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[Clinical studies on 35 patients with infection-related acute encephalopathy]
1Department of Pediatrics, Urafune Hospital of Yokohama City University School of Medicine.
Insights
This study categorizes imaging findings in children with acute encephalopathy (AE) due to infections, linking specific patterns like brain edema and cortical necrosis to outcomes such as death or severe brain damage.
Area of Science:
- Pediatric Neurology
- Neuroradiology
- Infectious Diseases
Context:
- Acute encephalopathy (AE) in children presents a diagnostic challenge, with varied neurological sequelae.
- Understanding the correlation between early imaging findings and patient outcomes is crucial for prognosis.
Purpose:
- To categorize and analyze magnetic resonance imaging (MRI) or computed tomographic (CT) scan findings in children with infection-induced acute encephalopathy (AE).
- To correlate specific neuroimaging patterns with clinical outcomes, including mortality, epilepsy, and severe brain damage (SBD).
Summary:
- Thirty-five children with infection-induced AE were classified into five imaging groups: normal, mild atrophy, severe edema, cortical necrosis, and thalamic lesions.
- Outcomes varied significantly by group, with severe edema and thalamic lesions associated with higher mortality and SBD rates.
- Elevated serum AST and Reye syndrome-like liver histology were observed in some cases, particularly those with severe imaging findings.
Impact:
- Provides a framework for interpreting neuroimaging in pediatric AE, aiding in early prognostication.
- Highlights the severity and potential long-term consequences of specific AE-related brain pathologies.
- Informs clinical management and resource allocation for children affected by severe neurological complications of infections.
Abstract:
The findings on magnetic resonance imaging (MRI) or computed tomographic scan in 35 children with acute encephalopathy (AE) induced by infections were categorized into five groups: (1) normal findings (11 cases), (2) normal findings in the acute phase followed by mild brain atrophy (1 case), (3) severe brain edema which developed within 48 hours after the onset of AE (7 cases), (4) diffuse cortical necrosis which appeared around 4 days after the onset of AE (9 cases), and (5) symmetric thalamic lesions (7 cases). Their outcomes were as follows: three cases developed epilepsy in (1) and (2); six died and one had a sequel of severe brain damage (SBD) in (3); all cases survived but had SBD in (4), and four died, one had SBD, and 2 recovered in (5). Serum AST were elevated in 7.7 and 6 cases in (3), (4) and (5), respectively. In all of them, there were more than one case having liver histologies consistent with Reye syndrome.