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2C H A P T E R L. John Greenfield, Jr., MD, PhD Approaching the EEG: An Introduction to Visual Analysis

The Approach to Reading Your fi rst exposure to reading EEGs was probably a daunting experience. How should you approach the complex patterns of waves? It may have been even more discouraging to see your attending, an experienced EEG reader, rapidly page through a study, spending a sec- ond or less on pages that took you minutes to analyze. The ability to read EEGs correctly and with confi dence comes with experience, as you learn an orderly approach to reading and develop skills of pattern recognition that make your examination more effi cient. The goal of this book is to provide the knowledge base necessary to understand what you are looking at and to help you develop the analytical and pattern recognition skills that will make you a competent EEG reader. You will need to learn how not to miss pathological waveforms (underreading) without agonizing over every defl ection of the pen and also not to misclas- sify normal waveforms, variants, or artifacts as pathological (overreading), which can cause problems as well.

So, how do we begin? The goal of reading EEGs is to identify abnormal electrical activ- ity and determine its signifi cance. But the only way to know what is abnormal is to begin by identifying what is normal. And before learning what is normal, we fi rst have to learn how to look at an EEG. This may sound trivial, but it is a critical skill that most readers develop over months to years of experience. While there is no substitute for experience, the techniques experienced readers use to analyze EEGs effi ciently can be broken down into a few simple procedures. First, you need to know how to analyze waveforms visually and break them down into their component parts. The next step is to learn what patterns to look for in patients of different ages and different states of wakefulness and sleep. Finally, you need to “tune” your eyes to recognize abnormalities in those patterns, to determine whether those abnormalities were generated in the brain rather than extraneous sources (artifacts), and to interpret the sig- nifi cance of the abnormal fi ndings.

Visual Analysis of EEG Waveforms When you begin to read EEG recordings, you will need to look for characteristics of the activity that will allow you to describe it in precise terms. Even if you do not completely understand the signifi cance of the activity you see, being able to describe it in a consistent fashion may help you (and others) to interpret your fi ndings later, perhaps when more clinical information is available. EEG activity is described in the following terms: frequency, amplitude, distribution or location, symmetry, synchrony, reactivity, morphology, rhythmicity, and regulation. We will defi ne each of these in detail below.

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39CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

Frequency Frequency is defi ned as the number of complete waveforms that occur per second, expressed as cycles per second (cps) or Hz. If brain waves were composed of uniform single frequencies and amplitudes, the task of interpreting cerebral activity would be much simpler. More commonly, though, each channel of EEG activity is the sum of multiple frequencies of different ampli- tudes. One of the fi rst skills you need to learn is how to identify and categorize the frequencies in a given waveform.

Frequencies recorded in standard EEG recordings are divided into four standard frequency ranges or “bands,” as noted in Table 2-1 and shown in Figure 2-1.

In Figure 2-1A, we can determine the frequency by counting the number of waves between the 1-s vertical bars. But the frequencies represented in an EEG waveform are not always simple. Figure 2-1B shows several examples of more complex waveforms that can be seen when two or more frequencies occur at the same time at the same electrodes. If the frequen- cies are widely separated, it may be possible to discern the component frequencies underly- ing the combined waveform, but it becomes more challenging when multiple frequencies are represented, particularly if they are close together. The bottom trace in Figure 2-1B is an

Band Frequency Range Usual Location

Alpha 8 to <13 Hz Occipital Beta >13 to 25 Hz Frontal, central Theta 4 to <8 Hz Central, diffuse Delta <4 Hz Focal or diffuse

EEG Frequency RangesTA B L E 2 - 1

(15 Hz)

(10 Hz)

(5 Hz)

(2.5 Hz)

5 + 15

5 + 2.5

2.5 + 15

10 + 2.5

Sum/4

A

B

FIGURE 2-1. A: Sine waves demonstrating sample frequencies in the beta, alpha, theta, and delta ranges. Vertical bars mark 1-s divisions. B: Mixtures of frequencies can produce complex waveforms. The fi rst four traces show the sums of two sine waves: 5 Hz + 15 Hz, 5 Hz + 2.5 Hz, 2.5 Hz + 15 Hz, and 10 Hz + 2.5 Hz. Widely sepa- rated frequency components (as in trace 3) are more easily separated by eye. Trace 5 shows the sum of all four frequencies divided by four, which produces a complex waveform in which the indi- vidual components are very diffi cult to resolve.

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40 Reading EEGs

average of 2.5, 5, 10, and 15 Hz, in which individual frequencies are diffi cult to distinguish. Moreover, frequency components do not remain constant but may shift from moment to moment. Complex mixtures of frequencies may not be as easily susceptible to visual frequency analysis, but you should train your eye to recognize the components that may be lurking in EEG waveforms.

Amplitude Amplitude is the size of the waveforms, measured in microvolts (μV). There are minor com- plexities here as well. Amplitude is often measured “peak to peak,” i.e., from the highest to the lowest point of the sinusoidal wave. However, this can be misleading if there is a drift of the waveform due to slow oscillations (e.g., alpha waves superimposed on delta waves, as in Fig. 2-1B). The different frequency components may have different amplitudes associated with them. The breakdown of amplitudes for different frequencies can be done by sorting out the waveforms into the sum of sine waves of different frequencies by Fourier analysis (often done by computer using fast Fourier transform or FFT), which produces a graph of power versus frequency (recall from Chapter 1 that power is voltage times current and is thus proportional to the amplitude of the signal for each frequency component). In reporting the amplitude of the activity, you may choose to describe the overall amplitude of all components or the amplitude of each frequency component. Amplitude can be reported as a numerical range (e.g., 20 to 40 μV) or in descriptive terms as low (0 to 25 μV), moderate (25 to 75 μV), or high (>75 μV) amplitude. Some pathological conditions are associated with enormous amplitudes of hundreds of microvolts, such as hypsarrhythmia, a chaotic pattern seen in severe infantile epilepsies.

Distribution or Location In the previous chapter, we discussed the basics of waveform localization by mapping the electrical potential fi eld. Recall that in a bipolar montage, the derivation(s) where a reversal of polarity occurs is likely the source of the fi eld, while in a referential montage, the highest amplitude at the exploring electrode is the likely source, unless the reference is involved in (contaminated by) the potential, in which case all bets are off. These principles are used to determine the location of a specifi c type of activity. While some EEG signals can be precisely localized (e.g., some epileptiform activity can be localized to a single electrode), other activities may be regional (e.g., right anterior temporal, bifrontal), lobar (e.g., occipital), hemispheric, or global. Even diffuse activity may have patterns of expression, with greater emphasis over the temporal lobes bilaterally or the parasagittal regions on either side of the midline. The signifi cance of certain types of EEG activity depends heavily on where that activity is located. For example, frontal intermittent rhythmic delta activity (FIRDA) over both frontal lobes is a nonspecifi c abnormality associated with a variety of brain disorders, while the same rhythmic delta located over a single temporal lobe (temporal intermittent rhythmic delta activity or TIRDA) can be highly predictive of epilepsy.1,2

Symmetry Symmetry refers to a comparison of the amplitudes and frequencies on either side of the mid- line. Typically, comparisons are made between homologous (same named) derivations from each side. Activity may be asymmetrical due to differences in frequency components between hemispheres, with similar overall amplitudes, or due to a signifi cant difference in amplitude (defi ned as >50% difference between sides) but similar frequencies, or both. Asymmetry can result from a variety of conditions, either due to altered cortical function over one hemisphere (due to stroke, tumor, hemiencephalitis, or other focal conditions) or due to structural lesions between the brain and recording electrodes (subdural hematoma or hygroma, scalp edema, a skull fracture resulting in a breach rhythm, etc.).

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41CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

Synchrony Synchrony is the simultaneous occurrence of similar waveforms over each hemisphere. Normal EEG activity is usually synchronous over the left and right hemispheres, both for relatively continuous background activities and more sporadic waveforms (e.g., “K complexes,” the large amplitude biphasic slow waves seen in stage 2 sleep, should have simultaneous onset over both hemispheres). Loss of synchrony can occur when communication between the hemispheres is impaired by damage to the corpus callosum or in severe disorders of cortical function. Lack of synchrony can also indicate that the location where the waveform appears fi rst may be closer to the origin of that activity, and thus help with the localization of abnormal or epileptiform activity.

Reactivity Reactivity is a change in EEG activity in response to sensory stimulation or a sudden change in the internal state. One of the most prominent examples is visual input to the occipital cortex, which attenuates or blocks the occipital alpha frequency rhythm when the eyes are open. An example is seen in Figure 2-2. When the eyes open, the alpha activity in the occipital leads disappears, and when the eyes close again, it reappears. Other kinds of reactivity include slow- ing of the background frequencies during hyperventilation and blocking of the mu rhythm (an alpha frequency activity over the centrotemporal region often unmasked by eye opening) by moving, or even thinking about moving, the opposite arm.3 Reactivity also includes changes

1 s

eyes open eyes close

mu

Fp2-F8

F8 - C3

C3 - P3

P3 - O2

Fp2-F8

F8 - T4

T4 - T6

LLC

T6 - O2

RUC

100μV

FIGURE 2-2. Effect of eye opening and closure on the PDR. A well-formed alpha frequency posterior dominant rhythm is attenuated by eye opening (fi rst arrow) and returns with eye closure (second arrow). During the time that eyes are open, an alpha-frequency activity is seen over the central and (to a lesser degree) midtemporal regions; this is termed mu activity.

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42 Reading EEGs

in EEG activity in comatose patients induced by painful stimulation and occipital waveforms induced by a fl ashing strobe light known as the posterior photic driving response. Reactivity is usually a normal response, but its absence is not always abnormal unless it is asymmetrical. For example, absence of the photic driving response over one hemisphere suggests a lesion inter- rupting the optic tract on that side, which is known as Bancaud’s phenomenon.4

Morphology Morphology is a physical description of the waveform, which includes its shape (e.g., sinu- soidal, saw-toothed, cone-shaped, spindle-shaped, and epileptiform), the number of phases (e.g., biphasic, triphasic, polyphasic), and the polarity of those phases. The consistency of the shape may also be described; for example, repeated waveforms with inconsistent shape may be described as polymorphic, while trains of identical waveforms would be considered mono- morphic. Figure 2-3 shows some model waveforms and examples of actual EEG waves that are described using these terms. Some waveforms have such a distinctive morphology that a diag- nosis can almost be made on the basis of its appearance alone; for example, the centrotemporal spikes in benign rolandic epilepsy (benign childhood epilepsy with centrotemporal spikes) have a characteristic symmetrical V shape and an anteroposterior (and sometimes horizontal) dipole not seen in other spike-and-wave discharges (Fig. 4-9, p. 106).5

Rhythmicity Rhythmicity is the continuous repetition of similar waveforms and frequencies over time. The rhythmic repetition of waves creates the background activity upon which sporadic waveforms are superimposed. When such superimposed waves occur at regular intervals, they are called periodic activity (if the period is irregular, the term pseudoperiodic is used). Waveforms that occur without any regular period can be called aperiodic or arrhythmic. Such activity is sometimes

A

B

C

D

E

F

FIGURE 2-3. Some EEG wave mor- phologies. Model waveforms and sample EEG activity associated with that morphol- ogy. A: Sine wave associated with alpha frequency posterior dominant rhythm. B: Arciform shape associated with wicket spikes (a normal variant). C: Spindle mor- phology associated with sleep spindles. D: Sawtooth morphology associated with sawtooth waves (seen in REM sleep). E: Biphasic morphology associated with a POST wave (slowed for clarity). F: Tripha- sic morphology associated with a frontal triphasic wave.

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43CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

also called polymorphic since the wave shapes tend to differ as well, and the distinction is minor. Examples are shown in Figure 2-4.

Regulation Regulation is the degree to which amplitude and frequency change over time. A rhythm can be described as “well-regulated” if the amplitude varies smoothly in a waxing and waning pattern (more on this later) and the average frequency does not vary more than ±0.5 Hz during a 2-s epoch (without an obvious change of state).6 The gradual variation in amplitude and frequency is also known as “modulation,” similar to the modulation of amplitude and frequency used to carry radio signals on AM and FM radio stations.

Describing EEG Activity As you have seen, there are many different characteristics that apply to EEG activity. Does each of these need to be described for every waveform? The short answer is, yes! This can lead to some pretty lengthy descriptions when several different activities are present during the course of a recording. Perhaps owing to the Germanic origin of EEG, the usual convention is to string together all of the adjectives that apply to the activity you are describing. So it would not be unusual to state that you observed a frontally dominant, 2- to 3-Hz, 75-μV, inter- mittent rhythmic delta activity with sharply contoured morphology, in runs lasting 3 to 4 s. Fortunately, many such patterns are seen frequently enough that they can be described in well- understood acronyms, so frontally dominant intermittent rhythmic delta activity becomes FIRDA, pseudoperiodic lateralized epileptiform activity becomes PLEDs, etc. These shortcuts do not relieve you of the responsibility of describing the activity you observe, but they do make life easier for transcriptionists.

A

B

C

D

E

F

G

FIGURE 2-4. EEG waveform periodicity and rhythm. A: Sporadic waveforms occur without periodicity. B: Periodic activity occurs at regular intervals (2 s). C: Pseudoperiodic activity is not perfectly regular but, on average, the period is about 2 s. D: Aperiodic activity occurs frequently but without a clear pattern. E: Rhythmic alpha activity as seen in occipital alpha-frequency activity; there is some intermixed faster and slower activity but the primary alpha frequency consistently occurs at 10 Hz. F: Polymorphic or arrhythmic activity. A 5-Hz theta pattern is occasionally seen but broken up by faster and slower frequency waves of variable morphology. G: Evolving activity in two bipolar temporal leads during a temporal lobe seizure. Activity begins with low-amplitude fast activity and then slows from 6 to 4 Hz while increasing in amplitude.

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44 Reading EEGs

QUESTION 2.1: What are the primary characteristics by which EEG waveforms should be evaluated?

ANSWER: All EEG activities can be described in terms of frequency, amplitude, morphology, symmetry, synchrony, rhythmicity, reactivity, and regulation.

Evolution Evolution is a gradual change in amplitude, frequency, or spatial distribution of rhythmic activ- ity over time. Such evolution may be normal, as seen with the gradual slowing and anterior spread of background frequencies during the transition from wakefulness to drowsiness. More often, changes of state are fairly sudden, such as the shift from sleep to arousal, and within a given state activity remains relatively consistent over time. Gradually evolving changes in frequency, amplitude, or spatial distribution, particularly when all of these parameters evolve at once, are a hallmark of seizure activity. An example of evolving seizure activity is shown in Figure 2-4G. This will be covered in greater detail in Chapter 4.

Normal Wakefulness: The Posterior Dominant Rhythm What frequencies and patterns are “normal?” The answer to this question depends on a number of factors, including the location of the activity, the patient’s age, and the clinical state (wake- fulness, drowsiness, or other stages of sleep). The most important EEG pattern of wakefulness is the posterior dominant rhythm, or PDR. This activity is primarily located at the occipital poles but can be prominent more anteriorly, particularly as the patient becomes drowsy or with a sudden arousal from sleep. It is rhythmic and usually sinusoidal in character. The amplitude may vary signifi cantly between patients, but it is often the highest amplitude activity observed in normal awake subjects. The frequency of the PDR gradually increases during development from infancy through childhood and reaches a plateau in the early teen years. In adults and children older than 9 years of age, this activity should be in the alpha frequency range (8 to 12.5 Hz). Indeed, the alpha frequency band was defi ned based on the usual frequencies seen in the adult posterior dominant rhythm. A study of healthy young adults (24- to 35-year-old Air Force personnel) showed a mean frequency of 10 Hz, with less than 1% having a frequency less than 9 Hz.6 Thus, PDR frequencies slower than 9 Hz in young adults are greater than two standard deviations from the mean and are more likely to represent an abnormality than the low end of normal. On the other end of the spectrum, supranormal frequencies of 13 Hz or faster are occasionally seen, and are not considered abnormal, though one must be careful not to confuse a fast PDR with increased activity in the beta frequency range.

The PDR frequency should ideally be measured at two symmetrical occipital derivations (e.g., T5–O1 and T6–O2) within the same 1-s period, and should be counted “by hand,” not relying on digital frequency measurements that are often inaccurate. Only the “best” (fastest) alpha frequency in the record is used to determine the value of the PDR, likely occurring at the patient’s most alert state. If the subject is drowsy, the technician should stimulate alertness by asking the patient to perform a mental alerting task (count from one to ten, name the Great Lakes, etc.) with eyes closed.

Other faster and slower frequencies may be represented in the waking EEG. Faster beta frequencies are sometimes seen, particularly over frontal and central regions, but they should be low in amplitude. Beta activity of more than 25 μV is considered abnormal,6 though the cause is nonspecifi c, and in normal adults, it is often related to CNS active medications such as the benzodiazepines or barbiturates. Theta activity is frequently present, often in the con- text of a transition to drowsiness, and is almost never abnormal. Slow wave (delta) activity is generally considered abnormal in awake adults. A certain amount of delta activity is accept- able in younger children through the teenage years, particularly in the occipital region, where individual delta slow waves with overriding alpha are frequently observed in normal children.

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45CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

These “posterior slow waves of youth” should not be considered pathological delta activity unless they are unilateral or disrupt the alpha background.

PDR Frequency Changes in Childhood The development of the PDR through childhood has been well studied since the early days of EEG recording.7,8 The ontogeny of the PDR will be covered in more detail in Chapter 5, but we can briefl y summarize the major milestones in the development of PDR frequency as follows6:

A 3-Hz rhythmic posterior activity is usually seen by 3 months of age (in children born • at 40 weeks gestational age). The PDR frequency increases to 5 to 6 Hz by 1 year of age.• Average PDR in children 3 years of age is 8 Hz.• Average PDR reaches 9 Hz by 8 years of age and 10 Hz by 15 years of age.•

This can be summarized in the “rule of 3’s and 8’s” in which most of the milestones are con- veyed in terms of multiples of 3 or 8:

3 Hz by 3 months, 6 Hz by 1 year, 8 Hz by 3 years, and 9 Hz by 8 years.•

While this “rule” is not completely accurate, it does provide a convenient mnemonic to help you remember the PDR frequencies expected at different ages during childhood.

QUESTION 2.2: Can you add an additional line to the“3’s and 8’s” mnemonic for later development of the PDR?

ANSWER: “10 Hz by 15 years”—15 is a multiple of 3. In practice, the range of normal extends down to 9 Hz, so this “milestone” is not always met.

PDR Amplitude, Synchrony, and Symmetry The PDR amplitude is normally in the moderate range, from 15 to 45 μV, often higher in chil- dren and lower in the elderly.9 The waveforms should be synchronous between hemispheres and symmetrical in amplitude, though amplitude differences of up to 20% are not uncommon in normal patients. Most often, such differences in amplitude are due to variations in skull thick- ness, which is usually greater on the left side causing right side amplitudes to be slightly higher.

Slow Alpha Versus Slow Alpha Variant If the PDR is slower than 9 Hz in young adults, this is generally considered abnormal but nonspecifi c and suggests a mild diffuse disturbance of cortical function, as seen in metabolic encephalopathies and primary neuronal disorders. However, patients with normal alpha fre- quencies will sometimes have brief episodes (several seconds) in which the PDR is suddenly reduced by half and increased in amplitude. This is “slow alpha variant,” a subharmonic of the normal alpha frequency, which is thought to be of no clinical signifi cance. An example is shown in Figure 2-5. Longer runs of slow alpha variant can occur, but a patient with only 5-Hz PDR and no faster alpha rhythm likely has pathological slowing of the background rather than slow alpha variant.

Mu Rhythm Mu is an alpha frequency activity with arciform (arc-shaped) appearance located over the central regions that is not blocked by eye opening. It may be unilateral or bilateral, may be synchronous or asynchronous, and may or may not be present at any given time. It is likely generated in the sensorimotor cortex and can be suppressed by moving a contralateral extrem- ity (or sometimes by thinking of moving a contralateral extremity). An example is shown in Figure 2-2.

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46 Reading EEGs

Lambda Waves Lambda waves are sharply contoured surface-positive waves observed in the occipital leads during wakefulness with eyes open, which correlate with visual fi xation to a target after a sac- cadic eye movement. They usually have a prominent initial positive component (seen as an upstroke in bipolar derivations with the occipital electrode at input 2) followed by a down- stroke that may go past the baseline giving it a biphasic appearance (Fig. 2-6; see also Fig. 4-3). Since they occur with eyes open, when the alpha PDR is suppressed, they stand out clearly from the background. They have no clinical signifi cance.

Origin of the PDR The posterior dominant alpha rhythm is generated by intrinsic oscillators within the occipi- tal cortex and heavily infl uenced by thalamocortical projections from the lateral geniculate nucleus. There are likely multiple cortical oscillating circuits with similar but not identical frequencies, which may be synchronized by thalamocortical interactions. Studies with intracra- nial electrodes have shown multiple alpha generators, not only in the occipital region but also in central and temporal areas.10 We see evidence of multiple oscillators in the modulation of the PDR, i.e., the gradual waxing and waning of amplitude and (to a lesser extent) frequency seen to some degree in most normal records. Figure 2-7 demonstrates how modulation can result from the interactions of multiple oscillators. Part A shows a normal 10-Hz posterior dominant alpha frequency rhythm, which tends to wax and wane in amplitude over the course of a few seconds. Part B examines how this could occur using pure sinusoidal waves. The fi rst trace is a 10-Hz sine wave, which, in the second trace, is added to itself out of phase (shifted by π/2 or ¼ or a wavelength). The addition of the phase-shifted rhythm reduces the amplitude but does not reproduce the varying amplitude as seen in the recorded PDR. However, if the phase

FIGURE 2-5. Slow alpha variant. The 10-Hz posterior dominant rhythm is at times replaced by a notched waveform representing the partial fusion of two alpha waves, appearing as a 5-Hz theta activity. The fusion may be more com- plete without the notching between the two fused waves, sometimes with a spiky appearance, but the slower wave- form should be exactly half the frequency of the PDR and should remain in phase with the rest of the background activity. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York: Raven Press, 1995:69, Fig 2-27, with permission.)

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47CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

FIGURE 2-6. Eye opening with posterior lambda waves. Eye opening blocks the posterior dominant alpha rhythm, which is replaced by low-amplitude electropositive, diphasic triangular-shaped waves in the occipital region (lambda waves) associated with visual fi xation on a target. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York: Raven Press, 1995:97, Fig 3-55, with permission.)

10 Hz

10 + π/2

9 Hz

10 + 9

50 μV

1 s

C3 - P3

P3 - O2

A

B

FIGURE 2-7. Modulation of the PDR. A: Waxing and waning amplitude with relatively constant frequency in two anteroposterior derivations from normal 27-year-old female. B: Modulation of the PDR may result from interactions between multiple alpha oscillators. The sum of 10 Hz (trace 1) and itself displaced by π/2 (trace 2) is a slightly lower amplitude signal at the same fre- quency, which could result in amplitude modula- tion if there were a shifting phase relationship between multiple oscillators. The sum of 10 plus 9 Hz (trace 4) is a mixed frequency waveform with dramatic amplitude modulation with a period of 1 s—the difference in frequencies between the two oscillators.

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48 Reading EEGs

of multiple oscillators of the same frequency were to shift over time, some waxing and waning of amplitude could occur. The third trace shows a rhythm of the same amplitude but slightly slower at 9 Hz. When the 10-Hz and 9-Hz signals are added, the summation of out-of-phase components results in a waxing and waning pattern, as shown in the fourth trace. Hence, the PDR is likely composed of several different oscillators at slightly different frequencies or with shifting phase relationships. This concept should be familiar to musicians; instruments that are slightly out of tune (the same note played at slightly different frequencies) will cause a rhythmic change in the loudness of the tone called “beating” when the out-of-tune notes are played together.

The infl uence of thalamocortical interactions on the PDR can be seen in two phenomena we have already discussed: the blocking of the alpha background with eye opening and the photic driving response. The fact that visual input associated with eyes being open desyn- chronizes the EEG and blocks the PDR suggests that the cortical alpha rhythm in the awake state may be a receptive state that facilitates visual processing, which is co-opted when visual stimuli are present. The infl uence of light on the PDR is complex and state-dependent. Alpha can persist in dim illumination with eyes open, and individuals can train themselves using biofeedback to infl uence the amount and amplitude of alpha activity.11 In some instances, eye opening can increase alpha by producing a sudden increase in alertness. In congenitally blind adults, the alpha frequency power is reduced, suggesting that the brain structures like the geniculostriate pathway might be reorganized or less developed in people who are blind from birth.12 Another clue is that when the eyes close again, there is a transient increase in the PDR frequency in the fi rst second after eye closure, a phenomenon known as “squeak” possibly due to the Doppler-like shift to a higher frequency after a period of suppression or from the sound of EEG pens suddenly making a high-pitched noise against the paper when the eyes close after a period of relative quiet during eye opening.13 This rebound increase in frequency suggests an intrinsic cortical drive to oscillate that is suppressed by visual input and recurs more forcefully when blocking is released. Photic driving (which will be discussed in more detail below) can synchronize the alpha activity when it is delivered at the same frequency as the PDR or can replace it with faster or slower driven frequencies.

QUESTION 2.3: What features of the PDR suggest that it is generated by multiple independent cortical oscillators?

ANSWER: Intracranial recordings have shown multiple distinct oscillating circuits, and the waxing and waning modulation of amplitude suggests the interaction of multiple oscillators.

Drowsiness and Sleep The principles of formal sleep scoring (analyzing an EEG or polysomnogram record for fea- tures of sleep) will be covered in greater detail in Chapter 11. This introduction will help you understand the waveforms associated with sleep as they are found in routine EEG recordings. The EEG undergoes dramatic and specifi c changes during the transitions from wakefulness to drowsiness and sleep. Drowsiness, also known as stage 1 sleep, is characterized by several distinctive features:

Slowing and anterior spread of alpha activity, followed by• Dropout of the posterior dominant rhythm• Slow lateral eye movements seen in the lateral eye and frontal leads• Vertex sharp waves•

These changes may occur nearly simultaneously or gradually over tens of seconds. Anterior spread and then loss of the alpha activity are among the earliest signs, usually accompanied by slow “rolling” side-to-side eye movements (Fig. 2-8). These movements can be detected on frontal EEG electrodes and electrodes placed at the outer “corners” of the eyes, usually at the

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49CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

right upper canthus (RUC) and left lower canthus (LLC). Eye movements can be detected at these electrodes due to the fact that the globes (eyeballs) have a front-to-back potential, with the cornea positive and the retina negative. A positive wave at the LLC electrode occurring simul- taneously with a negative wave at the RUC would indicate that the left cornea is moving closer to the left canthal electrode while the right retina is moving closer to the right canthal electrode; hence, the eyes are looking conjugately to the left. Positioning the right electrode higher and the left electrode lower helps to indicate upward and downward eye movements as well. This will be covered in more detail below—for now, it is suffi cient to know that side-to-side, slowly drifting lateral eye movements are a sign of drowsiness.

When the posterior alpha activity drops out, it is usually replaced by a disorganized, low- amplitude mixture of frequencies, with theta activity predominating. Often there will be bursts of centrally dominant rhythmic theta activity and/or increases in faster beta frequencies in the frontal or central regions. Patients may oscillate between wake and drowsy states. Vertex sharp waves, a sign of late drowsiness, usually have maximal amplitude (on referential montages) and reverse phase (on bipolar montages) at the Cz electrode, though their spread may involve the central and sometimes frontal electrodes as well. They are usually monophasic, surface- negative waves that last 70 to 200 ms, with highly variable amplitude. They can be quite sharp, particularly in children, but are rarely considered epileptiform. They usually occur as drowsi- ness is about to transition into stage 2 sleep (see Fig. 2-12 and Fig. 4-2, p. 95).

Hypnogogic Hypersynchrony In children and adolescents, drowsiness may be associated with dramatic bursts of paroxysmal high-amplitude theta to delta frequency slowing (usually around 4 Hz but sometimes faster or slower) with amplitudes as high as 300 μV or more. This is often referred to as “hypnogogic hypersynchrony” and is a normal fi nding in children, even when there are associated faster

FIGURE 2-8. Drowsiness with slow lateral eye movements. Out-of-phase positivity at F7 and negativity at F8 indicate conjugate lateral eye movements. Anterior spread of the alpha posterior dominant rhythm is also typical of drowsiness. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalogra- phy. New York: Raven Press, 1995:19, Fig. 2-3, with permission.)

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50 Reading EEGs

“spikelike” components. Hypnogogic hypersynchrony or “drowsy bursts” should not be used to support a diagnosis of generalized epilepsy (e.g., absence epilepsy with 3-Hz spike-and-wave) unless the spike-and-wave pattern also occurs in states other than drowsiness (see Fig. 5-11 for an example of generalized 3-Hz spike-and-wave).

Stage 2 Sleep As somnolence progresses, the next deeper phase is stage 2 sleep, which is characterized by the presence of well-defi ned but sporadic waveforms:

K complexes• Sleep spindles•

K complexes are moderate to high amplitude diffuse to centrally predominant biphasic slow wave transients that last at least 0.5 s and are at least 75 μV in amplitude (see Fig. 11-6, p. 266). They are usually solitary and stand out from the background. The initial phase is usually nega- tive (upward) and the second phase positive (downward). K complexes help defi ne stage 2 sleep but may also indicate brief partial arousals; indeed, it is possible to trigger K complexes in a patient in stage 2 sleep by lightly tapping with a pen on a table, as EEG or sleep technicians are fond of demonstrating.

Sleep spindles are very regular rhythmic sinusoidal or spindle-shaped (pointy at the ends) waves at 12 to 14 Hz, usually of low amplitude, seen most prominently in the frontal or central regions, though they may occur anywhere or be quite diffuse (Fig. 2-9; see also Fig. 11-7, p. 266 showing stage 2 sleep on a 30-s page). They typically last 1 to 3 s but may last only a fraction of a second or go on for many seconds. They may occur asymmetrically, particularly in young

100 mV 1 s

Fp1-F7

F7 - T3 T3 - T5

T5 - O1

Fp1- F3 F3 - C3 C3 - P3

P3 - O1 Fz - Cz

Cz - Pz

Fp2-F8

F8 - C3 C3 - P3

P3 - O2

Fp2-F8

F8 - T4

T4 - T6 T6 - O2

FIGURE 2-9. Stage 2 sleep. Stage 2 sleep is marked by the presence of sleep spindles, here seen symmetrically in the parasagittal regions (outlined by dashed lines) associated with delta slow waves.

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51CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

children or the elderly, sometimes oscillating from side to side, but the overall amount should be the same on either side. Sleep spindles may be superimposed on a K complex or stand alone. They are the defi ning waveform for the state, and once they are seen, the patient is consid- ered to remain in stage 2 sleep until a state-changing event is seen, such as the return of alpha activity indicating an arousal to wakefulness, an increase in rhythmic delta activity indicating progression to slow wave sleep, or other evidence of a state change.

For many EEGers, despite the defi nition of stage 1 as the fi rst stage of sleep, the recording is not considered to have shown sleep unless stage 2 sleep is achieved. This curious discrepancy in defi nitions may be due to the “transitional” quality of drowsiness, the deeper loss of aware- ness in stage 2, and the greater likelihood of stimulating interictal epileptiform activity (spike- and-wave discharges) in stage 2. The fact that stage 2 sleep brings out epileptiform activity is the main reason that sleep-deprived EEGs are ordered, to ensure that the patient falls asleep during the study and both wake and sleep are recorded. It is not necessary for the patient to stay awake the entire night before the recording; staying up a few hours later than usual, com- bined with an early morning recording time, is usually suffi cient to guarantee that the patient will sleep during the study. Sleep can thus be considered one of the “activating procedures” (described below) used to bring out epileptiform activity.

Slow-Wave Sleep and REM Sleep As sleep deepens, an increasing amount of delta activity is observed, and when more than 20% of the activity on a 30-s page is delta, the patient has entered stage 3 or slow-wave sleep (Fig. 2-10; see also Fig. 11-8, p. 267). Sleep-scoring rules defi ne delta activity differently

FIGURE 2-10. Stage 3 sleep. Frontally dominant rhythmic high-amplitude polymorphic delta waves predominate in deeper non-REM sleep. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electro- encephalography. New York: Raven Press, 1995:180, Fig. 3-138, with permission.)

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52 Reading EEGs

than EEG rules; it must be 2 Hz or less (rather than 4 Hz) and of at least 75 μV amplitude, using a contralateral ear referential montage. Rapid eye movement (REM) sleep is marked by rapid eye movements, a low voltage, mixed frequency EEG, and very low-amplitude EMG activity, usually recorded at the chin (see Fig. 11-9). These stages are rarely encountered in routine EEG recordings, as the patient is seldom recorded for long enough to enter the deeper non-REM or REM sleep stages. REM may be encountered in narcoleptic patients or during long-term continuous EEG monitoring. However, EMG electrodes are not usually included in routine EEG recordings; hence, determination of REM sleep is quite diffi cult in routine EEGs even when it does occur.

Positive Occipital Sharp Transients of Sleep Positive occipital sharp transients of sleep (POSTS) are surface-positive, monophasic sharp transients seen in the occipital leads that may occur singly or in trains, often four to fi ve per second, though usually not rhythmic in appearance (Fig. 2-11; see also Fig. 4-4). They should be synchronous when seen bilaterally but may be asymmetrical in amplitude in normal indi- viduals. Despite the sharp contour of these waveforms, they are not considered epileptogenic. They can occur in either stage 1 or stage 2 sleep.

Arousal Patterns When the adult patient arouses from sleep, a variety of EEG changes can be seen. Arousals from light drowsiness (stage 1) are often marked only by return of the alpha PDR. From stage 2 or deeper NREM sleep, there is often a high-amplitude biphasic or triphasic transient lasting 0.5 s or longer, reminiscent of an exaggerated K complex (though probably not from the same

FIGURE 2-11. POSTS. These sharply contoured occipital waves can occur in clusters in drowsiness (stage 1) or stage 2 sleep. Asterisk shows a “small sharp spike” or benign epileptiform transient of sleep (BETS), which is not associated with epilepsy. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electro- encephalography. New York: Raven Press, 1995:109, Fig. 3-67, with permission.)

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53CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

generator), often followed by a burst of diffuse alpha activity and intermixed muscle artifact (Fig. 2-12). In children, arousals tend to occur more slowly with the diffuse alpha activity gradually slowing into the theta and delta range before being replaced by the PDR.6

Activating Procedures Much of the information we acquire during EEG recording is passive; we simply attach the electrodes, turn on the EEG machine, and record what happens. But there are a number of procedures used to infl uence EEG activity, some of which are standard and essential for most recordings. Such procedures may reveal abnormalities that would not be seen otherwise.

Mental Alerting Alerting is performed by the technician when the patient appears to be drowsy (by physical appearance or EEG criteria) and the background alpha frequency is slower than expected. It is usually performed early in the study, so the subject can subsequently become drowsy and fall asleep if possible. Alerting tasks are designed to provide enough stimulus to focus mental activity, which usually enhances the PDR alpha frequency. This procedure is thus designed to determine whether a slower-than-expected PDR is due to drowsiness (i.e., state-dependent) or is pathological. The task can be chosen at a level appropriate to the patient’s age, level of

FIGURE 2-12. Vertex waves followed by an arousal. Sharply contoured repetitive vertex waves in light sleep, reversing at the Cz electrode, are followed by a high-amplitude slow transient and then a diffuse alpha frequency pattern indicative of arousal. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Elec- troencephalography. New York: Raven Press, 1995:194, Fig. 3-67, with permission.)

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54 Reading EEGs

education and native language, and should be able to be performed with eyes closed. Counting slowly from one to ten, serial subtractions, spelling “world” forward and backward, or simply calling the patient’s name may each be appropriate for different patients. The verbal answer will create speech related artifacts involving temporal and tongue muscles, but between words or after completion, the patient should be at maximal alertness.

Hyperventilation Hyperventilation causes a complex physiological response that is refl ected in the EEG activity. Increased minute ventilatory volume depletes CO

2 resulting in a respiratory alkalosis, cerebral

vasoconstriction, and a corresponding reduction of cerebral blood fl ow,14,15 though the under- lying mechanisms for the EEG changes remain controversial.16 The effects on EEG may be subtle or quite dramatic, particularly in children. After 30 to 60 s of hyperventilation, there can be slowing of the PDR into the theta range with diffuse spread of rhythmic polymorphic theta activity. With continued hyperventilation, the amplitude of the rhythmic slowing may increase dramatically to several hundred μV, and waves may slow into the delta frequency range (Fig. 2-13). This effect is sometimes known as “buildup,” hyperventilation hypersyn- chrony, or hyperventilation-induced high-amplitude rhythmic slowing (HIHARS). This effect persists for tens of seconds after hyperventilation ceases, which sometimes allows a better view of cerebral activity if the EEG is obscured by muscle artifact during overbreathing.

In addition to the normal physiological changes that can occur with hyperventilation, it can also bring out focal slowing or epileptiform activity, particularly the 3-Hz spike-and-wave of absence epilepsy. This can get confusing for two reasons. First, HIHARS itself can cause impaired consciousness in normal children who do not have absence epilepsy.17 Second, the spike component of 3-Hz spike-and-wave can sometimes be diffi cult to discern in the high- amplitude rhythmic delta activity, or other superimposed waveforms may appear spike-like. Hence, only clearly defi ned repetitive spike-and-wave discharges should be considered evidence of epileptiform activity during hyperventilation (ideally supported by additional discharges at other times in the record). Similarly, the generalized slowing during hyperventilation may

FIGURE 2-13. Hyperventilation hypersynchrony in a 17 year old. The alpha pattern prior to hyperventilation with some intermixed slow alpha variant and mu activity (left panel) slows to theta frequency with superimposed high- amplitude frontally dominant sharply contoured waves after 1 min of hyperventilation (middle panel), with further slowing and high-amplitude theta and delta activity after 2.5 min of hyperventilation (right panel). These responses are normal and most prominent in youth. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York: Raven Press, 1995:94, Fig. 3-52, with permission.)

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55CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

be slightly more prominent over one hemisphere than the other, and only clearly lateralized slowing should be considered abnormal.

Younger children can be induced to perform continuous overbreathing by asking them to keep a pinwheel spinning by blowing on it. Sustained crying can also duplicate hyperventilation. The movements associated with breathing may cause artifacts as well, including a “rocking” arti- fact in the occipital leads as the patient leans forward and back during deep breaths, and increased temporalis muscle tone. The technician will encourage the patient to continue overbreathing for up to 3 min, though some patients will be unable to comply. Contraindications include COPD or other chronic lung or heart disease, pregnancy, recent stroke or subarachnoid hemor- rhage, sickle cell disease, moyamoya disease, and patients incapable or unwilling to cooperate.

Sleep Sleep is activating for nearly all forms of epilepsy, sometimes dramatically so. The most striking example is electrical status epilepticus of sleep, in which spike-and-wave discharges occur during more than 85% of slow-wave sleep. Children with benign childhood epilepsy with centrotem- poral spikes may have a normal EEG in wakefulness, but characteristic centrotemporal spike- and-wave discharges appear once the patient is asleep. Seizures are also more likely during sleep or upon awakening, particularly in some epilepsy syndromes like juvenile myoclonic epilepsy.

The desire to record EEG during sleep and to facilitate performing studies on potentially uncooperative patients (children or patients with mental retardation/developmental delay) led to the frequent use of sedating agents prior to EEG recordings. Chloral hydrate was often the drug of choice due to its relatively minor effect on EEG patterns compared to other sedatives (benzodiazepines, etc.). Chloral hydrate was fairly well tolerated in most patients, but rare cases of respiratory depression and even mortality have occurred with accidental overdoses (most often when a second dose is given after failure of the fi rst dose to sedate the patient). For this reason, most hospitals and EEG laboratories now require extensive training and continuous monitoring by a physician for any patient undergoing light anesthesia (more commonly known as “conscious sedation”). This is impractical for most EEG laboratories, and the use of chloral hydrate and other sedatives has declined signifi cantly in recent years. However, the use of behav- ioral techniques including sleep deprivation prior to the study and timing studies to correspond to nap times has largely replaced the use of sedatives, with nearly the same success rate.

Eye Opening and Closure We have already mentioned the ability of eye opening to block the PDR (see Fig. 2-2), and the return of the PDR with a slightly faster frequency in the fi rst second after eye closure (called “squeak”). Eye opening and closure should be performed several times during the course of the study to assess reactivity of the PDR. In children who have childhood epilepsy with occipital paroxysms (CEOP), the occipital spikes are sometimes suppressed by eye opening.18

Photic Stimulation The photic driving response is one of the most robust and dramatic ways that external stimuli can affect brain activity. With each strobe fl ash, an excitatory synaptic potential is generated in the striate cortex that can sometimes be directly seen over occipital EEG leads (Fig. 2-14A). The potential recorded at occipital derivations is essentially the same positive waveform that occurs 100 ms after the fl ash that is generated in visual evoked potential studies. Repetition of the fl ash at specifi c frequencies increases the response, likely due to the creation of a “standing wave” that reinforces thalamocortical rhythms. Stimulation frequencies at or near the native alpha back- ground frequency will increase its amplitude, and other fl ash frequencies may or may not cause a photic driving response that supplants or is superimposed on the PDR. The most effective frequencies will vary from patient to patient, but often include frequencies that are “harmonics” (multiples) or “subharmonics” (divisions) of the PDR. For example, a patient with a PDR at

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56 Reading EEGs

10 Hz might have the best driving responses at 5, 10, and 20 Hz. “Overdriving” is also frequently seen, in which the photic driving response is only present at frequencies higher than the PDR. Most laboratories perform photic stimulation through a range of frequencies from 1 Hz to as high as 30 Hz, for up to 10 s at each stimulation frequency. Some laboratories perform this twice, once with eyes open and once with eyes closed (the fl ash has suffi cient intensity to illuminate through closed eyelids). As previously noted, the absence of a response is only abnormal if it is unilateral. It is important to distinguish photic driving from the photomyoclonic response (stim- ulated blinking or facial twitching in response to each fl ash, seen in the frontal electrodes, which is usually not epileptic) (Fig. 2-14B) and the photoelectric response (a rare fi nding in which the light itself triggers an electrical impulse from its interaction with the frontal electrodes).

10 Hz

Fp1- F7

F7 - T3

T3 - T5

T5 - O1

Fp1- F3

F3 - C3

C3 - P3

P3 - O1

photic

14 Hz 18 Hz A

B Fp2 - F8

F8 - C3

C3 - P3

P3 - O2

Fp2 - F8

T6 - O2

F8 - T4

T4 - T6

FIGURE 2-14. Photic driving and photomyoclonic response. A: Posterior photic driving response seen at 10-Hz, 14-Hz, and 18-Hz stimulation rates. Note that although the posterior dominant rhythm is close to 10 Hz, driving is still clearly evident as synchronization of the alpha activity with the light stimulus (marked by the bottom trace). B: Low-frequency photic stimulation (3 Hz) evokes a repetitive frontal slow transient associated with fl ash-induced blinking, termed a photomyoclonic response. No posterior photic driving is observed. Calibration bar is 1 s, 20 μV.

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57CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

Photoparoxysmal Response Photic stimulation can induce epileptiform activity, termed a photoparoxysmal response (PPR), particularly associated with idiopathic generalized epilepsies (IGE). The mechanism is not entirely understood but likely refl ects an increase in occipital cortical excitability, as indi- viduals who demonstrated PPR were also more likely to show inhibition of visual perception in response to occipital transcutaneous magnetic stimulation.19 The PPR has been linked to chromosome 6p21.2 in families without IGE and to chromosome 13q31.3 in families with IGE.20 The PPR consists of fl ash-induced spike-and-wave or polyspike-and-wave discharges tracking each fl ash, initially in the occipital leads but often spreading anteriorly as photic stimulation continues (Fig. 2-15). Such discharges can evolve into a clinical seizure, known as a photoconvulsive response, with spike discharges that outlast the photic stimulation and clinical

FIGURE 2-15. Photoparoxysmal Response. Photic stimulation at 15 Hz evokes symmetrical 3- to 4-Hz generalized spike-and-wave discharges. Note that discharges began after 5 s of stimulation at the fi rst presentation, but within 200 ms after the start of the second presentation, due to lowering of the threshold for spike generation. Calibration bar is 1 s, 100 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York: Raven Press, 1995:320, Fig. 5-42, with permission.)

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58 Reading EEGs

features ranging from loss of awareness to convulsions. Patients with juvenile myoclonic epilepsy and the progressive myoclonic epilepsies appear to be particularly susceptible to photic stimulation.

Painful Stimulation In unresponsive or comatose patients, sternal rub or forceful pinching of the fi ngernail or toe- nail may cause a partial arousal that alters the EEG background. The change can be subtle or dramatic and varies from patient to patient. Reactivity to pain is usually a favorable prognostic sign suggesting that the cortex can respond to sensory stimuli.

QUESTION 2.4: A 16-year-old boy with moderate mental retardation is suspected of having seizures. What activating procedures could be used to increase the likelihood that a routine EEG will show epileptiform activity?

ANSWER: The patient should be sleep deprived on the night before the study to increase the odds that he will fall asleep during the recording. Mental alerting (perhaps by asking him his favorite foods) should be performed early to ensure that the fastest alpha PDR activity is observed. Early in the course of recording (or later, after sleep has been obtained), hyperventilation can be requested by asking him to blow on a pinwheel. Photic stimulation should be deferred until the end of the study in case he reacts badly to the flashing light (so that this does not abort the rest of the recording).

Artifacts and Noise: EEG Signals Not Produced by the Brain One of the challenges in EEG interpretation is separating out signals that appear to be of cerebral origin but are in fact derived from other sources. One example of how a reader can be misled by EEG appearances occurred during a long-term epilepsy monitoring session. The EEG showed a slow rhythmic discharge with an apparent fi eld involving a single electrode, which then increased in frequency, spread to adjacent electrodes, gradually increased in ampli- tude over the course of 15 to 20 s, and then abruptly ceased. This might have been the classic appearance of a partial onset seizure. It was not until reviewing the video taken during the event that the explanation became clear—the patient had been scratching an itchy scalp elec- trode! Sometimes the sources are less obvious, and it is important to be aware of the possible sources of noise and artifact in EEG recordings.

Sources of noise can be divided into several different types: (i) electrode-related noise and potentials, (ii) noncerebral biological potentials, (iii) electrical device and power supply–related artifacts, and (iv) patient movement and extraneous physical artifacts. It is important for the technician to seek out and eliminate these problems as much as possible and, when not pos- sible, to note when they occur and their etiology on the EEG record. For greater detail, readers are referred to the excellent chapter on this topic in Ebersole and Pedley’s Clinical Practice of Electroencephalography (3rd Ed.).21

Electrode-Related Noise Electrode “Pops” One of the most common sources of noise is a sudden increase in the impedance of the electrode known as an electrode “pop,” due to a head movement or the drying of the conductive paste. These appear as sudden disconnects or jumps in the voltage potential with a drift back to base- line. Electrode pops are distinguished by their absence of a fi eld, with the disturbance affecting only a single electrode. In a bipolar montage, they are made obvious by “mirror image” activity on adjacent channels within a chain, due to the electrode being connected to the negative input of one channel and the positive input of the next. The hallmark of an electrode artifact is the

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59CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

absence of involvement of other electrodes, or in EEG parlance, the lack of a “fi eld,” though artifactual electrode problems can involve more than one electrode in a scalp region giving the false impression of that a cerebral fi eld exists (Fig. 2-16). Once identifi ed, such electrodes should be tended to by the technician (often mildly abrading the scalp through the hole in the electrode while adding conductive gel can lower impedance and fi x the problem). Until the situation is corrected, the information from that electrode should be viewed with caution and skepticism.

Salt Bridges As previously mentioned, low-impedance connections can result from sloppy application of conductive gel, sweating, or other situations, resulting in a slow undulating potential (usually 0.5 Hz or slower) involving the electrodes affected by the low-impedance connection.

High Impedance Increased electrode impedance causes several different kinds of noise. The mismatch of imped- ances between inputs of the differential amplifi er prevents suppression of 60-Hz AC noise and can amplify pickup of other extraneous signals including EKG. These problems can be mini- mized by ensuring that the impedance of all electrodes is less than 5,000 Ω.

Photoelectric Response During fl ash photic stimulation, electrodes with high impedance will sometimes generate an electrochemical response in which the fl ash stimulates a very brief photoelectric potential in the Fp (and sometimes other frontally placed) electrodes. This potential has virtually no delay as it is the direct result of the action of light on the electrodes, which helps distinguish it from the photomyoclonic response generated by refl ex blink activity at the orbicularis oculi in response to the fl ashing light.

FIGURE 2-16. Electrode “pop” and impedance artifacts. Sudden changes in impedance cause “pops” at the F8 electrode, which appear as mirror image sharp potentials in the adjacent Fp2–F8 and F8–T4 derivations. Pops also involve the T4 electrode (late in this sample), hence the delta activity at both electrodes may be artifactual. Calibra- tion bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York: Raven Press, 1995:8, Fig. 2-2, with permission.)

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60 Reading EEGs

Noncerebral Biological Signals (Artifacts) The high-gain amplifi cation required to record EEG potentials can pick up other patient-generated biological potentials. Many of these are obvious to experienced EEGers, but some can pose interpretive problems. All are more prominent at high sensitivity settings (high gain) and with long interelectrode distances as occur with referential montages or double- distance bipolar montage recordings. Some can be reduced or eliminated by appropriate fi lter- ing, while others must simply be recognized and noted.

Electrocardiogram Electrocardiogram (ECG/EKG) potentials generated by ventricular contraction (the QRS com- plex) may be large enough in amplitude to be detected by cerebral electrodes. These usually cause a regular spiky-appearing potential (Fig. 2-17) that may be more prominent at some electrodes than others (particularly those near the skull base or over the left hemisphere) that may vary in amplitude and even in frequency (if there are intrinsic cardiac problems like atrial fi brillation or sinus arrhythmia). Patients with hypertension-induced myocardial hypertrophy may generate larger voltage potentials with greater likelihood of contaminating the EEG. This activity occurs independently from cerebral potentials, and does not alter cerebral activity, but occasionally the coincidental occurrence of an ECG-related sharp wave with an “aftergoing” slow

FIGURE 2-17. ECG artifact. Cardiac electrical fi elds extend to the skull base and may be seen in EEG tracings, particularly in ipsilateral ear reference recordings. The large R wave of the ECG causes a positive fi eld at A1 and negative at A2, resulting in out-of-phase signals over the left and right hemispheres. The ECG trace at the bottom confi rms the cardiac origin of these potentials. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York: Raven Press, 1995:31, Fig. 2-25, with permission.)

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61CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

wave can lead to the erroneous diagnosis of a spike-and-wave complex. Concurrent recording of a single channel of ECG allows comparison of cerebral and ECG-generated potentials. It should be standard procedure to examine the timing of the QRS complex when evaluating possible spike-and-wave activity, and when these are simultaneous, the cerebral origin of such a complex must be questioned. It should be noted that the presence of an ECG lead in the EEG montage serves an additional purpose by allowing the detection of arrhythmias, which may help distinguish between epilepsy and syncopal disorders with similar presentations. If an ECG anomaly is found during the recording, its presence and potential signifi cance should be noted in the report.

Pulse Artifact A related issue is artifact due to pulse. These potentials are generated by subtle physical move- ment of the scalp or the brain due to cardiac pulsations (Fig. 2-18). They are thus slower than the QRS waveform and occur at a fi xed delay after the QRS complex. Since pulsation artifacts are rhythmic and often sinusoidal in character, they can be mistaken for cerebral potentials. They can be very prominent in patients who have undergone neurosurgery, in whom the cra- nium is no longer intact. A tight correlation with the ECG waveform is usually suffi cient to make the diagnosis.

Eye Movements The eyes, like several other body parts, have an associated electrical potential that causes elec- trical fi eld fl uctuations with eye movements. Due to the electrical activity of retinal neurons,

FIGURE 2-18. Pulse artifact. Rhythmic delta-frequency activity exclusively at the C3 electrode due to placement at or near a superfi cial scalp artery. Note that the waveform has a consistent phase relationship to the QRS complex of the ECG trace. The higher voltage positive potential may be an electrode “pop” due to movement. Pulse artifacts are common after neurosurgery, which allows artery or brain pulsations to be translated to scalp electrodes. Calibra- tion bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York: Raven Press 1995:33, Fig. 2-27, with permission.)

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62 Reading EEGs

there is a DC potential associated with the globe of the eye in which the retinal/posterior end is negative and the cornea is positive (Fig. 2-19). Since this is a DC potential, it does not affect the EEG when the eyes are still, but eye movements create moving or changing fi elds that generate signals detected by nearby EEG electrodes, predominantly Fp1/Fp2 and F7/F8, which sit above the medial and lateral orbit, respectively. At times, the eye muscles also gen- erate fast “spiky” potentials known as “rectus spikes” at the onset of eye movements. The potentials generated by eye movements depend on the direction, nature, and speed of the movements. Fast saccadic movements to a target, both during wakefulness and in REM sleep, cause sudden stepwise movements with a decay to baseline consistent with the time constant of the recording. Lateral saccades are sometimes accompanied by a brief spiky myogenic potential from the lateral rectus muscle (on the side to which the eyes are deviated), seen best in F7- or F8-linked derivations. In drowsiness, slow lateral eye movements cause drifting potentials that shift gradually from side to side over several seconds.

In the longitudinal bipolar montage, these movements are easily discerned due to the bipolar connections between Fp1–F7 and F7–T3 on the left and Fp2–F8 and F8–T4 on the right. In Figure 2-19, we see that either a saccadic or slow drifting eye movement to the left causes the front part of the eye, with its positive charge, to move toward F7 and away from Fp1, while the negatively charged retina moves toward Fp1 and away from F7, both mak- ing F7 relatively positive compared to Fp1. The opposite occurs at the right eye. The cornea moves toward Fp2 and the retina toward F8, making Fp2 positive to F8. These opposite polarities cause mirror image effects in the temporal chains. The negativity at Fp1 relative to F7 causes an upward defl ection while the positivity at F7 relative to T3 causes a downward defl ection. The positivity at F7 forms another kind of phase reversal, this time positive with waveforms pointing away from each other. This is easy to remember as you can imagine a plus sign fi tting in between the opposite-pointing waveforms. On the right side, the positiv- ity at Fp2 compared to F8 causes a downward defl ection while the negativity of F8 relative to T4 causes an upward defl ection, revealing a phase reversal with negativity at F8. Again, a mnemonic for the negative potential at the shared F8 electrode is that only a “minus sign” will fi t in the narrow space between the two waveforms pointing at each other. These two events will occur simultaneously since eye movements are tightly coordinated. Examples of conjugate left, right, up, and down eye movement potentials in the anteroposterior bipolar montage are shown in Figure 2-20.

Fp1 Fp2

F7 F8

+

- +

- Fp2-F8

F8 – T 4

Fp1-F7

F7 – T 3 + +

- -

Fp1 Fp2

F7 F8

+

- +

-

Fp2-F8

F8 – T 4

Fp1-F7

F7 – T 3

+ +

- -

A

B

FIGURE 2-19. Generation of eye movement voltage signals. A: The positive charge at the cornea and negative charge at the retina gen- erate potentials at nearby frontal and frontopolar electrodes. Looking left creates a positive voltage at F7 and negative potential at F8. Sac- cadic movements cause a rapid rise followed by a decay to baseline, while slow lateral eye movements cause more gradual potential shifts. B: Rightward eye movements cause a negative potential at F7 and posi- tive at F8.

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63CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

Look up look down look up 1 s

1 s

100 mV

100 mV

Fp1- F7 F7 - T3 T3 - T5 T5 - O1

Fp1-F3

F3 - C3 C3 - P3 P3 - O1 Fz - Cz Cz - Pz

Fp2-F8 F8 - C3 C3 - P3

P3 - O2

Fp2-F8 F8 - T4 T4 - T6 T6 - O2

T1 - A1 T2 - A2

Fp1- F7

F7 - T3 T3 - T5 T5 - O1 Fp1-F3

F3 - C3 C3 - P3 P3 - O1 Fz - Cz Cz - Pz Fp2-F8 F8 - C3 C3 - P3 P3 - O2 Fp2-F8

F8 - T4 T4 - T6

T6 - O2 T1 - A1 T2 - A2

look right look leftA

B

FIGURE 2-20. Lateral and horizontal gaze in anterior bipolar montage. A: Right gaze causes a negative potential at F7 and positive potential at F8, while left gaze causes the opposite. B: Upward gaze causes a positive poten- tial at Fp1 and Fp2, while looking downward causes a transient negative potential at the frontopolar and frontal electrodes.

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64 Reading EEGs

An old test of an EEGer’s prowess was to show a trace in which there are obvious saccadic eye movements over one side but not the other. The explanation is usually that the patient has a glass eye on the side lacking eye movement potentials (though it can also be caused by paralysis of the oculomotor nerve or other pathology)!

Blinking A different sort of eye movement potential is seen with blinking. With either volitional eye clo- sure or refl exive blinking, the eyes conjugately deviate upward as the eyes close (known as Bell’s phenomenon). Hence, the positive front part of both globes moves toward the Fp1 and Fp2 electrodes, resulting in a sudden positive potential at these electrodes and causing a large down- ward deviation of the signal (whether in a bipolar or referential montage) that can last several hundred milliseconds before decaying to the baseline (Fig. 2-21). Occasionally, this deviation has a rapid spiky component at the leading edge due to fi ring of the superior rectus muscle, known as a “rectus spike.” These potentials can be distinguished from cerebral potentials by the prominent involvement of canthal electrodes and lack of involvement of more posterior cerebral electrodes. While volitional blinking is limited to three or four blinks per second, some patients have fl uttering eye movements (particularly in response to the fl ashes of photic stimulation) that can be mistaken for frontal rhythmic cerebral activity (frontal intermittent rhythmic delta or FIRDA). However, rhythmic blinking is again restricted to only the most frontal electrodes, while FIRDA also involves more posterior derivations at lower amplitudes. Patients with uncontrolled persistent blinking during recording can sometimes be helped by placing a cloth loosely over the eyes.

Fp1-F7

F7 - T3 T3 - T5 T5 - O1 Fp1-F3 F3 - C3 C3 - P3 P3 - O1 Fz - Cz Cz - Pz Fp2-F8 F8 - C3 C3 - P3 P3 - O2 Fp2-F8 F8 - T4 T4 - T6 T6 - O2 T1 - A1 T2 - A2

100 mV 1 s

FIGURE 2-21. Blinks. With blinking, the eyes initially roll upward as the lids close, resulting in a positive potential at the frontopolar and frontal electrodes, followed by a negative potential as the eyes return to horizontal level with eye opening. These potentials can cause a sawtooth confi guration when blinks happen in rapid succession. Each arrow marks a blink. Note brief suppression of posterior alpha rhythm with eye opening and return with eye closure.

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65CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

Tongue Movement (Glossokinetic Artifact) The tongue also has a DC potential with the tip negative compared to the base. Movement of the tongue during speaking, chewing, or swallowing (Fig. 2-22B and C) can generate unusual (but generally symmetrical) potentials as the tip of the tongue moves up to the palate. The effect can be reproduced by having the patient say “La, la, la” during a test phase of the recording (Fig. 2-22A).

FIGURE 2-22. Glossokinetic, chewing, and swallow artifacts. A: Movement of the tongue to the hard palate generates a negative (upward) defl ection at the frontopolar electrodes due to the negative potential at the tip of the tongue. B: Chewing involves phasic contractions of temporalis, masseter, and other jaw muscles causing bursts of high-frequency spiky potentials with each forceful jaw closure (arrows). C: Swal- lowing involves complex interactions of tongue, jaw, and pharynx musculature with repeated glossokinetic and muscle potential signals.

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66 Reading EEGs

Muscle Artifact One of the most troublesome artifacts for EEG readers is the superimposition of high-amplitude continuous fi ring of motor units that obscure EEG signals. These potentials are most com- monly due to activity of the frontalis and temporalis muscles, often associated with unconscious anxiety over the test. Frontalis fi ring affects predominantly the Fp1/Fp2 and F7/F8 electrodes, while the temporalis covers a broad area of the lateral cranium covering the full extent of the temporal chain in the longitudinal bipolar montage and frequently extending to the parasagit- tal chain as well (Fig. 2-23). Technicians can often reduce these problems by instructing the patient to tense and then relax the jaw or by placing a damp cloth over the forehead and eyes. Muscle artifact tends to decrease as the patient relaxes into sleep but can occasionally be seen even in comatose patients. When severe myogenic artifact obscures low-amplitude EEG signals in a comatose patient who is being mechanically ventilated, it is possible to use short-acting paralytic agents to remove the artifact temporarily for diagnostic purposes. Movement artifacts tend to produce brief but often high-amplitude DC shifts, which can produce signals in the delta range (or in the case of fast tremor, into the theta range). Side-to-side head movements will produce an occipital delta synchronized with the movements (Fig. 2-23B).

