Abstract
A 4-year-old boy was admitted with disturbed consciousness following a convulsion. He developed bilateral pyramidal tract signs and showed a decerebrate posture. Laboratory findings revealed severe liver dysfunction and disseminated intravascular coagulation. On the eighth day eight in hospital he developed parkinsonism. However, 5 months from onset he had recovered almost completely. Brain CT on admission showed low density areas in the basal ganglia, thalamus, midbrain and pons. A T2-weighted scan in magnetic resonance imaging (MRI) showed almost symmetrical high signal intensities in both basal ganglia (including putamen, caudate nucleus, globus pallidus), external capsule, internal capsule, thalamus, midbrain, pons and white matter of the peribasal ganglia; but a T1-weighted scan showed low signal intensities in the same regions during all phases. Therefore hemorrhagic lesions or the presence of thalamic methemoglobin were excluded. It was considered that the pathogenesis may be cytotoxic cellular edema due to cytotoxic agents or acute metabolic factors. Clinical presentation, laboratory findings and radiological findings were most suggestive of acute necrotizing encephalopathy. As differential diagnoses, acute disseminated encephalomyelitis and brainstem encephalitis were considered.
Original language | English |
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Pages (from-to) | 454-458 |
Number of pages | 5 |
Journal | Pediatrics International |
Volume | 39 |
Issue number | 4 |
DOIs | |
Publication status | Published - Aug 1997 |
Externally published | Yes |
Keywords
- Acute disseminated encephalomyelitis
- Acute necrotizing encephalopathy
- Disseminated intravascular coagulation
- Magnetic resonance imaging
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health