late-onset BPEOP variant, seizures begin between the ages of 15 months and 17 years; the peak age at onset is between 7 and 9 years . Seizures nearly always begin with visual symptoms (amaurosis, phosphenes, illusions, or hallucinations) and are typically brief, lasting only seconds, without alteration in consciousness . In the immediate postictal period, about one-third of patients develop a severe diffuse headache, often with associated nausea and vomiting. Seizures tend to occur frequently, but response to medication is usually good. Although details of prognosis remain unresolved, the long-term outcome of the late-onset variant BPEOP is generally less favorable than that of BECTS. In the early-onset variant, the peak age at onset is between 3 and 5 years. In contrast to the late-onset variant, seizures lack the characteristic visual phenomena. Rather, stereotyped seizures consist of lateral gaze deviation and ictal vomiting, with a varying degree of alteration in consciousness . Seizures

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are exclusively nocturnal in about two-thirds of cases and are typically prolonged (5 to 10 minutes or longer in duration). Partial status epilepticus occurs in nearly half the patients. Despite the long duration of seizures and the high incidence of status epilepticus, prognosis in the early-onset variant is universally excellent. Up to 30% of patients experience only a single seizure, and in the remainder, seizures occur infrequently. Duration of the disease is typically 1 to 2 years, and nearly all patients become seizure free by age 12.

EEG findings EEG findings are indistinguishable in the two BPEOP variants. The interictal EEG demonstrates normal background activity and occipital epileptiform discharges that are morphologically stereotyped . The characteristic discharge consists of a diphasic spike or sharp wave with a high-voltage (200- to 300-µV) surface-negative peak, followed by a low-voltage surface-positive peak and an aftergoing surfacenegative slow wave . Although maximal in the occipital derivations, the discharges at times extend into the posterior temporal areas . In about 20% of discharges, the principal sharp component has a

duration longer than 70 milliseconds. In a similar percentage of discharges, spikes occur without aftergoing slow waves. Discharges occur in runs with a degree of rhythmicity and a frequency of 1-3 Hz. Typically, they are blocked or prominently attenuated with eye opening. They may be unilateral or bilateral and may occur independently on each side. Hyperventilation usually has no effect on epileptiform activity , although a few authors have reported activation. Similarly, in most patients, photic stimulation has no effect on epileptiform activity . In a few, however, photic stimulation can either activate epileptiform discharges or inhibit them. The inhibition effect seems to occur mainly with high flash rates. Occipital discharges are activated by NREM sleep and inhibited by REM sleep . In a minority of cases, occipital discharges may be evident only during sleep. In many patients-more than half in one series ,interictal epileptiform discharges persist after clinical remission of seizures, sometimes for several years. As in BECTS, some patients have other epileptiform abnormalities such as generalized spike-wave or centralmidtemporal discharges and frontal discharges.

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 highamplitude occipital (T6/02) spikes that have a stereotyped waveform.


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EEG of a 11-year old girl with type 2 BPEOP. Posterior bilateral spike-waves, very ample over temporal electrodes. The changes react to eye opening. Note the presence of a mu rhythm, more obvious with open eyes.

Cryptogenic or Symptomatic Focal Epilepsies Medial temporal lobe epilepsy This is the most common of focal epilepsies, and it typically associates a history of complicated febrile seizures followed by a period of latency before onset of epilepsy in the peri-pubertal period, and hippocampal sclerosis. Seizures may be simple, simple followed by complex, or complex from onset. Secondary generalization is usually observed before treatment, or during withdrawal, and mostly occurs during sleep. Impairment of consciousness may be preceded by an aura with a rising epigastric feeling, nausea, déjà-vu or jamis-vu. It is followed by staring, oral automatisms(chewing, lip smacking…), vocal and verbal automatisms, simple gestural automatisms, in a patient with more or less complete loss of contact. One may also find autonomic signs(pallor, flushing, tachycardia, breathing irregularities, mydriasis, bleching). The seizure lasts 30 seconds to 2 minutes,

and the post-ictal period is characterized by temporal and spatial disorientation and language deficit if the dominant side is involved. The patient resumes normal contact progressively and is amnesic of the seizure. Seizures occurs mainly during waking and particularly at awakening. The most common etiology is hippocampal sclerosis, but other causes may be found: dysplasias, tumors(ganglioglioma, low grade tumors), AVM, and a history of meningitis or encephalitis. Some cases are cryptogenic. These epilepsies are typically drug-resistant but may respond to surgical treatment.

EEG findings The interictal EEG shows spikes and spike-waves over the anterior and middle temporal leads, especially over the lower anterior temporal leads. There may also be theta activity and even slower waves in the same region. The changes are enhanced in nREM sleep, all the more if they are rare or even absent during waking. In nREM sleep , the changes tend to diffuse over adjacent regions and even contralaterally. In REM

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sleep, the changes become more focal. The frequency and morphology of the abnormalities is determined by the etiology. In cases with hippocampal sclerosis, spikes and spike-waves often occur in pairs or triplets, but they are not necessarily frequent. In other lesional cases, slow elements may predominante, with slow waves, theta waves, and slow spikes, and the abnormalities may occur more frequently. The ictal EEG shows a precise organization with flattening over the anterior and middle temporal region followed by rhythmic slow spikes at 6-7 Hz. The spikes become progressively less rhythmical and fade into slow wave over the same territory. The ictal activity may diffuse to adjacent regions contralaterally after a variable delay. The surface EEG shows an apparent seizure onset that is delayed with respect to the onset of the aura.

Lateral temporal lobe epilepsy Seizure originating in the external temporal cortex may or may not propagate to the limbic structures. The seizures are simple or complex and rarely generalized. They include simple auditory hallucinations, complex auditory hallucinations or illusions, but also an auditory dreamy state and language deficits if the dominant temporal lobe is involved. Complex seizures without aura are associated with behavioral arrest and non-oral automatisms, in contrast to internal temporal seizures. This may be followed by elements of propagation towards other structures. Seizures are seen

during waking but also during sleep, the latter being more common than in mesial temporal seizures. EEG findings Since the epileptogenic zone is external temporal, interictal changes are easily recorded by surface EEG over middle and posterior temporal leads. They are often frequent and high-voltage. According to the etiology, the changes include spikes, spike-waves, slow spikes, polyspikes, polyspike-waves, fast rhythms and theta activities. The changes are enhanced and become more diffuse during nREM sleep. In REM sleep, they become more lateralized again. The ictal EEG shows a flattening followed by fast recruiting rhythms over the middle and posterior temporal region, with rapid diffusion. This is followed by rhythmic slow waves that may be faster, slower or similar(6-7Hz) to those found in mesial temporal seizures.

Frontal Lobe Epilepsy Although neither the incidence nor prevalence of frontal lobe epilepsy (FLE) is known with certainty, large surgical series indicate that it is the second most common localization-related epilepsy, accounting for about 20% of patients undergoing epilepsy surgery. Unlike temporal lobe epilepsy, seizure symptoms are

Left temporal spikes in a 39 year old woman with TLE. Note asymmetrical alpha background rhythms between two hemisphere


heterogeneous, reflecting both the large size of the frontal lobe with its many functional and anatomical divisions, as well as the different pathways of propagation from different areas of the frontal lobe. As a result, several syndromes have been described as types of FLE referable to specific anatomical areas of presumed seizure onset within the frontal lobe. Although the ictal manifestations of frontal lobe seizures suggest particular localizations, no features are definitive for any. Recognizing significant overlap among the regions, the ILAE Commission classified the frontal lobe epilepsies by anatomical areas that produce relatively characteristic seizure symptoms: supplementary motor, cingulate, anterior frontopolar, orbitofrontal, dorsolateral, opercular, and motor cortex. All frontal lobe seizures share a number of features: (a) early and prominent motor manifestations, including clonic activity, asymmetrical tonic posturing, or complex semipurposeful, repetitive movements that often involve the legs (e.g., bicycling); (b) short duration with minimal or no postictal confusion; (c) occurrence in clusters; (d) frequent secondary generalization; and (e) predilection for occurring at night. Three manifestations are especially correlated with frontal lobe epilepsy: 1. Supplementary motor area seizures manifested by sudden asymmetrical tonic posturing of the limbs, usually with one arm extended upward, and contralateral head and eye deviation; consciousness may or may not be impaired. 2. Complex partial seizures with prominent motor activity, such as vigorous rocking, bicycling, circling, or vocalization; minimal or no impairment in consciousness; and no postictal confusion. Because of their frequently bizarre manifestations, nonepileptic psychogenic seizures are often first suspected. Although such seizures are typical of the medial frontal or orbital frontal areas, they may arise anywhere within the frontal lobe. 3. Simple partial motor clonic seizures, arising from regions within or adjacent to the primary motor cortex.

EEG findings Intericlal EEG: Diagnosis of FLE rests largely on clinical features, in as much as the EEG is often normal or non diagnostic. This is largely because much of the frontal lobe, including the orbital-frontal cortex, interhemispheric convexity and cingulum, and the sulcal depths are relatively inaccessible to scalp EEG recording. Consequently, small epileptogenic foci may be missed entirely; conversely, epileptiform abnormalities may appear widespread because of the often large distances and intervening cortex between the epileptogenic area and scalp electrodes.

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Furthermore, functional networks permit rapid propagation within and outside the frontal lobes, which results in the appearance of diffuse (secondary bilateral synchrony), multi focal, or falsely localizing epileptiform abnormalities .In contrast to temporal lobe epilepsy, the placement of additional, closely spaced scalp electrodes does not usually improve the localizing value of scalp EEG in FLE . lnterictal EEGs in FLE can demonstrate one of several patterns: 1. For the reasons just listed, epileptiform discharges are not identified on scalp EEG recordings in up to one-third of patients. This is most commonly seen in patients with medial frontal epilepsy. 2. Secondary bilaterally synchronous discharges may be seen in up to two thirds of patients with FLE; these discharges are especially frequent with medial frontal foci. The term secondary bilateral synchrony is used in describing the bilateral discharges seen in patients with parasagittal epileptogenic lesions. 3. Focal epileptiform discharges occurring over one frontal lobe are seen in 42% to 63% of cases of FLE . When these arise from epileptogenic cortex in the medial frontal lobe, the discharges are of highest voltage at or adjacent to the vertex. 4. High-voltage (up to 300µV), sharply contoured slow waves that are broadly distributed over the frontal regions but maximal at F3-F4 and Fp1-Fp2 are characteristic of orbital frontal foci. These discharges are almost always seen bilaterally to some extent, but they show voltage andf ield asymmetries that accurately indicate the epileptogenic hemisphere. Ictal EEG: The ictal EEG is nonlocalizing in more than half the patients with FLE . Often, there is no electrographic correlate to be seen in scalp electrodes. Equally problematic, however, is that the early and prominent motor activity of many frontal lobe seizures produces large amounts of muscle and movement artifact that obscures EEG activity. False localization, particularly to the temporal lobe, also occurs as a result of frontal-limbic connections. Although supplementary motor area seizures can be associated with a focal rhythmic discharge localized or adjacent to the vertex , most other seizures of medial frontal origin are not accompanied by a lateralized discharge; EEGs sometimes show only diffuse, bilateral frontal voltage attenuation followed by bilateral frontal or diffuse rhythmic theta or delta activity. Although diffuse, bilateral frontal voltage attenuation is frequently correlated with onset of orbital frontal seizures, focal rhythmic alpha or beta frequency activity is sometimes seen in the frontopolar electrodes. Seizures of dorsolateral frontal origin are usually associated with a localizing ictal discharge.

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Juvenile myoclonic epilepsy (JME)

EEG Findings

JME is a common idiopathic generalised epileptic syndrome . It is an inherited disorder (positive family history in 40% of cases). It is responsible for about 511% of the adult epileptic population with an equal distribution between sexes. It appears around puberty. Eighty percent of first seizures occur between ages 12 and 18 with a mean age of onset of 14.6 years; onset may, however, vary between 8 and 30 years. JME is frequently under-diagnosed and under-appreciated. Many patients do not mention that they are having myoclonic seizures until asked specifically about body jerks. Typically,myoclonic jerks appear 2-3 yrs before the first generalized T-C seizure,although it is almost always the latter that brings the patient to medical attention. JME is characterised by multiple seizure types; myoclonic seizures with short, bilateral, single or repetitive arrhythmic, irregular jerks, predominantly in the shoulders and arms, it mostly occurs after awakening from sleep. Myoclonic jerks are seen in 100% of JME cases and are the sine qua non of diagnosis. They occur as the only seizure type in about 3%–5% of JME patients. The amplitude and force of the jerks vary. They may cause some patients to suddenly fall. Some jerks occur unilaterally. Sometimes myoclonic seizures of JME are perceived only as a subjective electric shock sensation inside the body. Patients are sometimes reluctant, to volunteer information about their myoclonus unless specifically asked. Sometimes, the myoclonus is noticed only by the patient’s family. Myoclonus is especially marked in the setting of fatigue and sleep deprivation. GTCS occur in 90%–95% of patients with JME. GTCS are often preceded by a few minutes of generalised mild to moderate myoclonus of increasing frequency and intensity. They occur predominantly after awakening and are often precipitated by sleep deprivation. Absence seizures feature in 30-40% of patients. These seizures are relatively infrequent, brief, and not associated with automatisms. They may occur several times a day. Sometimes, they may be the first manifestation of the disorder, even preceding the development of myoclonic jerks . Absence seizures in JME are typically less frequent and less intrusive than those seen in childhood absence epilepsy and frequently go unnoticed. JME is the epilepsy syndrome which is most commonly associated with photosensitivity with a reported prevalence of 25–42% and with a female predominance. Photosensitivity is defined by the occurrence of generalised spikes, spike and wave or polyspike and wave in response to intermittent light stimulation (ILS). An earlier onset is seen in photosensitive patients.