Rhythmic or repetitive muscle artifacts can be caused by tremor (in essential/famil- ial tremor or Parkinson’s disease; see Fig. 2-23), hemifacial spasm, or other neurological conditions (e.g., the oculomasticatory myorhythmia of CNS Whipple’s disease) and may contribute toward diagnosis of these disorders. Myoclonic jerks associated with epilepsies (e.g., juvenile myoclonic epilepsy) may display cortical potentials a few milliseconds in advance of the movement artifact, but these may be diffi cult to distinguish from muscle and movement artifacts, even with advanced techniques for isolating these potentials (back- averaging of multiple events).

Chewing Chewing artifact is a complex phenomenon characterized by repetitive tension and relaxation of the temporalis muscle, often with a frequency of about 1 Hz, with contributions from glos- sokinetic movements as well, particularly in the complex action of swallowing (see Fig. 2-22B). Chewing artifacts are rarely seen in brief routine EEG recordings (though they might appear in a patient with orobuccal tardive dyskinesias!) but are common at mealtimes in patients admit- ted for long-term epilepsy monitoring.

Sweating We have already noted that sweating can cause salt bridges to form between electrodes, result- ing in low impedances and slowly drifting baselines. For reasons that should be obvious, this is more common in the summertime and frequently involves the occipital electrodes that contact the back of the chair or bed, which are less well ventilated.

Electrical and Device Artifact AC Power Supply Artifact We have already noted that 60 Hz “hum” is ubiquitous and may be diffi cult to eliminate. Due to the differing power supply design for different devices, each may radiate radio frequency (RF) noise after variable delay and thus out of phase, with different harmonic components (higher frequency multiples of 60 Hz). However, meticulous technique can reduce the likelihood of picking up 60 Hz, particularly ensuring that there is only a single well-connected ground path from the patient to the recording device (also important for safety reasons as we will discuss below) and no paths to an alternative ground. The presence of “ground loops” due to multiple different connections to ground is notorious for inducing AC noise into recorded signals. Judi- cious use of the “60-Hz notch” fi lter can reduce this signal when other methods fail.

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67CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

FIGURE 2-23. Muscle and movement artifacts. A: Muscle artifact is created by the fi ring of hundreds to thousands of individual muscle fi bers, each creating a rapid spiky potential that may obscure but not alter the underlying cere- bral activity. Together, the spiky activity forms a “hash” that overlies the EEG waves. Here, teeth grinding strongly and repeatedly activates temporalis, frontalis, and masseter to generate high-amplitude, high-frequency potentials. Normal alpha activity can be seen in the posterior derivations. B: Side-to-side movement of the head accelerates the EEG wires through space, generating slow (delta frequency) rolling potentials, most prominent at the occipital leads. Note that the “doll’s eye” phenomenon causes phasic lateral eye movement potentials at the canthal leads.

LLC, left lower canthus; RUC, right upper canthus.

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68 Reading EEGs

Patient Care Devices The number of these electrical devices has multiplied in recent years, from the ubiquitous IV fl uid and feeding tube pumps to pneumatic leg compression devices for prevention of deep venous thrombosis, heating or cooling blankets, bed position controls or pneumatic beds, etc. The intermittent nature of such devices can cause additional diffi culty since they may cycle on and off during the course of the recording. Technicians are encouraged to turn off and/or unplug any device not essential during the time of the recording. Certain settings are more problem- atic than others, and it may be impossible to eliminate AC noise sources in the intensive care unit or the operating room. In particular, electrocautery devices generate high-frequency/high- amplitude signals that completely obscure the EEG, and if the use of these devices is necessary, recording should be suspended during their operation. In addition to the IV pump motors, the drop chamber in gravity-fed IV infusions may also create a transient high-frequency potential with each drop. Such rhythmic artifacts can be notoriously diffi cult to fi gure out after the fact and should be documented by the technician if they cannot be eliminated.

Respirator Artifact Mechanical ventilation can create a variety of artifacts, some related to the electronics and others to the patient movement caused by chest wall activity that translates to subtle slow head move- ments. The electrical effects are likely to be seen at any or all of the electrodes, while movement- related artifacts typically affect the electrodes in contact with the bed. If such artifacts are severe, it is sometimes possible for the technician to lift the head off the bed by placing a rolled towel under the neck.

Internal Patient Devices Recent advances in technology have resulted in a proliferation of implantable patient devices. Cardiac pacemakers generate high-voltage signals that can be detected on EEG, often with variable detection by different electrodes or chains. Transients produced by pacemakers tend to be brief, repetitive, and correlate with ECG. They are sometimes more diffi cult to iden- tify when used in a demand mode, though correlation with the ECG is usually suffi cient. Other internally implanted devices including left ventricular assist devices, intra-aortic balloon pumps, and intravascular cooling devices may also generate stray potentials and should be considered when unidentifi ed sources of noise are found in patients with these devices. For neurological patients, the presence of a vagus nerve stimulator (VNS) or deep brain stimulator (DBS) causes intermittent high-frequency noise associated with the duty cycle of the device. Such devices should be turned off when possible during the period of EEG recording unless (in the case of DBS) the recurrence of tremor is more severe than the artifact produced by DBS.

Movement and Physical Artifacts Head and Patient Movement Movements create high-amplitude unpredictable artifact involving both large DC potentials and high-frequency muscle artifacts that often saturate the EEG recording system, making the record uninterpretable. Some of this noise is generated by motion of the EEG electrode wires and electrodes relative to the scalp or by movement of the wires through ambient electromag- netic fi elds including AC hum generated by fl uorescent lights, radio frequency waves, etc. Movement-related artifact can be enough of a problem with uncooperative patients or young children that sedation (or sleep deprivation) is sometimes needed to obtain usable recordings, even though most sedating medications can infl uence EEG activity (see Appendix A for a list of medications and their effects on the EEG). Restraint is seldom helpful since patients can still move their heads enough to disturb the recording. Measures to reassure the patients and make them comfortable (blankets, pillows, a warm cloth over the eyes, or a family member to hold the patient’s hand) may be more effective.

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69CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

Tremor Tremor can cause a rhythmic artifact due primarily to movement of the patient and electrodes, though muscle-related potentials may also play a role. The frequency of the movement or muscle potentials may have diagnostic signifi cance. For example, a 4- to 6-Hz tremor at rest may indicate Parkinson’s disease, while a side-to-side head tremor may be more suggestive of familial or essential tremor (Fig. 2-24). Addition of an EMG electrode can sometimes be helpful to confi rm the motor origin of these potentials if they appear suspicious for rhythmic seizure activity.

Shivering Artifact Shivering may occur in patients with fever or infection, therapeutic hypothermia, or other conditions and is generally of higher frequency than tremor, in the 10- to 15-Hz range. Docu- mentation of shivering activity by the technician is helpful for interpretation.

Patting, Rocking, Sucking, and Sobbing Recordings in infants pose a particular set of recording problems and unique artifacts. Moth- ers attempting to calm crying infants may rock or pat them rhythmically, which may create movement-related artifacts. Babies feeding will generate a rhythmic sucking artifact, which appears as a variant of glossokinetic artifact. Crying infants may have rhythmic respiratory artifacts induced by sobbing, again generating movement-related potentials. Good documen- tation of behavior by the technician can help the reader avoid interpretive pitfalls under these circumstances.

External Physical Artifacts Loud noises (doors slamming, loudspeaker paging systems, etc.) can affect the EEG in unpre- dictable ways, both by startling the patient (waking from sleep, sudden movement, etc.) and causing electrical transients. Walking in the vicinity of the recording may produce a rhythmic

FIGURE 2-24. Tremor artifact. Tremor generates a potential at 4 Hz with overlying bursts of spiky muscle artifact at F4 on the bipolar montage (left) but is more prominent on left hemisphere electrodes in the ipsilateral ear refer- ence (right). Use of multiple montages can help sort out artifact from cerebral potentials. Calibration bar is 1 s, 50 μV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York: Raven Press 1995:29, Fig. 2-23, with permission.)

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70 Reading EEGs

artifact that may resemble seizure activity if grounding is inadequate or in the intensive care unit setting associated with multiple electrical devices.

QUESTION 2.5: List the major categories of noncerebral artifacts commonly found in EEG recordings.

ANSWER: Artifacts can be grouped into the following categories: (i) electrode-related noise and potentials such as electrode pops and high- or low-impedance electrodes, (ii) noncerebral biological potentials such as eye movements and blinking, ECG and pulse artifact, chewing, and glossokinetic and muscle artifacts, (iii) electrical patient care device and power supply– related artifacts such as 60-Hz hum and respirator artifacts, and (iv) patient movement and extraneous physical artifacts.

Interpretation and Writing the Report

Biases and the Patient History When approaching the EEG, how much should we know about the patient’s history? If we know before looking at the EEG that the patient has seizures or had a recent stroke over one hemisphere, this introduces biases into our reading. Consciously or unconsciously, we will approach the study looking for evidence of seizures or focal slowing over one hemisphere, and our expectations may color our reading. Hence, it is better to form our opinion about the study before we know the details of the patient’s medical condition. There is one critical piece of information we do need in order to interpret the study—the patient’s age. The only way to know whether the PDR and other features are normal or pathological is to interpret them in the context of the patient’s age. Once you have committed to an interpretation, that a wave is sharp or not, or that there is focal slowing or not, only then is it appropriate to learn the patient’s history. Armed with that knowledge, the fi nal goal is to integrate the EEG fi ndings with the history. Sometimes the correlation is excellent; the patient with a history of seizures is found to have spike-and-wave discharges, and the stroke patient has slowing over the appropri- ate hemisphere. At other times, however, the fi ndings do not correlate. It is important that the interpretation accurately conveys the EEG fi ndings, even when they are not as expected. If the study is technically limited due to patient movement, muscle artifact, AC line noise, or lack of opportunity to observe both waking and asleep states, the reader may recommend that a repeat study be performed to address these issues.

An Approach to Writing the Report The report is meant to accomplish several goals. It must document that the study was per- formed and describe the major fi ndings. A brief and unequivocal statement of the results should be presented in the form of an EEG diagnosis. Finally, the reader must also interpret those results so that an ordering physician with little or no knowledge of EEG can understand the fi ndings and plan a course of action if necessary. The reader may also make recommenda- tions about the need for additional investigation or even treatment recommendations under some circumstances. For example, if the EEG is diagnostic of status epilepticus, the report should state that the physician or team caring for the patient was informed immediately after the diagnosis was made and suggest that anticonvulsant treatment be initiated and that further EEG monitoring may be indicated.

