| Literature DB >> 9258960 |
Abstract
Severe brain disorders can be expressed as markedly abnormal encephalopathic EEG patterns in neonates who are usually neurologically depressed, with abnormal levels of reactivity and tone. This symptomatic group is now a minority of medically ill neonates as a result of more vigorous fetal and neonatal resuscitative efforts. Most neonates alternatively express brain dysfunction as more pervasive alterations in EEG-sleep organization or maturation, usually in the absence or after resolution of abnormal clinical signs. One form of dysfunction is expressed as neurophysiologic dysmaturity. Brain dysmaturity may reflect altered rates of development in infants who sustained prenatal or postnatal stresses, as discussed in the first part of this review. We now summarize our findings of dysmature EEG-sleep development at conceptional term ages in an asymptomatic preterm cohort during a prolonged extrauterine period before discharge from the nursery. Dysmaturity of EEG-sleep function was expressed as delayed and/or accelerated physiologic behaviors, as compared with behaviors expected for the conceptional age. Dysmature brain function at conceptional term ages was also associated with poorer neurodevelopmental performances at 12 and 24 months of age. Neuronal pathways which subserve state-specific neurophysiologic behaviors will functionally adapt to stress by either slowing or accelerating neurological maturation. Through ontogenetic brain adaptation, which continues during postnatal development, a balance is maintained between the needs of the present developmental stage and anticipated needs during subsequent stages of maturation. How medical complications and environmental influences interact to promote greater brain dysmaturity in the neonate is still unknown. EEG sleep study can serve as a useful neurophysiologic screening procedure for the child suspected of having a subclinical presentation of an emerging static encephalopathy; longitudinal studies will then document deviations from expected ontogeny in the vulnerable child who is later stressed by environmental and socioeconomic factors.Entities:
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Year: 1997 PMID: 9258960 DOI: 10.1016/s0887-8994(96)00009-4
Source DB: PubMed Journal: Pediatr Neurol ISSN: 0887-8994 Impact factor: 3.372