The Pathogenesis of Neonatal Post-hemorrhagic Hydrocephalus

Authors

  • Shobha Cherian,

    1. Department of Clinical Science at South Bristol, University of Bristol, United Kingdom.
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  • Andrew Whitelaw,

    1. Department of Clinical Science at North Bristol, University of Bristol, United Kingdom.
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  • Marianne Thoresen,

    1. Department of Clinical Science at South Bristol, University of Bristol, United Kingdom.
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  • Seth Love

    Corresponding author
    1. Department of Clinical Science at North Bristol, University of Bristol, United Kingdom.
      Corresponding author: Seth Love, Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, United Kingdom (E-mail: seth.love@bristol.ac.uk)
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Corresponding author: Seth Love, Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, United Kingdom (E-mail: seth.love@bristol.ac.uk)

Abstract

Hydrocephalus after intraventricular hemorrhage (IVH) has emerged as a major complication of preterm birth and is especially problematic to treat. The hydrocephalus is usually ascribed to fibrosing arachnoiditis, meningeal fibrosis and subependymal gliosis, which impair flow and resorption of cerebrospinal fluid (CSF). Recent experimental studies have suggested that acute parenchymal compression and ischemic damage, and increased parenchymal and perivascular deposition of extracellular matrix proteins—probably due at least partly to upregulation of transforming growth factor-β (TGF-β)—are further important contributors to the development of the hydrocephalus. IVH is associated with damage to periventricular white matter and the damage is exacerbated by the development of hydrocephalus; combinations of pressure, distortion, ischaemia, inflammation, and free radical-mediated injury are probably responsible. The damage to white matter accounts for the high frequency of cerebral palsy in this group of infants. The identification of mechanisms and mediators of hydrocephalus and white matter damage is leading to the development of new treatments to prevent permanent hydrocephalus and its neurological complications, and to avoid shunt dependence.

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