Blume's Atlas of Pediatric and Adult Electroencephalography, 1st Edition

Chapter 3

Normal EEG

The electroencephalograms (EEGs) of infants and children are normally characterized by a greater mixture of waveforms and frequencies than is found in adults. The relative predominance of these wave types varies with age. There may be considerable intersubject variability, possibly because of differences in maturation. Several waveforms, such as the initial response to hyperventilation and posterior slow rhythms of youth, may be normally asymmetrical. Moreover, infants and young children tend to become drowsy during the recording, and the electrographic alterations with drowsiness are greater than those with adults.

These factors create wider limits of normality than might be expected in adults. In addition, the superimposition of two or more waveforms often creates sharply contoured waves that can be mistaken for spikes.

Fortunately, most of the clinically significant EEG abnormalities in children are morphologically well defined. However, to identify abnormalities in children's EEGs with confidence, it is first necessary to sharpen one's concept of normal features and their variations.

For each state of alertness (wakefulness, drowsiness, sleep, and arousal), the electroencephalographer interpreting a child's recording should ask the following questions:

  1. Is the electrical maturation adequate?
  2. Are there any marked nonartifactual asymmetries beyond those normally accepted for certain waveforms?
  3. Are there any spikes?
  4. Is there any excessive focal or diffuse delta activity?

For adults, similar criteria apply:

  1. Are normal phenomena present: alpha, mu, theta, V waves, spindles?
  2. Are such features symmetrical or almost so?
  3. Are states (wakefulness, drowsiness, sleep, and arousal) easy to identify and do they contain normal features?
  4. Are abnormal spikes present?
  5. Is there focal or diffuse excess delta activity for state?


Awake Recordings

Background Activity

Hans Berger was the first to recognize that the frequency of background activity in childhood increases with age, (Gloor, 1969). Studies by Dreyfus-Brisac (1975), Hagne et al. (1973),Pampiglione (1972), Petersen and Eeg-Olofsson (1971), and Samson-Dollfus and Goldberg (1979) have provided the frequency milestones outlined below.

There is no discernible dominant occipital activity until the age of 3 months, at which time a rhythm of 3 to 4 Hz can be seen. Its frequency increases to approximately 5 Hz at age 6 months; a 6 to 7 Hz rhythm is characteristic from 9 to 18 months. By age 2 years, a 7 to 8 Hz rhythm is usual; this increases to 9 Hz by 7 years. The mean frequency at age 15 years is 10 Hz.

Background activity can be appreciated best by passive eye closure, as the background can be attenuated by eye opening as early as age 3 months. Gentle passive closure of the eyes can be maintained for a few seconds. A low frequency filter (LFF) of 1 Hz might be helpful to decrease the quantity of movement artifact at such times. The occipital rhythm may also be seen during crying, as this is often associated with eye closure.

In estimating the background frequency, it is important to assure that the patient is not drowsy. Drowsiness should be suspected if there is less than the usual quantity of muscle artifact for age. During drowsiness, the background activity can be 1 to 2 Hz less than that for wakefulness; in children, this can persist for prolonged periods after sleep, even when the


child appears alert. Thus, passive eye closure should be performed at times when complete alertness is assured.

There is moderate intersubject variability of background amplitude. The following data will help to assess whether abnormal amplitudes exist, particularly if they are too low, suggesting a focal or diffuse paucity of cortical activity. Recording with the eyes open, Hagne (1968) found an amplitude of 10 to 20 µV in the first months of life, increasing to 20 to 40 µV at 6 to 12 months. Using the passive-eye-closure technique, Pampiglione (1972) found an amplitude of 50 to 100 µV at age 3 months, increasing to 100 to 200 µV at age 9 months. During passive eye closure, we have found considerable wave-to-wave amplitude variability in the first year of life, usually from 30 to 100 µV, with occasional waves reaching 200 µV in the latter part of the first year. Pampiglione (1972) reported amplitudes of 50 to 80 µV at age 2 years. The alpha amplitude in the study of Petersen and Eeg-Olofsson (1971)increased to a maximum at 6 to 9 years and then declined. In their study, the average alpha amplitude for children between 3 and 15 years was 56 µV, the amplitude of 90% of their children falling between 30 and 100 µV. The alpha exceeded 100 µV in 9% and remained between 20 and 30 µV in 1%. All of the latter were 12 to 15 years of age. None of the normal subjects showed a background activity less than 20 µV.

Most studies (Corbin & Bickford, 1955; Cornil & Gastaut, 1947) report that alpha activity tends to be higher on the right side. Petersen and Eeg-Olofsson (1971) found alpha-amplitude asymmetries in nearly all children, usually higher on the right. Five percent of their normal population showed an amplitude asymmetry exceeding 20% on the higher side. They found no relationship between alpha asymmetry and handedness.

Posterior Slow Waves and Lambda

The alpha rhythm in youth normally and commonly is interrupted by slower rhythms that occasionally combine with the alpha rhythm to create complex and often sharply contoured waveforms. These waveforms appear in the occipital, parietal, and posterior temporal regions. They attenuate with eye opening and may be augmented by hyperventilation. Their prominence may shift from side to side.

Polyphasic Potentials

Polyphasic potentials consist of 250 to 500 ms, medium to high-voltage waves occurring singly or repeating at 2 to 4 Hz. The main body of these waves is usually electropositive. It is often preceded and followed by an alpha wave whose negative-going deflection is greater than usual. Low-amplitude alpha waves may be superimposed upon this 250 to 500 ms potential. These features together create the polyphasic morphology of the phenomenon. Occasionally the accentuated alpha component, together with the after-coming slow wave, can resemble superficially a spike–wave complex, which it is not.

Some polyphasic potentials were found in nearly all of the normal controls reported by Petersen and Eeg-Olofsson (1971), although these potentials were present in only minimal amounts in 30%. The quantity increases gradually during the first decade of life, to peak from ages 9 years to the early teens. This increase in polyphasic potentials may give the false impression of deterioration in sequential EEGs carried out during this age period. Their prominence may be greater at the start of a recording than later. Polyphasic potentials may be asymmetrical; if so, they are usually of higher voltage on the right. However, the asymmetry should not persistently exceed 50%.

Slow Posterior Rhythm or Posterior Rhythmic Waves

Slow posterior rhythm (SPR) is sinusoidal, of low to medium voltage, 2.5 to 4.5 Hz, and may appear in brief sequences or prolonged runs. Less commonly, it may appear in medium- to high-voltage bursts. This rhythm was originally thought to be associated exclusively with absence attacks, but Petersen and Eeg-Olofsson (1971) found this rhythm in 25% of their normal population. It occurred more commonly in younger children; its incidence increased from 1 year of age to a maximum at 5 to 7 years. The SPR amplitude was 50 to 100 µV in 90% of the children, but it exceeded 100 µV in 10%. In 25% of the children, the SPR episodes lasted 3 s or more. In 16% of the children, this rhythm occupied more than 10% of the posterior activity; in approximately half, it constituted 2% to 10%.

The distinction between this normal phenomenon and a series of rhythmic waves that are actually abortive spike waves is not always clear. Rarely, such rhythmic waves can merge into clearly defined posteriorly situated spike waves; this may occur under the influence of hyperventilation. Thus, if the patient is referred for a question of absence attacks and the SPR is seen, a second attempt at hyperventilation may be indicated. However, unless clear spike waves are seen, no statement ascribing epileptogenic significance to such waves should be made.

Slow Alpha Variant

This waveform appears to be created by the partial fusion of two alpha waves, creating a notched waveform at half the alpha frequency, as described by Goodwin (1947). Unlike the first two posterior slow waves, this is not peculiar to children. Petersen and Eeg-Olofsson (1971) found such waves in 3.5% of their normal childhood population.



Lambda Waves

Lambda waves are sharply contoured occipital transients evoked by saccadic eye movements scanning a well-illuminated picture or complex design. The most constant and prominent phase is surface positive, whose duration is 75 to 150 ms; a subsequent 200 to 250 ms negative phase also may occur (Kooi et al., 1978). In early childhood, blinking or other eye movements may evoke sharply contoured occipital transients whose major phase is electronegative; this lasts 200 to 400 ms and may attain 100 to 200 µV. It may be preceded and followed by lower-voltage electropositive phases (Westmoreland & Sharbrough, 1975). This phenomenon occurs mainly from age 6 months to 10 years, attaining a maximum incidence and prominence between 2 and 3 years of age. Their association with scanning well-illuminated, interesting objects links these transients with lambda waves.

Lambda waves may attain higher amplitudes in children, giving them a spike-like configuration. Their occasional asymmetry in normal children furthers this resemblance to occipital spikes. Darkening the room, staring at a blank card, and eye closure will eliminate lambda waves.

Theta and Delta Activity

Varying amounts of diffuse theta activity are seen in the awake records of all pediatric age groups. Theta is seen as a central rhythm at age 3 weeks. The total quantity of theta increases sharply throughout the first years of life, reaches a peak at approximately age 5 to 6 years, and declines thereafter (Hagne, 1968; Corbin & Bickford, 1955). However, as noted in the previous section on posterior slow waves, theta appearing in the posterior head regions may be more prominent at later ages. With the eyes closed or open, theta is the dominant diffuse activity in recordings in the 2- to 5-year-old age group. With eyes closed, its total quantity is approximately equal to that of alpha activity at ages 5 to 6 years, after which alpha very gradually becomes more predominant. However, the relative proportion of alpha and theta varies considerably among normal children. It is often more prominent over the left hemisphere than the right at all ages. The area of theta distribution is widespread in younger children and tends to be confined to temporal and occipital regions in older children. Despite the aforementioned variations, there is little change in theta frequency with age.

Despite its normal prevalence, or perhaps because of it, cerebral disease very rarely manifests itself as focal or diffuse excess theta activity. The rare exceptions are (a) diffuse bursts of 3 to 4 Hz waves not related to drowsiness, which may herald the later appearance of generalized spike–wave discharges, and (b) an awake tracing containing only theta activity in chronic, static, severe encephalopathies. In older children and adolescents as in adults, focal excess theta may be an abnormality. However, its predominance in one region should be consistent before definite clinical significance is ascribed. Therefore, the electroencephalographer reading the child's EEG does not have to worry about the quantity of diffuse theta activity as long as there is some variability in its quantity and other normal frequencies are present.

Perhaps the major reason why the quantity of diffuse or even regionally accentuated theta is difficult to correlate with disease processes is the considerable intersubject variability in theta quantity in all age groups (Petersen & Eeg-Olofsson, 1971; Samson-Dollfus & Goldberg, 1979).

Although frequency analysis indicates that delta activity dominates during the entire first year of life (Hagne et al., 1973; Pond, 1963), delta and theta appear approximately equally prominent to visual inspection in the first year. The absolute quantity of delta activity increases throughout the first year (Hagne, 1968) and actually continues to do so until the fifth year (Corbin & Bickford, 1955). However, this increase is less than that for theta; for this reason, theta activity becomes more prominent as the first year progresses and is the dominant diffuse awake activity in the 2- to 5-year-old age group. Delta activity is commonly diffuse in early childhood but may be transiently asymmetrical, the side of maximum expression shifting over the course of the EEG recording. Therefore, it is important to examine long stretches of the recording before concluding that delta clearly predominates in one region. Small amounts of diffuse delta activity can normally be identified in older age groups, even into adolescence.

Beta Activity

Petersen and Eeg-Olofsson (1971) found beta activity at 10 to 20 µV in various quantities in all awake recordings of their 743 unmedicated normal children. Amplitudes above 20 µV appeared in only 1%. Other principles concerning beta activity in awake recordings for adults also apply to children.

Central Rhythms

Sustained runs of activity develop earlier in the central regions (C3, C4) than in any other area (Hagne et al., 1973). Pampiglione (1972) found a 6 to 7 Hz rolandic rhythm before 3 months of age whose frequency


increases to 8 to 10 Hz after 3 months. Its quantity augments further between 6 and 12 months (Hagne, 1968). Even in the 1 to 5 year-old age group, the most prominent activity while awake with eyes open resides in the central region. Moderate asymmetries of such activity are acceptable. However, a complete and persistent unilateral absence of central rhythms usually reflects a lesion on that side.