As in other idiopathic generalized epilepsy syndromes, the interictal EEG in JME is characterized by two main features: 1. Normal or near-normal background activity, with a well-modulated alpha rhythm . 2. Spontaneous bursts of generalized, bisynchronous epileptiform discharges. Polyspikes and polyspike-wave discharges are characteristic of JME, although they are not pathognomonic, Such discharges are also common in other idiopathic generalized epilepsies. However, when polyspikes are abundant and are the predominant form of epileptiform activity, it is more likely that the patient has JME than another idiopathic generalized syndrome. The epileptiform discharge consists of a burst of generalized bisynchronous, symmetrical multiple spikes (polyspikes) that are of maximal voltage in the frontal and central regions, followed by high-voltage, irregular 2- to 5-Hz slow waves with intermixed spikes. The polyspike component is often evident only at the beginning of the epileptiform paroxysm. The number of repetitive spikes may be as high as 20; two to four spikes are more usual . Epileptiform activity can occur either as isolated polyspike-wave bursts or as prolonged paroxysms lasting up to 20 seconds . Spikewave complexes and polyspikes without associated slow waves are also frequent and may sometimes be the only epileptiform abnormality. The spike-wave and polyspike-wave discharges seen in JME are usually "fast"; that is, the repetition rate is higher than the 3-Hz spike-wave pattern seen in childhood absence epilepsy. The most common frequencies are 3.5 to 6 Hz, and the range is between 2 and 10 Hz . "Typical," stereotyped 2.5- to 3-Hz spike-wave discharges, indistinguishable from those seen in childhood absence epilepsy, are present in up to 25% of patients. Hyperventilation generally activates epileptiform activity , although there have been no quantitative studies of this effect. In a minority of patients, epileptiform activity is seen only during hyperventilation. A relatively high percentage of patients, demonstrate photosensitivity. Photosensitivity is two to three times more common among girls with JME than among boys with JME. Photic stimulation, commonly at a frequency of 10-20 Hz, will elicit a photoparoxysmal response that often may outlast the duration of the photic stimulation or even induce a seizure Ictal EEG: Myoclonic seizures are always associated with polyspike or polyspike-wave bursts that are generally indistinguishable from those that are not accompanied by clinically detectable jerks. Sometimes the number of multiple spikes is higher (10


to 16 Hz) with ictal discharges, and the voltage may increase from the first spike to the last. The intensity of the myoclonic jerks correlates with a higher number of repetitive spikes . The polyspikes are of medium to high voltage, maximally expressed over the frontal regions, and followed by high-voltage, 1- to 3-Hz rhythmic slow waves . While the jerk itself is extremely brief ("lightning-like"), the associated EEG discharge is typically 1 to 2 seconds in duration and

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may last as long as 4 seconds. Absence seizures in JME are associated with generalized, somewhat irregular 2.5- to 4-Hz spike and polyspike-waves that last several seconds and may be interrupted with discontinuities lasting 1 second or less. The repetition rate of the spike-wave and polyspike-wave discharges can range from 2 to 7 Hz. A classical 3-Hz spike-wave pattern is uncommon.

Polyspike and wave discharges seen in juvenile myoclonic epilepsy

Spike and wave discharges in a patient with JME

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EEG of an 18-year-old woman with juvenile myoclonic epilepsy (JME). The interictal EEG demonstrates generalized spike-wave and polyspike-wave discharges.

EEG of an 18-year-old patient with juvenile myoclonic epilepsy (JME). A myoclonic jerk of the arms accompanies this burst of bilateral synchronous polyspikes.


Photoparoxysmal response in JME

Multispike and wave in JME

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Two discharges of fast, irregular spike-and polyspike-waves, both associated with myoclonic jerks(recorded on EMG leads over the deltoid muscles)

ILS in a patient with JME. Note the three photoparoxysmal responses, the first of which is associated with a myoclonic jerk(deltoid muscle surface EMG)


Epilepsy with Generalized Tonic-Clonic Seizures on Awakening The concept of awakening epilepsy was first developed by Janz. This type of idiopathic generalized epilepsy is less common than JME. Onset is generally in the second decade but earlier or later onset is possible (range: 5-25 years). There is a slight male predominance . A family history of epilepsy is frequent. Generalized tonic-clonic seizures occur within one hour of spontaneous morning awakening at the end of the nocturnal sleep period(90%), or during spontaneous or provoked intermediate awakenings. A lesser peak of occurrence is found during the evening relaxation period. Seizures are rare and are often elicited by sleep deprivation or excessive consumption of alcohol on the previous evening. Some patients may experience rare myoclonic jerks or absences. Prognosis is usually good, as seizures remain rare spontaneously and treatment is effective.

EEG Findgs Background is normal. There are rare generalized spike-waves and rare fast polyspike-waves(2-4Hz). Changes are activated at spontaneous or provoked awakening or during transitions between sleep stages. In some patients, interictal changes will never be recorded.

West,s Syndrome The west syndrome is one of the most frequent epileptic syndrome in infants, with an incidence of 2.94.9 per 100,000. This encephalopathy is characterized by a triad: 1.Infantile spasms 2.developmental retardation 3.hypsarrhythmia on EEG. Onset nearly always occurs in the first year of life, usually between the ages of 4 and 7 months . Nearly 90% of cases are associated with neurological abnormalities arising from a diverse array of structural, metabolic, and genetic disorders. Only 10% to 15% of cases are cryptogenic/idiopathic. Spasms are brief, symmetric, bilateral tonic contractions of muscles of trunk, neck and limbs(flexor spasms). Contractions are often followed by crying. Less frequently, there are extensor spasms with a sudden extension of trunk and neck with abduction and extension of the arms. Spasms can also be mixed (flexor-extensor), asymmetric or unilateral, and in the two latter cases often contralateral to a brain lesion. Spasms occur in series, often at awakening or at sleep onset, less commonly during nREM sleep and never during REM sleep. Associated focal seizures should

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always be sought, as these constitute an important element for etiological diagnosis and prognosis. Specific etiologies can be found in half of the cases, mainly a neurocutaneous syndrome(tuberous sclerosis), malformations, pre-, peri-, or postnatal encephalopathies, as well as metabolic, degenerative, or chromosomal diseases, or prenatal infections. Prognosis is in part related to the etiology. It has poor prognosis in most cases, often evolving into another epileptic encephalopathy, such as the lennox- Gastaut syndrome, or into another severe type of epilepsy associated with major mental retardation.

EEG findings The interictal EEG often shows typical "hypsarrhythmia". Hypsarrhythmia is seen in 75% of patients with West syndrome. Background is disorganized, with high-voltage, asynchronous and arrhythmic slow waves, in association with asymmetric and multifocal spikes and polyspikes. It is often necessary to lower the amplitude to have a better look at the EEG tracings. Hypsarrhythmia is mostly present at onset and can precede the occurrence of spasms. It is seen in waking and is fragmented during sleep. It can occur selectively during somnolence. In light nREM sleep,it becomes discontinuous. Spikes become more frequent and tend to be more diffuse and synchronouos. Irregular bursts of polyspike waves are separated by apparently fairly normal segments that may include sleep transients like spindles. Duration of REM sleep is shortened. Clinical spasms are associated with a marked suppression of the background that lasts for the duration of the spasm. This characteristic response is called the "electrodecremental response”. Spasms are associated with a brief tonic muscular contraction evidenced by surface EMG, that is symmetric or not according to the etiology. Serial spasms may occur at awakening, with or without interictal hypsarrhythmia. The presence of hypsarrhythmia between spasms may be characteristic of idiopathic cases and of a better prognosis. Focal seizures can initiate the series of spasms, occur during the series, or occur independently. EEG is useful in judging successful treatment of West syndrome. Typically, shortly after treatment with adrenocorticotropic hormone (ACTH) or vigabatrin is initiated, the spasms stop and hypsarrhythmia disappears.

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Hypsarrhythmia. High amplitude slowing with no organized background, and multifocal spikes (left and right frontal in this sample). This is a phenotype of the first year of life and is associated with West syndrome (infantile spasms).

Electrodecremental episode associated with infantile spasms (EEG during a spasm)


Typical hypsarrhythmia in an awake 5-month-old infant. The background activity is disorganized and replaced by a high-voltage activity with spikes, polyspikes and slow waves.

Hypsarrhythmia in a 5-month old child with a suprasellar hypothalamic hamartoma and tonic seizure

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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 The Lennox-Gastaut syndrome (LGS) encompasses a characteristic triad of severe generalized epilepsy, mental retardation,and an EEG pattern of slow-spikeand-wave discharges. Age at onset is usually between 1 and 8 years; most cases begin between the ages of 2 and 5 years. Onset after 10 years of age is rare. The ILAE Classification of Epilepsies and Epileptic Syndromes includes LGS among the generalized cryptogenic or symptomatic epilepsies. It is defined by the following criteria:

1. High seizure frequency; tonic, atonic, and atypical absence seizures are the most common. Myoclonic, generalized tonic-clonic, and partial seizures may also be present. As a rule, patients with LGS have multiple seizure types, and at least one episode of status epilepticus occurs in the majority . 2. Mental retardation, in general. More recently, some authors have argued that behavioral disorders, not accompanied by cognitive impairment, should be sufficient for diagnosis. 3. EEG demonstrating abnormal background activity with diffuse sharp slow waves that have a repetition


rate of less than 3 Hz. There are often multifocal spikes or sharp waves and, during sleep, frequent bursts of 10Hz and faster frequencies. LGS accounts for about 10% of all childhood epilepsies , although the actual prevalence may be much lower if rigorous criteria are used. Tonic, atonic, and myoclonic seizures can all result in the characteristic "drop attacks" seen in LGS, and differentiating among these on the basis of clinical features alone is often difficult. Moreover, there is significant overlap among the ictal patterns. Despite the consistent electroclinical triad, LGS cannot be attributed to a single cause or common pathological substrate. Diverse prenatal, perinatal, and postnatal disorders have been implicated. About two-thirds of cases are considered symptomatic, because a preexisting neurological condition can be identified. One-third of cases are classified as cryptogenic.

EEG findings EEG features of LGS may be divided into interictal and ictal. Interictal EEG features include: 1-Slow spike and wave pattern(SSW) that are bilateral,symmetrical and highest voltage in frontocentral with frequency of 1.5-2.5 Hz . SSW discharges can vary, both between and within individual bursts, in morphological appearance, distribution,voltage, and frequency. The repetition rate of SSW discharges can be quite erratic, with frequencies ranging from I to 4 Hz. The extended runs of SSW discharges commonly lack discrete onsets or terminations; sometimes they are nearly continuous during the greater part of an entire recording. Most SSW discharges are not accompanied by obvious clinical manifestations. Although usually symmetrical, SSW complexes sometimes show shifting asymmetries. Persistent focal or lateralized asymmetries of SSW discharges usually occur in symptomatic cases with focal neurological abnormalities. NREM sleep dramatically enhances SSW discharges in the great majority of patients . This effect is not universal,

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however, and in some patients, the discharges may actually decrease in both NREM and REM sleep . On occasion, SSW discharges are prominent during sleep even when they are infrequent during wakefulness, which underscores the importance of obtaining an adequate sleep recording . Polyspikewave discharges may emerge during sleep. In a minority of patients, sleep causes fragmentation of SSW bursts and a pseudoperiodic or burstsuppression appearance, with 2- to 3-second paroxysms of SSW alternating with diffuse voltage attenuation of background activity. 2-Paroxymal fast activity(PFA)or polyspike discharges: the second defining electrographic feature of LGS, is present mainly or exclusively during sleep in nearly all patients . PFA consists of diffuse, bilaterally synchronous bursts of 15- to 20Hz 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 from 25 to 250 µV The duration of PFA bursts ranges from 2 to 12 seconds . Bursts of PFA occur up to hundreds of times each night, but only in NREM sleep; they are absent during REM . Although indistinguishable from the ictal pattern associated with tonic seizures , the majority of PFA discharges are not accompanied by any visually discernible clinical changes. Autonomic changes, including tachycardia and apnea, can occur in association with PFA, even when motor manifestations are absent . Thus, it can be argued that PFA is not, strictly speaking, an interictal finding, although the ictal manifestations may be subtle and not visually detectable. 3-Background slowing: Diffuse abnormalities of background activity occur in up to 90% of patients with LGS . In two-thirds of cases, background slowing is moderate to severe and is generally correlated with the degree of cognitive impairment. Ictal EEG features: Electrographic accompaniment varies with the seizure type.However, there is significant overlap among the ictal patterns between the various type of seizures.

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Eleven-year-old boy with moderately severe mental retardation and intractable generalized tonic, atonic, myoclonic,and atypical absence seizures since age 4 years. Awake EEG showed generalized sharp- and slow-wave complexes.

EEG of a 29-year-old woman who had Lennox-Gastaut syndrome (LGS) since early childhood. Interictal EEG recording demonstrating diffuse background delta frequency slowing and nearly continuous 1.5- to 2.0-Hz bilateral synchronous slow-spike-and-wave (SSW) discharges. During this time, the patient was attentive and interactive.


Atypical absence seizure in a patient with LGS. Clinically characterized by decreased responsiveness and gaze deviation to the right. Although very similar to the interictal recording shown in previos recordind, the SSW discharges appear more organized and sustained at a consistent 2-Hz frequency.

