title: Neonatal posthemorrhagic hydrocephalus: neuropathologic and immunohistochemical studies.
abstract: A neuropathologic study was undertaken to examine associated brain damage in patients with fetal and neonatal posthemorrhagic hydrocephalus (PHH). In PHH the association of periventricular leukomalacia and pontosubicular necrosis was not increased, but that of cerebellar subarachnoid hemorrhage and olivo-cerebellar pathology was significantly increased. All patients with the olivocerebellar pathology exhibited associated cerebellar subarachnoid hemorrhage and loss of Purkinje cells. Ferritin-positive glia were increased in the molecular layer of most patients, and glial fibrillary acidic protein-positive glia and/or fibers were increased in the molecular layer, granular layer, and white matter in older infants. Neonates with PHH had more severe brain lesions than those with only intraventricular hemorrhage. At 2 weeks of age in PHH, the ventricular wall displayed hemosiderin deposits and nodular gliosis, with ependymal cell loss and subependymal rosette formation. These findings may be closely related to the underlying pathogenesis and neurologic sequelae of PHH.
authors.affiliation: Department of Mental Retardation and Birth Defect Research; National Institute of Neuroscience, Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Fukumizu
authors.forename: S
authors.initials: S
authors.lastname: Takashima
authors.forename: L E
authors.initials: LE
authors.lastname: Becker
mesh_terms: D001933:Brain Stem / Q000378:metabolism / Q000473:pathology*; D002531:Cerebellum / Q000378:metabolism / Q000473:pathology*; D002543:Cerebral Hemorrhage / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D006849:Hydrocephalus / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D007150:Immunohistochemistry; D007223:Infant; D007231:Infant, Newborn; D007234:Infant, Premature; D007235:Infant, Premature, Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology*