Atlas of Neonatal Electroencephalography, 3rd Edition

Chapter 6

Electroencephalographic Abnormalities of Premature and Term Neonates

TIMING OF ELECTROENCEPHALOGRAPHIC STUDIES

Ideally, the initial electroencephalogram (EEG) examination should be done within the first 24 hours after birth or after a suspected brain insult. The best estimate of the degree of damage or dysfunction can be made when the EEG documents the evolution of the abnormality over time. Typically, as time passes, the degree of abnormality lessens. The slower this change, the more severe the underlying brain abnormality. If serial studies document the rate and character of changes, the prognostic information will be more reliable than that obtained from a single study (Chequer et al., 1992; Douglass et al., 2002; Graziani et al., 1994; Holmes and Lombroso, 1993; Holmes et al., 1982; Klinger et al., 2001; Kumar et al., 1999; Selton and Andre, 1997; Takeuchi and Watanabe, 1989; Tharp et al., 1981; Tharp et al., 1989; Watanabe et al., 1999; Zeinstra et al., 2001). Serial studies also afford greater opportunity to detect electrical seizures (Glauser and Clancy, 1992), the presence of which may be of prognostic significance (see Chapter 7).

Failure to recognize that EEG findings evolve over time may lead to a less than accurate determination of prognosis. For example, an EEG of an infant might show a suppression-burst pattern on the first day after birth, a finding generally indicating the presence of severe brain dysfunction. However, hours later, after the infant's physiological condition has stabilized, the EEG activity may become continuous, with relatively normal background activity. Such changes drastically alter statements concerning the prognosis. On the other hand, a suppression-burst pattern that is sustained over several days or that changes to a depressed and undifferentiated pattern implies a poor prognosis for recovery of brain function. Failure to recognize the importance of the time course has led to contradictory statements in the literature concerning the prognostic significance of suppression-burst activity.

With this caveat, however, some statements can be made concerning the significance of the first EEG recorded early in the course of neurologic illness. In infants requiring intensive care, the EEG findings obtained within the first 24 hours after birth can provide reliable prognostic information (Pezzani et al., 1986); a normal EEG on the first day, or one with only minimally abnormal findings, reliably indicates a good prognosis unless further brain injury occurs later.

DIFFUSE ABNORMALITIES

Dyschronism: Disordered Maturational Development

An experienced neurophysiologist can usually determine CA to within 2 weeks between 27 and 33 weeks CA, and within ±1 week between 34 and 37 weeks CA, based on expected developmental features (see Chapter 4) (Tharp, 1990). Disordered maturational development is referred to as “dyschronism” and, if present, is an important abnormality of the neonatal EEG (Hrachovy et al., 1990).

External Dyschronism

This term refers to an EEG in which the developmental characteristics in all states of sleep and wakefulness are immature for the reported gestational or CA. If the

P.118


developmental features of an EEG are immature for the stated gestational or CA and the features of the background activity in all states are normal, the following questions must be addressed: (a) Is the age as determined by clinical evaluation overestimated? or (b) Are the immature EEG features evidence of delayed maturation? The latter explanation suggests that a cerebral insult may have occurred during intrauterine life. A discrepancy of 2 weeks or less between EEG age and estimated CA most likely indicates the presence of a transient central nervous system (CNS) dysfunction. However, discrepancies of more than 3 weeks usually indicate persistent impairment of CNS function and are frequently accompanied by other EEG abnormalities, including marked suppression of background activity or multifocal sharp waves.

Internal Dyschronism

This term refers to different maturational characteristics between the EEG awake and in the deepest stages of non-rapid eye movement (NREM) sleep (Fig. 6-1). For example, characteristics of the waking EEG might be consistent with a CA of 38 weeks, whereas the background activity during deep NREM sleep might be consistent with a CA of 34 weeks. If a dyschronism of 3 or more weeks occurs between the awake record and deep sleep, other EEG abnormalities are often present. These abnormalities are usually most apparent in NREM sleep, the state that always shows the least mature characteristics (Fig. 6-2). Such findings suggest significant brain dysfunction. Therefore, an EEG of any infant should include a period of the deepest stages of NREM sleep.

Transient Maturational Abnormalities

Maturational abnormalities may occur transiently in a newborn with acute or ongoing hypoxia-ischemia. Immature EEG characteristics can disappear rapidly when the patient is well oxygenated and the period of hypoxia-ischemia has been short. Therefore, the prognostic significance of an EEG whose developmental features are immature for the stated CA can be determined only by making serial recordings.

Abnormalities of Background Activity in Diffuse Brain Disturbance

Prolongation of Interburst Intervals in Premature Infants

The range of the duration of normal interburst intervals is CA dependent and, in older premature infants, state dependent (Fig. 6-3). The longest acceptable single interburst interval duration according to CA has been reported to be 26 weeks CA, 46 seconds; 27 weeks, 36 seconds (Selton et al., 2000); less than 30 weeks CA, 30 to 35 seconds; 31 to 33 weeks CA, 20 seconds; 34 to 36 weeks CA, 10 seconds; 37 to 40 weeks CA, 6 seconds (Hahn et al., 1989). In general, the longest interval within an individual record is measured, rather than assessing an average of intervals. Although a prolongation of the interburst interval may be secondary to a CNS insult, it may also be due to the use of sedative medications such as morphine (Young and da Silva, 2000) and sufentanil (Nguyen et al., 2003).