On occasion, such central rhythms can become even more sharply contoured than the mu they resemble, giving the appearance of spikes. To assure that such forms are not spikes, look for similar sharply contoured waves that are clearly central or mu rhythms. Unless a definite qualitative distinction can be made, call them both normal central rhythms.

Frontal Activity

During wakefulness, there is normally a relative paucity of activity over the frontal regions in the early years (Hagne, 1968). Subsequently, theta activity predominates. This rarely attains a voltage equal to that in the central regions except in drowsiness.


In adults, a chronic, mild focal lesion can be detected by careful side-to-side comparisons. However, this is more difficult to accomplish in children because (a) transient asymmetries occur more commonly (especially in the very young) and (b) some types of activity are normally asymmetrical. Such activities include the following. Theta activity is usually more abundant over the left hemisphere (Petersen & Eeg-Olofsson, 1971); posterior slow waves often appear maximally on the right, particularly over the right posterior temporal region (T6), as compared with the left (T5) (Aird & Gastaut, 1959). Central rhythms may be asymmetrical (see previous). Hyperventilation may initially cause a greater buildup over one hemisphere, usually the left; this left–right difference is usually seen principally over the temporal regions. In infants, brief runs of delta activity may shift from side to side throughout the recording.

Activation Procedures

Any method that may elicit an EEG abnormality which has not occurred in a routine recording falls into the broad category of an activation procedure.


From age 4 years, children can cooperate with hyperventilation; their enthusiasm for the procedure usually is greater than that of adults.

The main role of hyperventilation is to elicit generalized spike–wave discharges when they are not present on the “resting” recording. Less commonly, focal spikes appear. Other focal abnormalities may also be revealed.

The “buildup” of slow waves is characteristically greater in children than in adults, particularly in children around 10 to 12 years of age (Petersen & Eeg-Olofsson, 1971). The first effect is usually an accentuation of the dominant frequency in the resting recording (e.g., alpha), followed by augmentation of theta; finally, 3-Hz rhythmic waves appear (Corbin & Bickford, 1955). These slower waves may occur posteriorly before becoming diffuse and maximum anteriorly. A slightly greater buildup on one side, usually the left, may occur in healthy subjects.

Sometimes hyperventilation creates sharply contoured waveforms whose differentiation from true spikes is difficult. This occurs particularly when the resting record contains a rich mixture of waves, such as beta and theta. In this situation, it is better to read the hyperventilation response as normal unless clear identification of spikes can be made. Revealing your uncertainty by terms such as “spikey” may mislead the reader of your report.

No pathological significance can be given to the abruptness or amount of buildup or to its persistence after the apparent end of hyperventilation. The quantity of slow waves depends primarily on the degree of hypocapnea produced and the blood sugar level (Kellaway, 1990). Moreover, many subjects continue to hyperventilate despite the technologist having asked them to stop.

Photic Stimulation

Four types of results occur with photic stimulation: (a) “driving”—i.e., response of varying morphology that is time-locked to the flash rate; (b) frontal myoclonic potentials, also time-locked, reflecting myoclonus of periocular and scalp musculature; (c) photoparoxysmal response, described in Chapter 4; and (d) no apparent effect.

Sleep Recordings

The reliable interpretation of pediatric and adult EEGs requires a thorough appreciation of drowsy, sleep, and arousal phenomena, as patterns


occur in these states that do not appear in normal subjects. In addition, the morphology of common sleep patterns may differ between children and adults. Lack of a clear correlation between clinical and EEG manifestations of state reflects a diffuse encephalopathy in children and adults.


Electroencephalographic signs of drowsiness commonly appear before the child, particularly an infant or younger child, appears drowsy to the technologist. A drowsy child's eyes may be wide open, and he or she may be restless.

The technologist should record the entire process of falling asleep so that the electroencephalographer can interpret the many changes that occur. A child may drop quickly from light drowsiness to deep sleep; intermittent recording would miss lighter sleep stages. It is common for young children to fluctuate fairly rapidly between drowsiness, sleep, and arousal. Continuous recording will assure that an abnormality that occurs only once or during one state of alertness or sleep will not be missed.

The most common drowsy pattern in children is diffuse rhythmic to sinusoidal theta, which gradually replaces the awake pattern and may persist for several minutes. This may be maximal centrally, more posteriorly, or frontocentrally. It is present from age 3 months to 4 years and then declines in prominence, to be only minimally evident after 6 to 7 years(Dale & Busse, 1951; Kellaway & Fox, 1952; Brandt & Brandt, 1955). The frequency is 3 to 5 Hz in the first year of life, increasing gradually to 4 to 6 Hz by age 4 to 5 years. Its amplitude is variable, up to 200 µV. Delta may augment slightly in drowsiness, but less so than theta.

Less common but more dramatic are generalized bisynchronous bursts of 2 to 5 Hz, rhythmic to sinusoidal, high-voltage waves that may exceed 350 µV (Kellaway & Fox, 1952). They are usually maximal frontocentrally. They first appear at 14 to 18 months and are most common between the ages of 3 and 5 years. However, they may be a component of drowsiness and light sleep to age 11 years. The frequency of such waves gradually increases with age. Because of the superimposition of some background activity upon such bursts, they may be confused with generalized spike waves, which may also appear preferentially with drowsiness. Identification of a burst as a spike–wave complex should be reserved for instances where the spike is clearly distinct from background activity. These normal bursts disappear in moderate sleep, unlike spike–wave complexes, which usually persist or may become more frequent in sleep.

The continuity of any occipital rhythm of wakefulness may break up in early drowsiness without initial slowing. On other occasions, there is slowing and increasing amplitude of the occipital rhythm; this may then merge with continuous sinusoidal theta rhythm described previously. Indeed, combinations of all these drowsy patterns commonly occur.

From age 5 to 6 months, beta activity at 25 Hz occasionally may become more prominent in drowsiness and light sleep, distributed diffusely or with an anterior or a posterior maximum. Transient and shifting beta asymmetries may normally occur. Beta, which occurs initially at about 5 µV, increases to a maximum of 30 µV at 12 to 18 months, following which there is a gradual decline. Unmedicated children older than 7 years of age show little beta in early sleep (Kellaway & Fox, 1952). Sedative medication will promote the appearance of beta at any age.

Vertex Waves

Rudimentary vertex waves (V waves) appear in light sleep as early as 3 to 4 months of age but usually are well developed by 5 months (Kellaway & Fox, 1952). They achieve their maximum expression at 3 to 4 years, following which there is a modest decline until adolescence, when the adult form is attained. Compared with those in adults, V waves in children are higher in voltage and briefer. Moreover, spontaneous V waves may occur in sequences, a phenomenon seen less often in adults. V waves may be electropositive, electronegative, or diphasic. They are often followed by a single slow wave that is opposite in polarity to the major deflection. shifting apparent asymmetries of V waves are commonly seen using bipolar anteroposterior or coronal montages. Such apparent asymmetries may be due to field cancellation effects and should be verified using an ipsilateral ear reference run. However, even then, shifting asymmetries may normally be seen. Unfortunately, there is no reliable relationship between the side of the larger or smaller V waves and a unilateral lesion.


Rhythmic sequences of 12 to 14 Hz waves appear in light sleep a few days after term (Kellaway & Fox, 1952). These may be the forerunners of spindles. Initially of low voltage and poorly defined, they become more clearly expressed by 3 to 4 months of age. From ages 3 to 9 months, spindles are almost invariably present during the non–rapid eye movement (non-REM) sleep of a normal child. They appear principally over central


parietal (C3,4; P3,4) and sagittal (Cz; Pz) regions but may extend frontally (F3,4) and diffusely. Spindles appear frontal–central in adults.

Several measures of spindle quantity indicate that they are most abundant at age 3 to 9 months. The quantity declines to a minimum at 22 to 54 months, after which there is a moderate increase (Lenard, 1970; Schulte & Bell, 1973; Tanguay, 1975). Thus, Tanguay found the maximum mean number of spindles per 10 s to occur at age 4 to 6 months; this decreased to a minimum at 27 to 54 months.

Similarly, these authors found the mean length of individual spindles to be 1.5 to 1.8 s at 4 to 6 months, falling to 0.5 to 0.6 s at 25 to 54 months. Spindle length later increased, reaching 0.9 s. Lenard (1970) found a mean spindle duration of 2.5 s at 3 months and 0.75 s at 22 months. Kellaway and Fox (1952) found spindles as long as 3 to 4 s in very young infants.

In contrast, the spindle wave frequency remains relatively consistent at 13 to 14 Hz from infancy to 4 to 5 years (Kellaway & Fox, 1952; Tanguay et al., 1975). After 3 to 5 years, a 10 to 12 Hz frontally dominant spindle occurs in about 5% of normal children (Kellaway, 1990). Its field may extend to the occipital region.

Unlike adults and older children, interhemispheric asynchrony of spindles occurs more commonly among subjects less than 1 to 2 years of age (Lenard, 1970; Tanguay et al., 1975). Although spindles tend to become more synchronous after this age, mild degrees of asynchrony may normally persist throughout the first decade. In addition to having the sinusoidal shape of adult spindles, the spindles of infants and young children may also be comb-shaped. Combined with V waves and other normal central rhythms of sleep, such comb-shaped spindles may create waveforms resembling spikes, which they are not.

Occipital Sharply Contoured Waves and Delta

These high-voltage diphasic occipital waves appear in moderate sleep and increase in incidence as sleep deepens. In deep sleep, such waves are associated with high-voltage, arrhythmic, posteriorly situated delta activity.

Such posterior phenomena are commonly seen in sleep of children less than 5 years of age; their prominence declines thereafter (Slater & Torres, 1979).

14- and 6-per-Second Positive Spikes

“Fourteen and six per second positive spikes” is a 60 to 70 µV comb-shaped phenomenon whose electropositive sharp components repeat at 14 and/or 6 to 7 per second. A burst may last as long as 3 s; rarely, only a single electropositive spike appears, principally in drowsiness or light sleep. Occurring independently in either hemisphere, the 14 and 6 field is widespread but centered over the posterior temporal regions. Thus, montages with long interelectrode distances, including interhemispheric linkages, best reveal their presence.

Much of the earlier work attributing clinical significance to this normal finding appears to be based on the assumption that a spike-containing phenomenon must be abnormal. Unfortunately, most of these earlier studies lacked precise criteria for the selection of normal control subjects. The following authors found 14 and 6 per-second positive spikes in their control populations: Schwartz and Lombroso (1968) 55%, Metcalf (1963) 26%, Gibbs and Gibbs (1964) 20%, Lombroso et al., (1966) 58%, and Demerdash et al. (1968) 7%. Schwartz and Lombroso (1968), Lombroso, et al. (1966), Reiher & Carmant, 1991 and Eeg-Olofsson (1971) did not find any correlation between the presence of “14 & 6” positive spikes and personality variables or vegetative-like complaints.

Most studies (Demerdash et al., 1968; Eeg-Olofsson, 1971; Petersen & Akesson, 1968) found an increased quantity with age of the child, with a peak incidence at early adolescence.Lombroso et al. (1966) found considerable intersubject variability in the quantity of “14 and 6.”

In EEGs of children with acute encephalopathies and a depressed level of consciousness, Drury (1989) identified 14 and 6 per-second positive spikes resembling those of normal sleep in duration, morphology, frequency, and repetition rate, but they differed in being evoked by stimulation.


At less than 2 months of age, arousal consists of a simple decrease in voltage of the tracing. At 2 to 3 months, a rudimentary diphasic slow wave may occur in response to stimuli. The initial diphasic component may be absent if arousal is spontaneous. Resembling a vertex wave, this phenomenon becomes better developed by 5 months; it may merge into a series of delta waves. If further arousal ensues, 4 to 8 Hz rhythmic waves appear diffusely, maximal frontocentrally, lasting 1 to 5 s or longer. First seen at 7 months (Kellaway & Fox, 1952), such waves become well developed at 13 months and remain prominent until age 3 to 4 years.