Sleep EEG of a patient with Lennox-Gastaut syndrome (LGS). There are frequent bursts of diffuse 16- to 20-Hz paroxysmal fast activity (PFA) without any visually detectable clinical changes.

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Generalized paroxysmal fast activity and electrodecrement. This pattern is characteristic of the the symptomatic/ cryptogenic epilepsies of the Lennox-Gastaut type, and may be subclinical or associated with tonic or atonic seizures.

Tonic seizure in Lennox-Gastaut syndrome (LGS). During sleep, the child exhibited abrupt onset of arm and neck stiffening, which lasted several seconds. The EEG shows an 8-second run of bilateral synchronous 16- to 20-Hz activity, which is the ictal discharge.


The Syndrome of Continuous Spike and Wave Discharges During Slow Sleep (CSWS)[electrical status epilepticus during slow sleep] This syndrome was first described by Patry et al as "subclinical electrical status epilepticus induced by sleep." It was later renamed because of the lack of typical clinical features associated with status epilepticus. The syndrome of CSWS is a rare condition, accounting for fewer than 0.5% of cases of childhood epilepsies . Age at onset ranges from 1 to 12 years, but onset peaks between the ages of 5 and 7 years. In primary school-age children, there is a more or less pronounced cognitive regression, psychomotor impairment, and epilepsy of varied severity, with focal or generalized seizures including atypical absences and falls. Boys are more concerned (63%). More than 1/3 of patients have abnormal neuroimaging, e.g; polymicrogyria, unilateral or diffuse cortical atrophy, or porencephalia. CSWS disappears in all cases after 1 to 5 years. In nearly all patients, seizures appear 1 to 2 years before the EEG abnormality of this syndrome . Simple partial motor and generalized tonic-clonic seizures predominate. Later, with appearance of the syndrome of CSWS, other seizure types emerge, including atypical absence seizures associated with atonia and falls. Most patients have frequent seizures, often multiple times in a week or even in a single day . Tonic seizures do not occur . With development of the syndrome, nearly all patients have a significant decline in IQ with deterioration in language, temporospatial disorientation, impaired memory, and reduced attention span. Behavioral changes such as aggressiveness or, rarely, psychosis also occur.

EEG findings At seizure onset, around age 4-5, EEG changes are non-specific. CSWS appear at around age 5 to 7. During the period of CSWS, the children will exhibit bursts of diffuse spike-waves at 2-3Hz, which can be associated with absences, during waking. CSWS appear as soon as the child falls asleep, and persist throughout the stages of nREM sleep, during which they occupy more than 85% of the total duration. However, a lesser proportion is accepted by some authors. Discharges can be asymmetric. During REM sleep, there is a fragmentation of spike-wave discharges and the percentage falls below 25%. The discharges can ever disappear, and focal, frontally predominant changes can be discerned. In REM sleep, subclinical frontal seizures can also be recorded and are a characteristic element of the syndrome. The EEG becomes progressively normal after remission of epilepsy.

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The Syndrome of Acquired Epileptic Aphasia (Landau-Kleffner syndrome) This syndrome, first described by Landau and Kleffner(LKS) , is characterized by acquired aphasia associated with epileptiform activity on EEG ("epileptic aphasia"). Although the nature of this syndrome is controversial, it is probably not fundamentally an epileptic disorder. It occurs in previously healthy children between the ages of 3- 9 years (peak incidence, 5 to 7 years), and never after age 12. Boys are affected twice as often.The first indication of aphasia is verbal auditory agnosia , but language function continues to deteriorate. Some children become mute and do not respond even to nonverbal sounds. Hyperactivity and personality changes appear as the aphasia worsens . Seizures occur in about 70% of patients; they tend to be relatively infrequent, although status epilepticus has been reported. Partial motor, atypical absence, generalized tonic-clonic, and atonic seizures have all been reported . More subtle seizures, such as eyelid myoclonia,ocular deviation, and head drops also occur. Type and frequency of seizures are not correlated with outcome . Similarly, treatment with antiseizure drugs does not clearly affect aphasia, EEG findings, or prognosis. About two-thirds of children have residual language impairment; cognitive and behavioral abnormalities are less frequent consequences. Total return to normal is possible in 10-20% of cases. In its typical forms, the landau-kleffner syndrome is cryptogenic.

EEG findings A paroxysmal EEG is one of the defining features of LKS, and epileptiform discharges are thus invariably present. Epileptiform activity is extremely variable in both location and amount. High-voltage multi focal spikes and spike-wave discharges occur both singly and repetitively . Discharges occur over the posterior temporal regions preferentially but are not limited to these areas . Epileptiform activity can be unilateral or bilateral. When bilateral, the discharges can be diffuse and bisynchronous and either symmetrical or asymmetrical. In the early stages of the disorder, epileptiform activity may be limited to sleep. The EEG abnormalities vary considerably over time, so that the distribution, abundance, and topography may change from one tracing to the next . NREM sleep activates epileptiform activity, often to a marked degree. Epileptiform discharges exhibit larger fields, tend to become generalized, and occur repetitively at frequencies of 1.5 to 3 Hz . During REM sleep, the slow spike-wave pattern fragments and focal or multi focal discharges appear in a pattern similar to that seen in the waking state . Sometimes there is continuous

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(occupying more than 85% of sleep time) spike-wave activity that is similar to that seen in the syndrome of CSWS . Seizure remit and the EEG normalizes in nearly all patients by the end of adolescence , but some

degree of language dysfunction persists in the majority. Most patients show improvement, but the degree of recovery is variable and unpredictable; some patients remain profoundly impaired.

A EEG of a 6-year-old boy with Landau-Kleffner syndrome (LKS). He had been neurologically normal until 9 months previously, when he developed rapidly progressive loss of language skills. He had only three seizures, all generalized convulsions. Results of brain imaging, cerebrospinal fluid studies, and metabolic evaluation were normal. A: EEG in the waking state demonstrates mild slowing of background activity and infrequent right midtemporal spikes.

B

B: EEG during non-rapid-eye-movement sleep shows nearly continuous spike-and wave discharges. Although broadly distributed bilaterally, they are maximal over the right temporal region

Chapter 10

Epileptiform Normal Variants

Epileptiform normal variants are EEG patterns that resemble epileptogenic abnormalities. Most of these patterns initially were thought to be associated with epilepsy or other neurological conditions but subsequently were demonstrated to have no such significance. They now are considered normal variants of no clinical significance. Their recognition is important to avoid overinterpretation or misinterpretation with regard to their significance. This chapter reviews the following such patterns: small sharp spikes (SSS), wicket spikes, 14- and 6-Hz positive spikes, phantom spike and waves, psychomotor variants, subclinical rhythmic EEG discharges of adults (SREDA), and midline theta.

Small Sharp Spikes(SSSs) Also known as benign epileptiform transients of sleep (BETS), SSSs occur in light sleep (stages I and II of nonrapid eye movement [NREM] sleep), usually sporadically. Location is temporal or frontotemporal , either unilateral or bilaterally independent, and with a broad field of distribution. Morphology is typically monophasic, occasionally diphasic or polyphasic, and the decline after the first negative peak is very steep.

SSSs have a single aftercoming slow-wave component or may be associated with an aftercoming dip in the background; however, they do not have the prominent aftercoming slow wave that temporal spikes have, and they do not occur in repetitive trains. The main features of SSSs are in their name: duration is short, amplitude is small, and an easy guideline states that SSSs generally should be less than 50 µV and less than 50 milliseconds. Rarely seen in children, they are seen most often in adults and the elderly. They can occur in epileptic patients but often are seen in healthy individuals. They may occur in patients with CVA, syncopal attacks,and psychiatric problems(manicdepressive). SSSs are generally easy to distinguish from spikes because of their short duration and small amplitude.

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Small sharp spikes or BETs. Note that these waveforms do not correspond to ECG see bottom trace.

Small sharp spikes


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Left temporal small sharp spike. Note low amplitude (<50mA)and short duration (<50msec)

Wicket spikes First described by Reiher and Lebel in 1977, Wicket spikes are trains of arch shaped or a single spike-like waveform that resembles a Mu rhythm. Wickets have a frequency of 6 to 11 Hz and range from 60 to 200 microvolts in amplitude. Wicket spikes occur bilaterally or independently over the temporal regions and there is usually no slow wave seen after the spikelike waveform. Wickets are best seen in drowsiness and light sleep when the alpha rhythm drops out. They occur perdominantly in adults older than 30 years . It can be difficult to differentiate temporal spikes from

wicket spikes especially when wicket spikes occur singly. Although wicket spikes are seen mainly during drowsiness and light sleep, but may be present during the awake recording and are often masked by other background rhythms and usually emerge or become apparent during drowsiness, when the alpha and other awake patterns disappear.

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Wickets

Wicket Spikes


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Wicket spikes in the left temporal region

14- and 6-Hz positive spikes These bursts occur predominantly during drowsiness and light sleep and consist of short trains of archshaped waveforms with alternating positive spiky components and a negative, smooth, rounded waveform that resembles a sleep spindle with a sharp positive phase. The bursts occur at a rate of 14 Hz or 67 Hz and last from 0.5 to 1 second. Usually, the faster frequency is the more prevalent, but the slower rate can occur either independently or in association with a train of 14-Hz positive bursts. The waveform is best displayed on a long-distance or referential montage to the ear. It usually has maximal amplitude over the posterior temporal region. The bursts can occur

asynchronously or independently over the two sides but may preferentially involve one side; they may also shift from side to side in predominance. In a normal population, 14- and 6-Hz positive bursts begin to appear in children between 3 and 4 years old, are maximally expressed in the adolescent age group (with a peak at age 13-14 years), and then progressively decrease in incidence with increasing age. Sleep spindles - 12 to 14 hertz bursts of rhythmic waves which often increase and decrease in voltage and are maximal in the central midline head region. 14 and 6 hertz positive spikes - surface-positive spikes most prominent in the posteriortemporal regions occurring at 14 Hz, 6 Hz, or a mixture of 14 Hz and 6 Hz

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14 and 6Hz positive spikes

14 and 6Hz positive spikes in the 6th and 7th second, seen in posterior temporal, temporal and central regions on this contralateral referential montage

Phantom spike and waves (6Hz spike and wave) The 6-Hz spike-and-wave discharges have a repetition rate of 6 Hz, with a range of 5-7 Hz. The bursts are usually brief, lasting 1 or 2 seconds, although rarely they persist for 3 or 4 seconds. The pattern has also

been called the "phantom spike and wave" because of the evanescent nature of the spike, which is usually very brief and small in amplitude, in contrast to the more prominent slow-wave component, which has a higher amplitude and a more widespread distribution. The 6-Hz spike-and-wave pattern is seen in both adolescents and adults. It generally occurs during relaxed wakefulness and stage I sleep and disappears


during deeper levels of sleep. Location is usually diffuse, bisynchronous, and relatively symmetric. This pattern may predominate in the anterior and posterior head regions. Morphology is a typically small (<30 µV and <30 ms), evanescent diphasic spike followed by a higher (50-100 µV) slow wave component. Thus, at times the spike component may be difficult to see.

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Phantom spike and wave may be difficult to distinguish from the definitive clinically significant spike and wave complexes.A helpful way to distinguish them is by the tendency of benign phantom spike and waves to disappear during sleep while epileptic discharges(spike and wave complexes)tend to persist or become more prominent with deeper levels of sleep.

Six-Hertz spike-and-wave bursts in a 39-year-old woman

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EEG of a 26-year-old patient, showing 6 Hz spike wave paroxysms (phantom spike wave)

psychomotor variants (Rhythmic Midtemporal Theta of Drowsiness) A more useful and descriptive term is rhythmic midtemporal theta of drowsiness (RMTD). Frequency is theta (4-7 Hz). Location is maximum midtemporal, unilateral or bilaterally independent or bisynchronous. Morphology typically is notched, flat topped, or sharply contoured. It is an unusual form that occurs as asymmetrical runs of theta or delta activity primarily in the temporal regions, lasting for a few seconds or as long as 30-45 and thus resemble temporal lobe

seizures. Amplitude is medium to high. Psychomotor variant differs from a seizure discharge because it is usually a monomorphic or monorhythmic pattern that does not evolve into other frequencies or waveforms as usually occurs during seizures.


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RTMD

Subclinical rhythmic EEG discharges of adults (SREDA) This uncommon pattern is seen mainly in people older than 50 years. SREDA may occur at rest or during drowsiness, and occasionally occurs mainly during hyperventilation. This 40 to 100 microvolt discharge is a repetitive sharply

contoured waveform of 5 - 6 hertz. Once developed, the pattern sustains its rhythmic fashion until gradually dissolving into the background activity. SREDA may last from a brief 4 seconds to a prolonged 80 seconds in either the parietal and/or temporal head regions bilaterally. Once you have identified SREDA, you must distinguish it from epileptiform activity by having the patient perform various mental or physical activities during the discharge period to

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define the patients level of consciousness. Use such techniques as eye opening and closing, mental arithmetic, reading, answering questions, and hyperventilation. All patients with SREDA are fully responsive during the

discharges and bear no clinical motor manifestations or complaint of sensory symptoms, as might be found during a partial seizure.

SREDA

Another sample of SERDA


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Midline Theta This is a focal rhythm maximal at the midline, most prominently at Cz, which occasionally may spread to adjacent electrodes. It has a frequency of 5-7 Hz and typically has an arciform, spiky, mulike appearance. It waxes and wanes, can appear during wakefulness or

drowsiness, and is usually reactive to eye opening or limb movement. Although initially described in association with temporal lobe epilepsy, it probably represents a normal variant. Midline theta rhythm does not have any clinical significance and appears to represent a nonspecific variant of theta activity.