Episodes of Generalized and Regional Voltage Attenuation in Term Infants

Another finding of diffuse dysfunction in the term infant is the presence of generalized or regional episodes of voltage attenuation (Fig. 6-4). Although abnormal, this finding suggests relatively mild diffuse dysfunction compared with other findings listed later.

Depression and Lack of Differentiation

Depressed beta activity, either focal or diffuse, is often the first manifestation of abnormal cortical function. After hypoxia-ischemia, faster frequencies tend to be depressed or obliterated. Lack of differentiation (i.e., the “undifferentiated EEG”) refers to virtual or complete disappearance of the polyfrequency activity normally present (Fig. 6-5). A depressed and undifferentiated EEG background often accompanies other abnormalities (Fig. 6-6). However, in some instances, developmental milestones may persist (Fig. 6-7). A depressed and undifferentiated EEG in the newborn indicates that a severe brain insult has occurred. Disorders causing such an EEG include profound hypoxia-ischemia, severe metabolic disorders, infectious processes such as meningitis or encephalitis, cerebral hemorrhage, and intraventricular hemorrhage (IVH). A depressed and undifferentiated EEG within the first 24 hours after birth that persists signifies a poor prognosis.

Suppression-Burst Pattern

The suppression-burst pattern represents an intermediate degree of diffuse brain disturbance between the depressed and undifferentiated EEG and electrocerebral silence. Activity during the bursts consists primarily of delta and theta frequencies, which at times is intermixed with sharp waves. The bursts are separated by periods of marked generalized voltage attenuation or electrocerebral silence (Figs. 6-8, 6-9, 6-10, 6-11, 6-12 and 6-13). Suppression-burst patterns persist unremittingly; no change in the EEG activity is seen during the entire recording, and the pattern does not react to

P.119


painful stimuli. Some infants with the suppression-burst pattern may experience periodic slow myoclonic jerks (Figs. 6-14 and 6-15).

Electrocerebral Silence

Electrocerebral silence represents the ultimate degree of depression and lack of differentiation in the neonate. The transition from a severely depressed and undifferentiated background to isoelectric may be difficult to determine (Fig. 6-16), and serial EEGs may be required to demonstrate a persistent degree of cortical inactivity (Fig. 6-17). An isoelectric EEG (i.e., “electrocerebral silence”) is evidence of death only of the cortex, not of the brainstem, which, in the infant, may sustain vital functions for prolonged periods. Indeed, prolonged survival may occur in infants whose EEGs continue to show electrocerebral silence (Mizrahi et al., 1985).

Specialized Generalized Patterns

Hypsarrhythmia

The classic hypsarrhythmic pattern as described by Gibbs and Gibbs (1952) rarely appears before 44 weeks CA. However, one modification of this pattern in the neonatal period is the suppression-burst variant (Hrachvoy et al., 1984), characterized by periodic bursts of high-voltage activity (Fig. 6-15). The bursts consist of asynchronous, high-voltage, slow activity mixed with multifocal spikes and sharp waves. The primary features that distinguish this variant of hypsarrhythmia are the periodicity of the bursts and the high voltage of the activity within the bursts.

Patients with infantile spasms and this variant of hypsarrhythmia have a poor prognosis for long-term outcome, regardless of whether the pattern develops in the neonatal period or in later months of life (Maheshwari and Jeavons, 1975). In addition, when this pattern does appear in the neonatal period, it is closely associated with the presence of inborn errors of metabolism, most notably nonketotic hyperglycinemia.

Holoprosencephaly

The term holoprosencephaly is applied to a spectrum of related cerebral malformations resulting from faulty diverticulation of the prosencephalon. The malformation varies in severity, from arhinencephaly (in which the olfactory bulbs and tracts are absent but the brain is otherwise normal) to alobar holoprosencephaly (in which lobes are not demarcated and the cerebrum is monoventricular, with or without a dorsal cyst). A variety of median facial defects (including cyclopia, orbital hypotelorism, cleft lip, cleft palate, and hypoplasia of the premaxilla) are associated with the cerebral malformations (DeMyer and Zeman, 1963; Yakovlev, 1959).

The EEG findings associated with holoprosencephaly were described by DeMyer and White (1964). They include (a) multifocal spike and polyspike activity mixed with slow waves; (b) periods of monorhythmic beta-, alpha-, theta-, or delta-frequency activity, occurring singly or in various combinations; (c) asynchrony between hemispheres; (d) isoelectric or relatively low voltage activity; (e) periodic patterns; and (f) lack of any normal organization (Figs. 6-18 and 6-19). These findings occur in various combinations in a single patient. Equally dramatic are the repeated and abrupt changes from one pattern to another, such that in a few minutes, most or all of the aforementioned features can be visualized. This constellation of findings is not seen in other disorders of infancy and is therefore diagnostic for holoprosencephaly. Infants with holoprosencephaly often have unusual or stereotyped movements suggestive of seizures. However, no correlation exists between these movements and EEG changes. The prognosis is poor; about 50% of infants die within the first month of life; about 80% will be dead within the first year.

