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Updated: May 21, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

Delayed hypoxic-ischemic leukoencephalopathy.

Hipólito Nzwalo¹, Francisca Sá, Inês Cordeiro

¹Neurology Department, Hospital de Faro, Faro, Portugal. nzwalo@gmail.com

BMJ Case Reports

|June 9, 2012

Summary

A delayed hypoxic-ischemic encephalopathy diagnosis followed benzodiazepine exposure. This rare condition caused severe neurological deficits, including a vegetative state, but showed some recovery with supportive care.

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Area of Science:

Neurology
Toxicology

Background:

Benzodiazepine intoxication can present with diverse neurological symptoms.
Delayed neurological complications following toxic exposure are rare but significant.

Observation:

A 55-year-old female presented with unconsciousness after exposure to benzodiazepines.
Initial presentation included altered mental status, with subsequent development of catatonia, immobility, and a vegetative state.
Neurological deterioration was marked by pyramidal signs and decerebration.

Findings:

Brain imaging revealed diffuse leukoencephalopathy.
Cerebrospinal fluid and metabolic studies were largely unrevealing.
Brain biopsy indicated chronic cerebral hypoxia/anoxia, leading to a diagnosis of delayed hypoxic-ischemic leukoencephalopathy.

Implications:

This case highlights a rare sequela of benzodiazepine exposure, emphasizing the importance of considering delayed hypoxic-ischemic encephalopathy.
The findings underscore the potential for severe, delayed neurological damage and the need for comprehensive diagnostic workups.
Despite severe deficits, gradual improvement suggests the potential for some recovery with intensive supportive care.