Polarity Localization

Proper electrode placement and montage choices allow accurate comparisons between homologous brain regions. In this way, the neurologist can localize EEG data on an anatomic basis and can standardize regional or hemispheric findings over multiple EEG recordings. An understanding of the principles of polarity is essential in using the localization technique [Ebersole and Pedley, 2003].

Inputs for two electrodes for one EEG channel are generated by two differential amplifiers, called input terminal one and input terminal two. With a differential amplifier, the output is proportional to the voltage difference between these two input terminals. The direction of the pen deflection depends on differences in polarity of this voltage difference. By convention, when input terminal one is relatively more negative, there is an upward deflection. Other possibilities include a downward deflection if input terminal one is relatively more positive. The reverse situation pertains to input terminal two; when input terminal two is relatively more negative, there is a downward deflection [Cooper et al., 1980].

An EEG waveform recorded on the scalp surface is assumed to arise from an electrical dipole within the brain. This hypothetical dipole arises from a network of neurons whose dendritic processes are ideally oriented perpendicular to the scalp. An electrical field is represented on the scalp, with the maximum voltage potential near the center and decreasing levels of voltage denoted by concentric rings that successively enlarge from this central point. Most abnormal electrographic potentials are represented by a dipole with the negative end toward the surface and the positive end inward. Depending on the particular orientation of the dipole in relation to the surface, its field representation on the scalp has different shapes. Occasionally, surface positive waveforms are observed, such as positive sharp waves in newborn recordings or dipoles represented on the scalp in patients with rolandic epilepsy.

Given the common practice of comparing groups of electrodes in a linear fashion, the amplitude and polarity expressed for each electrode in a bipolar recording may demonstrate a phase reversal in adjacent electrodes. This reversal is represented by a simultaneous pen deflection in opposite directions in two adjacent bipolar channels. By this technique, the electroencephalographer can localize focal EEG phenomena, assuming sources of artifact are not suspected. For accurate localization, two linear electrode arrays at right angles to each other should intersect through the region to be examined. This technique can effectively localize most waveforms that are considered to have vertical dipoles in relation to the scalp.

Instrumental Control Settings

Each EEG recording must clearly indicate all instrumental settings at the beginning of the study. Any adjustments in sensitivity, paper speed, or filter settings must be marked. Calibration signals should begin and conclude the recording to demonstrate to the electroencephalographer how the amplifier and pen-writing apparatus respond at all instrumental settings.

Physiologic Noncerebral Channels

Important information can be derived from recording muscle movement, respiratory activity, eye movements, and cardiac activity. These monitors can assist in defining specific portions of the sleep cycle. Noncerebral physiologic observations, such as respiratory pauses or cardiac arrhythmias, may also have relevance for the clinical problem that prompted the request for an EEG study. Sleep state-dependent apnea and congenital heart block are two clinical situations in which noncerebral physiologic monitoring can be crucial to the diagnosis. Important sources of artifact can be more readily identified and eliminated by using noncerebral monitors; cerebral activity can be more accurately displayed.

Artifact Recognition

As with adults [Richey, 1976], physiologic and nonphysiologic artifacts must be properly identified in pediatric recordings because either may interfere with the interpretation of cerebral activity. Three basic forms of artifacts have been classified: instrumental, external, and physiologic. Accurate descriptions by the technologist can assist the neurologist in the diagnosis of a neurologic disorder in adults [Klass and Reiher, 1968], children [Blume, 2002], and neonates [Scher, 1985] (Figure 12-1). Such artifacts may help define normal and abnormal sleep and waking behaviors. The technologist should try to identify the source of any artifacts, initially to reproduce them and subsequently to eliminate artifacts that were identified during the recording.

Fig. 12-1 EEG of a term neonate and older child demonstrating artifacts that could affect interpretation.