Accompanying or immediately following this rhythmic theta is diffuse 1 to 3 Hz, semirhythmic to arrhythmic diffuse delta. This delta


component of arousal may initially be accentuated anteriorly but tends to persist longer posteriorly. Such delta waves may appear simultaneously anteriorly and posteriorly as independent activity. The posterior delta is usually the slower. Over the next several seconds, the frequency of this rhythm increases to 4 to 5 Hz, when it becomes indistinguishable from a drowsy rhythm. This slower rhythm first appears at 2 to 3 months, is well established at 4 to 5 months, is maximally expressed at 12 to 18 months, and declines after 4 to 5 years. Of course, this sequence may abort at any point if the child returns to sleep.

Drowsiness and Arousal from 7 to 16 Years and in Adulthood

Medium-voltage, 5 to 7 Hz rhythmic waves lasting 5 to 30 s appear anteriorly in drowsiness; the frequency tends to increase with age within this range. During this period, the arousal gradually attains the adult form. Its rhythmicity–that is, its sinusoidal waveform–distinguishes such theta from abnormal theta bursts that are semirhythmic, reflecting the superimposition of multiple theta frequencies.

Except for arousal from deep, non-REM sleep, where a brief delta/theta burst may occur, adolescent and adult arousal should consist of conversion from sleep to awake EEG characteristics within 1 to 2 s. A childlike arousal pattern at this age indicates an encephalopathy or a postictal state.

Normal Electroencephalogram of Adults

The point-form notes preceding the illustrations of normal phenomena adequately describe EEG features of adults. These evolve far less than they do in children.


Normal Awake: Pediatrics

3 to 12 months (Figs. 3-1 to 3-10)

  • Delta and theta equally prominent with eyes open.
  • Transient asymmetries common.
  • Central rhythms develop during first year.
  • Passive eye closure elicits posterior rhythms equivalent to alpha of older age groups.
  • Eyes open unless indicated.

14 months to 2 years (Figs. 3-11 to 3-18)

  • Pace of development slows in second year.
  • Theta and central rhythms better developed.
  • Delta still prominent.
  • Relative paucity of frontal rhythms.
  • Eye closure elicits posterior rhythms at higher frequency than in first year.
  • Eyes open unless indicated.

3 to 4 years (Figs. 3-19 to 3-23, 3-25 to 3-27)

  • Diffuse theta is prominent; exceeds delta.
  • Diffuse delta present.
  • Alpha moderately developed when eyes are closed.
  • First manifestation of “posterior slow waves” as polyphasic potentials and posterior rhythmic waves.

5 to 10 years (Figs. 3-24, 3-28 to 3-39)

  • Slow pace of development.
  • Well-developed alpha with eyes closed
  • Variable quantity of posterior theta and delta that may be asymmetrical.
  • Variable quantity of diffuse theta.
  • Delta persists at about 20 to 30µV, principally with eyes open.
  • Prominent central rhythm (mu) that may resemble spikes and may be asymmetrical.

11 to 16 years (Figs. 3-40 to 3-43, 3-50)

  • Well-developed alpha.
  • Variable quantity of posterior slow waves that may be asymmetrical.
  • The previous two features in combination create sharply contoured waves that are not spikes.
  • Diffuse theta has diminished but continues.
  • Minimal diffuse delta, principally with eyes open.



Hyperventilation (Figs. 3-25, 3-44 to 3-49, 3-51)

  • Initially accentuates background including posterior slow waves.
  • Posterior build-up usually precedes anterior build-up.
  • Asymmetrical bursts normally occur, usually maximum left.
  • Sharply contoured waves common.

Normal Awake: Adults

Alpha Rhythm (Figs. 3-52 to 3-60, 3-63, 3-64, 3-66 to 3-71)

  • 9 to 13 Hz; slows to 7 to 8 Hz in drowsiness.
  • Sinusoidal or sharply contoured if beta present.
  • Waxing and waning–that is, “beating”–if composed of two close frequencies, such as 9 and 10 Hz.
  • Same dominant frequency in each hemisphere.
  • Highest amplitude O1,2; P3,4; T5,6.
  • Commonly extends to C3,4; A1,2; T3,4.
  • Bilaterally symmetrical or higher right most common. Higher left also normal.
  • Persistent symmetry >50% produced by artifact or abnormality.
  • Symmetry is variable within recording.
  • Ear referential recording is the best measure of symmetry.
  • Partial or complete “blocking” by eye opening or alerting; attenuation normally symmetrical.
  • Low voltage (<15 µV) in some normals.

Posterior Slow Waves of Youth (Figs. 3-61 and 3-62)

  • 250- to 400-ms monophasic waves.
  • Principally O1, O2.
  • Interrupts alpha activity, creating sharply contoured waves.
  • Adolescents, children, young adults.

Slow Alpha Variant

  • Saw-toothed waveforms at about one-half alpha frequency from partial fusion of two alpha waves.
  • Same location and reactivity as alpha.

Mu Rhythm (Figs. 3-58 and 3-65)

  • Arciform–apiculate negative and rounded positive phases.
  • 10 (9 to 11) Hz.
  • Intermingled with 20-Hz beta.
  • C3,4 and Cz location; occasionally involves P3,4.
  • Long epochs of unilateral expression common.
  • Normal if other central rhythms symmetrical.
  • Side-to-side shifts in maximal amplitude occur.
  • Movement of contralateral or ipsilateral extremities (or its contemplation) blocks rhythm.
  • Eye opening has no effect.
  • High voltage over skull defect–breach rhythm.
  • Apiculate phase may resemble spikes.

Beta (Figs. 3-68, 3-72 to 3-76)

  • Any rhythmic activity >13 Hz.
  • Some beta in all normals; amount varies.
  • 14 to 40 Hz, 15 to 25 Hz most common.
  • Usually sinusoidal; apiculate or arciform if competing frequencies; “beating” if close frequencies.
  • May occur in bursts.
  • Locations
  • Frontal: common.
  • Central: common, mixed with mu.
  • Posterior: fast alpha variant.
  • Diffuse: when abundant medication effect.
  • Usually <20 µV; occasionally 20 to 30 µV.
  • Amplitude and distribution increased by:
  • Drowsiness, light sleep, rapid eye movement (REM) sleep.
  • Skull defect.
  • Medication; especially benzodiazepines, barbiturates.
  • Diffuse theta may accompany medication-induced excess beta.


  • Low-voltage (<30 µV) 4 to 7 Hz diffuse theta is a common component of normal recordings.
  • It is more common in children and young adults than in older adults.



  • Temporal theta.
  1. ≤10% of awake records in normal subjects over 60 years.
  2. Equal distribution bilaterally or twice as abundant on left.
  3. Single wave or brief bursts separated by normal background.

Hyperventilation (Figs. 3-78 to 3-80)

  • Sequence:
  1. Increase in diffuse theta.
  2. Rhythmic delta in bursts.
  3. Continuous rhythmic delta.
  • Effect maximal anteriorly in most adolescents and adults.
  • Maximal amplitude of delta bursts may shift from side to side.
  • Multiple frequencies may create apiculate waveforms.
  • Effect greatest in youth, with maximal effort and low serum glucose.
  • Effect subsides in 60 to 90 s after hyperventilation (HV).
  • May abnormally elicit focal spikes, generalized spike–waves, and focal delta or theta.
  • Post-HV period may contain newly appearing focal delta or theta as abnormalities.

Lambda Waves (Fig. 3-81)

  • O1,2 principally; involve P3,4 and T5,6.
  • Bilaterally synchronous.
  • Diphasic or triphasic.
  • Largest wave electropositive, lasting 100 to 200 ms.
  • Usually <20 µV; rarely >50 µV.
  • Evoked by scanning well-illuminated, patterned visual field.
  • Present in 50% of normal EEGs.

Photic Stimulation (Figs. 3-82 to 3-84)

  • ≤3 flashes per second.
  1. Electropositive evoked response.
  2. 100-ms delay.
  3. Maximum O1,2 and T5,6.
  4. Variable anterior extension.
  5. Resembles lambda.
  • ≥6 flashes per second.
  1. More rhythmic response.
  2. Time-locked to flash with harmonic or subharmonic frequencies.
  3. Initial response may resemble (a) response of ≤3 flashes per second, (b) lambda, or (c) V-wave.
  • Responses larger in children and the elderly.
  • Responses symmetrical or asymmetrical, usually higher right.
  • Responses not visible in many normal subjects.

Wicket Spikes (See Chapter 4)

  • Arciform waves.
  • Negative phase apiculate.
  • Positive phase rounded.
  • Single or clusters.
  • T3,4, or T3,4 to F7 or F8.
  • Unilateral or independent bilateral.
  • No distortion of background rhythms.

Psychomotor Variant–Rhythmic Temporal Waves

  • 5 to 7 Hz.
  • Sharply contoured, often notched.
  • Mid-anterior temporal regions.
  • Parasagittal spread.
  • Bursts or runs.
  • Gradual onset and offset.
  • Monomorphic; that is, without evolution.

Subclinical Rhythmic EEG Discharge of Adults (SREDA) (See Chapter 4)

  • Sequential monophasic or biphasic apiculate waves mixed with rhythmic theta or delta.
  • No morphological evolution.
  • Abrupt onset; abrupt or gradual offset.
  • Usually in wakefulness, occasionally in sleep.
  • May occur after HV.
  • Principally parietal, posterior temporal.



  • Bisynchronous or unilateral.
  • Occurs principally in elderly or middle age.

Normal Drowsiness, Sleep, Arousal: Pediatrics

Drowsy Patterns (Figs. 3-85 to 3-92)

  • Slight increase in ongoing theta and delta in some patients in first year.
  • Spontaneous eye closure may elicit posterior rhythms in early drowsiness, but slower than when awake.
  • Trains of diffuse rhythmic theta may be maximum centrally, posteriorly, or anteriorly. Principally 3 months to 4 years. Most common pattern.
  • Beta accentuation, diffuse or maximal anteriorly or posteriorly, maximal at 5 to 18 months.
  • Decrease in ongoing activity: delta, beta.
  • Combinations of the previous features may occur in sequence: Certain combinations may occur simultaneously.

Burst Drowsy Pattern (Figs. 3-93 to 3-96)

  • Bursts of 2 to 5 Hz sinusoidal waves, usually maximal frontocentrally.
  • Superimposed on other drowsy patterns.
  • Begin at 14 to 18 months; most common at 3 to 5 years; seen until age 11 years.

V Waves (Figs. 3-97 to 3-103, 3-107, 3-110)

  • Of higher voltage and briefer than in adults, therefore spike-like.
  • Variable morphology and polarity.
  • May occur sequentially.
  • Shifting asymmetries.
  • Begin at 3 to 4 months, maximal at 3 to 4 years.

Spindles (Figs. 3-104 to 3-110, 3-114, 3-116)

  • First clearly expressed at 3 to 4 months.
  • More numerous and longer at 3 to 9 months than later.
  • Asynchrony common in first year.
  • Central–parietal location in early childhood.
  • May be comb-shaped.

V Waves and Spindles (Figs. 3-107, 3-110, 3-115)

  • V waves, spindles, and other central sleep rhythms combine to create sharply contoured waves that are not spikes.

Positive Occipital Sharp Transients of Sleep (POSTS) (Figs. 3-147 to 3-148)

  • Also known as lambdoid waves.
  • Monophasic.
  • Sharply contoured.
  • Electropositive.
  • Bioccipital.
  • Singly or in 4 to 5 s sequences.
  • Occur in most normal subjects.

Occipital Sharply Contoured Waves and Delta (Figs. 3-112 to 3-114)

  • Normal component of moderate to deep sleep under 5 years.

