Classifying brain damage in preterm infants  

Oleh:

Paneth, Nigel

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Journal of Pediatrics vol. 135 no. 05 (Nov. 1999), page 527-529.
Topik: CT ; Computed tomography; IVH ; Intraventricular hemorrhage; PVL ; Periventricular leukomalacia; VE ; Ventricular enlargement; WMD ; White matter damage

Ketersediaan

Perpustakaan FK Nomor Panggil: J45.K.1999.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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The importance of better understanding brain damage in preterm infants cannot be overstated. The direct costs of low birth weight were estimated to be $7.4 billion annually in the United States in 1992, a figure more than double the estimated direct costs of acquired immunodeficiency syndrome that year. These costs are largely driven by the high costs of managing and remediating neurodevelopmental disorders in survivors. The remarkable advances in neonatal care of the past 2 decades have greatly reduced the mortality rate but have not made a parallel dent in the high frequency of neurodevelopmental sequelae or in the brain disorders that underlie them. Prevention of brain damage, unfortunately not yet in our grasp, should be the ultimate goal of every neonatologist. Two articles in this issue of The Journal help advance our understanding of preterm brain damage but also highlight one reason that progress is slow. Although no field can advance unless there is agreement on nomenclature, the 2 sets of authors use different terminology to describe the brain damage they address. Kuban et al refer to “white matter damage,” whereas Inder et al speak of “periventricular leukomalacia.” WMD is a term that encompasses a variety of pathologic entities, held together by one common feature: they tend to target developing white matter. PVL is just one form of WMD. First described and named by Banker and Larroche in 1962, the main feature of PVL is bilateral focal coagulation necrosis in the periventricular region, sometimes including multiple small cavities. Using diffusion-weighted magnetic resonance imaging, Inder et al have detected broad evidence of white matter dysfunction, which they call the “diffuse component of periventricular leukomalacia,” in the brain of a premature infant in whom PVL later developed, before any abnormal ultrasound image was evident. It may well be that disturbances of oligodendrocyte precursors, or of other mechanisms required for timely myelination, are a common feature of all forms of WMD. Delayed or permanently deficient myelination is a common finding on magnetic resonance imaging in children previously shown to have WMD on neonatal ultrasound scans.

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