A, Electroencephalogram (EEG) of an infant of 40 weeks’ gestation 1 day after birth. The infant had severe asphyxia caused by a ruptured vilamentous cord with exsanguination. Background activity is markedly suppressed with superimposed physiologic artifact from excessive tremulousness. Readjustment of the patient’s head lessened this artifact. B, An 11-year-old female with brainstem encephalitis. On neurologic examination, the right pinnae displayed myoclonic movements. Myogenic potentials on the EEG (in the region of the right temporal area [T4]) represent the segmental myoclonus noted on examination.

(A, From Scher MS. Physiologic artifacts in neonatal electroencephalography. Am J EEG Technol 1985;25:257. B, Courtesy of Dr. P Crumrine, Children’s Hospital, Pittsburgh.)

Recording Setting

The pediatric EEG laboratory should be within easy access of inpatients and outpatients. Technologists must also be able to travel rapidly to areas within the medical facility to perform portable EEG studies in the emergency department, intensive care units, or patients’ hospital rooms. Pediatric epilepsy monitoring units (PEMUs) represent specialized settings where detailed behavioral and neurophysiological recordings can efficiently document seizure and nonseizure behaviors over arbitrarily assigned recording periods of hours to days.

To obtain quality recordings, efforts must be made to elicit the child’s most cooperative behavior. A well-illuminated, neatly organized room with a friendly decor assists in preparing the child. Ample time should be arranged for proper electrode application and recording. Obtaining unmedicated, awake, drowsy, and natural sleep recordings on all children is highly recommended. Despite the special challenge provided by the infant and young toddler, it is possible to obtain quality tracings without the use of sedative medications.

A minority of children may require sedation. The need for sedation can be substantially reduced by adequate preparation of the child, including the creation of a less-threatening environment in which to perform the study. One report described a decreased proportion (32 to 2 percent) of 513 children who needed sedation over a 4-year period when appropriate preparation was provided [Olson et al., 2001]. Chloral hydrate (50–80 mg/kg; maximum dose, 2 g) has historically been the most commonly used sedative, but should be administered only to a child who has not been recently fed and cannot tolerate the study in the natural state. Rectal administration may be advantageous for the encephalopathic or extremely uncooperative child who requires the study [Thoresen et al., 1997]. Psychotropic or sedative drugs should be avoided because they produce more profound behavioral and EEG effects. Infant recordings should be obtained around a scheduled feeding or nap. At least 90 minutes should be scheduled for electrode application, EEG recording, and clean-up. With some exceptions, the parents’ presence during the recording session should be discouraged. A child-life specialist or similarly trained individual can provide developmentally appropriate and child-friendly support. The technologist should accurately record the pertinent clinical evaluation of the child that explains the reason for obtaining the EEG study. Information from parents or the medical record should include the child’s age; gestational and postconceptional ages should be included for neonates. The ordering physician should be identified, and the written request for an EEG study should clearly state the clinical problem that prompted the EEG request.

Notations by the technologist of the recording conditions must include the state of arousal and cooperation of the patient. Skull defects, vital signs, pertinent laboratory studies, and medications should be listed, because each may affect the technical recording and clinical correlation of the EEG recording. For instance, cephalohematomas, hypothermic states, or barbiturate overdosage may attenuate the EEG activity on a regional or bihemispheric distribution, but they have dramatically different clinical interpretations.

Frequent and accurate annotations by the technologist must describe changes in state throughout the spontaneous and activation portions of the record. Passive or active eye opening and closure are essential, and repositioning of the patient may be required to eliminate or minimize artifacts. Consensual validation of suspicious cerebral activity with an encephalographer must always be a high priority.

Monitoring within the pediatric or neonatal intensive care settings and PEMUs requires special considerations, because of the need to obtain quality recordings in the hostile electronic and physical environment. Nursing personnel and physicians assigned to the intensive care unit or PEMU teams should receive appropriate instructions on the documentation of events in question and on rudimentary pattern recognition to identify major bihemispheric ictal patterns and how to differentiate them from artifact.