PATTERNS THAT MAY BE FOCAL OR GENERALIZED

Sustained Rhythmic Alpha-Theta Activity

Sustained, rhythmic, 4- to 7-Hz activity (theta) and/or 8- to 10-Hz (alpha), 40- to 100-µV activity that is generalized or focal is an abnormal finding. However, precise correlations to specific etiologic factors have not, for the most part, been determined. This activity may occur almost continuously or paroxysmally in brief runs and may occur as only theta, alpha, or mixed activity (Figs. 6-20, 6-21, 6-22, 6-23, 6-24 and 6-25).

When alpha activity occurs focally, it is most prevalent in the central or temporal regions, where it may occur independently on the two sides. Although this activity may be most prominent in the awake state, it is usually present in all states and is accompanied by other abnormalities, such as abnormal sharp waves. Generalized rhythmic alpha and/or theta activity has been associated with various underlying abnormalities, most commonly congenital heart disease; however, it also may be seen in infants who have received CNS-active drugs such as diazepam and phenobarbital (Hrachovy and O'Donnell, 1996). It is important to distinguish this pattern from the alpha seizure pattern (see Chapter 7).

Sustained Rhythmic Delta Activity

In some instances, bifrontal slow (delta) activity is considered an abnormal finding. Abnormal bifrontal slow activity can be differentiated from normal bifrontal slow activity by its presence in all stages of sleep and wakefulness and its unrelenting

P.120


character (Fig. 6-26). Abnormal rhythmic slow (delta) activity also may be present in the occipital regions bilaterally (Fig. 6-27).

FOCAL ABNORMALITIES

Periodic Complexes

Focal periodic and quasiperiodic discharges in a newborn's EEG have been reported to be suggestive of neonatal herpes simplex encephalitis (HSVE) (Mizrahi and Tharp, 1982) (Fig. 6-28). Although such periodic discharges may be associated with HSVE, such discharges also may be interpreted as electrical seizures of the depressed-brain type (see Chapter 7). In addition, periodic discharges are not, however, peculiar to HSVE and may occur with various other CNS insults such as infarction (Scher and Beggarly, 1989).

Unilateral Depression of Background Activity

Mild shifting asymmetry of the background EEG activity between hemispheres is a common finding in the newborn, particularly during quiet sleep. However, an abnormal finding is a marked voltage asymmetry of background rhythms between hemispheres that persists in all states (Figs. 6-13 and 6-29, 6-30 and 6-31). Unilateral depression may occur in association with a wide range of structural cerebral lesions such as infarction, hemorrhage, focal cystic lesions, and rarely, congenital malformation. In addition, other intracranial abnormalities such as subdural fluid collections may be associated with this EEG finding. However, focal depression of the background activity may persist for variable periods after electrical seizures. A marked asymmetry of the background activity also may result from nonintracranial causes such as subgaleal swelling, scalp edema, or technical error.

Focal Slow Activity

Just as in older infants, the finding of focal slow activity that persists at a specific site may indicate the presence of a focal destructive lesion such as infarction, hemorrhage, or, more specific to neonates, congenital anomalies of the brain (Fig. 6-32).

Central Positive Sharp Waves

These waves are 50- to 250-µV surface-positive transients lasting 100 to 250 milliseconds and occurring either unilaterally or bilaterally in the central regions (Figs. 6-33, 6-34, 6-35,6-36 and 6-37). A lower-voltage aftergoing surface-negative component may be present. The waves usually occur singly or in brief runs. Central positive sharp waves are not epileptiform discharges, and the physiological processes causing them remain unknown. They have been described most notably in infants with IVH (Blume and Dreyfus-Brisac, 1982;Cukier et al., 1972; Lomboso, 1982; Tharp et al., 1981) and white-matter necrosis (periventricular leukomalacia) (Lomboso, 1982; Marret et al., 1986; Novotny et al., 1987); as well as other conditions, including meningitis, hydrocephalus, aminoaciduria (Tharp, 1980), and asphyxia (da Costa and Lombroso, 1980). Current thought is that central positive sharp waves are specific not for IVH but rather for white-matter necrosis, which may result from a variety of insults, including IVH (Novotny et al., 1987). In addition, the abundance and rate of recurrence of central positive sharp waves within a single record of an infant appears to correlate with long-term neurologic outcome; a rate of greater than two per second has been reported to be associated with a poor outcome (Blume and Dreyfus-Brisac, 1982).

Temporal Sharp Waves

The problems of determining whether focal temporal sharp waves are normal or abnormal have been previously discussed (see Chapter 5). Whereas some sharp waves occurring in the temporal regions are considered normal, others may not meet the criteria to be called abnormal and are thus of questionable significance. However, some temporal sharp waves are clearly abnormal. Criteria for abnormality include morphology, polarity, rate of recurrence, and persistence at one site (Figs. 6-38 and 6-39).

Extratemporal Focal Sharp Waves

Abnormal sharp waves that appear as slow sharp transients or rapid spikes may occur in the frontal (Figs. 6-40, 6-41, 6-42, 6-43, 6-44, 6-45 and 6-46), central (Figs. 6-47, 6-48and 6-49), and occipital (Figs. 6-50, 6-51 and 6-52) regions. When persistently focal, they may indicate focal brain injury, although often no well-defined structural lesion can be documented by neuroimaging.