Midline theta rhythm

Chapter 11

Nonepileptic Abnormalities

It is an obvious but important fact that the electroencephalogram (EEG) evaluates brain function, not structure. Although many different pathological processes disturb brain function, the repertoire of resulting EEG abnormalities is limited. As with other physiological tests, EEG abnormalities, although reliable indicators of brain dysfunction, cannot, except in rare instances, distinguish etiology or pathology. Advances in neuroimaging have fortunately reduced dependence on the EEG for information that it cannot reliably provide, while new methods of data processing have led to further development of its usefulness in examining brain physiology.Although at one time authors discussed the application of EEG in

differentiating various types of lesions, this clearly has not been clinically useful in the modern era. The exercise of describing EEG abnormalities by pathology which is common in EEG texts, is therefore not followed here. Instead, the different patterns of abnormal EEG and their clinical significance are reviewed. The abnormal nonepileptic EEG abnormalities may be broadly divided into four catrgories: 1. 2. 3. 4.

Abnormalities of the background rhythms Abnormal sleep patterns Focal or generalized abnormal slow activity Abnormal periodic patterns

1. Abnormalities of the background rhythms Alterations in rate, rhythm, distribution, symmetry, amplitude, or reactivity of the background activity may occur during various CNS disorders. The alterations may involve one or more of the physiological rhythms, namely, the alpha, beta, or mu rhythms.

Alpha rhythm Generally, absent or scanty posterior alpha rhythm may be due eye opening, attention, anxiety, or drowsiness.Some asymptomatic individuals normally have little or no alpha rhythm,perhaps on a genetic basis.

In the awake adult an alpha rhythm of less than 8Hz is abnormal. Since a number of clinical conditions can produce slowing of the alpha rhythm, the slowing is considered a nonspecific abnormality. Thus, bilateral 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 dementia irrespective of the underlying cause. The degree of slowing often parallels alterations in the mental status of the patient. It should also be noted that the alpha rhythm slows down in patients with hypothyroidism and can become normal when a euthyroid state results from adequate treatment. Asymmetrical slowing of the alpha rhythm with a consistent difference of greater than 1.5Hz between

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the two sides is abnormal and should suggest the possibility of a lesion on the slower side. However, such a finding does not necessarily indicate the presence of a lesion in the occipital lobe itself; asymmetrical slowing of the alpha rhythm is known to occur even with lesions that are more anteriorly located. A difference in amplitude of the alpha rhythm between the two sides is considered significant if it exceeds 50%. Since the alpha rhythm in most normal persons is of higher amplitude on the right side, even a 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 fluid between the brain and the recording electrode, as in the case of subdural or scalp edema, may lead to attenuation of alpha rhythm ipsilaterally. Markedly diminished background amplitude on one side of the EEG, compared to homologous channels of the contralateral hemisphere, is found with abnormalities of cortical gray matter, or with excess fluid between the cortex and recording electrodes. This finding is characteristic of ischemic stroke with gray matter involvement or subdural hematoma. In patients with gray matter involvement, concurrent white matter involvement causing delta activity is typical. Decreased background amplitude also may occur with congenital lesions, such as porencephalic cysts, or with Sturge-Weber syndrome. Transient background attenuation also is characteristic of the postictal EEG of patients with focal-onset seizures. Focal suppression will usually involve multiple electrodes. Focal suppression which is confined to one electrode is more likely to be due to smear of electrode paste, or some other artifact which affects the recording system. Less commonly, increased amplitude of background waveforms (alpha rhythm, sleep spindles, beta activity, or mu rhythm) can be seen ipsilateral to cerebral lesions. Abnormalities may also occur in the distribution of the alpha rhythm. Normally, it is distributed in the occipital, parietal, and, to some extent, posterior temporal areas; however, activity may occur over widespread areas, including the frontal regions. Such an alpha patterns is abnormal and is seen in alpha coma, which may result from a number of conditions such as brain stem infarct or cerebral anoxia, or it may 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 , and this should not be mistaken for an alpha coma pattern. Lack of reactivity to eye opening is a significant finding, particularly if consistently demonstrated on one side. This may be an early finding in occipital lobe lesions. A total lack of reactivity of the alpha rhythm is a feature that may be seen in alpha coma, particularly in cases of diffuse cerebral anoxia due to

cardiac arrest. In the case of alpha coma resulting from lower brain stem lesions, there may be some degree of reactivity. This contrasts with findings in psychogenic unresponsiveness where reactivity to eye opening is normal. A focal increase in amplitude and or frequency of the alpha rhythm is known to occur in patients with structural lesions, particularly tumors; but this is quite an uncommon finding. Remember that a localized increase in amplitude may also be seen over a skull defect.

Unilateral failure of alpha blocking on eye opening: often referred to as bancaud,s phenomenon, occurs with lesions of the parietal and temporal lobe on the side which fails to block.

Bilateral failure of alpha blocking: Normal subjects show great variability of alpha blocking and may have only very brief reductions of alpha amplitude in response to eye opening and alerting. Unilateral cerebral lesions located in the frontal or temporal lobes that abolish the blocking of alpha activity are usually associated with an impairment of consciousness, prominent neurological deficits, or both. In contrast, lesions located in the parietal or occipital lobes that abolish blocking of the alpha rhythm are often not associated with impaired consciousness or severe deficits. Binocular blindness, when acquired after the development of alpha, leads to a loss of the reactivity of alpha rhythm to eye opening. The alpha rhythm in this condition may have a central or unusually wide distribution. Like congenitally blind persons, persons with acquired blindness may have no alpha rhythm and may develop occipital spikes even in the absence of occipital lesions. Monocular blindness or loss of discrimiminative vision can cause failure of alpha blocking in both hemisphere when the blind eye is opened; opening of the seeing eye produces normal bilateral alpha blocking.

Beta activity Beta activity in normal controls may be up to 35% lower on one side, but a greater asymmetry, especially if combined with other abnormalities, is a sensitive indicator of cortical injury underlying the region of lower amplitude. Both attenuation and accentuation of beta activity may be abnormal. Beta attenuation is often seen in


Epilepsy with Generalized Tonic-Clonic Seizures on Awakening The concept of awakening epilepsy was first developed by Janz. This type of idiopathic generalized epilepsy is less common than JME. Onset is generally in the second decade but earlier or later onset is possible (range: 5-25 years). There is a slight male predominance . A family history of epilepsy is frequent. Generalized tonic-clonic seizures occur within one hour of spontaneous morning awakening at the end of the nocturnal sleep period(90%), or during spontaneous or provoked intermediate awakenings. A lesser peak of occurrence is found during the evening relaxation period. Seizures are rare and are often elicited by sleep deprivation or excessive consumption of alcohol on the previous evening. Some patients may experience rare myoclonic jerks or absences. Prognosis is usually good, as seizures remain rare spontaneously and treatment is effective.

EEG Findgs Background is normal. There are rare generalized spike-waves and rare fast polyspike-waves(2-4Hz). Changes are activated at spontaneous or provoked awakening or during transitions between sleep stages. In some patients, interictal changes will never be recorded.

West,s Syndrome The west syndrome is one of the most frequent epileptic syndrome in infants, with an incidence of 2.94.9 per 100,000. This encephalopathy is characterized by a triad: 1.Infantile spasms 2.developmental retardation 3.hypsarrhythmia on EEG. Onset nearly always occurs in the first year of life, usually between the ages of 4 and 7 months . Nearly 90% of cases are associated with neurological abnormalities arising from a diverse array of structural, metabolic, and genetic disorders. Only 10% to 15% of cases are cryptogenic/idiopathic. Spasms are brief, symmetric, bilateral tonic contractions of muscles of trunk, neck and limbs(flexor spasms). Contractions are often followed by crying. Less frequently, there are extensor spasms with a sudden extension of trunk and neck with abduction and extension of the arms. Spasms can also be mixed (flexor-extensor), asymmetric or unilateral, and in the two latter cases often contralateral to a brain lesion. Spasms occur in series, often at awakening or at sleep onset, less commonly during nREM sleep and never during REM sleep. Associated focal seizures should

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always be sought, as these constitute an important element for etiological diagnosis and prognosis. Specific etiologies can be found in half of the cases, mainly a neurocutaneous syndrome(tuberous sclerosis), malformations, pre-, peri-, or postnatal encephalopathies, as well as metabolic, degenerative, or chromosomal diseases, or prenatal infections. Prognosis is in part related to the etiology. It has poor prognosis in most cases, often evolving into another epileptic encephalopathy, such as the lennox- Gastaut syndrome, or into another severe type of epilepsy associated with major mental retardation.

EEG findings The interictal EEG often shows typical "hypsarrhythmia". Hypsarrhythmia is seen in 75% of patients with West syndrome. Background is disorganized, with high-voltage, asynchronous and arrhythmic slow waves, in association with asymmetric and multifocal spikes and polyspikes. It is often necessary to lower the amplitude to have a better look at the EEG tracings. Hypsarrhythmia is mostly present at onset and can precede the occurrence of spasms. It is seen in waking and is fragmented during sleep. It can occur selectively during somnolence. In light nREM sleep,it becomes discontinuous. Spikes become more frequent and tend to be more diffuse and synchronouos. Irregular bursts of polyspike waves are separated by apparently fairly normal segments that may include sleep transients like spindles. Duration of REM sleep is shortened. Clinical spasms are associated with a marked suppression of the background that lasts for the duration of the spasm. This characteristic response is called the "electrodecremental response”. Spasms are associated with a brief tonic muscular contraction evidenced by surface EMG, that is symmetric or not according to the etiology. Serial spasms may occur at awakening, with or without interictal hypsarrhythmia. The presence of hypsarrhythmia between spasms may be characteristic of idiopathic cases and of a better prognosis. Focal seizures can initiate the series of spasms, occur during the series, or occur independently. EEG is useful in judging successful treatment of West syndrome. Typically, shortly after treatment with adrenocorticotropic hormone (ACTH) or vigabatrin is initiated, the spasms stop and hypsarrhythmia disappears.

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Focal EEG waveform abnormalities. This EEG of a 62-year-old patient with a right parietal glioblastoma . As you see it demonstrates decrease in amplitude of the ongoing background activity on right side, indicating that an abnormality of cortical gray matter is present as well.

Left background suppression in 7y-old boy with a large left frontotemporal porencephalic cyst. Note a well developed alpha rhythm is seen occipitally in both sides.


Focal attenuation of posterior alpha rhythm on the right side after a seizure

Increased beta activity over a right frontal skull defect(breach effect)

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Excess beta activity. This patient has been treated with clonazepam

Excessive beta activity in a comatose patient


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Generalized suppression background with intermittent bursts in a 76 year-old man with anoxic encephalopathy

2. Abnormal sleep patterns Amplitude asymmetry of sleep spindles is suggestive of a lesion on the side with the lower amplitude. This may happen both in structural lesions and also when there is abnormal collection of fluid between the brain and the recording electrode, as in subdural hematoma. By contrast, sleep spindles may appear with higher amplitude over a skull defect. The V waves may also be asymmetrical in amplitude. The presence of consistently asymmetrical V waves indicates a structural lesion,a subdural hematoma or effusion on the side of a skull defect.

Another group of sleep- pattern abnormalities includes disorders of sleep architecture. A person normally goes through stage 1 and 2 sleep before the first phase of REM sleep occurs,usually 90 minutes after the onset of sleep. But the REM phase can occur at the onset of sleep,and this abnormality is a feature of narcolepsy. Polysomnographic studies are needed to evaluate such sleep disorders.

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Asymmetry of sleep spindles in a 36-year-old patient with a right thalamic glioma.

Asymmetric reduced sleep spindle in left hemisphere in a 29 year old man with TLE


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3. Focal or generalized abnormal slow activity

One of the commonest abnormalities in EEG is the occurrence of abnormal slow activity. It must be understood that certain forms of slow activity are entirely normal. These include the delta activity that occurs in stages 3 and 4 sleep,the theta activity that is present in the background activity of children during wakefulness,and also the theta or delta activity that may be seen during hyperventilation. The distinction between normality and abnormality is less precise in the case of theta than delta activity. With theta activity, asymmetries in amplitude and frequency may be more significant than the mere presence of the activity. This is due to the variable occurrence of theta activity in drowsiness and in the waking state of normal young and very old persons. Slow activity may occur intermittent or persistent. It can be generalized, focal, or regional. It may be rhythmic (means monomorphic and regular) or arrhythmic (means polymorphic and irregular). Arrhythmic or polymorphic delta activity consists of delta waves that are irregular in shape and have a variable duration and frequency without a stable predominant frequency. Rhythmic delta activity consists of delta waves that are regular in shape and have a fairly constant duration and stable predominant frequency. Focal slowing is most commonly seen with structural lesions. Generalized slowing is most commonly seen with encephalopathy. Regional slowing is uncommon, and usually manifest as intermittent rhythmic delta activity. Although this might be considered focal, it is bihemispheric, so should be considered regional. For convenience , the discussion of slowing is divided into these sections: A. B. C. D.