Potential Fields and Neuronal Networks

A variety of neuronal elements contributes to the extracellular currents that generate field potentials recorded at the surface of CNS structures, as discussed in the previous section. Spatial arrangements of neuronal elements and the position of recording electrodes play an essential role in establishing and detecting extracellular potential fields. There are two principal types of neuronal arrangements. The first is a parallel type in which the somata are in one layer and dendrites in the opposite layer. The second type consists of the somata in the center of a pool and dendrites extending to its periphery; the first type of organization is found in the cortex, and the second is observed in brainstem nuclei.

Each neuronal arrangement generates opened and closed fields. In open fields, one electrode largely integrates potentials of the neuronal population, whereas the other electrode sees only the positive or negative field, permitting the recording of the field potential. In a closed field, external electrodes do not appear to see potential differences because currents within the pool compensate for each other [Niedermeyer and Lopes da Silva, 2005]. Several types of field potentials can be differentiated, depending on the time constant of the amplifying recording device. Amplified EEG recordings at a time constant of 1 second or less can be contrasted with an infinite time constant using a direct current (DC) amplifier, permitting additional recording of baseline shifts and wavelike potentials without filtering of slow-frequency activities.

On conventional EEG studies, the generation of a wavelike potential consists of summated excitatory postsynaptic potentials, which occur in the dendrite. With sustained regular activity, a depolarization shift of the membrane potential appears, and changes in the membrane potential in the upper dendritic layers lead to an action potential. When amplifiers with a finite time constant, such as on conventional EEG recordings, are used, fluctuations in field potential are recorded without recording shifts in membrane potentials. In contrast, baseline shifts or EEG/DC potentials reflect sustained values of the membrane potential of neuronal elements that are being recorded. Using a sufficiently high upper-frequency limit, DC recordings comprise conventional EEG waves and slow potential deviations. Glial cells are involved in the generation of baseline shifts, as are neuronal cells, because of the functional coupling between neurons and glial cells. However, field potential changes are thought to be generated primarily by neuronal structures.

Neurophysiologic Basis of Abnormal Electrical Patterns

Several electrical patterns appear to correlate with specific clinicopathologic situations in adults and children. In general, epileptiform and nonepileptiform abnormalities are subdivided because of presumably different neurophysiologic or neuropathologic substrates. The following sections describe selected experimental findings that help explain certain abnormal patterns relevant to pediatric and adult EEG studies, which are addressed in a later section.

Interictal spike discharges, the hallmark of the epileptic neuron in experimental models of epilepsy, involve a specific type of membrane depolarization, referred to as a paroxysmal depolarization shift. There are general similarities between the neuronal events underlying this interictal epileptogenic process [Jeffreys, 1990]. In hippocampal and neocortical slice recordings taken after penicillin application [Ayala et al., 1973], high-voltage discharges appear in the EEG recording and are associated with an intracellularly recorded paroxysmal depolarization shift. These phenomena appear in intracellular recordings of experimental animals and human cortices. The depolarization is of relatively high voltage (10–15 μV) and long duration (100–200 msec), and it is associated with a burst of spike discharges. The event produces a train of action potentials that conduct away from the neuron along the axon. The interictal paroxysmal depolarization shift is followed by a period of hyperpolarization. Over time, this depolarization can summate to form a prolonged depolarization with a persistent loss of hyperpolarization, which is recorded on the surface as continuous spike discharges coinciding with the tonic phase of a generated tonic-clonic seizure. Subsequently, large inhibitory potentials alternate with recurrent rhythmic depolarization, which coincides with the clonic phase of the seizure. Despite the higher threshold necessary to achieve depolarization and the longer refractory period observed in immature animals [Prince and Gutnick, 1972], an understanding of paroxysmal depolarization shift is crucial to an appreciation of maturational aspects of epileptogenesis.

Based on these experimental observations, several hypotheses have been advanced to explain the mechanism by which normal neuronal activities convert to those of abnormal interictal discharges [Prince, 1985]. One mechanism involves intrinsic membrane abnormalities that promote burst-generating properties in individual neurons by an imbalance of calcium and sodium ion movements [Schwartzkroin and Prince, 1978]. Another mechanism involves the loss of inhibition by a group of neurons because of the absence of the inhibitory neurotransmitter, GABA [Prince, 1985]. A third mechanism of summated excitatory postsynaptic potentials helps explain how large groups of neurons generate depolarization shifts [Prince, 1978].