Multifocal Sharp Waves

As already noted, sharp waves in the newborn EEG are common, with certain sharp-wave activity being considered normal. Multiple foci of high-voltage,

P.121


long-duration, sharp-wave activity are commonly seen in infants who have had a diffuse CNS insult (Figs. 6-53, 6-54, 6-55 and 6-56). Such abnormal sharp waves usually predominate in the temporal regions and may persist over one hemisphere. Multifocal sharp waves usually accompany various other EEG abnormalities, including depressed and undifferentiated background activity and episodes of attenuation. However, multifocal sharp waves may be the only abnormality after a CNS insult and also may be the last remaining evidence of CNS dysfunction in serial tracings. This abnormality is usually maximal in quiet sleep, and in some infants, it may occur only in this state (Fig. 6-2). Multifocal sharp waves cannot be used as evidence that a seizure has occurred or will occur, because the sharp waves do not show a significant association with neonates with seizures.

P.122

LIST OF FIGURES

Dyschronism

Fig. 6-1. Internal dyschronism

Fig. 6-2. State-dependent abnormality of the EEG

Prolongation of Interburst Intervals

Fig. 6-3. Excessive discontinuity

Voltage Attenuation

Fig. 6-4. Generalized and regional episodes of voltage attenuation

Depression and Lack of Differentiation

Fig. 6-5. Moderately undifferentiated background activity

Fig. 6-6. Undifferentiated background activity with periods of generalized voltage attenuation

Fig. 6-7. Undifferentiated background with episodes of generalized voltage attenuation, but with preservation of some developmental milestones

Suppression-Burst Pattern

Fig. 6-8. Suppression-burst activity with sharp and slow waves within the bursts and variable durations between bursts

Fig. 6-9. Suppression-burst activity with activity of normal character within the bursts

Fig. 6-10. Suppression-burst activity with bursts of asynchronous, very slow, and superimposed fast activity

Fig. 6-11. Suppression-burst activity with predominance of fast activity within the bursts

Fig. 6-12. Suppression-burst activity with rhythmic alpha activity within the bursts

Fig. 6-13. Suppression-burst activity with persistent asymmetry of activity within the bursts

Fig. 6-14. Suppression-burst activity with synchronous bursts

Fig. 6-15. Suppression-burst variant of hypsarrhythmia with periodic bursts

Severe Depression of Background

Fig. 6-16. Depressed and undifferentiated background activity

Fig. 6-17. Depressed and undifferentiated background activity evolving to suppression-burst activity

Holoprosencephaly

Fig. 6-18. Dynamic pattern of holoprosencephaly

Fig. 6-19. Dynamic pattern of holoprosencephaly with persistent focal features

Sustained Rhythmic Alpha-Theta Activity

Fig. 6-20. Rhythmic bifrontal theta activity

Fig. 6-21. Paroxysmal bifrontal theta activity

Fig. 6-22. Rhythmic bifrontal theta activity followed by rhythmic bifrontal alpha activity

Fig. 6-23. Generalized rhythmic alpha activity with variable interhemispheric asynchrony

Fig. 6-24. Generalized rhythmic alpha and theta activity

Fig. 6-25. Generalized rhythmic theta activity

Sustained Rhythmic Delta Activity

Fig. 6-26. Rhythmic, monomorphic, bifrontal delta activity

Fig. 6-27. Rhythmic bioccipital slow activity

Periodic Complexes

Fig. 6-28. Periodic lateralized discharges associated with HSV encephalitis

Unilateral Depression of Background Activity

Fig. 6-29. Voltage asymmetry in prematurity

Fig. 6-30. Voltage asymmetry with mildly abnormal background activity

Fig. 6-31. Voltage asymmetry associated with abnormal background activity

Focal Slow Activity

Fig. 6-32. Focal slow activity in the left occipital region

Central Positive Sharp Waves

Fig. 6-33. Surface-positive sharp waves

Fig. 6-34. Surface-positive sharp waves in the premature

Fig. 6-35. Occurrence and location of surface-positive sharp waves

Fig. 6-36. Asynchronous, independent surface-positive temporal sharp waves

Fig. 6-37. Surface-positive sharp wave of moderate voltage

P.123

Temporal Sharp Waves

Fig. 6-38. Surface-positive sharp waves in the temporal region with complex morphology

