Clinical examination findings in neonates with the absence of electrocerebral activity: an acute or chronic encephalopathic state?

Although the presence of an isoelectric electroencephalogram (EEG) in an older patient may reflect brain death caused by an acute brain injury, this electrographic abnormality may appear in more diverse clinical situations in the neonate with encephalopathy. During a 6-year period, 20 neonates were identified with a severe encephalopathy on neurologic examination who had at least one isoelectric EEG during their treatment in a neonatal intensive care unit. Seventy-four EEG recordings were obtained including 36 isoelectric EEG records. Partially preserved clinical brain function was present in 15 (75%) of 20 infants at the time an isoelectric EEG was obtained. The initial EEG was isoelectric in 16 of 20 infants. Although electrographic activity reemerged in nine of these infants, significant clinical improvement was seen in only two patients. Thirteen of 20 neonates also had electrographic or other evidence of clinical seizures. Of the five survivors (25%), three had severe neurologic sequelae. The remaining two had either transient or persistent neurologic deficits. An isoelectric EEG may be obtained in the neonate with partially preserved brain function and, therefore, may not be a reliable confirmatory test of neonatal brain death. In addition, serial EEGs not only can help assess the severity of a neonatal encephalopathy but also may correlate with chronic and acute neurologic insults.

Timing of brain insults in severe neonatal encephalopathies with isoelectric EEG.

In a neonatal intensive care unit of a large obstetric hospital, 20 neonates (7 preterm, 9 term, 4 postterm) with at least one isoelectric recording were treated over a 6-year period. Seventy-four EEGs were obtained in this cohort, including 36 isoelectric recordings. Seven infants in this group had evidence of a predominant antepartum component of a pathologic process based on placental, postmortem examination findings, or clinical history. Of the 16 placentas available for review, chronic lesions were observed in 13 of 16 specimens, including villitis, infarction, dysmaturity, and thrombosis. Seven of 9 patients with postmortem neuropathologic examinations had evidence of chronic lesions, principally neuronal necrosis, infarction, and microcalcifications. An additional 10 infants had evidence of an antepartum contribution to a pathologic process that continued into either the intrapartum or neonatal periods, based on maternal and/or neonatal medical factors. Clinical findings supportive of antepartum insults included intrauterine growth retardation, antepartum hemorrhage, abnormal antepartum fetal heart rate patterns, and maternal medical complications. Three patients had either intrapartum- or neonatal-onset of injury. Clinical signs of severe encephalopathy, however, were present in the immediate postnatal period in most patients (18 of 20; 90%). Assessment of clinical and pathologic information on neonates with isoelectric EEGs may estimate the timing of brain injury to the antepartum period, as opposed to, or in addition to, the labor and delivery periods. A neonate who suffered brain injury before parturition may be neurologically depressed after birth with absence of electrocerebral activity on EEG.