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Delayed neuropsychiatric syndrome in a child following carbon monoxide poisoning
Akiko Kondo1, Yoshiaki Saito, Ayumi Seki
1Divisions of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Japan. holbergs@nifty.com
Insights
Carbon monoxide (CO) poisoning can cause delayed neuropsychiatric syndrome in children, even after hyperbaric oxygen therapy. This case highlights atypical cortical laminar necrosis, suggesting complex CO poisoning pathomechanisms.
Area of Science:
- Neurology
- Toxicology
- Pediatrics
Background:
- Carbon monoxide (CO) poisoning is a significant public health concern, particularly in pediatric populations.
- Hyperbaric oxygen (HBO) therapy is a standard treatment for CO poisoning, aiming to accelerate CO elimination and tissue oxygenation.
- Delayed neuropsychiatric sequelae following CO poisoning, while known, are less commonly reported in children.
Observation:
- A five-year-old boy presented with symptoms of CO poisoning and initially improved with HBO therapy.
- He later developed delayed neurological deficits including lethargy, visual and gait disturbances, hemiparesis, and mood lability.
- Electroencephalography showed slow frontal activity, and MRI revealed lesions in the hippocampus and cerebral cortex.
Findings:
- The patient exhibited persistent neurological deficits despite a 10-day course of HBO therapy.
- Follow-up MRI demonstrated lesions in the globus pallidum and characteristic cortical laminar necrosis.
- These findings, particularly cortical laminar necrosis, are atypical for CO poisoning and suggest a broader pathomechanism.
Implications:
- This case underscores the importance of vigilant, long-term neurological monitoring in children following CO exposure.
- The atypical imaging findings challenge current understanding of CO poisoning's neuropathology.
- Further research is warranted to elucidate the mechanisms underlying delayed neuropsychiatric syndrome and cortical lesions in pediatric CO poisoning.
Abstract:
Here, we report the case of a five-year-old boy with carbonic monoxide (CO) poisoning. The patient initially recovered after the initiation of hyperbaric oxygen (HBO) therapy, but lethargy as well as visual and gait disturbances appeared two days later. Left hemiparesis and mood lability also subsequently appeared. Slow frontal activity was noted on electroencephalography, while fluid-attenuation inversion recovery and diffusion-weighted magnetic resonance imaging (MRI) revealed high signal-intensity lesions in the hippocampus and deeper layers of the occipital and frontal cerebral cortex. The neurological symptoms subsided gradually during the 10-day course of HBO therapy, but the left-hand paresis and quadrantic hemianopsia persisted, in association with impaired attention, slow mental processing, and incontinence. Lesions in the globus pallidum were noted on follow-up MRI at 14 days, and cortical lesions became evident as linear, low signal-intensity areas on T1-weighted imaging 4 months after presentation. Delayed neuropsychiatric syndrome in CO poisoning is rare in childhood, although children should be carefully monitored after CO exposure. The finding of cortical laminar necrosis in this patient is quite atypical in CO poisoning, and suggests a broader and previously nonpredicted pathomechanism in this condition.
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