Fig. 6-39. Temporal sharp waves with complex morphology

Extratemporal Focal Sharp Waves

Fig. 6-40. Abnormal frontal sharp wave

Fig. 6-41. Burst of abnormal frontal sharp waves

Fig. 6-42. Independent bilateral abnormal frontal sharp waves

Fig. 6-43. Bilateral frontal spikes

Fig. 6-44. Bilateral frontal sharp waves

Fig. 6-45. Frontal sharp waves and independent central spikes

Fig. 6-46. Midline and lateralized frontal spikes

Fig. 6-47. Central rapid spike

Fig. 6-48. Repetitive midline central spikes

Fig. 6-49. Central midline, rhythmic theta, and lateralized central spikes

Fig. 6-50. Occipital spikes and slow waves

Fig. 6-51. Occipital spikes and independent temporal and central sharp waves

Fig. 6-52. Bilateral, independent occipital spikes

Fig. 6-53. Multifocal sharp waves

Fig. 6-54. Multifocal spikes and sharp waves

Fig. 6-55. Multifocal sharp waves with rhythmic morphology

Fig. 6-56. Surface-positive and surface-negative multifocal sharp waves

P.124

FIG. 6-1. Internal dyschronism. A: The developmental features of the EEG in this term infant in transitional sleep are consistent with a CA of 38 to 40 weeks and are within the range of normal variation. B: In deep non-rapid eye movement (NREM) sleep, during the same recording of the infant, the developmental features of the EEG are consistent with the CA of 33 weeks, with central beta-delta complexes, temporal alpha bursts, and a discontinuous background. This NREM sleep recording also is without abnormalities.

P.125

FIG. 6-1. (Continued)

P.126

FIG. 6-2. State-dependent abnormality of the EEG. A: The awake EEG of this term infant, suspected of having hypoxic-ischemic encephalopathy, is within the range of normal variation, and its developmental features are consistent with that CA. B: During non-rapid eye movement sleep, the EEG is abnormal, with excessive discontinuity, asynchronous activity including sharp waves and spikes, and no well-defined developmental milestones. This differs from internal dyschronism, because the features of the sleep recording are abnormal.

P.127

FIG. 6-2. (Continued)

P.128

FIG. 6-3. Excessive discontinuity. During non-rapid eye movement sleep, the degree of discontinuity is excessive for the infant's CA of 35 weeks. This is shown in two contiguous segments (A) and (B). In addition, there is an absence of beta-delta complexes. This infant was found to have grade III intraventicular hemorrhage bilaterally.

P.129

FIG. 6-3. (Continued)

P.130

FIG. 6-4. Generalized and regional episodes of voltage attenuation. Brief episodes of generalized voltage attenuation lasting 1 to 2 seconds and episodes of similar character and duration appear independently in leads from the left and right hemispheres. The background activity also is abnormal with multifocal sharp waves. The EEG is from a 40-week CA infant who is lethargic and with computed tomography neuroimaging findings of biparietal white-matter lucencies. No specific etiology was identified.

P.131

FIG. 6-5. Moderately undifferentiated background activity. The background EEG activity is undifferentiated, with a lack of developmental milestones, a lack of faster frequencies, and brief episodes of generalized voltage attenuation. The EEG comprises almost exclusively moderate-voltage slow activity. The infant is 43-week CA with the inborn error of metabolism, methylmalonic acidemia.

P.132

FIG. 6-6. Undifferentiated background activity with periods of generalized voltage attenuation. The background activity is low in voltage with no alpha or beta activity. Periods of generalized voltage attenuation appear early and late in the sample. The EEG is from a 41-week CA infant with renal failure and metabolic acidosis. The patient was on renal dialysis at the time of recording.

P.133

FIG. 6-7. Undifferentiated background with episodes of generalized voltage attenuation, but with preservation of some developmental milestones. The background activity is depressed and undifferentiated with intermittent rhythmic theta activity between episodes of generalized voltage attenuation. Early in the sample, abnormal sharp waves occur in the frontal regions. However, later in the sample, normal frontal sharp transients are present. Such findings can be distinguished from a suppression-burst pattern when other portions of the EEG are continuous and by the presence of normal developmental milestones. The EEG is from a 39-week CA infant with congenital heart disease and chronic hypoxemia.

P.134

FIG. 6-8. Suppression-burst activity with sharp and slow waves within the bursts and variable durations between bursts. The brief bursts are characterized by high-voltage slow activity with superimposed theta and alpha activity. The bursts are followed by high-voltage very slow wave transients. The periods of suppression are variable in these contiguous samples (A, B), lasting from 3 seconds to >10 seconds. This EEG was recorded from a 35-week CA infant who was lethargic with hypoxic-ischemic encephalopathy, microcephaly, and the finding of periventricular leukomalacia on head computed tomography.

P.135

FIG. 6-8. (Continued)

P.136

FIG. 6-9. Suppression-burst activity with activity of normal character within the bursts. The bursts are characterized by moderate-voltage activity of mixed slow and faster frequencies, which, if continuous, would be considered normal for this term infant. However, the background activity is suppression-burst. This term infant had meconium aspiration, required ventilatory support and, by the time of this recording, was maintained with extracorporeal membrane oxygenation.

P.137

FIG. 6-10. Suppression-burst activity with bursts of asynchronous, very slow, and superimposed fast activity. The bursts are characterized by high-voltage, very slow activity with superimposed very low voltage faster activity. This occurs asynchronously on the two sides. The infant is 37 weeks CA, with hypoxic-ischemic encephalopathy, multisystem organ failure, and intracerebral hemorrhage on the left—in this instance with no consistent lateralizing findings on EEG.

P.138

FIG. 6-11. Suppression-burst activity with predominance of fast activity within the bursts. Runs of moderate-voltage fast activity are present asynchronously on the two sides during periods of bursting. The infant is 35 weeks CA with metabolic acidosis, cardiac failure, pulmonary edema, peritonitis, and microcephaly.