14 and 6 per Second Positive Spikes (Figs. 3-117 to 3-120)

  • Electropositive sharp components repeat at 14 and/or 6 to 7 Hz per second.
  • Positive component apiculate or arciform.
  • Negative component smooth.
  • Occur singly or in bursts.
  • 13 to 17 Hz or 6 to 7 Hz; principally 14 or 6 Hz.
  • Posterior temporal and adjacent areas.
  • Widespread field.
  • Best recorded with coronal or referential montages.
  • Duration: <1 to 2 s.
  • Seen in adolescents and young adults.
  • Occur during drowsiness and sleep.
  • Normal.

Arousal Sequence (Figs. 3-121 to 3-124)

  • Initial stimulus evokes one or more broad V waves.
  • Then 4 to 8 Hz diffuse rhythmic waves, maximum frontal-central occasionally mixed with delta.



  • Then 1 to 3 Hz diffuse delta.
  • Posterior delta is independent of anterior delta and persists longer.
  • Then delta merges with 4 to 5 Hz waves.

Normal Drowsiness, Sleep, Arousal: Adults

Drowsiness (Figs. 3-125 to 3-130)

  • Theta augments in amplitude and distribution and is rhythmic.
  • Alpha augments in amplitude and distribution, then disappears.
  • Beta increases, occasionally in bursts, then may decrease.
  • Slow lateral eye movements.
  • Occasional 2 to 4 Hz waves, in bursts, in the elderly.
  • Brief epochs of drowsiness common in senility.

Vertex (V) Waves (Figs. 3-131 to 3-133, 3-135 to 3-140)

  • Bilaterally synchronous.
  • Maximal amplitude at vertex (Cz).
  • Extend to Fz, Pz; F3,4; C3,4; P3,4.
  • May appear in sequences.
  • Shifting asymmetries occur.
  • Principal component is usually a sharply contoured electronegative wave.
  • Principal component may be positive.
  • May be preceded and/or followed by smaller waves of opposite polarity.
  • Highest amplitude and sharpest in youth; become more blunt with age.
  • Appear principally in light sleep but also in wakefulness, drowsiness, and at onset of high-frequency flash stimuli.
  • Rarely suppressed by focal pathology.

Spindles (Figs. 3-136, 3-137, 3-139 to 3-141)

  • Rhythmic or arciform waves.
  • In 2 to 3 s bursts, waxing and waning, giving spindle shape.
  • Bilaterally synchronous and symmetrical or asynchronous with symmetry of total spindle quantity.
  • 13 to 14 Hz, Cz,3,4 with frontal spread in light stage 2 sleep.
  • 10 to 12 Hz, Fz,3,4 in deeper stage 2 and stage 3 sleep.

Mitten Pattern (Figs. 3-138 and 3-139)

  • High-voltage 400 to 500 ms waves at Fz-Cz with parasagittal spread.
  • Notched in ascending phase by 100 to 125 ms wave.

K Complexes

  • Diphasic wave.
  1. Initial brief wave.
  2. Subsequent slower wave.
  • Spindles superimposed on slower wave.
  • Stage 2 sleep.

Rapid Eye Movement (REM) Sleep (Figs. 3-144 to 3-146)

  • Low voltage.
  • Mixed frequencies: theta, beta, delta.
  • Clusters of rapid conjugate vertical and/or horizontal eye movements.

Deep Sleep (Figs. 3-142 and 3-143)

  • Diffuse delta.
  • Minimal spindles, no V waves.

Arousal (Figs. 3-155 and 3-156)

  • Number, complexity, and duration of phenomena vary directly with depth of sleep.
  • From drowsiness: abrupt with minimal or no intermediate theta/delta waves or frontocentral beta.
  • From light sleep:
  1. V waves.
  2. Frontocentral alpha–theta.
  • From deep sleep:
  1. High-voltage delta.
  2. Frontocentral alpha–theta.
  • Duration: 1–2 s from light sleep; 3–5 s in deep sleep.

Small Sharp Spikes (Figs. 3-149 to 3-152)

  • Abrupt ascending slope.
  • Steeper descending slope.



  • Followed by low-amplitude slow wave, same polarity as spike; or low-amplitude potential as “dip” in background, polarity opposite to spike.
  • Brief: <50 ms.
  • No disruption of background activity.
  • Widespread field; dipole between hemispheres or within hemisphere.
  • Cancellation between ear (Al,2) and posterior temporal lead (T5,6) common.
  • Often appear bilaterally with maximal amplitude in one hemisphere.
  • Single events; rarely as doublets.
  • Appears in adults and adolescents.
  • Light, non-REM sleep.
  • Appears in multiple channels on common average reference montage (CAR).

6-per-Second Spike Waves (Figs. 3-153 and 3-154)

  • 5 to 7 Hz.
  • <1 s duration.
  • Brief, low-amplitude spike.
  • Awake or drowsy; not sleep.
  • Waves are bisynchronous.
  • <1 s duration
  • Two forms:
  1. Low-amplitude, posterior.
  2. High-amplitude, anterior.

Fig. 3-1. Theta and delta. Patient's age, 3 months. Eyes open. A mixture of theta and delta diffusely with transient asymmetries. Calibration signal 1 s, 100 µV.


Fig. 3-2. Theta and delta. Patient's age, 4 months. Eyes open. Diffuse mixture of theta and delta. Three to 4 Hz background moderately developed posteriorly. Minimal beta activity, greater right, which waxed and waned on either side in other parts of this recording. Paucity of activity anteriorly. Calibration signal 1 s, 100 µV.


Fig. 3-3. Theta and delta. Patient's age, 4 months. Eyes open. Note increased sensitivity. Mixture of diffuse delta and theta; intermittent 4 Hz background posteriorly. Greater quantity of delta activity in the left posterior head region in this segment was a transient phenomenon occurring intermittently on either side during the recording. Calibration signal 1 s, 70 µV.


Fig. 3-4. Normal awake. Patient's age, 4 months. Eyes closed. A normal rich mixture of delta and theta diffusely. Note 4 Hz background activity at O1,O2.


Fig. 3-5. Posterior rhythm. Patient's age, 8 months. Eyes open. Similar mixture of theta and delta, but a better developed posterior rhythm. Calibration signal 1 s, 100 µV.


Fig. 3-6. Central activity better developed. Patient's age, 9 months. Eyes open. Good development of central rhythms on both sides underlying a normal quantity of diffuse delta activity. Calibration signal 1 s, 70 µV.


Fig. 3-7. Asynchrony of central rhythms. Patient's age, 9 months. Eyes open. Better development of central–parietal rhythms, which occur in runs on either side. Muscle artifact in the first channel. Calibration signal 1 s, 70 µV.


Fig. 3-8. Asymmetrical central rhythms. Patient's age, 9 months. Eyes open. Central rhythms may be transiently asymmetrical in normal subjects. Calibration signal 1 s, 100 µV.


Fig. 3-9. Passive eye closure. Patient's age, 4 months. Passive eye closure (↑) reveals a 3 to 4 Hz posterior rhythm, which was not apparent with eyes open. Calibration signal 1 s, 100 µV.


Fig. 3-10. Passive eye closure. Patient's age, 7 months. Passive eye closures (↑) reveal a 5 Hz posterior rhythm whose predominance waxes and wanes on either side at different epochs. This attenuates on eye openings (*). Muscle, truncated eyeblink, and movement artifact are nearly inevitable during this procedure. Calibration signal 1 s, 100 µV.


Fig. 3-11. Mixture of waveforms. Patient's age, 14 months. Eyes open. Increased quantity of central rhythms and diffuse theta and delta as compared with illustrations of 8 and 9 months (Figs. 3-5, 3-6 to 3-8). Note the spike-like waveform in channels 1 and 5, which is artifact. Calibration signal 1 s, 100 µV.


Fig. 3-12. Well-developed central activity. Patient's age, 14 months. Eyes open. Same patient as shown in Fig. 3-11. This coronal run emphasizes the predominance of central rhythms and their shifting asymmetry. Note the relative paucity of frontal rhythms. Calibration signal 1 s, 150 µV.


Fig. 3-13. Paucity of frontal activity. Patient's age, 18 months. Note the predominance of parietal rhythms with the eyes closed on the coronal run. Once again, the paucity of frontal rhythms is evident. Calibration signal 1 s, 100 µV.


Fig. 3-14. Asymmetrical central rhythm. Patient's age, 15 months. Eyes open. Well-developed central rhythm on left and minimal on right; a normal asymmetry when transient, as in this case. Calibration signal 1 s, 100 µV.


Fig. 3-15. Passive eye closure. Patient's age, 14 months. Passive eye closure (↑) elicits a well-developed, 7 Hz occipital rhythm, which was not present while the eyes were open. Note central rhythm in the initial seconds. Calibration signal 1 s, 150 µV.


Fig. 3-16. Clear posterior rhythm. Patient's age, 2 years. Eyes closed. Note the more posteriorly dominant rhythm and less diffuse theta and delta. This could represent intersubject variability or slightly greater alertness in this tracing, as evidenced by more muscle artifact. The posterior delta is normal at this age. Calibration signal 1 s, 100 µV.


Fig. 3-17. Eye closure elicits normal posterior rhythm. Patient's age, 2 years. Drowsy. Spontaneous eye closure during light drowsiness (↑) elicits well-developed 7 to 8 Hz posterior rhythm and diffuse theta. Eye opening (*) attenuates these rhythms, particularly 7 to 8 Hz posterior waves. Calibration signal 1 s, 150 µV.


Fig. 3-18. Normal after sleep. Patient's age, 2 years. The background frequency may be lower than that of wakefulness for several minutes after arousal, indicating that full alertness has not yet been attained. Spontaneous eye closure in the 2nd second. Calibration signal 1 s, 150 µV.


Fig. 3-19. Well-developed alpha. Patient's age, 3 years. Eyes closed. Well-developed 8 Hz alpha. Moderate central rhythms. Minimal diffuse delta. Calibration signal 1 s, 150 µV.


Fig. 3-20. Normal asymmetry. Patient's age, 4 years. Alpha here is less interrupted by slower waves than often occurs normally. Such appearance would be normal well into adolescence. The slight asymmetry (higher left) is entirely normal for age. Calibration signal 1 s, 100 µV.


Fig. 3-21. Posterior slow waves. Patient's age, 3 years. Eyes closed. Similar to Figs. 3-19 and 3-20 except for the addition of 200 to 400 ms waves constituting the first prominent appearance of posterior slow waves of youth as polyphasic potentials. Calibration signal 1 s, 150 µV.


Fig. 3-22. Posterior rhythmic waves. Patient's age, 4 years. Eyes closed. Rhythmic 3 to 4 Hz posterior waves can be seen from this age to mid-adolescence. Their significance is not always certain. Such waves may be seen in normal subjects, whereas in others these waves may merge into posteriorly situated spike waves. Their presence, therefore, indicates a more prolonged recording and perhaps a second hyperventilation seeking spike waves. Eye opening (↑) attenuates these waves. Calibration signal 1 s, 200 µV.


Fig. 3-23. Posterior rhythmic waves. Patient's age, 4 years. Eyes closed. Rhythmic 3 to 4 Hz posterior waves may shift from side to side, as in this example. Their sharply contoured appearance in this segment does not necessarily indicate hidden spike waves and simply may be the result of a combination of waveforms. Calibration signal 1 s, 150 µV.


Fig. 3-24. Eye closure elicits posterior rhythmic waves. Patient's age, 6 years. Eye closure and then eye opening (*) elicit and abolish such normal potentials. Calibration signal 1 s, 70 µV.


Fig. 3-25. Hyperventilation. Patient's age, 3 years. Hyperventilation (HV) may elicit posterior slow waves. This example shows early appearance of semirhythmic posterior theta and the late appearance of rhythmic 3 Hz waves. Segments shown are pre-HV, 30 s of HV, and 2 min of HV. Calibration signal 1 s, 100 µV.


