TY - JOUR
T1 - Prognostic value of neonatal EEG following therapeutic hypothermia in survivors of hypoxic-ischemic encephalopathy
AU - Koskela, Tuomas
AU - Kendall, Giles S
AU - Memon, Sara
AU - Sokolska, Magdalena
AU - Mabuza, Thalitha
AU - Huertas-Ceballos, Angela
AU - Mitra, Subhabrata
AU - Robertson, Nicola J
AU - Meek, Judith
AU - Whitehead, Kimberley
N1 - Copyright © 2021 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.
PY - 2021/9
Y1 - 2021/9
N2 - OBJECTIVE: Early prediction of neurological deficits following neonatal hypoxic-ischemic encephalopathy (HIE) may help to target support. Neonatal animal models suggest that recovery following hypoxia-ischemia depends upon cortical bursting. To test whether this holds in human neonates, we correlated the magnitude of cortical bursting during recovery (≥postnatal day 3) with neurodevelopmental outcomes.METHODS: We identified 41 surviving infants who received therapeutic hypothermia for HIE (classification at hospital discharge: 19 mild, 18 moderate, 4 severe) and had 9-channel electroencephalography (EEG) recordings as part of their routine care. We correlated burst power with Bayley-III cognitive, motor and language scores at median 24 months. To examine whether EEG offered additional prognostic information, we controlled for structural MRI findings.RESULTS: Higher power of central and occipital cortical bursts predicted worse cognitive and language outcomes, and higher power of central cortical bursts predicted worse motor outcome, all independently of structural MRI findings.CONCLUSIONS: Clinical EEG after postnatal day 3 may provide additional prognostic information by indexing persistent active mechanisms that either support recovery or exacerbate brain damage, especially in infants with less severe encephalopathy.SIGNIFICANCE: These findings could allow for the effect of clinical interventions in the neonatal period to be studied instantaneously in the future.
AB - OBJECTIVE: Early prediction of neurological deficits following neonatal hypoxic-ischemic encephalopathy (HIE) may help to target support. Neonatal animal models suggest that recovery following hypoxia-ischemia depends upon cortical bursting. To test whether this holds in human neonates, we correlated the magnitude of cortical bursting during recovery (≥postnatal day 3) with neurodevelopmental outcomes.METHODS: We identified 41 surviving infants who received therapeutic hypothermia for HIE (classification at hospital discharge: 19 mild, 18 moderate, 4 severe) and had 9-channel electroencephalography (EEG) recordings as part of their routine care. We correlated burst power with Bayley-III cognitive, motor and language scores at median 24 months. To examine whether EEG offered additional prognostic information, we controlled for structural MRI findings.RESULTS: Higher power of central and occipital cortical bursts predicted worse cognitive and language outcomes, and higher power of central cortical bursts predicted worse motor outcome, all independently of structural MRI findings.CONCLUSIONS: Clinical EEG after postnatal day 3 may provide additional prognostic information by indexing persistent active mechanisms that either support recovery or exacerbate brain damage, especially in infants with less severe encephalopathy.SIGNIFICANCE: These findings could allow for the effect of clinical interventions in the neonatal period to be studied instantaneously in the future.
KW - Child Development/physiology
KW - Electroencephalography/trends
KW - Female
KW - Follow-Up Studies
KW - Humans
KW - Hypothermia, Induced/trends
KW - Hypoxia-Ischemia, Brain/diagnosis
KW - Infant, Newborn
KW - Male
KW - Prognosis
KW - Retrospective Studies
KW - Survivors
U2 - 10.1016/j.clinph.2021.05.031
DO - 10.1016/j.clinph.2021.05.031
M3 - Article
C2 - 34284244
SN - 1872-8952
VL - 132
SP - 2091
EP - 2100
JO - Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
JF - Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
IS - 9
ER -