Related Experiment Video
Updated: Aug 20, 2026

Continuous Video Electroencephalogram during Hypoxia-Ischemia in Neonatal Mice
Published on: June 11, 2020
Cortical electroencephalogram suppression is associated with post-ischemic cortical injury in 0.65 gestation fetal
Mhoyra Fraser1, Laura Bennet, Mark Gunning
1The Liggins Institute, University of Auckland, Private Bag 92019, Auckland, New Zealand.
Suppression of electroencephalogram (EEG) spectral edge (SE) is a suggested marker for preterm white matter (WM) injury; however, there are few specific data. We examined the relationship between SE and EEG intensity and white and grey matter injury after a severe ischemic insult, induced by 30 min carotid occlusion (n=10) compared with sham-control (n=7) in preterm fetal sheep at 95-96 days of gestation (term=147 days). Fetuses were instrumented with a microdialysis probe placed within the left periventricular region and with EEG probes over the parietal cortex bilaterally. Fetuses that showed only brief suppression of the EEG during bilateral carotid occlusion (Mild group, n=4) were compared with those who exhibited persistent suppression (Severe group, n=6). After 72 h recovery, the severe ischemia group showed parasagittal cortical neuronal loss accompanied by diffuse WM damage in the right hemisphere, whereas the mild group showed little or no neuronal loss, either with (n=2) or without diffuse (n=2) WM damage. Left sided focal periventricular WM infarction corresponding with probe placement was seen in all groups. EEG intensity and SE were profoundly suppressed in the severe group, with only partial recovery after 72 h (P<0.01), in contrast with transient suppression in the mild group. There was no difference in baseline SE values or post-ischemic responses between the left and right hemisphere. These findings suggest that persistent suppression of EEG SE is primarily a consequence of cortical grey matter injury.
Suppression of electroencephalogram (EEG) spectral edge (SE) is a suggested marker for preterm white matter (WM) injury; however, there are few specific data. We examined the relationship between SE and EEG intensity and white and grey matter injury after a severe ischemic insult, induced by 30 min carotid occlusion (n=10) compared with sham-control (n=7) in preterm fetal sheep at 95-96 days of gestation (term=147 days). Fetuses were instrumented with a microdialysis probe placed within the left periventricular region and with EEG probes over the parietal cortex bilaterally. Fetuses that showed only brief suppression of the EEG during bilateral carotid occlusion (Mild group, n=4) were compared with those who exhibited persistent suppression (Severe group, n=6). After 72 h recovery, the severe ischemia group showed parasagittal cortical neuronal loss accompanied by diffuse WM damage in the right hemisphere, whereas the mild group showed little or no neuronal loss, either with (n=2) or without diffuse (n=2) WM damage. Left sided focal periventricular WM infarction corresponding with probe placement was seen in all groups. EEG intensity and SE were profoundly suppressed in the severe group, with only partial recovery after 72 h (P<0.01), in contrast with transient suppression in the mild group. There was no difference in baseline SE values or post-ischemic responses between the left and right hemisphere. These findings suggest that persistent suppression of EEG SE is primarily a consequence of cortical grey matter injury.
More Related Videos
06:58Non-restraining EEG Radiotelemetry: Epidural and Deep Intracerebral Stereotaxic EEG Electrode Placement
Published on: June 25, 2016
09:00Investigating the Function of Deep Cortical and Subcortical Structures Using Stereotactic Electroencephalography: Lessons from the Anterior Cingulate Cortex
Published on: April 15, 2015