Elana F Pinchefsky1, Cecil D Hahn2, Daphne Kamino2, Vann Chau3, Rollin Brant4, Aideen M Moore5, Emily W Y Tam2. 1. Division of Neurology, Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada; Program in Neurosciences and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada. Electronic address: elana.pinchefsky.hsj@ssss.gouv.qc.ca. 2. Division of Neurology, Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada; Program in Neurosciences and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada. 3. Division of Neurology, Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada; Program in Neurosciences and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada; BC Children's Hospital Research Institute, Vancouver, British Columbia, Canada. 4. BC Children's Hospital Research Institute, Vancouver, British Columbia, Canada; Department of Statistics, The University of British Columbia, Vancouver, British Columbia, Canada. 5. Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada.
Abstract
OBJECTIVES: To investigate how glucose abnormalities correlate with brain function on amplitude-integrated electroencephalography (aEEG) in infants with neonatal encephalopathy. STUDY DESIGN: Neonates born at full term with encephalopathy were enrolled within 6 hours of birth in a prospective cohort study at a pediatric academic referral hospital. Continuous interstitial glucose monitors and aEEG were placed soon after birth and continued for 3 days. Episodes of hypoglycemia (≤50 mg/dL; ≤2.8 mmol/L) and hyperglycemia (>144 mg/dL; >8.0 mmol/L) were identified. aEEG was classified in 6-hour epochs for 3 domains (background, sleep-wake cycling, electrographic seizures). Generalized estimating equations assessed the relationship of hypo- or hyperglycemia with aEEG findings, adjusting for clinical markers of hypoxia-ischemia (Apgar scores, umbilical artery pH, and base deficit). RESULTS: Forty-five infants (gestational age 39.5 ± 1.4 weeks) were included (24 males). During aEEG monitoring, 16 episodes of hypoglycemia were detected (9 infants, median duration 77.5, maximum 220 minutes) and 18 episodes of hyperglycemia (13 infants, median duration 237.5, maximum 3125 minutes). Epochs of hypoglycemia were not associated with aEEG changes. Compared with epochs of normoglycemia, epochs of hyperglycemia were associated with worse aEEG background scores (B 1.120, 95% CI 0.501-1.738, P < .001), less sleep-wake cycling (B 0.587, 95% CI 0.417-0.757, P < .001) and more electrographic seizures (B 0.433, 95% CI 0.185-0.681, P = .001), after adjusting for hypoxia-ischemia severity. CONCLUSIONS: In neonates with encephalopathy, epochs of hyperglycemia were temporally associated with worse global brain function and seizures, even after we adjusted for hypoxia-ischemia severity. Whether hyperglycemia causes neuronal injury or is simply a marker of severe brain injury requires further study.
OBJECTIVES: To investigate how glucose abnormalities correlate with brain function on amplitude-integrated electroencephalography (aEEG) in infants with neonatal encephalopathy. STUDY DESIGN: Neonates born at full term with encephalopathy were enrolled within 6 hours of birth in a prospective cohort study at a pediatric academic referral hospital. Continuous interstitial glucose monitors and aEEG were placed soon after birth and continued for 3 days. Episodes of hypoglycemia (≤50 mg/dL; ≤2.8 mmol/L) and hyperglycemia (>144 mg/dL; >8.0 mmol/L) were identified. aEEG was classified in 6-hour epochs for 3 domains (background, sleep-wake cycling, electrographic seizures). Generalized estimating equations assessed the relationship of hypo- or hyperglycemia with aEEG findings, adjusting for clinical markers of hypoxia-ischemia (Apgar scores, umbilical artery pH, and base deficit). RESULTS: Forty-five infants (gestational age 39.5 ± 1.4 weeks) were included (24 males). During aEEG monitoring, 16 episodes of hypoglycemia were detected (9 infants, median duration 77.5, maximum 220 minutes) and 18 episodes of hyperglycemia (13 infants, median duration 237.5, maximum 3125 minutes). Epochs of hypoglycemia were not associated with aEEG changes. Compared with epochs of normoglycemia, epochs of hyperglycemia were associated with worse aEEG background scores (B 1.120, 95% CI 0.501-1.738, P < .001), less sleep-wake cycling (B 0.587, 95% CI 0.417-0.757, P < .001) and more electrographic seizures (B 0.433, 95% CI 0.185-0.681, P = .001), after adjusting for hypoxia-ischemia severity. CONCLUSIONS: In neonates with encephalopathy, epochs of hyperglycemia were temporally associated with worse global brain function and seizures, even after we adjusted for hypoxia-ischemia severity. Whether hyperglycemia causes neuronal injury or is simply a marker of severe brain injury requires further study.
Authors: Jana Krystofova Mike; Katherine Y Wu; Yasmine White; Praneeti Pathipati; Blaise Ndjamen; Rachel S Hutchings; Courtney Losser; Christian Vento; Kimberly Arellano; Oona Vanhatalo; Samuel Ostrin; Christine Windsor; Janica Ha; Ziad Alhassen; Brian D Goudy; Payam Vali; Satyan Lakshminrusimha; Jogarao V S Gobburu; Janel Long-Boyle; Peggy Chen; Yvonne W Wu; Jeffrey R Fineman; Donna M Ferriero; Emin Maltepe Journal: Dev Neurosci Date: 2022-05-19 Impact factor: 3.421
Authors: Daphne Kamino; Asma Almazrooei; Elizabeth W Pang; Elysa Widjaja; Aideen M Moore; Vann Chau; Emily W Y Tam Journal: Clin Neurophysiol Date: 2020-10-22 Impact factor: 3.708
Authors: John Madar; Charles C Roehr; Sean Ainsworth; Hege Ersda; Colin Morley; Mario Rüdiger; Christiane Skåre; Tomasz Szczapa; Arjan Te Pas; Daniele Trevisanuto; Berndt Urlesberger; Dominic Wilkinson; Jonathan P Wyllie Journal: Notf Rett Med Date: 2021-06-02 Impact factor: 0.892