The Normal Adult EEG

L. John Greenfield Jr

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 and the patient’s age and clinical state (wakefulness, 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 significantly 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 (8-12.5 Hz). Indeed, the alpha frequency band was defined based on the usual frequencies seen in the adult PDR. A study of healthy young adults (24- to 35-year-old Air Force personnel) showed a mean frequency of 10 Hz, with <1% having a frequency <9 Hz.¹ 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 (eg, T5-O1 and T6-O2) within the same 1-second 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 1 to 10, name the months of the year, etc.) with eyes closed.

Other faster and slower frequencies may be represented in the waking EEG. Beta frequencies (13-25 Hz) are sometimes seen, particularly over frontal and central regions, but they should be low in amplitude. Beta activity of >25 µV is considered abnormal,¹ though the cause is nonspecific and, in normal adults, is often related to CNS-active medications such as the benzodiazepines or barbiturates. Theta (4 to <8 Hz) activity is frequently present, often in the context of a transition to drowsiness, and is almost never abnormal. Slow-wave (delta, <4 Hz) activity is generally considered abnormal in awake adults. A certain amount of delta activity is acceptable 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. These “posterior slow waves of youth” should not be considered pathologic 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.²^,³ The ontogeny of the PDR will be covered in more detail in Chapter 7, but we can briefly summarize the major milestones in the development of PDR frequency as follows¹:

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 5-6 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 and 10 Hz by 15 years.

This can be summarized in the “rule of 3s and 8s” in which most of the milestones are conveyed 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.

PDR Amplitude, Synchrony, and Symmetry

The PDR amplitude is normally in the moderate range, from 15 to 45 µV, often higher in children and lower in the elderly.⁴ The waveforms should be synchronous between hemispheres and symmetrical in amplitude, though amplitude differences of up to 20% are common in normal patients. Most often, such differences in amplitude are due to variations in skull thickness, which is usually greater on the left side causing right side amplitudes to be slightly higher.

Slow Alpha vs Slow Alpha Variant

If the PDR is slower than 9 Hz in young adults, this is generally considered abnormal but nonspecific and suggests a mild diffuse disturbance of cortical function, as seen in metabolic encephalopathies and primary neuronal disorders. However, patients with normal alpha frequencies 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 significance. An example is shown in Figure 6.1. Longer runs of slow alpha variant can occur, but a patient with only 5-Hz PDR and no faster alpha rhythm likely has pathologic 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, 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 extremity (or sometimes by thinking of moving the extremity). An example is shown in Figure 4.2 in which mu activity is revealed by eye opening, which suppresses the PDR but not the central alpha frequency mu activity.

Lambda Waves

Lambda waves are sharply contoured surface-positive waves observed in the occipital leads during wakefulness with eyes open, which correlate with visual fixation to a target after a saccadic 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 downstroke that may go past the baseline giving it a biphasic appearance (see Figs. 6.2 and 9.3). Since they occur with eyes open, when the alpha PDR is suppressed, they stand out clearly from the background. They can sometimes be confused with occipital sharp waves, but the association with eye movement artifacts and suppression with eye closure can help to distinguish them as nonpathologic. They have no clinical significance.

Origin of the PDR

The posterior dominant alpha rhythm is generated by intrinsic oscillators within the occipital cortex and heavily influenced 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 intracranial electrodes have shown multiple alpha generators, not only in the occipital region but also in central and temporal areas.⁵ We see evidence of multiple oscillators in the modulation of the PDR, that is, the gradual waxing and waning of amplitude and (to a lesser extent) frequency seen to some degree in most normal records. Figure 6.3 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 first 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 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- 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.

FIGURE 6.1. 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 complete without the notching between the two fused waves, sometimes with a spiky appearance, but the slower waveform 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 second, 50 µV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York, NY: Raven Press; 1995:69, Figure 3-27, with permission.)

The influence 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 desynchronizes 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 influence 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 influence the amount and amplitude of alpha activity.⁶ 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.⁷ Another clue is that when the eyes close again, there is a transient increase in the PDR frequency in the first 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).⁸ 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.

FIGURE 6.2. 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 fixation on a target. Calibration bar is 1 second, 50 µV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York, NY: Raven Press; 1995:97, Figure 3-55, with permission.)

FIGURE 6.3. Modulation of the PDR. A. Waxing and waning amplitude with relatively constant frequency in two anteroposterior derivations from a 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 frequency, which could result in amplitude modulation if there were a shifting phase relationship between multiple oscillators. The sum of 10 Hz plus 9 Hz (trace 4) is a mixed frequency waveform with dramatic amplitude modulation with a period of 1 second—the difference in frequencies between the two oscillators.

DROWSINESS AND SLEEP

The principles of formal sleep scoring (analyzing an EEG or polysomnogram record for features of sleep) will be covered in detail in Chapter 20. This introduction will help you understand the waveforms associated with sleep as they appear in routine EEG recordings.

The EEG undergoes dramatic and specific 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
Dropout of the PDR
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 (see Fig. 6.4). These movements can be detected on frontal EEG electrodes and electrodes placed at the outer “corners” of the eyes, usually at the right upper canthus (RUC) and left lower canthus (LLC). Eye movements can be detected at these electrodes because 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 simultaneously 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 right. Figure 5.4 shows how the globe dipole generates these waves. Positioning the right electrode higher and the left electrode lower helps to indicate upward and downward eye movements as well. This is occasionally helpful for determining whether a frontal potential is of cerebral or ocular origin. For now, it is sufficient 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 70-200 ms, with highly variable amplitude. They can be quite sharp,
particularly in children (see Fig. 9.2), but are rarely considered epileptiform. They usually occur as drowsiness is about to transition into stage 2 sleep.

FIGURE 6.4. 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 second, 50 µV. (Example from Blume WT, Kaibara M. Atlas of Adult Electroencephalography. New York, NY: Raven Press; 1995:19, Figure 2-3, with permission.)

Hypnagogic 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 “hypnagogic hypersynchrony” and is a normal finding in children, even when there are associated faster “spikelike” components. Hypnagogic hypersynchrony or “drowsy bursts” should not be used to support a diagnosis of generalized epilepsy (eg, absence epilepsy with 3-Hz spike-and-wave) unless the spike-and-wave pattern also occurs in states other than drowsiness (see Fig. 9.7 for examples of generalized 3-Hz spike-and-wave). A similar pattern of high-amplitude delta frequency slowing can be induced by rapid deep breathing, one of the “activating procedures” done in routine EEG recording to bring out
abnormalities (see below). This hyperventilation-induced high-amplitude rhythmic slowing (“HIHARS”), which is most commonly seen in children and young adults, may rarely induce transient loss of awareness associated with cessation of activity, staring, and oral and manual automatisms in normal subjects without an underlying seizure disorder.⁹

Stage 2 Sleep

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

K-complexes
Sleep spindles

FIGURE 6.5. Stage 2 sleep. Stage 2 sleep is marked by the presence of sleep spindles, here seen symmetrically in the parasagittal regions (outlined by boxes) associated with delta slow waves.

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