P.139

FIG. 6-12. Suppression-burst activity with rhythmic alpha activity within the bursts. Runs of moderate-voltage rhythmic alpha activity in the frontotemporal regions appear asynchronously within the bursts of this suppression-burst recording. This EEG is from a 35-week CA infant with hypoxic-ischemic encephalopathy.

P.140

FIG. 6-13. Suppression-burst activity with persistent asymmetry of activity within the bursts. The bursts are characterized by moderate-voltage theta and delta activity. Persistent voltage asymmetry of the bursts is present with the amplitudes of waves lower in leads from the left centrotemporal region compared with homologous regions on the right. This term infant was born by emergency cesarean section, had persistent cyanosis, and required support by extracorporeal membrane oxygenation. The asymmetry on EEG is most likely owing to dependent scalp edema on the left.

P.141

FIG. 6-14. Suppression-burst with synchronous bursts. The bursts recur periodically every 3 to 5 seconds, but are brief, lasting 1 to 2 seconds, with fairly synchronous activity on the two sides. This term infant experienced generalized myoclonic and focal clonic seizures with the eventual finding of the inborn error of metabolism, nonketotic hyperglycinemia. (From Mizrahi EM, Kellaway P. Diagnosis and management of neonatal seizures. Philadelphia: Lippincott-Raven, 1998:181, with permission.)

P.142

FIG. 6-15. Suppression-burst variant of hypsarrhythmia with periodic bursts. This is a suppression-burst variant of hypsarrhythmia in a 43-week CA infant with an inborn error of metabolism and a clinical diagnosis of early myoclonic encephalopathy. The infant had infantile spasms accompanied by generalized voltage attenuations in the EEG (not shown).

P.143

FIG. 6-16. Depressed and undifferentiated background activity. The background activity is severely depressed and undifferentiated in all regions with only electrocardiogram artifact and occasional very low voltage slow waves present. This EEG is from a 37-week CA infant with hypoxic-ischemic encephalopathy (Apgar scores, 1 at 1 minute, 1 at 5 minutes), multiorgan system failure, and intracerebral hemorrhage.

P.144

FIG. 6-17. Depressed and undifferentiated background activity evolving to suppression-burst activity. A: The EEG is depressed and undifferentiated with artifact from electrocardiogram and extracorporeal membrane oxygenation instrumentation. This EEG was recorded on day 3 of life from this term infant with hypoxic-ischemic encephalopathy. B: On day 10 of life, the EEG had evolved to a suppression-burst pattern. Although this represented a change in the EEG findings with some improvement, the rate of improvement and the change to only suppression-burst suggested a poor prognosis in terms of neurologic outcome.

P.145

FIG. 6-17. (Continued)

P.146

FIG. 6-18. Dynamic pattern of holoprosencephaly. These are samples from a single EEG recorded from a term infant with holoprosencephaly diagnosed by clinical and magnetic resonance imaging findings. A: Multiple foci of spike and polyspike activity are mixed with slow-wave activity, with independent delta activity with superimposed beta activity. B: A sudden transition occurs to sustained rhythmic theta and alpha activity. C: A sudden transition to high-voltage rhythmic slow activity is seen predominantly on the left. Note the voltage calibration that indicates the very high voltage of this activity.

P.147

FIG. 6-18. (Continued)

P.148

FIG. 6-18. (Continued)

P.149

P.150

FIG. 6-19. Dynamic pattern of holoprosencephaly with persistent focal features. The EEG features that are typical in infants with holoprosencephaly are present in this term infant who, as part of the brain malformation, also has a dorsal cystic lesion that is characterized on EEG by marked depression of activity in the affected regions. A: High-voltage, rhythmic, alpha and theta frequency activity is mixed with some slower waveforms. B: High-voltage, rhythmic fast activity is present. C: High-voltage very slow activity is present on the right with the persistence of fast activity on the left until a sudden transition to slower frequencies on that side. D: Asynchronous, high-voltage very slow activity with superimposed fast activity is present.

P.151

FIG. 6-19. (Continued)

P.152

FIG. 6-20. Rhythmic bifrontal theta activity. Moderate-voltage rhythmic 5- to 6-Hz activity is present in the frontal regions bilaterally in the EEG that is otherwise normal in this term infant.

P.153

FIG. 6-21. Paroxysmal bifrontal theta activity. Paroxysmal moderately high voltage 5- to 6-Hz activity appears in the frontal regions bilaterally. The EEG is otherwise normal in this term infant.

P.154

FIG. 6-22. Rhythmic bifrontal theta activity followed by rhythmic bifrontal alpha activity. There is a burst of rhythmic high voltage 5- to 6-Hz activity in the frontal regions bilaterally followed by a run of low-voltage rhythmic 8- to 9-Hz activity. The background EEG activity is otherwise normal in this term infant.

P.155

FIG. 6-23. Generalized rhythmic alpha activity with variable interhemispheric asynchrony. Runs of rhythmic 8- to 9-Hz activity occur both synchronously and asynchronously in the left and right central regions in a term infant with a chromosomal abnormality and multiple congenital anomalies. (From Hrachovy RA, Mizrahi EM, Kellaway P. Electroencephalography of the newborn. In: Daly DD, Pedley TA, eds. Current practice of clinical electroencephalography, 2nd ed. New York: Raven Press, 1990:201-241, with permission.)

