EEG background findings (Table 1.1) are also frequently employed to assess the functional integrity of the neonatal brain and to aid in the evaluation of neurologic prognosis. At the same time, however, many patterns are nonspecific and of uncertain clinical significance.

TABLE 1.1 EEG Background in Prematurity

Source: Adapted from Refs. 5, 8, 9.

Excessive Sharps

A depressed and undifferentiated pattern (Figure 1.1) is most commonly associated with severe underlying neurologic injury to the cortical generators of electrocerebral activity. Low voltage is considered to be background activity persistently less than 10 µV without normal background features. The recording will also show poor reactivity, no alteration in frequencies with external stimulation, and no sleep-wake cycling.

SEIZURE DETECTION

Seizure is the most common neurologic disorder in the neonatal period. There are numerous potential etiologies for neonatal seizures, and timing of presentation as well as electrographic findings can be of potential use in elucidating their etiology. Seizures can be transient due to an acute injury, markers of an underlying genetic or metabolic disorder, or signs of an underlying structural abnormality.

EEG evaluation and confirmation of seizure activity is particularly important in the neonatal population, given the high rate of subclinical or subtly clinical seizures and because newborns may often have unusual movements that can be mistaken for seizure activity. For instance, a systematic video review of 526 electrographic seizures in nine infants revealed that only 34% of seizures were associated with clinical manifestations, and only 27% of these clinical seizures (9% of overall seizures) were recognized by nursing staff. Of more concern, 73% of “seizures” documented by the neonatal intensive care unit (NICU) nursing staff were not epileptic seizures. Rather, the events marked by NICU nursing were not epileptic in nature. Instead, these movements commonly consisted of likely nonepileptic events such as jitteriness, mouthing, and fisting (10). Therefore neonatal seizure quantification solely by clinical observation is plagued by both high false-positive and high false-negative rates. To ensure an accurate assessment of seizure detection and treatment response, EEG monitoring is essential.

EEG confirmation of seizure cessation following anticonvulsant treatment is also recommended. Neonates are particularly vulnerable to the phenomenon of electroclinical uncoupling, in which clinical evidence of seizure activity ceases, following the administration of seizure medications, while subclinical electrographic seizure activity continues unabated. Although subclinical seizures are known to occur in critically ill children and adults (11,12), features of chloride homeostasis unique to the immature brain contribute to a high likelihood of electroclinical uncoupling. The potassium-chloride cotransporter (KCC2), which is the predominant type of chloride channel in the adult brain, transport chloride ions outside of neurons and have a hyperpolarizing effect. In contrast, the predominant chloride channel in the immature brain is the sodium-potassium-chloride cotransporter (NKCC1), which transports chloride ions into neurons and has a depolarizing effect. Gamma aminobutyric acid (GABA), a neurotransmitter that activates chloride channels, can therefore have a paradoxically excitatory effect in developing neurons due to the predominance of NKCC1 channels (13). Because the transition from NKCC1 to KCC2 chloride channels occurs in a caudal-to-rostral progression, GABA initially becomes inhibitory in subcortical structures such as the brainstem and basal ganglia while remaining excitatory in the cortex. Commonly used medications such as phenobarbital, which exert their effects through GABA agonist activity, may therefore suppress brainstem motor output, while allowing electrographic seizure activity to continue in the cortex.

Seizure semiology in the newborn is variable but can be grouped into the following categories: clonic, tonic, and myoclonic (Table 1.2). These are focal, repetitive, and cannot be suppressed by the examiner. Due to incomplete myelination, infants cannot generate generalized tonic-clonic seizures, but they can have multifocal seizures that can appear generalized to the untrained or inexperienced examiner. Infants can also have generalized epileptic spasms that are hypothesized to be more subcortically driven.

Because infants often have repetitive movements which can be difficult to interpret, EEG is often relied upon to distinguish stereotyped or rhythmic movements as epileptic or nonepileptic. Oral automatisms, bicycling, roving eye movements, and other nonrhythmic but repetitive movements are often seen in critically ill infants. Without clear electrographic correlate, these had been previously termed clinical only seizures, but are now more commonly presumed to be nonepileptic in nature. These movements tend to occur more often in encephalopathic infants and are also associated with poor prognosis (19).

Related posts:

Clinical Neurophysiology in Pediatric Peripheral Neuropathy Intraoperative Considerations in the Pediatric Patient Clinical Evaluation in Pediatric Peripheral Neuropathies Epileptic and Nonepileptic Paroxysmal Events in Childhood Autonomic Disorders in Children EEG Interpretation in Childhood Epilepsies

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