Although overshadowed by factors influencing seizure initiation, seizure termination is a critical step in the return to the interictal state [Lado and Moshe, 2008]. Understanding the mechanisms contributing to seizure termination could potentially identify novel anti-ictal and antiepileptogenic drugs, as well as highlighting the pathophysiology contributing to both seizure initiation and termination.

Proposed mechanisms unfortunately do not yet fully explain the transformation from an interictal to an ictal event. Other mechanisms have been proposed based on additional experimental studies, including changes in the ionic microenvironment that result in enhanced neuronal excitability, axonal burst generation, and cholinergic alteration of neuronal properties [Prince, 1985]. A systems biology approach from membranes to synapses to networks and finally circuits may better elucidate pathways to normal or abnormal neurobehavior [Grillner et al., 2005].

Metabolic factors related to glucose or electrolyte imbalance or noncerebral factors, such as trauma or fever, also facilitate the onset of seizures, particularly in children. Additional biochemical and anatomic alterations within a seizure focus may further promote seizure generation by neuronal destruction or glial proliferation [Aird et al., 1984].

Abnormal Suppression or Slowing of Electroencephalographic Activity

In addition to the presence of spike or sharp-wave discharges for the diagnosis of seizure disorders, other types of abnormal EEG patterns coincide with different neuropathologic substrates [Ebersole and Pedley, 2003]. Unfortunately, little information exists that correlates altered neuronal properties, such as the mechanisms discussed for epileptogenesis, with specific neuropathologic entities. Instead, clinical interpretations of the following EEG patterns are empirically based on correlative neuropathology.

Local suppression or absence of background rhythmic activity is a strong indication of brain dysfunction, irrespective of age or location in the brain. Complete absence of activity usually implies cortical necrosis that is close to the surface [Goldensohn, 1979a; Goldensohn, 1979b]. However, incomplete depression of background activity is the more common situation. The presence of symmetric suppression of frontal beta activity, central rhythms, dominant alpha activity, or sleep spindles in association with polymorphic delta waves strongly indicates a destructive process in the brain underlying those electrodes (Figure 12-6A) [Arfel and Fischgold, 1961]. EEG recordings of neonates showing asymmetric background activities usually suggest that the brain lesion is in the attenuated location [Scher, 1982].

Fig. 12-6 EEG findings demonstrating focal suppression or slowing of activity.

A, EEG of a 2-year-old female, with marked attenuation in the right hemisphere occurring above and below the sylvian fissure, demonstrates an absence of vertex waves and suppression of sleep spindles. Extensive right hemispheric encephalomalacia is documented on imaging studies. B, EEG of a 9-year-old female with slowing in the left posterior quadrant demonstrates an arteriovenous malformation in the left hemisphere, which was depicted on imaging studies.

Continuous polymorphic delta waves constitute a category of EEG abnormality that may suggest a structural brain lesion on an acquired or congenital basis (see Figure 12-6B). Irregular delta waves between 0.5 and 2.5 Hz do not react to eye opening, arousal, or sleep. Correlations with brain lesions in animals [Gloor et al., 1968] and in humans at postmortem examination have been described [Rhee et al., 1975]. Focal slowing may imply focal destructive lesions of white matter by a congenital, vascular, neoplastic, or infectious process. Polymorphic delta waves can commonly appear immediately after a seizure of focal onset and with reversible conditions, such as migraine [Hockaday and Whitty, 1969]; both are common occurrences in children. The combination of bilateral, synchronous rhythmic discharges and polymorphic delta waves occurs in diffuse encephalopathies involving white and gray matter. Certain brain regions, such as the frontal, temporal, and occipital areas, are more likely to express polymorphic delta waves. The association of background rhythm depression and polymorphic delta waves increases the likelihood of destructive lesions, especially tumors. Parasagittal and parietal lesions often are associated with attenuation of rhythms or prominent theta rhythms.