Fig. 3-26. Diffuse delta. Patient's age, 3 years. Eyes closed. As is the case until mid-adolescence, diffuse delta courses through many normal recordings, as in this one. Comparing this illustration with others of the same age demonstrates the wide variations of normal delta. Calibration signal 1 s, 100 µV.


Fig. 3-27. V waves while awake. Patient's age, 4 years. Occipital alpha indicates that this patient is awake or in very light drowsiness. V waves of various morphologies appear in each of the three segments, their appearance accentuated by the ear referential montage. Calibration signal 1 s, 100 µV.


Fig. 3-28. Normal apiculate temporal waves. Channels 1 through 8; patient's age, 5 years, drowsy. Channels 9 through 16, patient's age, 12 years, awake, eyes open. Broad, sharply contoured waves appearing in temporal leads, principally T3,T4, are normal components in childhood. Calibration signal 1 s, 100 µV.


Fig. 3-29. Delta and theta with eyes open. Patient's age, 6 years. The normal quantities of delta and theta are evident when the eyes are open. Calibration signal 1 s, 100 µV.


Fig. 3-30. Moderate posterior theta. Patient's age, 6 years. Eyes closed. Although there is a moderate amount of diffuse theta, maximum posteriorly, the approximately 8 Hz alpha can be discerned in this normal recording. Calibration signal 1 s, 100 µV.


Fig. 3-31. Alpha and theta. Patient's age, 7 years. Awake. Diffuse theta and well-developed alpha. Calibration signal 1 s, 100 µV.


Fig. 3-32. Posterior slow of youth. Patient's age, 6 years. Awake. Eyes closed. The 300 to 400 ms waves combine with alpha to produce the sharply contoured features of this phenomenon. Unilateral accentuation of “posterior slow of youth,” right in this example, commonly occurs. Note the normal diffuse delta activity. A similar picture can normally extend to age 12 years. Calibration signal 1 s, 70 µV.


Fig. 3-33. Prominent theta and delta. Patient's age, 8 years. Eyes closed. There is a greater quantity of theta and delta in this figure as compared with some others in this age group. Note the sensitivities when comparing samples. Calibration signal 1 s, 100 µV.


Fig. 3-34. Normal occipital delta. Patient's age, 6 years. Awake. In childhood, the appearance of bioccipital delta with eye opening (*) has never been associated with any other EEG abnormality and can, therefore, be considered normal for this age. This activity does not represent movement or electrode artifact at O1–O2. Calibration signal 1 s, 100 µV.


Fig. 3-35. Posterior theta and alpha. Patient's age, 6 years. Eyes closed. The posteriorly situated theta combines with alpha to create sharply contoured waveforms whose prominence shifts from side to side. Calibration signal 1 s, 100 µV.


Fig. 3-36. Minimal posterior theta. Patient's age, 8 years. Eyes closed. The alpha activity appears better “regulated” in this sample because of the lower quantity of posterior theta relative to alpha. Calibration signal 1 s, 150 µV.


Fig. 3-37. Asymmetry of posterior slow waves. Patient's age, 5 years. Eyes closed. Posterior slow waves of youth are more prominent on the right in this example; note the diffuse delta and theta. Calibration signal 1 s, 100 µV.


Fig. 3-38. Central rhythms. Patient's age, 10 years. The 10 Hz bicentral rhythm dominates this sample with the eyes open. Diffuse delta is evident. The central rhythm may occasionally be sharply contoured, as in this example, and looks superficially like spikes, which it is not. In contrast, rolandic spikes (not present) have a prominent after-coming slow wave in the same phase as the spike and are less likely to be strictly localized to C3 or C4. Calibration signal 1 s, 70 µV.


Fig. 3-39. Sharply contoured mu. Patient's age, 10 years. Eyes open. Another example of sharply contoured central rhythms (mu). Calibration signal 1 s, 100 µV.


Fig. 3-40. Sharply contoured frontal rhythms. Patient's age, 16 years. Theta combined with beta at the superior frontal regions (F3,4) creates the sharply contoured appearance. None of these could be identified as a spike. Calibration signal 1 s, 70 µV.


Fig. 3-41. Sharply contoured frontal rhythms with drowsiness. Patient's age, 16 years. Same frontal rhythm as shown in Figure 3-40 depicted on coronal montage in this normal recording. Note the slow lateral eye movements at F7 and F8. Calibration signal 1 s, 70 µV.


Fig. 3-42. Posterior rhythms. Patient's age, 13 years. Posterior slow waves of youth continue to be prominent in adolescence. Once again, they create sharply contoured waves, as seen here in the left occipital region, which are not spikes. Broad, sharply contoured posterior temporal waves occur normally at this age. These are often more abundant in the right posterior temporal region (T6), as seen in the first part of this tracing. Calibration signal 1 s, 100 µV.


Fig. 3-43. Asymmetrical mu. Patient's age, 12 years. Eyes open. A mu rhythm may be considerably asymmetrical for certain stretches of the recording as seen maximally on the left here. Movement of the left hand may have attenuated mu on the right. This asymmetry may transiently create the false impression that a focal delta activity is present on the contralateral side: the normally appearing delta is more evident in the absence of the central rhythm. Note the presence of minimal delta on the left as well, underlying the central rhythm. Calibration signal 1 s, 70 µV.


Fig. 3-44. Hyperventilation—start. Patient's age, 8 years. The beginning of hyperventilation may be manifested by accentuation of the background rhythms. Calibration signal 1 s, 150 µV.


Fig. 3-45. Hyperventilation—initial buildup. Patient's age, 8 years. Until age 11 to 12 years, the initial buildup is usually posteriorly situated, as in this example. Calibration signal 1 s 150 µV.


Fig. 3-46. Hyperventilation—maximal buildup. Patient's age, 8 years. The maximum is often considerable. Intrusion of the background activity between the rhythmic delta can create sharply contoured waves to produce a pattern superficially resembling spike waves, which it is not. When a spike wave occurs in hyperventilation, its form is clearly more apiculate than the preceding background activity, and it is seen simultaneously in two or more channels. Calibration signal 1 s 150 µV.


Fig. 3-47. Asymmetrical burst in hyperventilation. Patient's age, 6 years. Hyperventilation commonly elicits bursts confined to or clearly maximum in one hemisphere, as in this example. Thus, if such lateral accentuation is unsustained, it is a normal finding. Calibration signal 1 s, 100 µV.


Fig. 3-48. Asymmetrical posterior slow waves in hyperventilation. Patient's age, 10 years. Previous samples have shown that posterior slow waves of youth may be normally asymmetrical. As this phenomenon is accentuated in hyperventilation, its asymmetry also may be accentuated, particularly in the posterior temporal regions. Greater prominence on the right is the more common, as in this example. Calibration signal 1 s, 70 µV.


Fig. 3-49. Sharply contoured waves in hyperventilation. Patient's age, 13 years. The complex mixture of waveforms accentuated by hyperventilation in children and adolescents creates many sharply contoured waves (as seen here), which are not spikes. Calibration signal 1 s, 100 µV.


Fig. 3-50. Posterior slow waves. Patient's age, 13 years. Eyes closed. A further example of posterior slow waves of youth. Note the 400 to 600 ms waves posteriorly, with superimposed alpha activity, creating a sharply contoured appearance. Calibration signal 1 s, 100 µV.


Fig. 3-51. Posterior slow of youth. Patient's age, 14 years. Awake. Eyes closed. These abrupt 250 to 600 ms O1–O2 waves interrupt the alpha activity to create sharply contoured waves that are not spikes. This phenomena may normally be about two to three times as abundant as seen here and are commonly asymmetrical. Rare young adults normally retain this phenomenon. Calibration signal 1 s, 70 µV.


Fig. 3-52. Normal alpha activity. Patient's age, 62 years. Well-regulated 9 Hz alpha activity. Its slight asymmetry, higher right, is well within normal limits. Beta activity is slightly lower in the left frontal region than the right, but a greater quantity of EEG would have to be assessed before ascribing any significance to this asymmetry. Note the ocular movements in the second and tenth seconds. Calibration signal 1 s, 50 µV.


Fig. 3-53. Normal alpha activity. Patient's age, 83 years. Alpha rhythm of 8 to 9 Hz in an awake adult. Its waxing and waning amplitudes (“beating”), particularly in derivations C3–P3 and C4–P4, together with the incompletely sinusoidal nature of the rhythm, suggest more than one frequency, in this case 8 and 9 Hz. The relative contributions of alpha and mu rhythm to the potentials in derivations F3–C3 and F4–C4 are not clear with the eyes closed. Alpha may extend to the central regions and rarely to the superior frontal areas. Calibration signal 1 s, 70 µV.


Fig. 3-54. Normal. Patient's age, 80 years. Awake. Eyes closed. Alpha rhythm does not necessarily decrease in frequency with normal aging. The small amount of theta is easily acceptable for age. Calibration signal 1 s, 50 µV.


Fig. 3-55. Beating of alpha. Patient's age, 17 years. Awake. Eyes closed. Alpha rhythms of adjacent frequencies (e.g., 9 and 10 Hz) may summate when in the same phase to create high-voltage potentials, then proceed to opposite phases producing relative cancellation. Calibration signal 1 s, 70 µV.


Fig. 3-56. Paradoxical alpha. Patient's age, 52 years. Drowsy. Eye opening (indicated by upward [negative] deflections at FP1,2) during drowsiness elicits alpha activity. Calibration signal 1 s, 50 µV.


Fig. 3-57. Central alpha. Patient's age, 50 years. This coronal montage illustrates the extension of alpha activity to the central regions, although contribution by a mu rhythm cannot be excluded, since the eyes remain closed. The small amount of theta activity centrally (fourth second) is not an abnormality. Note the relative paucity of frontal activity, which is usual with this montage. Calibration signal 1 s, 50 µV.


Fig. 3-58. Alpha and mu. Patient's age, 23 years. Awake. Eyes closed. Alpha and mu frequencies overlap considerably or are identical. This illustration fails to distinguish the relative contributions of these elements to potentials at F3,4–C3,4 and C3,4–P3,4. Calibration signal 1 s, 50 µV.


Fig. 3-59. Normal alpha asymmetry. Patient's age, 25 years. No clinical significance can be ascribed to even moderate alpha asymmetries if (a) the alpha on each side is in itself normal, (b) there are no frequency differences exceeding 1 Hz, and (c) there are no other electrographic abnormalities. Note how the degree of asymmetry between P3 and P4 fluctuates with time. Slow eye movements create the delta activity of anterior derivations. The brief eye opening attenuates the alpha transiently (*). Calibration signal 1 s, 70 µV.


Fig. 3-60. Shifting alpha asymmetries. Patient's age, 25 years. The common average reference (CAR) also depicts alpha symmetry or shifts in asymmetry. Note the shifting alpha asymmetry from right dominant to left dominant in this tracing. This is clearly normal, because the alpha is normal on each side and there are no other electrographic abnormalities. Low-voltage delta activity underlying the alpha in the P3-CAR and O1-CAR derivations does not represent an abnormality as it is unassociated with any “background” disturbance. Calibration signal 1 s, 70 µV.


Fig. 3-61. Posterior slow waves of youth. Patient's age, 32 years. Posterior slow waves of youth as polyphasic potentials (Aird & Gastaut, 1959) may disrupt the alpha rhythm, creating a posteriorly situated spike–wave-like phenomenon, as seen here (*). The 1 Hz activity underlying normal background rhythms in many derivations is not abnormal in youth. Youthful waveforms may normally persist into adulthood. Calibration signal 1 s, 50 µV.


Fig. 3-62. Sharply contoured alpha. Patient's age, 32 years. The negative component (downward deflection) of the alpha may appear sharply contoured. Eyeblinks appear in the frontal polar derivations. Calibration signal 1 s, 50 µV.


Fig. 3-63. Alpha attenuation with eye opening. Patient's age, 45 years. Awake. Eye opening. Eye opening (*) completely abolishes the alpha activity leaving a transient central rhythm. Calibration signal 1 s, 70 µV.


