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Updated: Aug 10, 2026
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A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
[Delayed postanoxic encephalopathy]
F J Gascón Jiménez1, B Navarro Gochicoa, M J Velasco Jabalquinto
1Facultad de Medicina, Unidad Docente de Pediatría, Hospital Universitario Reina Sofía, Departamento de Pediatría, Córdoba.
Anales Espanoles De Pediatria
|November 21, 2000
Summary
Delayed postanoxic encephalopathy can occur after benzodiazepine intoxication, causing a relapse of neurological symptoms. This rare condition, affecting the basal ganglia, leads to permanent neurological deficits.
Area of Science:
- Neuroscience
- Toxicology
- Pediatric Neurology
Background:
- Benzodiazepine intoxication can lead to coma and acute respiratory distress syndrome.
- Delayed postanoxic encephalopathy is a rare, unexplained neurological condition.
- This syndrome manifests after an initial hypoxic-ischemic event.
Observation:
- A 9-year-old boy experienced delayed postanoxic encephalopathy following benzodiazepine intoxication.
- Initial recovery was followed by the onset of extrapyramidal rigidity and involuntary movements.
- Brain MRI revealed ischemic changes in the basal ganglia, consistent with anoxic-ischemic encephalopathy.
Findings:
- The patient presented with lead-pipe rigidity and cogwheel quality in passive movements.
- Neurological impairment progressed over weeks to months.
- The basal ganglia were disproportionately affected compared to the cerebral cortex and white matter.
Implications:
- This case highlights the potential for delayed postanoxic encephalopathy, particularly affecting the basal ganglia.
- The pathogenesis of this delayed neurological sequela remains unknown.
- Understanding this phenomenon is crucial for managing patients with severe intoxication and hypoxic events.
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