Periventricular Leukomalacia of Infancy

Banker, Betty Q.

doi:10.1001/archneur.1962.04210050022004

Cited by 668 publications

(147 citation statements)

References 23 publications

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“…Although early routine neuropathological studies did not generally show evidence of apparent cortical neuronal injury in PVL (Banker and Larroche, 1962;DeReuck et al, 1972), the frequently observed cognitive and movement disorders, classically attributable to neuronal dysfunction, suggest an impaired development of cortical and deeper neurons in brains with PVL. Axonal swelling and injury around the foci of white matter necrosis and the neuronal damage of the adjacent cortex, predominantly in the pyramidal neurons of the cortical layer 5, have been found in the prenatal-onset PVL patients (Deguchi et al, 1999;Meng et al, 1997).…”

Section: Discussionmentioning

confidence: 91%

α-Phenyl-n-tert-butyl-nitrone attenuates lipopolysaccharide-induced neuronal injury in the neonatal rat brain

et al. 2008

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Although white matter damage is a fundamental neuropathological feature of periventricular leukomalacia (PVL), the motor and cognitive deficits observed later in infants with PVL indicate the possible involvement of cerebral neuronal dysfunction. Using a previously developed rat model of white matter injury induced by cerebral lipopolysaccharide (LPS) injection, we investigated whether LPS exposure also results in neuronal injury in the neonatal brain and whether α-phenyl-n-tert-butylnitrone (PBN), an antioxidant, offers protection against LPS-induced neuronal injury. A stereotactic intracerebral injection of LPS (1 mg/kg) was performed in Sprague-Dawley rats (postnatal day 5) and control rats were injected with sterile saline. LPS exposure resulted in axonal and neuronal injury in the cerebral cortex as indicated by elevated expression of β-amyloid precursor protein, altered axonal length and width, and increased size of cortical neuronal nuclei. LPS exposure also caused loss of tyrosine hydroxylase positive neurons in the substantia nigra and the ventral tegmental areas of the rat brain. Treatments with PBN (100 mg/kg) significantly reduced LPS-induced neuronal and axonal damage. The protection of PBN was associated with an attenuation of oxidative stress induced by LPS as indicated by the reduced number of 4-hydroxynonenal, malondialdehyde or nitrotyrosine positive cells in the cortical area following LPS exposure, and with the reduction in microglial activation stimulated by LPS. The finding that an inflammatory environment may cause both white matter and neuronal injury in the neonatal brain supports the possible anatomical correlate for the intellectual deficits and the other cortical and deep gray neuronal dysfunctions associated with PVL. The protection of PBN may indicate the potential usefulness of antioxidants for treatment of these neuronal dysfunctions.Keywords neuronal injury; tyrosine hydroxylase; microglial activation; oxidative stress; antioxidant Periventricular leukomalacia (PVL), the dominant form of brain injury in the preterm infant, is frequently associated with subsequent adverse neurological outcomes such as cerebral palsy and mental retardation (Rezaie and Dean, 2002;Volpe, 2003). Although white matter damage is a fundamental neuropathological feature of PVL, the motor and cognitive deficits observed later in these infants indicate possible cerebral cortical neuronal dysfunction. The precise nature Corresponding author: Dr. Zhengwei Cai Department of Pediatrics, Division of Newborn Medicine, University of Mississippi Medical Center, Jackson, MS 39216-4504, USA Tel.: +1-601-984-2786 Fax: +1-601-815-3666 E-mail address: zcai@ped.umsmed.edu (Z. Cai). Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Pleas...

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Section: Discussionmentioning

confidence: 91%

α-Phenyl-n-tert-butyl-nitrone attenuates lipopolysaccharide-induced neuronal injury in the neonatal rat brain

et al. 2008

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“…Pathologic abnormalities are characteristically localized to the white matter dorsal and lateral to the external angles of the lateral ventricles and involve primarily the centrum semiovale. 41 This white matter region is thought especially vulnerable to injury in the preterm infant because of the nature of its blood supply 42 and particular sensitivity to proinflammatory cytokines triggered by stimuli such as hypoxia-ischemia and infection. [43][44][45] Recently a role for low arterial partial pressure of carbon dioxide has been postulated as well.…”

Section: Dti and Injury During Brain Developmentmentioning

confidence: 99%

Diffusion tensor imaging of normal and injured developing human brain ‐ a technical review

et al. 2002

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The application of diffusion tensor imaging (DTI) to the evaluation of developing brain remains an area of active investigation. This review focuses on the changes in DTI parameters which accompany both brain maturation and injury. The two primary pieces of information available from DTI studies-water apparent diffusion coefficient and diffusion anisotropy measures-change dramatically during development, reflecting underlying changes in tissue water content and cytoarchitecture. DTI parameters also change in response to brain injury. In this context, not only does DTI offer the possibility of detecting injury earlier than conventional imaging methods, but also appears more sensitive to disruption of white matter than any other imaging method. DTI offers unique insight into brain injury and maturation, and does so in a fashion that can be readily applied in a clinical setting.

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“…In humans, certain stimuli such as excess phenylalanine or decreased circulating thyroxine affect the young brain more profoundly than they do the mature brain. The young brain also responds to anoxia very differently from the more mature brain [4]. Regional studies using these stimuli have not been done.…”

Section: -]:: Braimtemmentioning

confidence: 99%