Fig. 3-64. Transient and incomplete alpha attenuation. Patient's age, 80 years. Eye opening (asterisk) only transiently attenuates the alpha activity, but such attenuation is sufficient to reveal beta activity (F3–C3, F4–C4), which was not evident while the eyes were closed because of the very considerable anterior extent of the alpha field. Beta activity combines with muscle activity in Fp1,2–F3,4 derivations. Note the minimal parasagittal theta activity in recordings of most normal elderly subjects. Calibration signal 1 s, 50 µV.


Fig. 3-65. Asymmetrical mu rhythm. Patient's age, 16 years. Awake. Eye opening (*) blocks alpha but not C3 mu rhythm, which is subsequently blocked by right thumb movement (**). Calibration signal 1 s, 50 µV.


Fig. 3-66. Amorphous, then well-organized, normal EEG. Patient's age, 25 years. No abnormality appears in either the amorphous portion of this recording with the eyes open or in the more conventional-appearing portion with the eyes closed. Adequate central rhythms appear on either side with the eyes open; the slight left predominance has therefore no significance. At least part of the posterior delta activity may represent a pulse artifact; without any disturbance in posterior background activity, this delta activity should not be considered an abnormality. Calibration signal 1 s, 50 µV.


Fig. 3-67. Fast alpha variant on eye closure. Patient's age, 37 years. The fast alpha variant, a posteriorly situated beta rhythm that attenuates upon eye opening and may be particularly prominent upon eye closure, combines with usual frequency alpha activity to create sharply contoured waveforms. Note the principally electropositive lambda waves in the occipital derivations in the first second prior to eye closure. The prominent upward-deflecting potentials in the occipital and parietal derivations represent common average reference involvement of the eyeblinks and are opposite in phase to those in the frontal derivations. The diffuse theta and minimal beta are well within acceptable normal limits. Calibration signal 1 s, 50 µV.


Fig. 3-68. Alpha and beta. Patient's age, 56 years. Awake. Eyes closed. The diffuse beta activity interrupts, distorts, and renders apiculate the alpha activity of this normal recording with a medication effect. Calibration signal 1 s, 50 µV.


Fig. 3-69. Slow alpha variant. Patient's age, 60 years. An epoch where most of the alpha activity appears in the slow alpha variant form and is an entirely normal phenomenon. Delta activity in the frontal polar derivations represents slow eye movements. Calibration signal 1 s, 50 µV.


Fig. 3-70. Low-voltage alpha. 70 years. Minimal alpha activity allows other normal potentials to appear, such as diffuse beta and low-voltage delta. Calibration signal 1 s, 50 µV.


Fig. 3-71. Low-voltage normal EEG. Patient's age, 78 years. Awake. Eyes closed. Oscillation of cerebral potentials may be less apparent in some normal individuals. This may reflect anxiety and could disappear with HV. Scrutiny of such recordings will reveal low-voltage, high-frequency waves (alpha, beta), which distinguish this from true suppression. Calibration signal 1 s, 50 µV.


Fig. 3-72. Central beta. Patient's age, 39 years. Low-amplitude 20 Hz beta activity appears at the central vertex (Cz) and minimally diffusely in this coronal montage in an awake subject with the eyes closed. Its combination with a 9 Hz central rhythm produces occasional apiculate waveforms, which are not spikes. Note the relative paucity of frontal activity as recorded on this montage. Note also the partial cancellation of alpha activity at the P3–Pz and Pz–P4 derivations due to the widespread field of alpha activity. Calibration signal 1 s, 50 µV.


Fig. 3-73. No spikes. Patient's age, 23 years. Beta combines with diffuse theta and posteriorly situated alpha to produce many sharply contoured waves, none of which is a spike. These background components partially obscure the V wave in the fifth second. Calibration signal 1 s, 70 µV.


Fig. 3-74. Normal bursts of beta activity. Patient's age, 67 years. Amplitudes of beta activity can fluctuate suddenly, producing bursts superficially resembling polyspikes. The gradual crescendo of amplitude, the more sinusoidal waveform as opposed to spikes, and the lack of a prominent succeeding delta wave are clues that such phenomena are beta and not polyspikes. Muscle activity complicates the morphology in several channels. Calibration signal 1 s, 50 µV.


Fig. 3-75. Beating of beta. Patient's age, 55 years. As does alpha, the amplitude of beta activity may wax and wane in a regular fashion, producing a “beating” appearance. Note that its combination with 10 Hz alpha (or mu) produces a particularly apiculate appearance in the first 5 s. Calibration signal 1 s, 50 µV.


Fig. 3-76. Beta activity and muscle artifact. Patient's age, 55 years. Right frontal muscle artifact joins beta activity to produce a particularly dense appearance. This combination is only minimally present in the left frontal (Fp1–F3) derivation. Calibration signal 1 s, 70 µV.


Fig. 3-77. Amorphous normal EEG. Patient's age, 18 years. When no rhythm, such as alpha activity, dominates a recording, the virtually equal competition of other waves for prominence creates a disorganized appearance. Artifacts such as head movement and frontalis muscle complicate the occipital and frontal rhythms, respectively. The lack of alpha activity reveals a normal amount of posteriorly situated beta and theta activity. Consider whether any abnormality is clearly evident; if not, the EEG should be interpreted as normal, as in this instance. Calibration signal 1 s, 50 µV.


Fig. 3-78. Before, early, late hyperventilation. Patient's age, 17 years. Prior to hyperventilation (left), the background activity consists of alpha (far left), “slow alpha variant” (far right) and bilateral mu rhythm. Bursts of 200 to 300 ms high-voltage waves with intermingled sharply contoured waves characterize the early (1 min) hyperventilation period (center); none of these sharply contoured waves could be considered a definite spike. Such high-voltage waves appear more persistent during late (2½ min) hyperventilation (right). The magnitude of the hyperventilation response is not a criterion of its normality but is greater in youth, with hypoglycemia, and with ventilatory effort. Calibration signal 1 s, 50 µV.


Fig. 3-79. Normal, sharply contoured hyperventilation responses. Patient's age, 32 years. None of the bursts in these tracings contains a spike or spike–wave; instead, each is a result of the superimposition of hyperventilation-induced waveforms upon background activity. Calibration signal 1 s, 50 µV.


Fig. 3-80. Light sleep after hyperventilation. Patient's age, 46 years. Hyperventilation and photic stimulation can occasionally be followed by non-REM sleep, as occurred here. Note the symmetrical V waves and low-amplitude 12 Hz spindles, the latter slightly more evident in the right hemisphere compared to the left. Calibration signal 1 s, 70 µV.


Fig. 3-81. Prominent lambdas. Patient's age, 93 years. Awake. Eyes open. As in the case of single flashes, responses to scanning complex visual stimuli normally evoke higher-voltage lambda responses in the elderly than in younger adults. All of these often biphasic waves begin with an electropositive component at O1–O2, but lambdas may begin with a low-voltage, initially negative component, which did not appear here. none of these represented EKG (not shown). Calibration signal 1 s, 70 µV.


Fig. 3-82. Prominent photic “following.” Same patient as previous illustration. Awake. Eyes closed. As with lambda, responses to single flashes can be exaggerated in the elderly. Calibration signal 1 s, 50 µV.


Fig. 3-83. Lack of abnormality equals normality. Patient's age, 19 years. Prominent lambda waves combine with beta activity in the occipital derivations to create a highly irregular but normal background activity. Eye closure (*) has minimal effect because of the small amount of alpha activity present in this apparently anxious subject. Eye movements and frontal muscle potentials create irregular waves in the frontal polar derivations. A normal amount of theta activity, diffuse beta activity, and a burst of muscle potentials add to the havoc. However, no abnormality can be identified. Calibration signal 1 s, 70 µV.


Fig. 3-84. Photic “on” response and driving. Patient's age, 58 years. Awake. Eyes closed. The “on” response, the initial effect evoked by photic stimulation at a 12 Hz flash rate, has the same morphology as the 3 Hz following response, whereas the “driving response” morphology differs from these, reflecting their distinct physiologies (Perez-Borja, 1962). Calibration signal 1 s, 100 µV.


Fig. 3-85. Delta and theta augment in drowsiness. Patient's age, 4 months. At this age, the changes with drowsiness are modest and include a slight increase in the quantity of theta and delta activity, as seen here. The beta asymmetry was transient and normal. Calibration signal 1 s, 100 µV.


Fig. 3-86. More central–parietal activity than frontal. Patient's age, 4 months. Similar state of drowsiness as shown in Fig. 3-85, only with coronal montage. Note posteriorly situated delta and theta, well-developed theta rhythm centrally, and the relative paucity of activity anteriorly. Calibration signal 1 s, 100 µV.


Fig. 3-87. Early drowsiness with eye closure eliciting background rhythm. Patient's age, 8 months. The 4 to 5 Hz theta mixes with 2 Hz delta to create a sustained background rhythm in this state of reposelike drowsiness. Calibration signal 1 s, 100 µV.


Fig. 3-88. Theta and delta of drowsiness. Patient's age, 8 months. In addition to accentuating theta, drowsiness occasionally may accentuate delta, maximum on the left here. The delta shifted from side to side during drowsiness in this patient—a normal phenomenon. Calibration signal 1 s, 100 µV.


Fig. 3-89. Theta and delta of drowsiness. Patient's age, 8 months. Drowsy. Although the diffuse 1 Hz delta is more abundant than usually seen, this primarily 3 Hz drowsy pattern is not clearly abnormal for age. Calibration signal 1 s, 100 µV.


Fig. 3-90. Posterior rhythm. Patient's age, 11 months. Drowsiness may elicit a posterior rhythm similar to that revealed by passive eye closure at this age. Calibration signal 1 s, 70 µV.


Fig. 3-91. Theta with drowsiness. Patient's age, 13 months. Prolonged runs of theta constitute the most common drowsy pattern in early childhood. Note the low-voltage intermingled beta, which may be transiently asymmetrical, as in this example. The sensitivity is less than previous examples. Calibration signal 1 s, 150 µV.


Fig. 3-92. Beta with drowsiness. Patient's age, 13 months. Beta activity may become prominent in drowsiness–light sleep. It may normally appear principally in the central and posterior regions, as in this illustration. As in other examples, diffuse persistent delta activity is a normal component. Calibration signal 1 s, 150 µV.


Fig. 3-93. Prolonged burst of theta in drowsiness. Patient's age, 2 years. Prominent diffuse rhythmic theta is the most common drowsy pattern seen from infancy to 5 years of age. It may appear continuously or as brief or prolonged bursts. Calibration signal 1 s, 100 µV.


Fig. 3-94. Burst of delta and theta in drowsiness. Patient's age, 3 years. Prolonged burst of diffuse, synchronous delta and theta superimposed upon a drowsy pattern similar to those illustrated previously. Calibration signal 1 s, 150 µV.


Fig. 3-95. Bursts of theta in drowsiness. Patient's age, 4 years. Two examples of bursts of 3 to 5 Hz, high-voltage diffuse waves. Superimposed upon background activity, such waves create sharply contoured forms that are not spikes, as seen in both of these segments. Calibration signal 1 s, 150 µV.


Fig. 3-96. Burst of theta. Patient's age, 4 years. A burst drowsy pattern superimposed upon nonburst drowsy patterns. Calibration signal 1 s, 150 µV.


Fig. 3-97. A variable morphology of V waves as seen on a coronal montage. Patient's age, 2 years. Sleep. The high voltage and often brief duration of these create a resemblance to sagittal spikes, which they are not. The sharply contoured appearance occasionally can be enhanced by a combination of V waves with central theta and beta. Calibration signals 1 s, 100 µV; 1 s, 150 µV; 1 s, 100 µV.


Fig. 3-98. Variable morphology of V waves on referential montage. Patient's age, 3 years. Light sleep. Note that the fourth V wave is primarily electropositive. Shifting asymmetries of V waves occur commonly, as in this segment, where they are lower in the right frontal region as compared with the left. Calibration signal 1 s, 150 µV.