Generalized intermittent slow activity Focal and regional intermittent slow activity Persistent slow activity Encephalophatic patterns (theta coma, alpha coma, beta coma, spindle coma, triphasic waves)

A. Generalized intermittent slow activity This is a common and easily identified abnormal EEG pattern. It consists of intermittent rhythmic, usually monomorphic, slow activity most commonly occurring in the delta frequency band. The acronym IRDA (intermittent rhythmic delta activity) is often used for this pattern. The activity is characteristically bilateral and synchronous, showing frontal (FIRDA) or occipital dominance(OIRDA); rarely, it may be most prominent over the temporal areas. The dominance seems to be age related, OIRDA being more common in children. Intermittent rhythmic delta activity is usually of high amplitude; it stands out from the background and often has a frequency of 2to 3 Hz. These patterns attenuate with alerting or eye opening. On the other hand,eye closure, drowsiness, and hyperventilation accentuate IRDA. Although IRDA disappears in stage 2 and deeper non–rapid eye movement (NREM) sleep, it may reappear in REM sleep. IRDA is not specific for a single etiology and can occur in response to systemic toxic or metabolic disturbances as well as to diffuse or focal intracranial diseases. This may be due to diverse etiologies, such as infectious, inflammatory, degenerative, traumatic, vascular, or neoplastic disorders. IRDA is also the nonspecific type of slowing that occurs in normal individuals in response to hyperventilation. In such cases, it should not be interpreted as an abnormality, but rather as the response of a normal CNS to the stress of an acutely changing Pco2. Because IRDA may occur in response to systemic toxic or metabolic disturbances, diffuse intracranial pathology, or focal intracranial pathology, its localizing value obviously is limited. Even when it is due to a focal expanding lesion, the peak localization of the IRDA tends to be age-dependent[maximal frontal in adults and maximal posterior in children]. It is independent of the localization of the lesion, which may be at some distance, either in the supra- or infratentorial space, from the maximum expression of the IRDA. The recognition that IRDA is a nonlocalizing rhythm, even when associated with an intracranial lesion, led to its earlier designation as a “projected” or “distant” rhythm.

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Although frequently bilateral, IRDA may occur predominantly unilaterally. Even when it occurs unilaterally in association with a lateralized supratentorial lesion, the lateralization of the IRDA, although usually ipsilateral, may even be contralateral to the focal lesion . Therefore, when IRDA is present, 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 or even the laterality of IRDA. TIRDA(temporal intermittent rhythmic delta activity) is an important epileptogenic abnormality., highly pathognomonic for temporal lobe epilepsy. These rhythmical unilateral delta trains indicate a focal lesion. Thus, TIRDA markedly differs from FIRDA and OIRDA(and their mainly global significance). In summary, IRDA is nonspecific in that it can be seen in association with a wide variety of pathological processes varying from systemic toxic or metabolic disturbances to focal intracranial lesions. Even when associated with a focal lesion, IRDA by itself is nonlocalizing. The common denominator in the wide variety of pathological processes producing IRDA is that, when such an abnormality appears, it is likely to be associated with the development of widespread brain dysfunction ; the earliest clinical correlates are fluctuating levels of alertness and attention. With focal • • • • • •

lesions, the mechanisms may be sufficient distortion of the brain to produce secondary disturbances at both the subcortical and cortical levels. With primary intracranial encephalopathies, it appears to be due to widespread involvement of the gray matter at subcortical and cortical levels.

B. Focal and regional intermittent slow Activity These abnormalities have the same features as generalized intermittent delta activity except that they are limited to one area or to one side of the brain. Focal slow activity usually indicates a focal subcortical structural lesion. The slow activity typically has an irregular, polymorphic appearance, hence the name polymorphic delta activity (PDA). In general, the area of the slow activity is overlying the location of the structural lesion, but the anatomic correlation is not always exact. The differential diagnosis of focal irregular slow activity is large, with some of the possibilities including:

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 about the etiology of the slow activity from the appearance. While additional historical information may help the analysis, the diagnosis of focal structural lesions rests largely with imaging studies.

As previously pointed out one form of focal slow activity, temporal intermittent rhythmic delta activity (TIRDA), has a strong association with seizure activity.


Frontal intermittent rhythmic delta activity (FIRDA).

Frontal intermittent delta activity (FIRDA)

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OIRDA during hyperventilation in a 13 year old boy- this is a normal finding in this patient

Frontal intermittent delta activity


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Frontal intermittent delta activity

Bursts of high-voltage bilaterally synchronous frontal intermittent rhythmic delta activity in a 41-year-old lethargic patient with uremic encephalopathy.

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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.


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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).

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EEC of a 52-year old man who had a right parietal glioma. Note the polymorphic slow-wave focus in the right central region and the diffusely slowed background.

Intermittent slow activity, left temporal in a 20-yaer old patient with TLE

C. Persistent slow activity Persistent slow activity is usually in the delta frequency band. It may occur as monomorphic, rhythmic waves or as polymorphic, arrhythmic waves. It may be generalized, lateralized, or focal. In the case of the rhythmic delta activity, the waveforms resemble each

other and maintain a somewhat constant frequency. On the other hand, the polymorphic delta activity (PDA) usually has a frequency of 0.5 to 3 Hz, and the waveforms change in frequency, amplitude, and morphology in a continuous fashion. In other words, no two succeeding waves appear to be quite alike. Polymorphic delta activity (PDA) tends to show no reactivity to stimulation and persists both during


wakefulness and sleep. Even hyperventilation may not have much effect on PDA. Continuous PDA, especially when it is focal, is indicative of an underlying structural lesion unless proved otherwise. The finding often correlates well with other tests like the CT scan and MRI, but there are certain situations where the neuroimaging may be negative as, for example, in recent infarct or contusion. For the exact localization of the lesion, the frequency of the waveform is a better indicator than the amplitude; thus, the area showing the slowing activity is the most likely site of the lesion. The amplitude is often higher in the immediately surrounding areas. Sometimes the tracing from the area overlying a

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destructive lesion may be of such low amplitude that it appears to be flat, whereas the surrounding areas show large amplitude PDA. It is now believed that deafferentation of the cortex by a lesion that interrupts that thalamocortical afferents is the underlying mechanism in the genesis of PDA. Polymorphic delta activity is most likely to be associated with acute destructive lesions, but it gives no clues as to the specific etiology of the lesion. Sometimes PDA and rhythmic delta activity may coexist in the same tracing. This may conceivably depend on different degrees of involvement of the cortical and subcortical areas by the lesion.

Diffuse background slow activity in a 47 year old man with hepatic encephalopathy. Note EMG artifacts throughout the recording.

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(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.


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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.

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Continuous slowing, generalized. While some faster frequencies are present, this sample is dominated by generalized polymorphic delta activity. If this is "continuous" (greater than 80% of the recording), this usually goes along with a severe diffuse encephalopathy.

D. Encephalopathic patterns (alpha coma, theta coma, beta coma, spindle coma, triphasic waves) The terms alpha coma,theta coma, alpha-theta coma ana beta coma patterns are often used to denote patterns of rhythmical waves which have theta, alpha or beta frequency but differ from normal rhythms in that they occur in isolation without other accompanying waveforms in comatose patients. In addition, they usually do not demonstrate spontaneous variability or reactivity to sensory stimulation. Their topography(distribution over the head) is usually abnormal in that neither the alpha nor theta activities have a posterior dominant amplitude gradient and beta patterns are widespread. These waves show little variation in frequency and are either the only activity present or are clearly the dominant activity. Variants of these coma patterns occurs with less stable dominant frequency and with intermixed generalized slow waves. The beta coma patterns usually indicates a high likelihood of recovery from coma whereas the other coma patterns are more often associated with poor outcome. Regardless the dominant frequency of the pattern seen, in the absence of general anesthesia, hypotension, or hypothermia, non-reactivity and lack of spontaneous variability are the most important predictors of poor outcome.

Alpha coma: Unremitting 8- to 13-Hz EEG activity that is unresponsive to eye opening or other stimulation has been termed alpha coma. This activity differs in appearance from alpha rhythm (normal background activity) in its lack of reactivity and its spatial distribution. It is monorhythmic or diffuse, or it may have anterior or posterior accentuation. Only minor fluctuations in amplitude occur, and minimal to no reactivity to external stimulation can be elicited. Two kinds of alpha coma patterns have been distinguished which loosely correspond with different anatomical distributions of pathological involvement. a) The posterior dominant alpha coma pattern shows either no reaction or, rarely, a variable attenuation or increase in amplitude following altering maneuvers. This patterns is usually encountered in patients with brain stem lesions, particularly pontine infarction. It is important to attempt to differentiate patients with similarly located lesions who are in the so-called ‘locked-in syndrome’ from those who are comatose. A posterior dominant alpha background activity that attenuates with alerting in patients with little other evidence of response to stimulation(or in some cases only vertical eye movements)is indicative of the ‘locked-in syndrome’. Such patients may have nearly complete awareness, but are immobilized by an interruption of corticospinal motor pathways.


b) Generalized or predominantly frontal alpha activity without reaction to altering stimuli can be seen in patients with widespread cerebral damage, especially that following cardiac or respiratory arrest, prolonged hypoglycemia or bilateral destruction of midline thalamic nuclei. Variants present with intermixed focal or generalized slow waves or amplitude abnormalities. This alpha pattern is usually seen for up to 5 days after the insult and is then replaced by other abnormalities. The prognosis for complete recovery or survival is generally considered to be poor, particularly in

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cases of anoxic encephalopathy. However, complete recovery has been reported to occur frequently in cases of electrical injury and sedative intoxication uncomplicated by anoxia. Alpha coma patterns in patients who have overdose with sedative medications usually contain asynchronous and bisynchronous delta activity. As noted above, an alpha coma pattern without spontaneous variability or reactivity suggests a much worse prognosis than a reactive alpha pattern or a record with spontaneously changing patterns.

Alpha coma.This 29-year-old man sustained a closed head injury in an automobile accident. The patient was on a respirator, was deeply comatose, and responded to painful stimulation with decerebrate posturing. Later, he "improved" to a neurovegetative state. He could open his eyes and could breathe without the respirator, but he could not follow commands and made no purposeful movements.The EEG at one week contains high-voltage frontally predominant relentless alpha activity that was minimally responsive when stimulated. In this patient, reactivity did not suggest a good prognosis.

Alpha coma: The EEG is dominated by alpha activity, which is non-reactive in a patient in coma of unknown nature

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Alpha coma in a 33 year old man with severe diffuse anoxic encephalopathy following cardiovascular arrest

Theta coma: The theta coma patterns is characterized by generalized monorhythmic activity in the theta frequency range that shows little or no evidence of either spontaneous variability or reactivity to noxious stimulation. The clinical correlates of the theta coma patterns are similar to those of the generalized or frontal dominant alpha coma pattern. Interestingly, it is not unusual for the alpha coma pattern to be replaced by the theta coma pattern. Such transitions indicate a poor prognosis for normal recovery or survival. As with the alpha coma pattern, the theta coma or mixed alpha-theta coma patterns are not as reliable for

predicting a poor outcome as the absence of reactivity and spotaneous variability. Beta coma: The beta coma patterns consists of a generalized, sometimes frontal dominant, pattern of mainly rhythmic beta waveforms. It usually occurs in coma caused by or complicated by barbiturate or benzodiazepine intoxication. Unlike the alpha and theta coma patterns, the beta coma pattern is usually associated with a favorable outcome, because in most cases it is a demonstration of the ability of cortical structures to generate a ‘normal’ response to pharmacological stimulation. It may also occur in acute brainstem lesions .

Beta coma in a 69-year old comatose man who has received high doses of sedative medication


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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 diurnal EEG activity in comatose patients contain features of stage 2 sleep, including prominent spindlelike activity. This EEG pattern usually carries a good prognosis. It is often accompanied by other sleep patterns such as vertex waves or K complexes and appears to represent a sleep stage with impaired

Spindle coma

arousal. As pointed out, it is usually associated with a favorable outcome, but is not as good an electrographic prognostic sign as a reactive beta coma pattern. It is often seen following head trauma but has also been observed in patients recovering from anoxic encephalopathy or encephalitis.

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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.


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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 positive sharp transients, usually of greater than 70 microvolts amplitude. They consist of waveforms with 3 phases, each succeeding phase with longer duration than the one before, that clearly stand out from the background and other slow waves. They are bilateral

and occur in bursts of repetitive waves at 1-3 Hz. The total duration of each triphasic wave complex varies between approximately 0.25 and 0.5 s. The second phase is positive in polarity and usually has the greatest amplitude of the 3 phases. Occasionally a relatively low amplitude positive phase can be seen consistently proceeding the subsequent 3 phases.

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Triphasic waves may appear sporadically or periodically at 0.5-1s intervals. Although the amplitude distribution of triphasic waves varies in individual cases between either anterior or posterior dominance(with some individuals showing both simultaneously or at different times in the same record), in most cases triphasic waves are maximal over the anterior head regions. In instances in which maximal amplitudes occur at FP1 and FP2, triphasic waves may closely resemble vertical eye movement artifact. In longitudinal bipolar recordings triphasic wave phase reversals may occur over the anterior or posterior head regions. In many cases there is an apparent phase lag(time delay) of the second phase when comparing the anterior and posterior derivations of longitudinal bipolar montages. This delay can occur in either the anterior to posterior or posterior to anterior direction and may last more than 100 ms. In ear referential montage the time lag is usually not present. The pathophysiology of triphasic waves is poorly understood. As with other bisynchronous patterns, thalamic pacing probably plays an important role. Unilateral lesions that attenuate thalamically generated rhythms such as sleep spindles may also attenuate triphasic waves. It appears that triphasic wave

Triphasic waves. Note the near continuous pattern of periodic triphasic waveforms, with a large frontal positivity (downgoing) preceded and followed by smaller negative deflections. The wave marked near the middle of the sample illustrates the classic anteriorposterior lag. This pattern is typically unreactive. Note that a triphasic morphology is necessary but not sufficient to classify a pattern as triphasic waves.

generation is enhanced by biochemical and ultrastructural changes associated with aging; well developed triphasic wave patterns rarely occur in individuals less than 20 years of age, are infrequent before age 30, and increase in incidence thereafter. Clinical conditions associated with the triphasic wave pattern are mainly metabolic / toxic disturbances with the most common being hepatic failure, renal failure and anoxia. Sporadic triphasic waves are also not uncommon in elderly individuals with clinically advanced dementing disorders. The triphasic wave pattern has also been associated with other disorders including: hypo- or hypernatremia, hypercalcemia, hypoglycemia, stroke, hypertensive encephalopathy, cerebral abscess, encephalitis, congestive heart failure, septic shock, lithium intoxication and postictal state. The prognosis for patients with triphasic waves is mainly dependent on the degree of background slowing, suppression or reduced reactivity, not the presence or absence of triphasic waves. Many other patterns can have a triphasic morphology. Triphasic waves often are observed in the context of nonconvulsive status epilepticus. Often the decision whether to consider triphasic waves ictal must rely on the clinical information or the response to anticonvulsant treatment.