Intermittent rhythmic delta activity is another category of nonepileptiform abnormality with a variety of neuropathologic correlates. Runs of sinusoidal 2.5 Hz are generally reactive to eye opening, hyperventilation, or arousal. Two distinct distributions of rhythmic delta activity over the scalp have been identified. Frontal intermittent delta activity (Figure 12-7A) and occipital rhythmic delta activity (see Figure 12-7B) generally indicate modification of cortically generated EEG activity by midline subcortical structures. The thalamus, reticular activating system, and midbrain can contribute to the dysfunction between subcortical gray matter and cortical neurons [Daly, 1974]. These two types of rhythmic delta activity are largely age-related. Frontal intermittent delta activity usually occurs in adult patients, whereas occipital rhythmic delta activity is found mainly in children. Intermittent rhythmic delta activity does not necessarily indicate that the major pathologic condition is in that region. Occipital rhythmic delta activity and frontal intermittent delta activity have been documented in 53 percent of 145 children with posterior fossa tumors [Martinius et al., 1968]. As a rule, it has little localizing value for supratentorial masses, although it may be accentuated on the side of the tumor [Hess, 1975]. Intermittent rhythmic delta activity is nonspecific and may be observed with systemic metabolic disorders, increased intracranial pressure, encephalitis, and trauma. However, a subsequent report concerning frontal intermittent delta activity described this pattern as rare for children, observed in only 20 of 1500 EEG studies of children between 18 months and 17 years of age. Most patients were awake and showed no encephalopathic signs, but were cognitively impaired. Another 50 percent had a history of epilepsy, with epileptiform activity occurring in 55 percent of the cohort [Watemberg et al., 2003].

Fig. 12-7 EEG demonstrating frontal and occipital rhythmic activity.

A, EEG of a 2½-year-old male with frontal intermittent delta activity indicative of a diffuse encephalopathy on a hypoxic-ischemic basis. B, EEG recording of a 12-year-old male with a predominantly occipital intermittent rhythmic delta activity indicative of a diffuse encephalopathy on a metabolic basis.

Epileptiform discharges can be found in combination with slowing as an indication of a structural abnormality. Focal discharges during a seizure have better localizing value than interictal spikes [Hess, 1975]. In general, slow-growing neoplasms, such as oligodendrogliomas or astrocytomas, produce more epileptiform activity than rapidly growing tumors [Kershman et al., 1949]. Spike discharges are more common after surgery, such as for meningiomas, but neurologists are advised to exercise extreme caution concerning spike discharges as reliable guides to localization of destructive lesions. Imaging studies are far more reliable diagnostic guides for structural abnormalities.

Guidelines for Interpretation

EEG analysis requires a systematic, orderly process in which a series of steps are followed to reach a proper interpretation [Ebersole and Pedley, 2003]. The rhythmicity of spontaneous EEG signals gives a continuous admixture of scalp-generated oscillatory potentials. EEG frequencies used for clinical studies are classified in four band ranges. Delta activity is less than 4 Hz; theta activity is 4–8 Hz; alpha activity is 8–13 Hz; and beta activity is greater than 13 Hz. While DC (usually below 3 Hz) and gamma-frequencies (above 30 Hz) can be recorded with appropriate filter settings, these rhythms are currently applied only to research recordings. In general, the amplitude of EEG activity is inversely proportional to frequency.

For pediatric EEG studies, the amount of slow activity decreases with increasing age, and the persistence and frequency of slow activity vary in different brain regions. It is important to appreciate the presence and degree of expression of frequencies in various regions at different ages, and other parameters, such as waveform, manner of occurrence (e.g., random, continuous), and amplitude, are essential to visual analysis. By means of this cumulative analysis, using a list of parameters of EEG activity [Ebersole and Pedley, 2003; Kellaway and Crawley, 1964; Lombroso, 1980], the neurologist can attempt to assign normal or abnormal clinical significance to the EEG pattern. Critical information regarding age and state of the patient affects the ability of the neurologist to judge normality in the EEG record. It may require several EEG recordings and the persistence or resolution of abnormal electrical activity relative to the state of the patient to assess normality properly. Several recordings allow an appreciation of the ontogeny, or evolution, of significant age-specific EEG patterns. These guidelines must be repeatedly emphasized as the pediatric neurologist acquires an appreciation of the rich diversity of normal maturational patterns.