Fig. 3-99. Variable morphology of V waves. Not only the morphology but also the symmetry varies; each of these apiculate potentials is normal. Calibration signal 1 s, 100 µV.


Fig. 3-100. Sequential V waves. Patient's age, 8 years. Light sleep. In childhood, V waves tend to occur in sequences, as in this example, using a coronal montage. Note the greater involvement of Pz than Fz. Calibration signal 1 s, 100 µV.


Fig. 3-101. V waves merging into a central rhythm. Patient's age, 9 years. Light sleep. V waves are so sequential that they merge to form a central rhythm in the second half of this segment. Calibration signal 1 s, 150 µV.


Fig. 3-102. V waves. Patient's age, 5 years. Light sleep. Sequential V waves on bipolar anterior–posterior montage showing the variable morphologies and shifting asymmetries. Calibration signal 1 s, 100 µV.


Fig. 3-103. Central theta. Patient's age, 3 years. Light sleep. A 3 to 4 Hz central–frontal rhythm occasionally appears in light sleep. Note its resemblance (and perhaps identity with) a rhythm created by sequential V waves in previous figures. Calibration signal 1 s, 150 µV.


Fig. 3-104. Spindle. Patient's age, 4 months. Sleep. A relatively synchronous spindle lasting almost 5 s. This central–parietal location is more common in infants and younger children. Calibration signal 1 s, 100 µV.


Fig. 3-105. Asynchronous spindles and occipital delta. Patient's age, 4 months. Sleep. Prolonged asynchronous central parietal spindles. Spindle length is greater at ages 3 to 9 months than later. Spindles are commonly asynchronous at less than 2 years of age. Note prominent occipital sharply contoured delta, a normal finding in moderately deep sleep in early childhood; this creates the normal “frequency–amplitude gradient.” Calibration signal 1 s, 100 µV.


Fig. 3-106. Asynchronous spindles. Patient's age, 4 months. Asynchronous spindles lasting 3 to 4 s in channels 2 and 6. These are of low voltage relative to the background sleep activity. Calibration signal 1 s, 150 µV.


Fig. 3-107. V waves and spindle. Patient's age, 4 months. Sleep. Virtually bracketed by V waves, a 5 s central–parietal spindle occurs. Note the normal paucity of frontal activity. Calibration signal 1 s, 100 µV.


Fig. 3-108. Spindles, unilateral and bilateral. Patient's age, 4 months. Sleep, 2 samples. Spindles are often comb-shaped in youth and may transiently appear unilaterally (channels 1 through 8) in a shifting fashion. Note the posteriorly accentuated delta activity, also a normal phenomenon in early youth. Calibration signal 1 s, 100 µV.


Fig. 3-109. Asynchronous, comb-shaped spindles. Patient's age, 9 months. Sleep. A common configuration of spindles at this age. Calibration signal 1 s, 100 µV.


Fig. 3-110. V waves, spindles, and beta. Patient's age, 9 months (top), 2 years (bottom). Sleeping. These components combine to create a series of normal, sharply contoured waves. Calibration signal 1 s, 100 µV.


Fig. 3-111. Central rhythms; not artifact. Patient's age, 5 years. Delta activity is prominent in the central–parietal regions in deeper sleep. Combined with other central rhythms such as spindles, V waves, and theta, a chaotic artifact-like appearance is created. Calibration signal 1 s, 100 µV.


Fig. 3-112. Sharply contoured occipital delta. Patient's age, 9 months. Sleep. A prominent example of posteriorly accentuated delta activity with sharply contoured waves. Note asynchronous, comb-shaped spindles. Calibration signal 1 s, 100 µV.


Fig. 3-113. Sharply contoured occipital delta. Patient's age, 9 months. Similar to Fig. 3-112. Calibration signal 1 s, 100 µV.


Fig. 3-114. Occipital delta and minimal spindles. Patient's age, 3 years. Sleep. An additional example, on this referential montage, of normal, continuous, occassionally sharply contoured occipital delta. Note the minimal spindles (F3,4). Calibration signal 1 s, 200 µV.


Fig. 3-115. K complex and vertex sharp transients (V waves). Patient's age, 6 years. Sleep. The left portion of this segment contains a single V wave followed by high-frequency spindles. Subsequently, sequential V waves appear. Toward the right portion of the segment, an incidental right frontopolar (FP2) spike appears. Can you spot another? Calibration signal 1 s, 100 µV.


Fig. 3-116. Theta-like spindles. Patient's age, 16 years. Sleep. These 7 Hz apiculate waves in the superior frontal regions (F3,4) actually are spindles whose rate is halved as suggested by their notched appearance. Calibration signal 1 s, 70 µV.


Fig. 3-117. Typical 14/6. Patient's age, 13 years. Sleep. Well-defined 14 and 6 per second positive spikes (14 and 6 Hz positive burst) expressed best by the interhemispheric derivations. Calibration signal 1 s, 70 µV.


Fig. 3-118. Atypical 14/6. Patient's age, 13 years. Sleep. The superimposition of a greater quantity of background rhythms upon the 14 and 6 per-second positive spikes creates a phenomenon that could mistakenly be identified as abnormal polyspikes. Calibration signal 1 s, 70 µV.


Fig. 3-119. Fourteen- and six-per-second positive spikes. Patient's age, 13 years. Light sleep. “14 and 6” are minimally expressed on this anterior–posterior bipolar montage. Calibration signal 1 s, 70 µV.


Fig. 3-120. “Fourteen and six” and “N” waves. Patient's age, 6 years. Sleep. In some patients, the common patterns of 14 and 6 per-second positive spikes and V waves appears apposed, at which time the V-wave component appears as an N-shaped wave (Reiher & Carmant, 1991). Calibration signal 1 s, 150 µV.


Fig. 3-121. Arousal. Patient's age, 23 months. This arousal (↑) begins with a mixture of delta and rhythmic theta. The superior frontal delta appears more rhythmic and higher in frequency than the parietal–occipital delta; these two deltas do not characteristically occur in synchrony. Calibration signal 1 s, 200 µV.


Fig. 3-122. Arousal. Patient's age, 23 months. Same patient as shown in Fig. 3-121 a minute later. The 5 to 6 Hz rhythmic theta has been replaced by superior frontal–parietal, 3.5 to 4 Hz rhythmic waves. However, note the independently occurring frontopolar and occipital delta activity. Calibration signal 1 s, 200 µV.


Fig. 3-123. Early arousal. Patient's age, 3 years. The first auditory stimulus (↑) evokes a broad V wave followed by a brief run of delta and theta. The second stimulus (↑) causes a V wave followed immediately by diffuse 7 Hz rhythmic waves, indicating that arousal likely will ensue. Calibration signal 1 s, 200 µV.


Fig. 3-124. Continued arousal. Patient's age, 3 years. Five seconds later. Same montage as Fig. 3-123. The 7 Hz waves are replaced by 2 to 4 Hz semirhythmic, high-voltage, diffuse activity as the process of arousal continues. Calibration signal 1 s, 200 µV.


Fig. 3-125. Initial drowsiness. Patient's age, 29 years. Eyes closed. The rhythmic 6 to 7 Hz wave anteriorly may be the first indication of drowsiness. The rhythmicity distinguishes such bursts from abnormal ones. The slightly greater right hemispheric preponderance has no clinical significance provided that background activity is normal and symmetrical otherwise. Calibration signal 1 s, 50 µV.


Fig. 3-126. Normal adult drowsiness. Patient's age, 29 years. Drowsy. A normal 5 Hz background rhythm accompanies this drowsiness, which is also manifested by slow lateral eye movements. Muscle artifact can persist in drowsiness. Consider drowsiness before stating that the background activity is slow for age. Calibration signal 1 s, 50 µV.


Fig. 3-127. Drowsiness. Same patient as in the previous two illustrations. Intermittent runs of 7 then 5 Hz theta occur with a replacement of eyeblinks as slow ocular movements attest to drowsiness. Excessive daytime sleep or drowsiness should be commented upon in clinically interpreting a recording; excessive daytime sleep may be misinterpreted as absence or dyscognitive seizures. Calibration signal 1 s, 50 µV.


Fig. 3-128. Drowsiness and the ear reference montage. Patient's age, 20 years. Sinusoidal theta occurs in a burst before alpha activity recedes. Calibration signal 1 s, 70 µV.


Fig. 3-129. Drowsiness and bursting beta. Patient's age, 41 years. Beta activity can appear in alarming bursts during drowsiness. Some components of each burst are apiculate; yet, these are not polyspikes, in which all components are usually apiculate and are followed by a slow wave. The morphology of beta bursts is depicted in the square. Calibration signal 1 s, 70 µV.


Fig. 3-130. Drowsiness with beta and theta. Patient's age, 20 years. Beta and theta augment together to create an irregular sequence of often apiculate waves in this segment. Note the partial preservation of ongoing alpha activity, upon which the beta and theta are superimposed. Calibration signal 1 s, 70 µV.


Fig. 3-131. Varieties of V waves. Patient's age, 19 years. Sleep. This coronal run clearly depicts three varieties of normal V waves together with spindles. Six-per-second positive spikes also appear. Calibration signal 1 s, 50 µV.


Fig. 3-132. V-wave varieties on an ipsilateral ear reference montage. Patient's age, 19 years. Sleep. Same illustration as previous, depicting such V-wave variety. Note the 6/s positive spikes at P3 and elsewhere. Calibration signal 1 s, 70 µV.


Fig. 3-133. Drowsiness, beta, and a V wave. Patient's age, 25 years. This coronal montage using sagittal leads clearly illustrates augmentation of central beta activity and a V wave. Calibration signal 1 s, 70 µV.


Fig. 3-134. Delta bursts in drowsiness of an adult over 60 years. Patient's age, 67 years. Bursts of bilaterally synchronous delta lasting about 1 s may normally appear in light drowsiness at this age (Fisch, 1999). The maximum quantity of such waves that can be considered normal is not clear, but their appearance in about 10% of the drowsy recording would be acceptable. The third segment illustrates their association with a vertex wave at Cz. Calibration signal 1 s, 50 µV.


Fig. 3-135. Blunted V waves in the elderly. Patient's age, 83 years. Sleep. At this age, the duration of V waves increases and their sharpness decreases, so that they can become indistinct from bursts of delta and, therefore, straddle the border between normal and abnormal. Calibration signal 1 s, 70 µV.


Fig. 3-136. Spindles and V waves. Patient's age, 41 years. Sleep. Symmetrical and synchronous spindles interrupted by V waves. Possible A1/A2 “contamination” may have caused these spindles to appear more posterior than they are. Calibration signal 1 s, 70 µV.


Fig. 3-137. V waves, spindles, and ECG artifact. Patient's age, 39 years. Prominent ECG artifact combines with V waves to create a spike wave-like appearance, underscoring the importance of ECG monitoring. Calibration signal 1 s, 50 µV.


Fig. 3-138. Mitten pattern. Patient's age, 31 years. The combination of bursts of anterior rhythmic delta activity with relatively sharply contoured waves derived from the background activity may rarely create a complex appearing as a mitten pattern with the “thumb section” preceding. Although sharply contoured, this thumb section is considerably more blunt than the spike component of slow spike–wave discharges, the epilepti-form pattern most closely resembling the normal mitten. Calibration signal 1 s, 70 µV.


Fig. 3-139. Mittens and spindles of deep non-REM sleep. Patient's age, 35 years. High-voltage 400 to 500 ms waves centered near the vertex frontally and centrally may be notched in their ascending phase by a briefer, approximately 100 to 125 ms wave, creating a “mitten” pattern, as seen here (*). In this tracing, they are followed by irregular spindles which are not part of the mitten pattern. The greater frontal involvement of such vertex waves, the slightly slower frequency of the spindles, and the mitten pattern itself all attest to the deeper stage of sleep. Calibration signal 1 s, 50 µV.


Fig. 3-140. V wave and spindles. Patient's age, 34 years. Spindles and V waves are typical. Calibration signal 1 s, 70 µV.


