Abstract

Brain injury in the premature infant consists of multiple lesions, principally germinal matrix-intraventricular hemorrhage, posthemorrhagic hydrocephalus, and periventricular leukomalacia (PVL). The last of these now appears to be the most important determinant of the neurologic morbidity observed in survivors of birth weight <1500 g. Indeed, of these very low birth weight infants, ∼10% later exhibit cerebral palsy, and ∼50%, cognitive and behavioral deficits.1–5 The focal necrotic lesions of PVL deep in the cerebral white matter correlate well with the cerebral palsy, whereas the cognitive/behavioral deficits may relate to more diffuse white matter injury observed with PVL (see below). The nature of the relationship between the diffuse white matter injury and the cognitive/behavioral deficits is complex and not entirely understood (see below). The current report of the Hammersmith group by Counsell et al,6 published elsewhere in this issue, addresses the frequency and magnetic resonance imaging (MRI) characteristics of this diffuse white matter abnormality. The study of Counsell et al6 stimulates further a necessary change in the widely held concept of PVL as principally focal necrotic lesions in the periventricular white matter with subsequent cyst formation. This concept is based on the earlier classic neuropathological description in 1962 of the focal necrotic lesions by Banker and Larroche.7 That landmark work led to the appropriate descriptive term for focal softening in the periventricular white matter, ie, PVL. Indeed, innumerable later in vivo clinical and epidemiologic studies of PVL published in the last decade or so have used the ultrasonographic finding of focal periventricular echolucency as the hallmark of PVL (see ref. 1 for review). However, focal necrotic lesions evolving to cysts, readily identified by cranial ultrasonography, are no longer the principal feature of white matter injury in premature infants. Cystic PVL identified by brain imaging is a … Reprints requests to (J.J.V.) Department of Neurology, Fegan 1103, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115. E-mail: joseph.volpe{at}tch.harvard.edu

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.