Related Experiment Video
Updated: Dec 1, 2025
A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Abnormalities in evoked potentials associated with abnormal glycemia and brain injury in neonatal hypoxic-ischemic
Daphne Kamino1, Asma Almazrooei1, Elizabeth W Pang2
1The Hospital for Sick Children and University of Toronto, Department of Pediatrics (Division of Neurology), Toronto, ON M5G 1X8, Canada.
Objective:
To investigate how functional integrity of ascending sensory pathways measured by visual and somatosensory evoked potentials (VEP & SEP) is associated with abnormal glycemia and brain injury in newborns treated with hypothermia for hypoxic-ischemic encephalopathy (HIE).
Methods:
Fifty-four neonates ≥ 36 weeks gestational age with HIE underwent glucose testing, VEPs, SEPs, and magnetic resonance imaging (MRI) the first week of life. Minimum and maximum glucose values recorded prior to evoked potential (EP) testing were compared with VEP and SEP measures using generalized estimating equations. Relationships between VEP and SEP measures and brain injury on MRI were assessed.
Results:
Maximum glucose is associated with decreased P200 amplitude, and increased odds that N300 peak will be delayed/absent. Minimum glucose is associated with decreased P22 amplitude. Presence of P200 and N300 peaks is associated with decreased odds of brain injury in the visual processing pathway, with delayed/absent N300 peak associated with increased odds of brain injury in posterior white matter.
Conclusions:
Deviations from normoglycemia are associated with abnormal EPs, and abnormal VEPs are associated with brain injury on MRI in cooled neonates with HIE.
Significance:
Glucose is a modifiable risk factor associated with atypical brain function in neonates with HIE despite hypothermia treatment.