Newborn Electroencephalographic Patterns

Neonatal EEG studies have been reported for more than 60 years [Okamato and Kirikae, 1951]. Pioneering investigations by several independent researchers have all contributed information concerning the developmental neurophysiology of the immature brain. Some of these studies predate the development of the tertiary-care neonatal intensive care unit, and the neurologist using EEG recordings had an understandably limited role in the diagnostic assessment and clinical care of the sick neonate.

Improvements in recording equipment and standardization of the recording techniques are available in modern neonatal intensive care units. An internationally accepted system of electrode placement, adapted for the neonate and young infant, permits standardization of recordings between laboratories [AES, 1986]. Development of 16- and 21-channel EEG machines with improved filtering systems and electrode construction minimizes environmental and physiologic sources of artifacts. Synchronized video-EEG studies permit more accurate comparison between electrographic and behavioral changes in the assessment of seizures, movement disorders, and sleep cycles [Dyken et al., 1997; Scher, 2008; Scher and Barmada, 1987a].

Several fundamental principles for neonatal EEG studies serve as an introduction to an understanding of its chief clinical application [Scher, 2005a; Scher, 2008]. There are expected changes in the scalp-generated EEG patterns for neonates of different gestational ages. The experienced encephalographer can approximate the electrical maturity within 2 weeks of the gestational age. Changing electrical patterns reflect the postconceptional age of the neonate independent of birth weight. Maturation of the neonate’s sleep–wake behavior follows maturation of the CNS and is independent of the birth weight. Preterm neonates, when corrected to term postconceptional age, should have EEG patterns and sleep behavior similar to those of term, appropriate-for-gestational-age newborns.

Detailed electrographic and anatomic correlations that compare sulcal-gyral development with evolving electrical patterns have been correlated with clinical information concerning gestational maturity [Scher and Barmada, 1987a] (Figure 12-8 and Figure 12-9). Of 25 infants, 23 had maturational agreement within 2 weeks between electrical patterns and sulcal-gyral measurements of the inferior frontal, superior temporal, and calcarine gyri, and between the cytoarchitecture of various brain regions.

Fig. 12-8 Correlation of EEG and anatomical development in a 26-week-gestation preterm neonate.

A, Two age-appropriate electroencephalographic tracings of a 26-week-gestation, 3-day-old female are shown. Generalized theta and delta slowing is demonstrated, and vertex central slow activity is prominent (top left frame). Notice the bitemporal attenuation. Synchronous interburst intervals of less than 40 seconds’ duration and delta brush patterns in the vertex region are demonstrated (right frame). B, Lateral view of the brain of the patient in A. Underdeveloped frontal and temporal lobes with insulas are visible and indicate an immature sulcation pattern, especially of the rolandic, calcarine, and superior temporal sulci.

(From Scher MS, Ahdab-Barmada M. Gestational age by electrographic, clinical and anatomical criteria. Pediatr Neurol 1987;3:256.)

Fig. 12-9. Correlation of EEG and anatomical development in a 30 week-gestation preterm neonate.

A, Two samples of an EEG of a 30-week-gestation, 9-day-old female. A greater degree of spontaneous, continuous EEG activity is demonstrated (top left frame), including temporal delta and delta brush patterns. The occipital delta and delta brush patterns are shown (right frame). B, Lateral view of the brain for the patient described in A. There is a greater degree of sulcation evident. Observe the more complete elaboration of the rolandic, superior temporal, and calcarine sulci.

(From Scher MS, Ahdab-Barmada M. Gestational age by electrographic, clinical and anatomical criteria. Pediatr Neurol 1987;3:256.)

