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[Mid-term and long-term outcome in newborn infants with periventricular leukomalacia (53 cases)]
M Monset-Couchard1, O de Bethmann, B Kastler
1Unité de soins intensifs néonatals de Port-Royal, centre hospitalier universitaire Cochin-Port-Royal-Tarnier, université René-Descartes, Paris, France.
Insights
Cystic periventricular leukomalacias (CPVL) in neonates can lead to neurodevelopmental sequelae. Lesion thickness, especially in posterior regions, is a key predictor of severity, more so than extent.
Area of Science:
- Neonatal neurology
- Pediatric neuroimaging
- Developmental neuroscience
Context:
- Cystic periventricular leukomalacias (CPVL) are a common finding in preterm neonates.
- Brain ultrasonography is a primary tool for diagnosing CPVL.
- Neurodevelopmental outcomes in affected infants require long-term monitoring.
Purpose:
- To investigate the relationship between cystic periventricular leukomalacias (CPVL) and neurodevelopmental sequelae in neonates.
- To determine predictors of neurodevelopmental outcomes in infants with CPVL.
- To assess the role of lesion characteristics in predicting sequelae severity.
Summary:
- A cohort of 53 neonates with CPVL (mean gestational age 30 weeks) underwent 3-7 year neurodevelopmental follow-up.
- CPVL severity ranged from minor to major forms, with or without associated intraventricular hemorrhage.
- Lesion thickness, particularly in posterior regions, was found to be a significant predictor of neurodevelopmental sequelae, more so than lesion extent.
Impact:
- Identifies lesion thickness as a crucial factor in predicting neurodevelopmental outcomes in neonates with CPVL.
- Highlights the importance of posterior CPVL in determining the severity of neurological deficits.
- Informs clinical management and prognostic assessments for infants diagnosed with CPVL.
Abstract:
During the period 1983-1987, 53 neonates (30 boys, 23 girls, mean birth weight 1,438 +/- 317 g, mean gestational age 30 +/- 2 weeks) were found to have cystic periventricular leukomalacias (CPVL) detected by brain ultrasonography. The neuro-developmental follow-up was 3-7 years. Seventeen CPVL were isolated and CPVL were associated with minor peri-intraventricular hemorrhage (0-1 to II-II) in 36 cases. CPVL included 16 minor forms (11 normal children; 2 minor, 3 moderate sequelae), 29 moderate forms (15 normal children; 4 minor, 7 moderate, 3 major sequelae) and 8 major forms (7 major sequelae, one moderate mental retardation without motor deficit). According to reverse analysis, a normal evolution (26 cases) followed CPVL which were sometimes widely, but thinly spread over the ventricles (thickness 1/5-1/3 of the cerebral mantle); minor sequelae (6 cases) were associated with a 1/4-1/3 thickness, moderate sequelae (11 cases) with a 1/3-1/2 thickness, major sequelae (10 cases) with a 1/2-2/3 thickness of CPVL. The thickness of the lesions appeared to be more predictive of sequelae than the sagittal extent, in particular that of the posterior CPVL which played a major role in the severity of sequelae, and mainly in the presence of motor deficits.