P.156

FIG. 6-24. Generalized rhythmic alpha and theta activity. Runs of 8- to 9-Hz activity are mixed with 5- to 6-Hz activity in all regions in the EEG of this term infant with congenital heart disease.

P.157

FIG. 6-25. Generalized rhythmic theta activity. Sustained, monomorphic, rhythmic 5- to 6-Hz activity appears chiefly in anterior regions in this term infant with the inborn error of metabolism, citrullinemia.

P.158

FIG. 6-26. Rhythmic, monomorphic, bifrontal delta activity. Monorhythmic, monomorphic, 2.5- to 3-Hz activity in the frontal regions bilaterally and the background activity is depressed in this term infant with nonaccidental head injury.

P.159

FIG. 6-27. Rhythmic bioccipital slow activity. High-voltage, 1- to 1.5-Hz activity appears in the occipital regions of the EEG of this term infant. The background activity is undifferentiated.

P.160

FIG. 6-28. Periodic lateralized discharges associated with herpes simplex virus encephalitis. Low-volt-age, slow transients recur periodically in the left temporal region in this term infant with laboratory-confirmed herpes simplex virus encephalitis. The background activity is depressed and undifferentiated, with randomly occurring low voltage sharp waves in the left central region.

P.161

FIG. 6-29. Voltage asymmetry in prematurity. Voltage asymmetry is present, with the amplitude of waves lower in the leads from the left hemisphere compared with the right. The background activity on the right shows beta-delta complexes. This 35- to 36-week CA infant had a left frontoparietal intracerebral hemorrhage and an intraventricular hemorrhage with involvement of the germinal matrix on the left.

P.162

FIG. 6-30. Voltage asymmetry with mildly abnormal background activity. Voltage asymmetry appears with the amplitude of waves lower on the left compared with that in homologous regions on the right. Although frontal sharp transients (normal developmental milestones) persist on the right, the background activity is abnormal with a lack of faster frequencies. This term infant had a left frontoparietal intracerebral hemorrhage.

P.163

FIG. 6-31. Voltage asymmetry associated with abnormal background activity. A voltage asymmetry is seen with the amplitude of waves lower in leads from the right centrotemporal region compared with the homologous region on the left. Random moderate-voltage sharp waves are present bilaterally. The background activity is low in voltage. The infant is term with a right parietal infarction and diagnosis of hypoxic-ischemic encephalopathy.

P.164

FIG. 6-32. Focal slow activity in the left occipital region. Moderate to moderately high voltage, 1- to 3-Hz activity is found in the left occipital region in this term infant with a congenital cystic lesion in that region.

P.165

FIG. 6-33. Surface-positive sharp waves. During the second half of this EEG sample, an abnormal surface-positive high-voltage sharp wave is seen in the right temporal region. Earlier, moderate-voltage temporal sharp waves are repetitive with both surface-positive and surface-negative components. This sample is selected from a standard 12-channel EEG recording. (From Hrachovy RA, Mizrahi EM, Kellaway P. Electroencephalography of the newborn. In: Daly DD, Pedley TA, eds. Current practice of clinical electroencephalography, 2nd ed. New York: Raven Press, 1990:201-241.)

P.166

FIG. 6-34. Surface-positive sharp waves in the premature. After a period of quiescence, a high-voltage sur-face-positive sharp wave is present in the right central region. This is followed by abnormal spike and sharp-wave activity a few seconds later. Eventually, a temporal theta burst (a normal feature) is present. This EEG is from a 29- to 30-week CA infant with an intraventricular hemorrhage.

P.167

FIG. 6-35. Occurrence and location of surface-positive sharp waves. Surface-positive sharp waves may appear as a unilateral, single transient, as in the early portion of this sample, or they may recur at a relatively frequent rate and appear asynchronously on the two sides as in the latter portion of this sample. This sample is taken from the EEG of a 36-week CA infant with intraventricular hemorrhage. The background activity is depressed and undifferentiated; filtered electromyogram artifact is present in the frontal and temporal leads.

P.168

FIG. 6-36. Asynchronous, independent surface-positive temporal sharp waves. Surface-positive sharp waves are present independently in the left and right temporal regions in this 35-week CA infant with a chromosomal abnormality, dysmorphic features, and germinal matrix hemorrhage.

P.169

FIG. 6-37. Surface-positive sharp wave of moderate voltage. A surface-positive sharp wave of moderate voltage is present in the left central region. The background EEG activity is within the range of normal variation and consistent with a 34- to 35-week CA in this infant with periventricular leukomalacia.

P.170

FIG. 6-38. Surface-positive sharp waves in the temporal region with complex morphology. A sharp wave with both surface-positive and sur-face-negative components is present in the left temporal region in this 40-week CA infant with an intracerebral hemorrhage in the left temporal lobe.

P.171

FIG. 6-39. Temporal sharp waves with complex morphology. Abnormal temporal sharp waves with complex morphology are present in the left temporal region in the early portion of this sample of a term infant. The background EEG activity is normal and includes some intermittent, rhythmic delta activity in the frontal regions bilaterally. (SeeChapter 5 for additional samples of abnormal temporal sharp waves.)

