Elsevier

Clinics in Perinatology

Volume 40, Issue 4, December 2013, Pages 707-722
Clinics in Perinatology

Neuropathologic Studies of the Encephalopathy of Prematurity in the Late Preterm Infant

https://doi.org/10.1016/j.clp.2013.07.003Get rights and content

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Key points

  • The encephalopathy of prematurity comprises combined gray and white matter lesions underlying preterm brain injury, including periventricular leukomalacia (PVL).

  • The late preterm brain can develop PVL identical to that of the early preterm brain, and potentially with a higher incidence detected at autopsy.

  • There is an increased mean density of reactive astrocytes, as well as glia with the expression of the oxidative marker, 4-hydroxynonenal, in the damaged white matter of late preterm infants in

Brain development in the second half of human gestation

Brain development in the second half of human gestation, the time frame of prematurity, is nothing short of spectacular. At midgestation, the cerebrum is virtually smooth except for the indentation of the Sylvan fissure; by term, all primary, secondary, and tertiary sulci are in place, with different gyri differentiating at exquisitely timed periods over the second half of pregnancy (Fig. 2). The appearance of the central, cingulate, circular, calcarine, and superior temporal sulci follow on

The encephalopathy of prematurity further defined

The term “encephalopathy of prematurity” was coined to characterize the multifaceted gray and white matter lesions in the preterm brain that reflect acquired insults, altered developmental trajectories, and reparative phenomena in various combinations.5, 6, 37, 38 It encompasses damage to white matter (periventricular leukomalacia [PVL] and diffuse cerebral white matter gliosis), as well as to white matter neurons, axons, and gray matter (neuronal loss and/or gliosis in the cerebral cortex,

The encephalopathy of prematurity in the late preterm infant

In an attempt to elucidate the neuropathology of the late preterm infant at autopsy, the authors undertook an analysis of previously published data sets concerning various aspects of EP in preterm infants autopsied at Boston Children’s Hospital between 1997 and 2008.7, 8, 9, 10 This analysis compared several neuropathologic components of EP between early and mid preterm infants typically combined (<34 weeks at birth) and late preterm infants (34–36 weeks at birth), and, in some instances for

Summary

At 34 gestational weeks, the late preterm brain has attained approximately two-thirds of term weight, underscoring the distance yet to reach term maturation. This study attempts to begin to define the neuropathology of EP in the late preterm infant. In autopsied late preterm infants, the spectrum of brain damage has been found to be virtually the same as that found in early preterm infants (<34 weeks at birth), suggesting that if the insult(s) is severe enough, the same histopathologic changes

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    Disclosures: The authors/editors have identified no professional or financial affiliations for themselves or their spouse/partner.

    This work was supported by grants from the National Institute of Neurological Disorders and Stroke (PO1-NS38475), National Institute of Child Health and Development (P30-HD18655), and Cerebral Palsy International Research Foundation.

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