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Published on: February 7, 2025
Infant Abusive Head Trauma Induces Seizures and Cellular Stress in a Pre-Clinical Mouse Model
Sydney Harris1, Matt Hudson1, Marissa Sgro1
1Department of Neuroscience, School of Translational Medicine, Monash University, Melbourne, VIC, Australia.
Insights
Repeat abusive head trauma (AHT) in mice caused electrographic seizures and cellular stress, even without visible symptoms. This indicates subtle neurological damage from AHT, highlighting the need for sensitive detection methods.
Area of Science:
- Neuroscience
- Pediatrics
- Cellular Biology
Background:
- Abusive head trauma (AHT) involves forceful shaking, causing brain movement within the skull.
- Repeat AHT incidents are common, with affected children experiencing multiple episodes.
- AHT can cause underlying cellular and neurological damage, sometimes without obvious behavioral signs.
Purpose of the Study:
- To investigate electrographic seizures and cell stress indicators in a mouse model of repeat AHT.
- To determine if AHT leads to measurable cellular damage despite the absence of overt behavioral deficits.
Main Methods:
- Mice underwent hippocampal electrode surgery for electroencephalography (EEG) recording.
- AHT was modeled using a shaking device, followed by post-injury EEG.
- Gene expression and telomere length were analyzed in a separate cohort post-AHT.
Main Results:
- Electrographic seizures occurred in 35.7% of AHT-exposed mice, but none in sham controls.
- Repeat AHT altered gene expression related to cell stress in the hippocampus and olfactory bulbs.
- Telomere length was affected at postnatal day 21 following AHT exposure.
Conclusions:
- Repeat AHT induces electrographic seizures and cellular damage in a mouse model.
- These findings suggest measurable neurological harm from AHT, even without apparent behavioral deficits.
- The study underscores the importance of EEG for detecting subtle seizure activity post-AHT.
Abstract:
Abusive head trauma (AHT) occurs when a child is grasped and shaken with such force that the brain moves within the skull. AHTs are not isolated events; repetition occurs in 30-50% of cases, with affected children experiencing ∼10 episodes. While many AHTs appear asymptomatic, there is often underlying cellular and neurological damage. Notably, seizures following AHT may be solely electrographic without overt behavioral signs and detectable only via electroencephalography (EEG). Thus, we examined electrographic seizures and indicators of cell stress in a mouse model of repeat AHT. On postnatal day (P)8, mice underwent hippocampal electrode surgery. On P10-12, 5 min of baseline EEG was recorded, followed by an AHT and 15 min of postinjury EEG recording. AHTs were modeled by securing a mouse to a shaking device at 400 rpm (5g) for 60 s. Sham mice underwent the same surgery and EEG recording procedures but were placed on the shaking device while it remained stationary. A separate cohort of mice forewent surgery but were exposed to the same AHT procedure and were euthanized on P21 or P45 for gene expression and telomere length (TL) analysis. Electrographic seizures occurred following 35.7% of AHTs, while no sham mice exhibited electrographic seizures. Repetitive AHTs affected gene expression in the hippocampus and olfactory bulbs, in genes related to cell stress (TERT, Sod1, P53, Drd2, Dnmt3a, iNOS), and TL at P21. These findings suggest that despite the absence of observable behavioral deficits, repeat AHTs result in measurable cellular damage and electrographic seizure activity.