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.

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4. Abnormal periodic patterns These are defined as stereotyped recurrences of paroxysmal complexes at relatively fixed intervals. They should be present throughout the entire tracing or a major portion of it. The discharges should stand out from the background. They may be composed of slow waves, sharp waves, or sharp and slow wave complexes. Although they may appear to be epileptiform , they are not necessarily associated with a chronic seizure disorder. They often indicate severe encephalopathy and may or may not be associated with clinical seizures. Some of these patterns may suggest a specific diagnosis when taken in conjunction with the clinical picture, and for this reason it is important to recognize them. The discharges may be generalized, lateralized, or even focal. Generalized periodic paroxysmal patterns are seen classically in subacute sclerosing panencephalitis(SSPE), jakob-Creutzfeldt disease (JKD), and herpes simplex encephalitis(HSE). Electroencephalographic tracings with a burstsuppression pattern may also appear periodic, especially when the bursts occur at regular intervals. Lateralized and focal periodic paroxysmal patterns are seen in acute destructive lesions involving one hemisphere. These particular patterns are taken up in turn.

Generalized Periodic Paroxysmal Patterns I. Subacute sclerosing panencephalitis (SSPE) Subacute sclerosing panencephalitis (SSPE) is an inflammatory disease of children and adolescents caused by chronic infection with the measles virus. The characteristic EEG pattern, initially described by Radermecker and Cobb and Hill, consists of highvoltage (300-1500 µV), repetitive, polyphasic sharp and slow wave complexes of 0.5- to 2-second duration that recur every 4-15 seconds. Rarely, the complexes can occur at intervals of 1-5 minutes. The interval between complexes may shorten as the disease progresses. The periodic complexes may be present at any stage of the disease, but they usually are seen during the intermediate stages. Although the form and appearance of the periodic complexes are fairly constant and stereotyped in a single recording, the

shape of the complexes varies in different patients and can change in the same patient at different stages of the disease process. Although the complexes are usually symmetric and synchronous, they may be asymmetric with a time lag between hemispheres or lobes. The EEG background is slow and progressively more disorganized as the disease advances. The stages of sleep eventually become difficult to distinguish. A prominent feature of SSPE is the stereotyped motor jerks or spasms occurring with the periodic complexes. The movements are often described as myoclonic jerks; however, they do not have the momentary lightning-quick nature of true myoclonus; instead, the movements consist of an initial “shock-like abruptness” followed by a momentary arrest of the movement, and then a gradual melting away to the position of the rest. Abnormal movements, cognitive deterioration, and the diagnostic EEG characterize the clinical disease. Stereotypic jerking or other movement abnormalities occur with the periodic complexes. Rarely, the periodic complexes become apparent before the movements manifest. The movements often disappear in sleep, even though the complexes persist. 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 even be asymmetric. As the disease advances, the pattern becomes generalized and synchronous with continuous periodic stereotypic 200- to 400millisecond sharp waves occurring at intervals of 0.51.0 seconds. Myoclonic jerks often occur in association with the sharp waveforms, but the relationship is not constant. Late in the illness and during sleep, myoclonic jerks disappear, despite the persistence of the periodic EEG. The sharp waves typically react to external stimuli. Early in the disease, alerting the patient may elicit the periodic pattern; later, when the periodic pattern is readily apparent, rhythmic photic or other stimuli can "drive" the periodic frequency. Benzodiazepines or barbiturates can temporarily eliminate both myoclonic jerks and periodic patterns. As the disease progresses, there may be a shortening in the interval between the complexes. In the late stages of the disease, there is often a reduction in amplitude and abundance of the electroencephalographic activity, and the recording may become almost isoelectric. In some instances, however, alpha activity may still be present shortly before death.


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.

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Typical generalized periodic discharges in a child with SSPE. The interval between periodic complexes is 5-7 seconds

Another example of typical generalized periodic discharges(SSPE)

II. Creutzfeldt-jacob disease(CJD) CJD is one of the other prion diseases causing a diffuse disorder of the CNS that is characterized by progressive dementia, motor dysfunction, myoclonus, and a characteristic periodic EEG pattern. The earliest EEG changes consist of a disorganization and decrease of normal background activity and the development of progressive slow-wave abnormalities. The slow-wave abnormalities are usually generalized, but at times they occur in a more focal or lateralized fashion. As the disease progresses, diphasic or triphasic slow-wave discharges appear. Initially, these discharges occur in a sporadic or intermittent fashion and may be asymmetric or predominant over region, but eventually they evolve into the characteristric pattern, consisting of generalized and bisynchronous continuous periodic

stereotyped sharp waves, recurring at intervals of 0.5-1 second and having a duration of 200-400 msec. A majority of patients with CJD develops the characteristic EEG pattern by 12 weeks of the disease process. On a few occasions the discharges appear as periodic lateralized epileptiform discharges (PLEDs) before evolving into a bilateral pattern. Myoclonic jerks often occur in association with the periodic sharp waves; however, there is not always a constant relationship between the myoclonic jerks and periodic sharp waves; one can occur without the other. This is particularly true during sleep or late in the course of the disease, when the myoclonic jerks decrease or disappear, but the periodic sharp waves persist. One characteristric feature of the periodic discharges in CJD is the reactivity of the sharp waves to alerting or afferent stimuli. Prior to the time when the periodic pattern has been established or when the


sharp waves occur in a more intermittent or sporadic fashion, alerting the patient or arousing the patient out of sleep may bring out the periodic pattern. Loud noises and certain types of drugs such as diazepam and the barbiturates, can temporarily abolish the periodic sharp waves and myoclonic jerks. As the disease progresses, the interburst interval increases and the amplitude of the periodic sharp waves decreases. In the late stages of the disease, the EEG becomes almost isoelectric, with intermittent bursts of sharp or slow waveforms that finally disappear in the terminal stages of the disease. In Heidenhain,s variant of the disease, where there is a predominant involvement of the occipital head regions, the EEG often shows more focal abnormalities consisting of slowing and periodic

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complexes over the posterior head regions. Some lateralization of the abnormalities may occur in the early stages, but the abnormalities usually become bilateral as the disease progresses. The periodic complexes may become more widespread with a maximal amplitude over the posterior head regions. On occasion CJD may progress rapidly, and the typical EEG abnormalities may evolve over a period of 1-3 weeks, and serial EEGs are helpful in making or confirming the diagnosis. One should be aware, however, that some patients with CJD may not show the typical pattern of periodic sharp waves. The “mad cow” variant of CJD has been described as occurring at a younger age of onset than is typical for CJD and without the typical EEG changes of CJD.

CJD in a patient with encephalopathy and myoclonic jerks

Sporadic CJD in a 69-year-old.

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Periodic pattern in an 81-year old man with CJD. Note the EMG artifacts in anterior leads

The periodic discharges in a patient with CJD

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


III. Burst-suppression pattern The burst-suppression pattern is sometimes called the suppression-burst pattern when the duration of the suppression is greater than the duration of the burst. This may be considered as a periodic pattern, since it consists of periodic bursts of activity with intervals between in which the background activity is markedly attenuated. This subtype of periodic pattern consists of bursts of activity (mixture of sharp and slow waves) periodically interrupted by episodes of suppression (activity <10 µV). Typically, the episodes of suppression are longer (typically 5-10 s) than the bursts of activity (typically 1-3 s). Background suppression is a "nearly flat" EEG, with very low voltage activity (<10 µV) and no reactivity, but the activity is still too large to meet criteria for electrocerebral inactivity (ECI). They are usually widespread and bisynchronous, but they may be limited to one hemisphere or part of it. As previously mentioned, bursts last 1-3s and are separated from each other by low amplitude delta waves or by periods of no activity recognizable at regular gain. Successive bursts may vary in shape. The bursts usually have a polymorphic appearance, but may contain high voltage epileptiform activity in some patients who are placed in barbiturate coma because of

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refractory status epilepticus.The duration of the intervals between the bursts is often fairly regular in a given recording and ranges from 5 to 10s depending on the severity of the cerebral dysfunction. The duration increases as the patient,s condition worsens. Before death or with deepening anesthesia, bursts become shorter, simpler and of lower amplitude; periods of suppression become longer until complete eletrocerebral silence supervenes. The complexes are not responsive to stimuli. Seizure manifestations associated with this pattern are limited to myoclonus. However, a variety of behaviours have been associated with the bursts of activity, including chewing and tonic posturing. Clinical conditions causing burst-suppression patterns include a variety of severe disorders of cerebral structure or function. Structural lesions include acute strokes, postanoxic encephalopathy, head injury and encephalitis. Local burst-suppression patterns can be seen over abnormal cortical areas during surgical anesthesia. Commonly reversible disorders causing this pattern include deep anesthesia and coma due to barbiturates and other CNS depressant drugs, hypothermia, and Reye,s syndrome. The association of myoclonus, burst-suppression patterns and postanoxic coma suggests a very poor prognosis for survival.

Burst-suppression pattern. Suppression periods are characterized by activity less than 10 mV.

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Burst-suppression pattern recorded in the EEG of a 70- year-old man after a cardiac arrest from which he was resuscitated.

Burst suppression, in a 3-year-old boy with severe diffuse anoxic encephalopathy


Burst suppression from anoxic encephalopathy. This 54-year-old patient was seen 5 days after a coronary artery bypass complicated by a prolonged hypotension causing diffuse cerebral anoxia. The patient is deeply comatose and unresponsive to any stimulation. He has occasional episodes of rapid eye blinking. The EEG has high-voltage bursts of spikes and polyspikes lasting for less than 1 sec followed by low-voltage epochs. This type of abnormality is usually associated with anoxic encephalopathy. It carries a very poor prognosis

Burst suppression pattern in right hemisphere in a 5y old patient with refractory epilepsy

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Burst-suppression pattern after anoxic injury in a 76 year old man.

IV. Periodic Lateralized Epileptiform Discharges (PLEDs) Periodic lateralized epileptiform discharges (PLEDs) are EEG abnormalities consisting of repetitive spike or sharp wave discharges, which are focal or lateralized over one hemisphere, recur at intervals of 0.5-5 seconds, and continue through most of the duration of the EEG study. They are seen most frequently in the setting of acute unilateral lesions such as cerebral infarctions. They also may occur in other cerebral diseases, such as encephalitis or tumors(or in the setting of chronic lesions or long-standing epileptic disorders. PLEDs are usually self-limited and resolve after the acute phase of a cerebral insult. Rarely, they may persist on a chronic basis. Seizures often occur when PLEDs are seen on the EEG, but clinical and electrographic seizure manifestations typically differ from the baseline (PLEDs) condition. The seizures were either partial or generalized and the partial seizures were always contralateral to the PLEDs.Certain paroxysmal neurological symptoms,

such as epilepsia partialis continua or transient confusional states, may be associated with PLEDs. For clinical purposes the PLED pattern is generally regarded as a highly epileptogenic interictal pattern. There are case reports of PLED patterns persisting for years. Approximately 1% of all ischemic hemispheric non-lacunar infarctions are accompanied by PLEDs. More recently, PLEDs have been reported in mitochondrial encephalopathies(MERRF, MELAS) and in Jakob-Creutzfeldt disease. Bilateral independent PLEDs (BIPLEDs) are periodic complexes over both hemispheres. BIPLEDS are not synchronous and may differ in morphology and site of maximal expression on each side. This is an uncommon EEG finding. In a series of 18 patients, the most common etiologies were anoxic brain injury (28%) and CNS infection (28%). While BIPLEDs have been associated with herpes simplex encephalitis, the pattern can occur in other CNS infections as well. The clinical correlates of BIPLEDs differ somewhat from those of PLEDs. With BIPLEDs, incidence of coma is higher compared to PLEDs (72% vs 24%), mortality rate is higher (61% vs 29%), and likelihood of focal seizures or focal neurological deficits is lower.


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Focal EEG waveform abnormalities. This EEG demonstrates periodic lateralized epileptiform discharges (PLEDs) in the left hemisphere in a 54year-old patient with a history of left temporal ischemic stroke.

Examples of PLEDs seen from the left hemisphere. There is a slight reflection of PLEDs in the right hemisphere, which is not unusual. The patient developed confusion, aphasia, and witnessed focal motor seizure activity of the right arm and face, 10 days after a left carotid endarterectomy and was found to have a hyperperfusion syndrome.

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PLEDs pattern in right hemisphere

Right temporal PLEDs in a patient with herpes encephalitis and nonconvulsive SE recorded in the ICU.


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Left temporal PLEDs in a patient with left temporal lobe epilepsy immediately following serial complex partial seizure.

Left temporal PLEDs in a patient with an acute occipital ischemic infarction.