Regional changes in electrical activity clearly occur in the EEG of the premature neonate when recordings are obtained after 24–25 weeks’ estimated gestational age and at weekly intervals [Dreyfus-Brisac, 1979; Mizrahi and Kellaway, 2003; Scher, 2005a; Scher et al., 2003a; Tharp et al., 1981; Torres and Anderson, 1985] (Figure 12-10). Sleep–wake behavior cannot be distinguished for patients younger than 30 weeks of age, but other hemispheric or regional patterns demonstrate predictable, evolving characteristics.

Fig. 12-10 Regional EEG in the preterm neonate.

A, Relatively continuous background of slow and fast frequencies is shown for a 26-week-gestation, 5-day-old female. Rhythmic central delta occurs with superimposed delta brushes in the same region. Asymmetric or asynchronous occipital delta activity is demonstrated, and temporal attenuation is prominent. Myoclonic movement is indicated (arrow). B, For a 26-week-gestation, 1-day-old male, discontinuous background activity consists of central and vertex delta slow activity with superimposed delta brushes. Diffuse theta bursts occur with occasional occipital theta bursts. C, For a 28-week-gestation, 11-day-old female (postconceptional age of 29.5 weeks), background activity is largely continuous with predominant delta slowing. More active temporal activity includes prominent temporal theta bursts. Delta brushes also are seen in the occipital and vertex regions. D, For a 28-week-gestation, 7-day-old male (postconceptional age of 29 weeks), rhythmic occipital delta signals occur in different head regions with prominent temporal delta brushes. Periodic breathing is evident in the respiratory channel. E, For a 28-week-gestation, 51-day-old male (postconceptional age of 35 weeks), continuous background activity is appropriately of lower amplitude for the corrected age. This activity consists of fast frequencies with delta brushes in multiple head regions. An isolated frontal sharp wave and rapid eye movements are present. F, For a 34-week-gestation, 8-day-old female (postconceptional age of 35 weeks), a discontinuous background is demonstrated with age-appropriate, short interburst intervals. Rhythmic occipital delta activity occurs with good interhemispheric synchrony. Periodic breathing is evident in the respiratory channel. G, For a 39-week-gestation, 2-day-old female, a high-voltage slow wave (HVS) pattern of quiet sleep with scattered sharp waves is present, particularly in the temporal regions. Regular respirations with no movements are demonstrated in the polygraphic channels. H, For a 39-week-gestation, 2-day-old female, a tracé alternant pattern of quiet sleep is demonstrated with synchronous high-amplitude bursts; age-appropriate, brief interburst intervals; and a well-developed background.

Ontogeny of Electroencephalographic Features

The evolving EEG sleep patterns in the asymptomatic, presumably healthy preterm infant has been the subject of many excellent reviews [Ebersole and Pedley, 2003; Lombroso, 1985; Pope et al., 1992; Scher, 1993a; Scher, 1993b; Torres and Anderson, 1985]. Improvements in neonatal intensive care, however, require periodic revisions to include more preterm infants [Mizrahi and Kellaway, 2003; Scher, 2005a, 2008]. These revisions are particularly relevant for preterm infants younger than 32 weeks’ gestation, for whom substantial improvement in survival rates has occurred over the past decade. However, there is a greater prevalence of late preterm infants (34–37 weeks estimated gestational age [EGA]) who also remain at increased risk for neurodevelopmental deficits [Ramachandrappa and Jain, 2009]. Applying the principles of functional brain maturation using EEG is therefore relevant across the gestational age spectrum. It will always be important to verify which EEG-sleep patterns are within the range of normal by systematic neurodevelopmental assessment of such children at increasing postnatal ages.

In the following sections, regional and hemispheric EEG patterns for preterm and term neonates are arbitrarily assigned within specific gestational age ranges. Temporal, spatial, and state organization of the EEG recordings of cerebral activity during each age range is highlighted with appropriate illustrations. Greater details can be found in recent reviews [Scher, 2008; Scher and Loparo, 2009].