P.172

FIG. 6-40. Abnormal frontal sharp wave. An abnormal sharp wave, with polyphasic morphology, is seen in the left frontal region in this term infant. This is a selected sample from a 12-channel EEG. (From Hrachovy RA, Mizrahi EM, Kellaway P. Electroencephalography of the newborn. In: Daly DD, Pedley TA, eds. Current practice of clinical electroencephalography, 2nd ed. New York: Raven Press, 1990:201-241, with permission.)

P.173

FIG. 6-41. Burst of abnormal frontal sharp waves. A burst of abnormal sharp waves is present in the right frontal region in this term infant. This is a selected sample from a 12-channel EEG. (From Hrachovy RA, Mizrahi EM, Kellaway P. Electroencephalography of the newborn. In: Daly DD, Pedley TA, eds. Current practice of clinical electroencephalography, 2nd ed. New York: Raven Press, 1990:201-241, with permission.)

P.174

FIG. 6-42. Independent bilateral abnormal frontal sharp waves. Abnormal frontal sharp waves are present in the first half of this sample. Frontal sharp transients (an expected developmental milestone in this epoch) are present in the second half of the sample, although abnormal because of their asymmetry. In addition, the background EEG activity is undifferentiated in this 40-week CA infant with lactic acidosis and pulmonary insufficiency.

P.175

FIG. 6-43. Bilateral frontal spikes. High-voltage spikes are present in the frontal regions bilaterally, higher in amplitude on the left and well expressed in the midline frontal region. A temporal sharp wave on the left occurs earlier. The background EEG activity is discontinuous in this 38-week CA infant with cerebral dysgenesis, congenital ventriculomegaly, and choroid plexus hemorrhage.

P.176

FIG. 6-44. Bilateral frontal sharp waves. Intermittently occurring high-voltage sharp waves are seen in the frontal regions bilaterally. The background EEG activity is within the range of normal variation in this 42-week CA infant suspected of having seizures, but without clinical or electrical seizures documented by prolonged EEG.

P.177

FIG. 6-45. Frontal sharp waves and independent central spikes. There are independent high-voltage sharp waves in the right frontal region and runs of low-voltage spikes in the left central region in this 32-week CA infant.

P.178

FIG. 6-46. Midline and lateralized frontal spikes. Abnormal spikes appear in the left frontal region and, later in the sample, spikes appear in the right frontal region with expression in the midline central region in this term infant.

P.179

FIG. 6-47. Central rapid spike. A single spike discharge is present in the left central region with normal background EEG activity in this term infant. The sample is taken from a 12-channel EEG recording.

P.180

FIG. 6-48. Repetitive midline central spikes. A run of spikes in the midline central region is expressed in the Cz electrode in this 38-week CA infant with cardiac failure and grade I intraventricular hemorrhage.

P.181

FIG. 6-49. Central midline, rhythmic theta, and lateralized central spikes. In the early portion of the recording, rhythmic theta activity appears in the midline central region, and later, a run of rhythmic spikes in the right central region. The infant was born at 28 weeks CA and, at the time of EEG recording, was 35 weeks CA. An acute grade III intraventricular hemorrhage was resolving at the time of EEG recording, although posthemorrhagic hydrocephalus and a porencephalic cyst had extended into the left frontal ventricular horn.

P.182

FIG. 6-50. Occipital spikes and slow waves. Spikes and slow waves appear in the left occipital region, with some reflection of the slow-wave component on the right. The background EEG activity is within the range of normal variation in this term infant. This sample is selected from a 12-channel EEG.

P.183

FIG. 6-51. Occipital spikes and independent temporal and central sharp waves. Recurrent spikes are seen in the right occipital region early in this sample. Immediately after this burst, frontal sharp transients appear, a normal phenomenon. Then temporal sharp waves on the left are followed by an independent sharp wave on the right.

P.184

FIG. 6-52. Bilateral, independent occipital spikes. Spike and slow-wave complexes are seen independently in the left and right occipital regions in this 40-week CA infant with the peroxisomal disorder, Zellweger syndrome.

P.185

FIG. 6-53. Multifocal sharp waves. Sharp waves, with varying morphology, appear independently in the left and right central regions in a semiperiodic manner. The background activity is depressed and undifferentiated in this 44-week CA infant with the inborn error of metabolism, ornithine carbamylase transferase deficiency.

P.186

FIG. 6-54. Multifocal spikes and sharp waves. Spikes and sharp waves appear independently in the left and right central and right temporal regions. The background EEG activity is undifferentiated in this 40-week CA infant with congenital heart disease.

P.187

FIG. 6-55. Multifocal sharp waves with rhythmic morphology. Very brief bursts of rhythmic sharp theta activity appear independently in the left central and left and right temporal regions. The background activity is undifferentiated in this infant with laboratory confirmed herpes simplex encephalitis.

P.188

FIG. 6-56. Surface-positive and surface-negative multifocal sharp waves. Sharp waves are present in the left and right central, left and right temporal, and right frontal regions. Some of the waveforms are surface positive (left temporal early in the sample), and others are surface negative in this term infant with renal failure.

FIG. 4-31. (Continued)