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PLED in right hemisphere in a patient with Alzheimer,s disease

BiPLEDs in a 36-year-old man with severe diffuse anoxic encephalopathy after cardiovascular arrest.

Chapter 12

Reading and Reporting EEGs

To read a new language , needles to say, one needs first to learn the alphabet. The alphabet of the EEG consists of the various frequencies and waveforms that comprise the tracing. Just as the letters of the alphabet are combined in different permutations and combinations to form words and then sentences, so the EEG tracings are made up of combinations of waveforms of different frequencies and morphology. To carry the analogy further, it is not enough to be able just to read the words and sentences; one needs to understand quickly the meaning of what is written. In the same way, EEG reading involves analyzing the waveforms and deducing their significance. With experience, one uses a speed reading technique in which a whole page is rapidly scanned for evidence of normal and abnormal phenomena. How successfully this is done depends to a large extent on developing pattern-recognition skills.

Learning to Read How does one learn to read EEG? Like any other branch of medicine this involves a continuous process of learning for many months or sometimes even years. Often the intial learning is accomplished through observing an experienced electroencephalographer read EEGs. The next step involves reading under supervision; having seen how an experienced electroencephalographer interprets a record, and having gathered essential information regarding normal and abnormal patterns, the trainee interprets records in the precence of his or her instructor. Ideally, the instructor should regularly quiz the trainee on the various waveforms and artifacts in the tracings, and the trainee should complement this by seeking answers to the questions. Without at least an elementary knowledge of the basic principles of electricity, neurophysiology,

and the technique of recording, it is impossible to learn to read EEGs properly. One needs to know what calibration means, hoe the various frequency filters work, how various artifacts are identified, and how neurologic disorders produce alterations in electrical activity of the brain.

Description of the EEG The report should describe the essential normal and abnormal patterns appearing under the various recording conditions so that a person with some knowledge of EEG can imagine the findings on which diagnosis and interpretation are based. Sufficient detail should be given to enable the reader of a later EEG to estimate whether the major features of the two recordings are similar or different. The report should not be exhaustive in describing normal detail but 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 glossary of the International Federation of Societies for EEG and Clinical Neurophysiology. Judgments like ‘good’ and ‘ poor’ should be used only sparingly and only to characterize the overall composition of a record, but not to rate individual rhythm: persons not familiar with the EEG can not know that ‘poor’ driving has no different clinical significance than has ‘good’ or even ‘excellent’ driving. On the other hand, patterns should be described by indicating the frequency, amplitude, and distribution of the component waves. Wave shape, rhythmicity, symmetry, synchrony, persistence, reactivity, and periodicity, may be important for the description of abnormal patterns. Because the frequency of a rhythm often varies, it is usually indicated in terms of a frequency range or band of a few hertz in width rather than in terms of a single frequency. In most instances, it is not sufficient to use only the wide bands of delta,

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theta, alpha, and beta frequency to describe the frequencies of waves in a record; the frequency of alpha and beta rhythms and of theta and delta waves observed in a recording should be specified in narrower bands. Amplitude may be reported in absolute or relative measurements, preferably with the montage specified. Absolute units must be used in the diagnosis of electrocerebral silence in which no cerebral activity of over 2µV should be present. Even if activity of very low amplitude over 2µV is found in these cases, the amplitude should be specified to indicate the severity of the abnormality and to provide a basis for comparison with subsequent recordings. In most other instances, it is sufficient to characterize amplitude as low, medium, or high. To avoid omitting important features in the report, one should adhere to a standard sequence of reporting. Although many electroencephalographers do not include a summary of the clinical history, it is advisable to briefly state the referring complaint and any other information that is immediately relevant to the interpretation of the recording under a separate heading such as "history". This provides the referring physician with feedback as to the electroencephalographers, understaning of the referring complaint, facilitates future review of the EEG report, and helps in the interpretations of subsequent EEGs. It is also an important exercise for those who are training to become electroencephalographers. The general level of consciousness of the patient, other behavioral abnormalities(such as lack of cooperation, or persistent movement causing excessive artifact), the equipment used(e.g., digital or analog), the recording environment( e.g., outpatient, bedside, ICU, patient ventilator dependent), and whether or not sedation was given(e.g., chloral hydrate) should either be stated under a separate heading, such as "conditions of the recording" , or in the opening of the general body of the descriptive report.

The resting record 1. Description of normal background. Alpha, beta, mu and other rhythms and patterns, if present, are described in terms of their frequency range, relative amplitude and distribution. Wave shape, rhythmicity, symmetry, distribution, persistence and reactivity should be mentioned if they are abnormal. Excessive beta activity and unilateral blocking of the alpha rhythm must be reported. 2. Description of abnormal patterns. Epileptiform activity is characterized by its shape, amplitude, repetition rate, persistence, distribution, synchrony, symmetry, relationship between focal and generalized discharges and any other feature of possible clinical significance including the

association with behavioral seizure manifestations. Slow waves are described in terms of frequency, amplitude, shape, rhythmicity, regularity, persistence, distribution, symmetry, synchrony, and any other parameter of clinical importance. If more than one type of slow wave is present, the specifications for each type must be given. Abnormal generalized asynchronous slow waves must be distinguished by amplitude, frequency, distribution and persistence from the range of asynchronous slow waves normally seen at the age of the patient. Asymmetries and generalized changes of amplitude are usually noted when describing the normal background. Deviations from normal must be described by indicating the specific features which make a pattern abnormal, for instance the appearance of alpha activity which has a frontal maximum, lacks reactivity and is associated with coma. Hyperventilation. Normal responses can be described in one short sentence, for example ‘Hyperventilation produced no change’ or ‘Hyperventilation did not elicit any abnormalities.’ The performance of the patient may be mentioned. Symptoms induced by hyperventilation should be reported, particularly if the symptoms resemble episodic symptoms for which the patient is examined. Changes in the patient,s behavior such as jerking movements or loss of responsiveness, must be reported. Abnormal responses such as an asymmetrical buildup, enhancement of abnormalities of the resting record and induction of new abnormalities must be described in detail. Photic stimulation. Normal responses can be described briefly by stating ‘Photic stimulation did not elicit a driving response’ or ‘Photic stimulation elicited a symmetric driving response.’ Abnormal responses such as significant asymmetries and photoparoxymal responses should be described. Sleep. It is helpful to either briefly describe the major EEG findings during sleep or simply list the deepest stage of sleep that occurred. If the patient referred for the evaluation of a possible seizure disorder and epileptiform activity did not occur, then the depth and duration of sleep will be of particular importance. The report should also indicate whether sleep was induced with a sedative or occurred spontaneously. Abnormalities during sleep should be described in detail. Most important is the appearance of epileptiform activity.

Reading and Reporting EEGs

The report of an EEG The report of an EEG should consist of three principal parts: A. Introduction B. Description of the record, and C. Interpretation, including (a) impression regarding its normality or degree of abnormality and (b) correlation of the EEG findings with the clinical picture. A . Introduction. The introduction should start with a statement of the kind of preparation the patient had, if any, for the recording session. The initial sentence should state whether the patient received any medication or other preparation, such as sleep deprivation, as well as the patient,s state of consciousness at the onset of the record. If the patient was fasting, this should be stated. If the printed form used for the report does not provide a space for the regular medication the patient is receiving , as distinguished from medication given specifically for the recording, any medication that could influence the EEG should be included in the electroencephalographer,s report. If the number of electrodes used is not the standard 21 of the 10-20 system or if monitoring of other physiologic parameters is used, this should be stated in the introduction. B. Description. The description of the EEG should include all the characteristic of the record, both normal and abnormal, presented in an objective way, avoiding, as much as possible, judgment about their significance. The aim is to produce a complete and objective report that would allow another electroencephalographer to arrive at a conclusion concerning the normality or degree of abnormality of the record from the written report, without the benefit of looking at the EEG. This conclusion could conceivably be different from that of the original interpreter, since it is by necessity a subjective one. The description should start with the background activity, beginning with the dominant activity, its frequency, quantity(persistent, intermittent), location, amplitude, symmetry or asymmetry, and whether it is rhythmic or irregular. The frequency should be given preferably in hertz or cycles per second. For the purpose of standardizing the report, while recognizing that any decision on this point must be arbitrary, it is recommended that the amplitude of this activity be determined in derivations employing adjacent scalp electrodes placed according to the 10-20 system. It is desirable but not mandatory that the estimated mean amplitude be given in micrivolts. This will obviate the need for defining terms such as ‘low’, ‘medium’, and high. Enumeration of nondominant activities with their frequency, quantity, amplitude, location,

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symmetry or asymmetry, and rhythmicity or lack of it should follow, using the same units as for the dominant frequency. Responses to opening and closing eyes as well as to purposeful movement of the extremities when appropriate, should then be described. The responses should be described as symmetric or asymmetric, complete or incomplete , sustained or unsustained. Abnormal records, infants records, or recordes limited to sleep may not have clearly dominant frequencies. In those cases, the different activities with their amplitude, frequency, etc., should be described, in any order. When the record shows a marked interhemispheric asymmetry, the characteristics of each hemisphere should be described separately(i.e., dominant, nondominant frequency, etc., of one hemisphere first, followed by those of the other). The description of the background activity should be followed by description of the abnormalities that do not form part of this background activity. This should include a description of the type( spikes, sharp waves, slow waves), distribution (diffuse or focal), topography or location, symmetry, synchrony (intra- and interhemispheric), amplitude, timing (continuous, intermittent, episodic, or paroxysmal), and quantity of the abnormal patterns. Quantity has to be expressed in a subjective fashion, since in clinical, unaided interpretation of the EEG , no exact quantities or ratios can be given. When the abnormality is episodic, attention should be given to the presence or absence of periodicity between episodes and to the rhythmicity or irregularity of the pattern within each episode. The range of duration of the episodes should be given. In the description of activation procedures, a statement should be included pertaining to their quality( e.g., good, fair, or poor hyperventilation, duration of sleep, and stage attained). The type of photic stimulation used(i.e., stepwise) should be stated and the range of frequencies given. Effects of hyperventilation and photic stimulation should be described, including normal and abnormal responses. If hyperventilation or photic stimulation are not done, the reason for this omission should be given. If referring clinicians know that these procedures are used routinely, they may expect results even if they have not been specifically requested. There is no point in including in the description the absence of certain characteristics, except for the lack of normal features, such as low- voltage fast frequencies, sleep spindles, etc. Phrases such as ‘no focal abnormality’ or ‘ no epileptiform abnormality’ have a place in the impression when the clinician has asked for it either explicitly or implicitly in the request form. They have no place in the description. Artifacts should be mentioned only when they are questionable and could represent cerebral activity, when they are unusual or excessive (eye movements, muscle) and interfere with the interpretation of the record, or when they may provide valuable diagnostic information(e.g., myokymia, nystagmus, etc).

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C. Interpretation. (a) Impression. The impression is the interpreter,s subjective statement about the normality or abnormality of the record. The description of the record is directed primarily to the electroencephalographer who writes it for review at a later date, or to another expert, and should be detailed and objective. The impression, on the other hand, is primarily written for the referring clinician and should , therefore, be as succinct as possible. Most clinicians know that their information will not significantly increase by reading the detailed description and hence limit themselves to reading the impression. If this is too long and seemingly irrelevant to the clinical picture, the clinician will lose interest and the report of the record becomes less useful. If the record is considered abnormal, it is desirable to grade the abnormality in order to facilitate comparison between successive records for the person who receives the report. Since this part of the report is largely subjective, the grading will vary from laboratory to laboratory, but the different grades should be properly defined and the definitions consistently adhered to in any given laboratory. After the statement regarding normality or degree of abnormality of the record, the reasons upon which the conclusion is based should be briefly listed. When dealing with several types of abnormal features, the list should be limited to the two or three main ones; the most characteristic of the record. If all the abnormalities are enumerated again in the impression, the more important ones become diluted and emphasis is lost. If previous EEGs are available , comparison with previous tracings should be included. (b) Clinical correlation. The clinical correlation should be an attempt to explain how the EEG findings fit(or do not fit)the total clinical picture. This explanation should vary , depending on whom it is addressed to. More careful wording is necessary if the recipient is not versed in EEG or neurology. If an EEG is abnormal it is indicative of cerebral dysfunction, since EEG is a manifestation of cerebral function. However, the phrase "cerebral dysfunction" may sound too strong to some and it should be used only when the abnormality is more than mild and when enough clinical information is available to make the statement realistic within the clinical context. Otherwise , a sentence like, "the record indicates minor irregularities in cerebral dysfunction, " may be appropriate. Certain types of EEG patterns are suggestive of more or less specific clinical entities, a delta focus may suggest a structural lesion in the proper clinical context; certain types of spikes or sharp waves suggest potential epileptogenesis. If the EEG abnormality fits the clinical information containing the diagnosis or the

suspicion of the presence of a given condition, it may be stated that the EEG finding is consistent with or supportive of the diagnosis. In EEG reports, the term "compatible with" is frequently found. Strictly speaking, any EEG is compatible with practically any clinical picture. Therefore, the term is not helpful and should not be used. In cases in which the EEG is strongly suggestive of a certain condition that is not mentioned in the clinical history, it is prudent to mention the fact that such EEG abnormalities are frequently found in association with the clinical condition but are not necessarily indicative of it. An EEG can be said to be diagnostic of a certain condition only in the rare cases in which there is a clinical manifestation present at the time of the recording of an EEG and the record shows an electrical abnormality known to the generally associated with the specific clinical manifestation. Such a case would be one in which a patient presents a typical absence concomitant with a bilaterally synchronous 3/s spike-and-wave burst. In situations in which the diagnostic clinical impression seems at odds with the EEG findings, some possible reasons for the apparent discrepancy should be offered in the EEG report. These reasons should be presented cautiously, trying to avoid any impression of criticism of the clinical diagnosis, or to appear apologetic for an apparent failure of the EEG as a supplemental diagnostic test. If an EEG is abnormal, but the abnormal features could be produced, at least in part by medication or other therapeutic interventions such as recent electroconvulsive treatment, it should be so stated. Under no circumstances should the electroencephalographer suggest changes in medication or other clinical approaches. However, the clinical correlation statement could be followed by a recommendation pertaining to further EEGs with different added procedures, e.g., "in view of the clinical picture a sleep record could be useful", or " since the record was taken shortly after a clinical seizure, a follow-up EEG may be helpful in determining whether the slow wave focus present in this record is of permanent or of only transitory nature". A normal record does not, in general, require further explanation. However, when the clinical information suggests a serious question between two conditions, such as hysteria and epilepsy, a statement should be added that might prevent the clinician from jumping to a wrong conclusion. Such a statement could be: " a normal record does not rule out a convulsive disorder. If the clinical picture warrants , a recording with (some type of activation) may be helpful".