The report should be divided into sections roughly following the plan outlined below. Each institution has its own conventions for reporting, and this is meant only to serve as an example.

Patient and Study Identifi cation As trivial as it may seem, one of the most important aspects of writing the report is identify- ing the patient. This information should include the patient’s full name and age or birth date,

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71CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

his or her medical record number, the referring or ordering physician, the date the study was performed, and the study number assigned by the EEG technician.

History This should be a very brief description of the patient and the medical problem and the reason the study was ordered. If the patient has known seizures, it is useful to state when the most recent seizure occurred since that may infl uence the EEG fi ndings. This section should also include a list of any centrally active medications the patient is taking, whether sedation was used and whether the patient was sleep deprived for the study.

Procedure This section should describe the technique used for the recording, including the strategy for electrode placement (e.g., the International 10–20 system of electrode placement) and any extra electrodes that may have been applied, the state(s) of the patient during record- ing, and any activating procedures that were used. In the days of analog recording, it was usual to state that multiple montages were used, but now that montages can be varied at any time during or after recording, the montages used in recording are less critical. Still, it is a good habit to look at several montages for each study, particularly when a questionable waveform is seen.

Technical Description This section should ideally be presented in two parts. First, the presence and characteristics of the normal features of the EEG should be described. This will include a description of the PDR including its frequency, amplitude, regulation, synchrony, symmetry, and reactivity to eye opening and closure. Progression to drowsiness and/or stage 2 sleep should be documented with descriptions of K complexes, sleep spindles, and other normal sleep features that were seen. The arousal pattern, if observed, should be described. Responses to hyperventilation, photic stimulation, and any other activating procedures should be stated. Absence of normally expected activities for a given state should also be noted.

The second part should document and thoroughly describe any abnormal activities, including focal or generalized slowing, epileptiform activities (focal or generalized), seizure activity, status epilepticus, and any behavioral spells or other unexpected events that occur during the recording. Abnormalities in the ECG should also be noted. Abnormalities should be described in terms of their morphology, amplitude, frequency components, distribution, and how prevalent the abnormality is in the recording (using such terms as rare, occasional, frequent, persistent, or continuous). If abnormal waves occur at two or more separate loca- tions, it is important to distinguish whether they occur simultaneously or independently. The state in which the abnormal activity was observed or most prominent should be noted, and whether abnormalities were enhanced by activating procedures. Any epileptiform activity that was observed should be thoroughly described, and the absence of epileptiform activity should also be noted.

EEG Diagnosis This section should state whether the study is normal or abnormal, and if abnormal, it should briefl y list the abnormal fi ndings. If multiple, they should be numbered for clarity.

Clinical Interpretation This is where the fi ndings are discussed in light of the clinical history. Abnormalities should be noted as mild, moderate, or severe based on their intrinsic severity and prev- alence during the study. The relevance of abnormalities to patient’s history should be discussed. A brief differential diagnosis of the abnormal fi ndings may be appropriate,

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72 Reading EEGs

particularly if they do not fi t well with the clinical history. Attempts to reconcile these differences may also be appropriate, including conversations with the EEG technician, the referring physician, or, if possible, the patient or review of the patient’s record. If a diagno- sis is uncertain, recommendations for additional studies that might clarify the picture may be appropriate. For example, if no epileptiform activity was observed despite a history of seizures, it may be appropriate to recommend an additional study with sleep deprivation if sleep was not observed during the initial recording. If seizures or status epilepticus is observed, the report should document notifi cation of the referring physician and suggest additional investigation and treatment.

QUESTION 2.6: What are the major components of the EEG report?

ANSWER: The report must identify the patient and give a brief pertinent history or identify the reason the study was performed. A list of CNS-active medications is useful. The procedure should be described including the electrode placement. The technical description should describe both normal and abnormal features. The diagnosis section should list the abnormalities, and a clinical interpretation should put those findings into context with the clinical history.

In subsequent chapters, you will learn about the various abnormalities and their signifi - cance, which will enable you to generate an EEG report with confi dence. Now it is time to apply what you have learned. Figures 2-25 and 2-26 show sample EEGs with specifi c abnor- malities. While you may or may not know the signifi cance of the pathology shown, you should be able to describe the abnormal features with accuracy and confi dence.

Fp1-F7

F7 - T3 T3 - T5 T5 - O1 Fp1-F3 F3 - C3 C3 - P3 P3 - O1 Fz - Cz Cz - Pz Fp2-F8 F8 - C3 C3 - P3 P3 - O2 Fp2-F8 F8 - T4 T4 - T6 T6 - O2 EKG

FIGURE 2-25. Identifying EEG pathology—Test EEG 1. Using the terminology described in this chapter, describe the abnormality demonstrated in this EEG sample. This one should be easy! Calibration bar is 1 s, 50 μV.

ANSWER: A high-voltage surface positive spike-and-wave over the left frontotemporal region, reversing at the F7 and F3 derivations, with subsequent delta slowing over the left temporal and frontal areas extending to the contralateral frontal leads. Focal interictal spikes are highly predictive of epilepsy and will be discussed in greater detail in Chapter 4.

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73CHAPTER 2 | Approaching the EEG: An Introduction to Visual Analysis

REFERENCES 1. Geyer JD, Bilir E, Faught RE, et al. Signifi cance of interictal temporal lobe delta activity for localization of the

primary epileptogenic region. Neurology 1999;52:202–205. 2. Reiher J, Beaudry M, Leduc CP. Temporal intermittent rhythmic delta activity (TIRDA) in the diagnosis of

complex partial epilepsy: Sensitivity, specifi city and predictive value. Can J Neurol Sci 1989;16:398–401. 3. Chatrian GE, Petersen MC, Lazarte JA. The blocking of the rolandic wicket rhythm and some central changes

related to movement. Electroencephalogr Clin Neurophysiol 1959;11:497–510. 4. Bancaud J, Hecaen H, Lairy GC. Modifi cations de la reactivitie EEG, troubles de fonctions symboliques et

troubles confusionnels dans les lesions hemispherics localisées. Electroencephalogr Clin Neurophysiol 1955;7:179– 192.

5. Bancaud J, Colomb D, Dell MB. Rolandic spikes: An EEG reading characteristic of children. Rev Neurol (Paris) 1958;99:206–209.

6. Kellaway P. An orderly approach to visual analysis: Characteristics of the normal EEG of adults and children. In: Daly DD, Pedley TA, eds. Current Practice of Clinical Electroencephalography. 2nd Ed. New York: Raven Press, 1990:143.

7. Smith JR. The electroencephalograph during normal infancy and childhood. I: Rhythmic activities present in the neonate and their subsequent development. J Genet Psychol 1938;53:431–453.

8. Lindsley DB. Longitudinal study of he occipital alpha rhythm in normal children: Frequency amplitude stan- dards. J Genet Psychol 1939;53:431–453.

9. Maulsby RL, Kellaway P, Graham M. et al. The normal electroencephalographic Data Reference Library: Final Report 1968. Contract NAS 9-1200, National Aeronautics and Space Administration. Found in Kellaway P. “An orderly approach to visual analysis: Characteristics of the normal EEG of adults and children.” In: Daly DD, Pedley TA, eds. Current Practice of Clinical Electroencephalography. 2nd Ed. New York: Raven Press, 1990:198.

10. Perez-Borja C, Chatrian GE, Tyce FA, et al. Electrographic patterns of the occipital lobe in man: A topographic study based on use of implanted electrodes. Electroencephalogr Clin Neurophysiol 1962;14:171–182.

11. Cram JR, Kohlenberg RJ, Singer M. Operant control of alpha EEG and the effects of illumination and eye closure. Psychosom Med 1977;39:11–18.

12. Kriegseis A, Hennighausen E, Rösler F, et al. Reduced EEG alpha activity over parieto-occipital brain areas in congenitally blind adults. Clin Neurophysiol 2006;117:1560–1573.

FIGURE 2-26. Identifying EEG pathology—Test EEG 2. The pathology here is more subtle. ANSWER: In this sample from the same patient with the left frontotemporal spike discharge shown in Figure

2-25, subtle left frontotemporal delta slowing is observed between the third and fourth QRS complexes on the ECG trace. Such slowing is nonspecifi c but can indicate focal cortical dysfunction. Focal and generalized slowing will be covered in greater detail in Chapter 3.

Fp1-F7

F7 - T3

T3 - T5 T5 - O1 Fp1-F3 F3 - C3

C3 - P3

P3 - O1 Fz - Cz Cz - Pz

Fp2-F8 F8 - C3

C3 - P3 P3 - O2 Fp2-F8

F8 - T4 T4 - T6 T6 - O2 EKG

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74 Reading EEGs

13. Quigg M. EEG Pearls. Philadelphia, PA: Mosby, Inc., 2006:56. 14. Gotoh F, Meyer JS, Tagaki Y. Cerebral effects of hyperventilation in man. Arch Neurol 1965;12:410–423. 15. Jibikia I, Kurokawa K, Matsuda H, et al. Widespread reduction of regional cerebral blood fl ow during hyperventilation

induced EEG slowing (‘buildup’): Observation from subtraction of brain imaging with SPECT using Technetium- 99m hexamethyl-propyleneamine oxime. Neuropsychobiology 1992;26:120–124.

16. Patel VM, Maulsby RL. How hyperventilation alters the EEG: A review of controversial viewpoints emphasizing neurophysiological mechanisms. J Clin Neurophysiol 1987;4:101–120.

17. Epstein MA, Duchowny M, Jayakar P, et al. Altered responsiveness during hyperventilation-induced EEG slowing: A non-epileptic phenomenon in normal children. Epilepsia 1994;35:1204–1207.

18. Maher J, Ronen GM, Ogunyemi AO, et al. Occipital paroxysmal discharges suppressed by eye opening: Variability in clinical and seizure manifestations in childhood. Epilepsia 2005;36:52–57.

19. Siniatchkin M, Groppa S, Jerosch B, et al. Spreading photoparoxysmal EEG response is associated with an abnor- mal cortical excitability pattern. Brain 2007;130:78–87.

20. Tauer U, Lorenz S, Lenzen KP, et al. Genetic dissection of photosensitivity and its relation to idiopathic general- ized epilepsy. Ann Neurol 2005;57:866–873.

21. Brittenham D. Artifacts. In: Ebersole JS, Pedley TA, eds. Clinical Practice of Electroencephalography. 3rd Ed. Philadelphia. PA: Lippincott Williams & Wilkins, 2002:271–287.

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