TY - JOUR
T1 - EEG depression and germinal layer haemorrhage in the newborn
AU - Greisen, G
AU - Hellström-Westas, L
AU - Lou, H
AU - Rosén, I
AU - Svenningsen, N W
PY - 1987/5
Y1 - 1987/5
N2 - Amplitude integrated EEG (aEEG) recordings from 32 mechanically ventilated infants, gestational age 32 weeks or less, were analysed. All recordings were started within 24 h of birth and continued for at least 50 h. Germinal layer haemorrhage (GLH) was diagnosed by repeated ultrasonography. In six infants neither GLH nor hypocalcaemia were diagnosed; aEEG in these infants rapidly became more active after birth: at 30 h of age continuous background activity was present for more than 20% of the time, and a seizure-like pattern was exceptional. In seven infants without GLH but with hypocalcaemia and other signs of metabolic derangement, continuous background activity appeared later and seizure-like activity was frequent. In the infants with GLH, depression of the background activity was apparent. This finding was particularly distinct in the presence of severe haemorrhages. Four infants developed GLH after 30 h of age. All these infants had depressed aEEG before the development of GLH, with less than 20% continuous activity at 30 h of age. In ten infants an analysis of the aEEG during the occurrence of GLH was possible. In six of these, cortical electrical activity decreased. Due to the limitation of GLH timing, it was not possible to decide whether this decrease closely preceded or followed GLH. We suggest that GLH primarily occurs in brains with a preceding metabolic and neurophysiologic abnormality, and that further functional deterioration is caused by the most severe haemorrhages.
AB - Amplitude integrated EEG (aEEG) recordings from 32 mechanically ventilated infants, gestational age 32 weeks or less, were analysed. All recordings were started within 24 h of birth and continued for at least 50 h. Germinal layer haemorrhage (GLH) was diagnosed by repeated ultrasonography. In six infants neither GLH nor hypocalcaemia were diagnosed; aEEG in these infants rapidly became more active after birth: at 30 h of age continuous background activity was present for more than 20% of the time, and a seizure-like pattern was exceptional. In seven infants without GLH but with hypocalcaemia and other signs of metabolic derangement, continuous background activity appeared later and seizure-like activity was frequent. In the infants with GLH, depression of the background activity was apparent. This finding was particularly distinct in the presence of severe haemorrhages. Four infants developed GLH after 30 h of age. All these infants had depressed aEEG before the development of GLH, with less than 20% continuous activity at 30 h of age. In ten infants an analysis of the aEEG during the occurrence of GLH was possible. In six of these, cortical electrical activity decreased. Due to the limitation of GLH timing, it was not possible to decide whether this decrease closely preceded or followed GLH. We suggest that GLH primarily occurs in brains with a preceding metabolic and neurophysiologic abnormality, and that further functional deterioration is caused by the most severe haemorrhages.
KW - Cerebral Hemorrhage/diagnosis
KW - Electroencephalography
KW - Humans
KW - Infant, Newborn
KW - Infant, Premature, Diseases/diagnosis
KW - Respiration, Artificial/adverse effects
U2 - 10.1111/j.1651-2227.1987.tb10509.x
DO - 10.1111/j.1651-2227.1987.tb10509.x
M3 - Journal article
C2 - 3604671
SN - 0001-656X
VL - 76
SP - 519
EP - 525
JO - Acta Paediatrica Scandinavica
JF - Acta Paediatrica Scandinavica
IS - 3
ER -