References

1. Tatum, William.O: Handbook of EEG interpretation, Demos inc, USA, 2008 2. Neidermyer E, Lopes da Silva: Electroencephalography, basic principles,clinical applications and related fields, 3th edition, U&S inc, 1999 3. Bassel Abou-Khalil, Karl E, Misulis: Atlas of EEG and seizure semiology, Elsevier inc,2006 4. Aminoff, Michael J: Electrodiagnosis in clinical neurology, 4th edition, Churchill livingstone, USA, 1999 5. Wyllie, Elaine: The treatment of epilepsy, 4th edition, Lippincott Williams & Wilkins, USA, 2006

6. Karl E Misulis, Thomas C. Head: Essentials of clinical neurophysiology, Butterworth Heinemann, USA,2002 7. John S. Ebersole, Timothy A. pedley: current practice of clinical electroencephalography, 3th edition, Lippincott Williams & Wilkins, USA, 2003 8. Hans O. luders, Soheyl Noachtar: Atlas and classification of electroencephalography, W.B.Saunders, 2001 9. F.H.Duffy, V.G.Iyer, W.W Surwillo, Clinical electroencephalography and Topographic brain mapping, springer-verlag,USA, 1989 10. Selim R Benbadis, EEG atlas, www.emedicine.com, 2006

INDEX

EMG artifact, 39-41, 39f-41f photomyogenic response, 41 eye movement, 44-49, 44f-49f bell's phenomen, 44, 45f glossokinetic artifact, 42, 42f-43f chewing artifact, 43f pulse artifact, 51, 51f skin artifact, 52, 52f sweat artifact, 52, 52f

A - Abnormal EEG patterns, 83-178 - Abnormal sleep patterns, 145-146f sleep spindle asymmetry, 145-146f V wave asymmetry, 145 - Absence Epilepsy, 97-101, 99f- 101f photic stimulation, 41, 75, 78, 81, 98, 102, 108, 112, 180 -Acquired Epileptic Aphasia, 125-126, 126f clinical feature of, 125 EEG finding in, 125-126, 126f - Activation during sleep, 82 - Activation procedures in the EEG, 75-82, 76f-82f hyperventilation, 75-78, 76f-77f abnormal response, 75 photic stimulation, 75 response to, 78, 78f-82f photic driving response, 78-79, 79f photic evoked potential, 78 photoepileptiform response, 81 photomyogenic response, 79-80, 79f-80f photomyoclonic response, 79-80, 79f-80f photoparoxysmal response, 81-82, 81f-82f Visual evoked response, 78 sleep, 82 - Alpha coma, 158-159, 159f-160f - Alpha dropout, 58-60, 60f - Alpha rhythm (alpha activation), 23-29, 24f-29f abnormal, 139-140, 142f-143f characteristics of, 29 in breif, 29 reactivity of, 140 - Alpha variant pattern, 26-29, 26f-29f alpha squeak, 26 fast alpha variant, 28, 28f paradoxical alpha response, 29 slow alpha variant, 26-27, 26f-27f temporal alpha, 29 - Artifacts, 39-58, 39f-57f non physiologic artifact, 52-57, 52f-57f alternating current artifacts (60 Hz), 55, 55f electrodes and leads, 52-55, 52f-55f electrode pop artifact, 53, 53f interavenous artifact, 57, 57f movement artifact, 56, 56f physiologic artifacts, 39-52, 39f- 52f ECG artifact, 51f, 49-51

B - Bects, see benign epilepsy of childhood with central-midtemporal spike, 102 - Benign epilepsy of childhood with centrotemporal spike (Bects), clinical feature of, 102 EEG finding in, 102, 103f-107f - Benign epileptiform transient of sleep (Bets), 127, 127f-129f - Benign partial epilepsy of childhood with occipital paroxysm (Bpeop), activation during sleep, 82 clinical feature of, 107-108 EEG finding in, 108, 108f-109f familial occurrence of, 107 - Beta coma, 160, 160f-161f - Beta rhythm (Beta activity), 29-34, 30f-34f, 140-141 Excess Beta activity, 31, 31f focal attenuation of, 140 focal enhancement of, 141, 143f in brief, 32 - Breach rhythm, 36-37, 36f-37f - Burst suppression pattern, 171, 145f, 171f-174f

C - Chewing artifact, 43f - Childhood absence epilepsy, 97-101 clinical feature of, 97 EEG finding, 98, 99f-101f OIRDA, 98

186


- Complex partial seizure, activation during sleep, 82 - Continous spike and wave discharge during slow sleep, 125 - Craniotomy EEG of, 36-37 - Creutzfeldt- Jakob disease, 168-169, 169f-170f

D - Delta activity, polymorphic, 148, 154-155, 154f-150f, 156f-158f rhythmic, intermittent, 147 - Derivations of EEG, 10 - Excess Beta activity, 31, 86 - Drip artifact of EEG, 57, 57f

E - ECG artifact, 49-51, 51f - EEG, see under electroencephalogram - EEG, activation procedures of, 75-82, 76f-82f artifacts, 39-58, 39f-57f brain maps, 6-10, 6f-10f derivation in, 10 method of derivation, 13-14, 14f electrode placement in, 3-11, 4f-11f filters in, 3-4, 4f montage in, 14, 14f - Normal in adults, 23-39, 24f-39f physiological basis of, vii polarity conventions in, 11 - Principles in recording of, 1-4 instrument setting, 1 calibration, 3, 3f EEG filtering, 3, 4f paper speed, 3 sensitivity, 1 - Reading and report of, 179-182 - Techniques of EEG recording, 5-14, 6f-14f -Electrical status epilepticus during slow sleep, 125 - Electrode placements, 5-11, 6f-11f special electrodes, 9-10, 10f - Electrode popping, 53m 53f - EMG artifact, 39-41, 39f-41f - Encephalopathic pattern, 158-165 alpha coma, 158-159, 159f-160f beta coma, 160, 160f-161f spindle coma, 161, 161f-163f theta coma, 160 triphasic waves, 163-164, 164f-165f, 141 - Enhancement beta activity, 61 - Epilepsy, 85, 115 medication stop, 95 recurrence risk, 95 - Epilepsy syndrome, benign epilepsy of childhood with centrotemporal spiked, 102-107, 103f-107f

benign partial epilepsy of childhood with occiprtal paroxysm(BPEOP), 107-109, 108f-109f childhood absence epilepsy, 97-101, 99f-101f electrical status epilepticus during slow sleep, 125 epilepsy with generalized tonic-clonic seizure on awaking, 117 juvenile absence epilepsy, 97-101, 99f-101f juvenile myoclonic epilepsy, 112-116, 113f-116f landau-kleffner syndrome, 125-126, 126f lennox-gastaut syndrome,120-124, 122f-124f symptomatic focal epilepsy, 109-111, 110f west syndrome, 117-120, 118f-120f - Epilepsy with generalized tonic-clonic seizure on awaking, 117 - Epileptic discharge, 85-95 - Epileptiform normal variant, 127-138 mid line theta rhythm, 138 psychomotor variants, 134-135 rhythmic mid temporal theta of drowsiness, 134-135 small sharp spike, 127-129 subclinical rhythmic EEG discharge of adults (SREDA), 135-137 wicket spike, 129-131 6HZ spike and wave, 132, 134 14-and6-HZ positive bursts, 132-134 - Eye movement artifact, 44-49, 44f-49f eye blink, 45f eye closure, 45, 45f eye flutter, 46f-47f eye opening, 47, 47f lateral eye movement, 48, 48f-49f

F - FIRDA, see also frontal intermittent rhythmic delta activity (FIRDA) -FIRDA, 147, 149f-152f, 75 - Focal epilepsy, 109-111, 110f - Frontal lobe epilepsy, 110 clinical feature of, 110-111 EEG finding in, 111

G - Generalize periodic pattern, 166-170 SSPE, 166, 167f-168f CJD, 168-169, 169f-170f - Glossokinetic artifact, 42, 42f-43f

H - Hypnagogic hypersynchrony, 65, 65f - Hyperventilation, 75-78, 76f-77f - Hypsarrhythmia, 117, 118f-120f

index

I

M

- IED, see under interictal epileptiform discharges, 82 -Impedance artifact, 55 -Interictal epileptiform discharges, 85-94, 82 multiple spikes, 91, 91f-92f poly spikes, 91, 91f-92f sharp wave, 88, 89f-91f sharp and wave complex(swc), 92, 92f spike and wave complex(swc), 92, 92f-95f spike discharges, 86-88, 86f-88f - Intermittent rhythmic delta activity(IRDA), 147-154 FIRDA, 147, 149f-152f OIRDA, 148, 150f TIRDA, 148, 152f, 154f - Intermittent slow activity, focal, 148, 152f-154f - Intermitten slow activity,Generalize, 147-148, 149f-152f - International 10-20 system placement, 6-8, 6f-8f - Isoelectvic EEG, 141 - IV artifact, 57, 57f

-Medial temporal lobe epilepsy (MTLE), 109-110 - Methods of derivation, 10 - Midline theta rhythm, 138 - Montages of EEG, 14, 14f - Multiple spike, 91, 91f-92f - Mu rhythm, 32-34, 32f-34f characteristics of, 34 in brief, 34

187

N - Non physiologic artifacts, 52-57, 52f-57f - Normal EEG in adult, 23-39, 24f-39f - Normal sleep EEG, 58-74, 59f-74f - Non REM, 58

O J - Juvenile absence epilepsy, 97-101 clinical feature of, 97 EEG finding, 98, 99f-101f - Juvenile myoclonic epilepsy, 112-116 activation during sleep, 82 clinical feature of, 112 EEG finding in, 112-113, 113f-116f ictal, 112 interictal, 112

K - K complex, 68-70, 68f-70f

L - Lambda wave, 35, 35f - Landau-kleffner syndrome, 125-126 clinical feacture of, 125 EEG finding in, 125-126, 126f - Lateral eye movement artifact, 49f - Lateral rectus spike, 49f - Lateral temporal lobe epilepsy, 110 , 110f - Lennox- Gastaut syndrome, 120-124 clinical feature of, 120-121 EEG findin in, 121, 122f-124f inter ictal EEG, 121 ictal EEG, 121

- OIRDA, see under occipital intermitten rhythmic delta activity, -OIRDA, 148, 150f

P - Periodic patterern, 166-178 burst-suppression pattern, 121,145f, 171f-174f generalize periodic pattern, 166-170 SSPE, 166, 167f-168f CJD, 168-169, 169-170f - Periodic lateralized epileptiform discharge (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 photoepileptiform response, 81 photo myogenic response, 79-80, 79f-80f photo paroxysmal response, 80-81, 80f-81f visual evoked potential, 78 visual evoked response, 78 technique, 78 - Photomyoclonic response, 79-80, 79f-80f - Physiologic artifact, 39-52, 39f-52f - Physiologic basis of EEG, vii - Polarity convetions of EEG, 11 - Polymorphic delta activity, 148, 154-155, 153f-158f - Polyspike, 91-91f-92f - Positive occipital sharp transients of sleep, 61-62, 61f-62f - POST, 61-62, 61f-62f - Principles in recording of EEG, 1-4 - Psychomotor variant pattern, 134, 134f-135f - Pulse artifact, 51, 51f

188


R

T

- Reading and report EEG, 179-182 description of, 179-180 report, 181-182 - Referential technique, 14, 14f -REM sleep, 72-74, 74f - Rhythmic mid temporal theta of drowsiness, 134-135 - Rolandic epilepsy, 102-107 clinical feature of, 102 EEG finding in, 102, 103f-107f

- Technique of EEG recording, 5-14, 6f-14f - Temporal intermittent rhythmic delta activity (TIRDA), 148, 152f, 154f - Temporal lobe epilepsy, 109-110, 110f - TIRDA, see under temporal intermittent rhythmic delta activity, 72 - Theta coma, 160 - Theta rhythm, 34-35, 34f - Triphasic waves, 163-164, 164f-165f

S

V

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

- Vertex waves(V waves), 62-64, 62f-64f - Visual evoked response, 78

W - West syndrome clinical feature of, 117 EEG finding in, 117, 118f-120f - Wicket rhythm, 32 - Wicket spike, 129, 129f-131f

Z - Zygomatic electrode, 10 - 6 HZ spike and wave, 132-133, 133f-134f -14-and 6 HZ positive bursts, 131, 131f-132f

Review of Clinical EEG

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