Fig. 3-141. Asynchronous normal sleep spindles. Patient's age, 81 years. Although sleep spindles usually occur in a bilaterally synchronous fashion, they may normally appear independently in either hemisphere, as noted here and by Gibbs and Gibbs (1964). The overall quantity of spindles in this sample is normal. Calibration signal 1 s, 50 µV.


Fig. 3-142. Deep stage 3 sleep. Patient's age, 36 years. V-waves are less prominent in deep non-REM sleep (stage 3), which is dominated by diffuse delta and frontally predominant diffuse spindles. Calibration signal 1 s, 70 µV.


Fig. 3-143. Deep stage 3 sleep. Patient's age, 36 years. Deeper stage 3 sleep in the same subject as in Fig. 3-142 shows markedly augmented delta activity. The spindles have slowed to 11 to 12 Hz and appear principally frontally, although their field is diffuse. Calibration signal 1 s, 70 µV.


Fig. 3-144. Rapid eye movements (REMs) and muscle twitch. Patient's age, 70 years. Sleep. At any age, prominent REM sleep most likely represents sleep deprivation and occasionally narcolepsy. Such eye movements are synchronous, lateral, or vertical. The extremely brief FP1 potential in the first second is a periocular twitch, also characteristic of REM sleep. Calibration signal 1 s, 50 µV.


Fig. 3-145. Rapid eye movement (REM) sleep. Patient's age, 36 years. REM sleep may unexpectedly appear during routine recordings. As in this recording, a mixed frequency background occurs containing theta, beta, and minimal delta activity. Note the vertical rapid eye movements. A prominent rightward eye movement is also present (*). Calibration signal 1 s, 70 µV.


Fig. 3-146. Rapid eye movement (REM) sleep. Patient's age, 38 years. Bursts of synchronous vertical eye movements together with low-voltage continuous theta and minimal beta activity identify this epoch as REM sleep. Calibration signal 1 s, 50 µV.


Fig. 3-147. Positive occipital sharp transients of sleep (POSTS). Patient's age, 19 years. Drowsy. Eyes closed. These occipital positive potentials resembling lambda appear in normal sleep. Calibration signal 1 s, 50 µV.


Fig. 3-148. Positive occipital sharp transients of sleep. Patient's age, 25 years. The sequential spike-like occipital waves are POSTS and not conventional spikes because of the positive polarity of their spike-like potentials. Note the 14/6 per second positive spikes toward the end of the segment. Calibration signal 1 s, 100 µV.


Fig. 3-149. Small sharp spikes (SSS). Patient's age, 41 years. Small sharp spikes (SSS) (benign epileptiform transients of sleep) are well expressed by ear referential montages (A1, A2). There is partial cancellation between the active ear reference and the posterior leads, but the field is broad, like that of other normal apiculate waves. These diphasic or monophasic spikes have an abrupt ascending limb but an even steeper descending slope, with a relatively small aftercoming slow wave. Unlike epileptogenic spikes, there is no disruption of the background activity. Although these SSSs appear principally in the left hemisphere, note the moderate involvement of homologous regions of the right. The enlarged square depicts the typical morphology of the small sharp spike. Calibration signal 1 s, 70 µV.


Fig. 3-150. Small sharp spikes on coronal montage. Patient's age, 60 years. The transverse dipole field of SSS enhances their expression by coronal montages, where they may be confused with abnormal anterior temporal spikes. The widespread field including occasional deflections in derivations crossing the midline (F3–4, C3–4, P3–4), the relative cancellation in posterior temporal-ear derivations (A1–T5, T6–A2), the characteristic diphasic very apiculate morphology, and the lack of disruption of background activity all serve to distinguish these from anterior temporal spikes. Anterior temporal spikes (not depicted here) almost equally involve A1 and F7 but involve T5 only minimally. Calibration signal 1 s, 50 µV.


Fig. 3-151. Small sharp spikes, coronal montage and interhemispheric derivations. Patient's age, 39 years. The widespread gradual slope of SSS may create minimal deflections in bipolar coronal linkages but moderate deflections in interhemispheric derivations, because of the interhemispheric dipole. These principles are illustrated here. Calibration signal 1 s, 50 µV.


Fig. 3-152. Small sharp spikes on anterior–posterior bipolar montage. Patient's age, 29 years. Properties of SSSs, depicted previously, prepare one for the most likely encounter—on the commonly used anterior–posterior bipolar montage. Their distinct morphology, widespread field, prominent involvement in the midposterior temporal areas (T3 and T5 in this instance), and the lack of a prominent aftercoming slow wave or any disruption in background rhythms distinguish these discharges from anterior temporal spikes. The left temporal intermittent delta activity in this example bears no relationship to the SSSs. Calibration signal 1 s, 50 µV.


Fig. 3-153. 6-Hz spike and wave and 6-Hz positive spikes. Patient's age, 22 years. This coronal montage illustrates the co-existence of these two phenomena in the same recording as that described by Silverman (1967). The burst in the left segment appears principally as a 6 Hz spike–wave discharge with a minimal electropositive spike component, whereas that in the right segment more resembles a 6 Hz positive spike. The relatively prominent spike at the C3–C4 derivation with minimal deflections in adjacent channels suggests a broad electropositive field in the right hemisphere with a possible coexisting electronegative field in the left hemisphere. Clinically innocent phenomena such as these often have broad fields. Calibration signal 1 s, 50 µV.


Fig. 3-154. 6 Hz spike-wave/positive spikes: incomplete expression. Patient's age, 23 years. These tracings illustrate the minimal appearance of such discharges, which are more prominent in earlier figures. Calibration signal 1 s, 70 µV.


Fig. 3-155. Instantaneous arousal from drowsiness. Patient's age, 16 years. A light auditory stimulus evoked an instant change from diffuse theta and beta of drowsiness to an alpha-dominated awake pattern without intervening slow waves. The potentials recorded in the frontal polar leads represent eye opening to the auditory stimulus, then eye blinks with some frontal muscle artifact. Calibration signal 1 s, 70 µV.


Fig. 3-156. Normal arousal. Patient's age, 22 years. From light to moderate sleep, a V wave precedes instant high-frequency, diffuse activity. Calibration signal 1 s, 50 µV.


Aird RB, Gastaut Y. Occipital and posterior electroencephalographic rhythms. Electroencephalogr Clin Neurophysiol. 1959;11:637–656.

Berger H. On the electroencephalogram of man. Fifth report. In: Gloor P, ed. Electroencephalogr Clin Neurophysiol (suppl 28). Amsterdam: Elsevier; 1969:151–171.

Brandt S, Brandt H. The electroencephalographic patterns in young healthy children from 0 to five years of age. Acta Psychiatr Neurol Scand. 1955;30:77–89.

Corbin HPF, Bickford RG. Studies of the electroencephalogram of normal children: comparison of visual and automatic frequency analyses. Electroencephalogr Clin Neurophysiol. 1955;7:15–28.

Cornil L, Gastaut H. Donnees electroencephalographiques sur la dominance hemispherique. Rev Neurol. 1947;79:207.

Dale PW, Busse EW. An elaboration of a distinctive EEG pattern found during drowsy states in children. Dis Nerv Syst. 1951;12:122–125.

Demerdash A, Eeg-Olofsson O, Petersen I. The incidence of 14 and 6 per second positive spikes in a population of normal children. Dev Med Child Neurol. 1968;l0:309–316.

Dreyfus-Brisac C. The EEG during the first year of life. In: Lairy GC, ed. Handbook of Electroencephalography and Clinical Neurophysiology, vol 6B: The Evolution of the EEG from Birth to Adulthood. Amsterdam: Elsevier; 1975;25–30.

Drury I. 14 and 6 Hz positive bursts in childhood encephalopathies. Electroencephalogr Clin Neurophysiol. 1989;72:479–485.

Eeg-Olofsson O. The development of the electroencephalogram in normal children from the age of 1 through 15 years. 14 and 6 Hz positive spike phenomenon. Neuropadiatrie. 1971;2:405–426.

Fisch BJ. Fisch and Spehlmann's EEG Primer. Basic Principles of Digital and Analog EEG. 3rd ed. Amsterdam: Elsevier Science, 1999.

Gibbs FA, Gibbs EL. Atlas of Electroencephalography. Vol 3. Neurological and Psychiatric Disorders. Reading, PA: Addison Wesley; 1964:136.

Goodwin JE. The significance of alpha variants in the EEG and their relationship to an epileptiform syndrome. Am J Psychiatry. 1947:369–379.

Hagne I. Development of the waking EEG in normal infants during the first year of life. In: Kellaway P, Petersen I, eds. Clinical Electroencephalography of Children. New York: Grune & Stratton; 1968:97–118.

Hagne I, Persson J, Magnusson R, Petersen I. Spectral analysis via Fast Fourier transform of waking EEG in normal infants. In: Kellaway P, Petersen I, eds. Automation of Clinical Electroencephalography. New York: Raven Press; 1973:103–143.

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. New York: Raven Press, 1990:139–199.

Kellaway P, Fox BJ. Electroencephalographic diagnosis of cerebral pathology in infants during sleep. J Pediatr. 1952;41:262–287.

Kooi KA, Tucker RP, Marshall RE. Fundamentals of Electroencephalography. 2nd ed. Hagerstown, MD: Harper & Row; 1978:68.

Lenard HG. The development of sleep spindles in the EEG during the first two years of life. Neuropaediatrie. 1970;1:264–276.

Lombroso CT, Schwartz IH, Clark DM, Muench H, Barry J. Ctenoids in healthy youths. Neurology. 1966;16:1152–1158.

Metcalf DR. Controlled studies of the incidence and significance of 6 and 14 per sec positive spiking. Electroencephalogr Clin Neurophysiol. 1963;15:161(P).

Pampiglione G. Some criteria of maturation in the EEG of children up to the age of 3 years. Electroencephalogr Clin Neurophysiol. 1972;32:463(P).

Perez-Borja C, Chatrian GE, Tyce FA, Rivers MH. Electrographic patterns of the occipital lobe in man. Electroencephalogr Clin Neurophysiol. 1962;14:171–182.

Petersen I, Akesson HO. EEG studies of siblings of children showing 14 and 6 per second positive spikes. Acta Genet (Basel). 1968;l8:163–169.

Petersen I, Eeg-Olofsson O. The development of the electroencephalogram in normal children from the age of 1 through 15 years. Nonparoxysmal activity. Neuropadiatrie. 1971;2:247–304.



Pond DA. The development of normal rhythms. In: Hill C, Parr G, eds. Electroencephalography. 2nd ed. London: Macdonald, 1963:193–206.

Reiher J, Carmant L. Clinical correlates and electroencephalographic characteristics of two additional patterns related to 14 and 6 per second positive spikes. Can J Neurol Sci. 1991;18:488–491.

Samson-Dollfus S, Goldberg P. Electroencephalographic quantification by time domain analysis in normal 7–15-year-old children. Electroenc ephalogr Clin Neurophysiol. 1979;46:147–154.

Schulte FJ, Bell EF. Bioclectric brain development. An atlas of EEG power spectra in infants and young children. Neuropadiatrie. 1973;4:30–35.

Schwartz IH, Lombroso CT. 14 & 6/second positive spiking (ctenoids) in the electroencephalograms of primary school pupils. J Pediatr. 1968;72:678–682.

Silverman D. Phantom spike-waves and the fourteen and six per second positive spike pattern. Electroencelphalogr Clin Neurophysiol. 1967;23:207–213.

Slater GE, Torres F. Frequency–amplitude gradient. A new parameter for interpreting pediatric sleep EEGs. Arch Neurol. 1979;36:465–470.

Tanguay PE, Ornitz EM, Kaplan A, Bozzo ES. Evolution of sleep spindles in childhood. Electroencephalogr Clin Neurophysiol. 1975;38:175–181.

Westmoreland BF, Sharbrough FW. Posterior slow wave transients associated with eye blinks in children. Am JEEG Technol. 1975;15:14–19.