Related Experiment Video
Updated: Jun 16, 2026

Electromagnetic Source Imaging in Presurgical Evaluation of Children with Drug-Resistant Epilepsy
Published on: September 20, 2024
Fulminant sepsis-associated encephalopathy in two children: serial neuroimaging findings and clinical course
1Division of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan. holbergs@nifty.com
Insights
Sepsis-associated encephalopathy can cause severe, rapid brain damage in children, leading to coma and mimicking brain death. Neuroimaging reveals extensive edema and lesions, indicating profound neurological injury.
Area of Science:
- Pediatric Neurology
- Critical Care Medicine
- Neuroscience
Background:
- Sepsis-associated encephalopathy (SAE) is a serious complication of sepsis.
- Early recognition and understanding of SAE's neurological impact are crucial for pediatric critical care.
Observation:
- Two children presented with acute, severe neurological deterioration following sepsis.
- Clinical presentation included status epilepticus, deep coma, and near brain death.
- Initial CT scans showed diffuse brain edema, and EEG revealed severe brain dysfunction.
Findings:
- MRI demonstrated restricted diffusion in basal ganglia and white matter, indicating cytotoxic edema.
- Serial imaging over months showed progressive, severe lesions in cerebral white matter, cerebellum, and brainstem.
- MR angiography revealed diminished intracranial arteries, suggesting widespread vascular compromise.
Implications:
- SAE can lead to devastating, long-term neurological damage in children.
- Findings suggest a mechanism of severe brain injury due to rapid intracranial pressure elevation, mimicking "respirator brain".
- Highlights the need for advanced neuroimaging and monitoring in pediatric sepsis cases.
Abstract:
We report on two children with sepsis-associated encephalopathy. They presented with fulminant neurological damage on clinical, neuroimaging, and neurophysiological findings. At onset, both went into deep coma after status epilepticus, resulting in near brain death. Both patients showed diffuse brain edema on CT and severe brain dysfunction on electroencephalography within a day of onset. Brain magnetic resonance (MR) imaging of one patient on day 2 showed restricted diffusion in the basal ganglia and the subcortical white matter of the frontal and occipital lobes. Brain edema aggravated and lasted for a few months despite a variety of treatments. MR imaging in the chronic phase revealed cracking lesions extending to the cerebral white matter, the cerebellum, and the brainstem. MR angiography showed diminished intracranial major arteries. These serial neuroradiological findings suggested severe brain damage resulting from fulminant elevation of intracranial pressure, which mimicked "brain death" or "respirator brain".
Related Concept Videos
Encephalitis ll: Pathophysiology
Encephalitis l: Introduction
Brain Abscess l: Introduction
Bacterial Meningitis II: Pathophysiology
Hepatic Encephalopathy
Viral Meningitis

