Glial reaction in periventricular areas of the brainstem in fetal and neonatal posthemorrhagic hydrocephalus and congenital hydrocephalus

doi:10.1016/0387-7604(95)00103-4

Brain and Development

Volume 18, Issue 1, January–February 1996, Pages 40-45

https://doi.org/10.1016/0387-7604(95)00103-4 Get rights and content

Abstract

This immunohistochemical, neuropathological study was performed on the ventricular wall of the brainstem in children with fetal and neonatal posthemorrhagic and congenital hydrocephalus. In posthemorrhagic hydrocephalus (PHH), hemosiderin deposits, nodular gliosis, ependymal cell loss and subsependymal rosette formation developed subventricularly after 2 weeks of age. Ferritin-positive reactive microglia were well stained until about 2 weeks of age and thereafter diminished as reactive astrocytosis occurred. In congenital hydrocephalus (CH), the damage to the ventricular wall was less than in PHH at all ages and was associated with only mild astrogliosis. These differences in the neuropathological findings of periventricular regions, consisting mainly of glial reactions between PHH and CH, are due to differences in pathophysiology, and the timing of the insult in both conditions. The differences may be due to the effects of intraventricular hemorrhage and/or rapidly increased intracranial pressure in PHH. These results may have implications for the neurological prognosis in children with PHH.

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Cited by (39)

Pathogenesis of posthemorrhagic hydrocephalus of prematurity: New horizons
2022, Seminars in Perinatology
Citation Excerpt :
Chronic inflammation from PHHP appears to disrupt ependymal motile cilia maturation.24 Failure of ependymal cell maturation leads to replacement of ependymal cells by astrogliosis, termed ventricular disruption.34 Ependymal echogenicity on HUS is a well-known finding after sIVH35 (Fig. 1C), and likely represents hemosiderosis, gliosis and/or ependymal inflammation.
Posthemorrhagic hydrocephalus of prematurity (PHHP) remains a vexing problem for patients, their families, and the healthcare system. The complexity of the pathogenesis of PHHP also presents a unique challenge within the fields of neonatology, neurology and neurosurgery. Here we focus on pathogenesis of PHHP and its impact on the development of CSF dynamics including choroid plexus, ependymal motile cilia and glymphatic system. PHHP is contrasted with infantile hydrocephalus from other etiologies, and with other types of posthemorrhagic hydrocephalus that occur later in life. The important concept that distinguishing ventricular volume from brain health and function is highlighted. The influence of the pathogenesis of PHHP on current interventions is reviewed, with particular emphasis on how the unique pathogenesis of PHHP contributes to the high rate of failure of current existing interventions. Finally, we discuss emerging interventions. A thorough understanding of the pathogenesis of PHHP is essential to developing effective non-surgical therapeutics to prevent the transformation from severe IVH to PHHP
Preterm Intraventricular Hemorrhage/Posthemorrhagic Hydrocephalus
2018, Volpe's Neurology of the Newborn
Germinal matrix hemorrhage–intraventricular hemorrhage (GMH-IVH) is the most common variety of neonatal intracranial hemorrhage and is characteristic of the premature infant. This form of brain injury affects around 25% of all very low birthweight (<1500 g) premature infants, resulting in an increased risk for neurodevelopmental disability. Its occurrence can lead to impact on subsequent brain development because of destruction of the immature germinal cerebral region resulting in loss of progenitor cells, acceleration of white matter injury via pressure and oxidative stress, and direct parenchymal injury. Finally, hydrocephalus can complicate IVH, resulting in a further increased risk of neurodevelopmental disability. In this chapter, the neuropathology, pathogenesis, clinical features, diagnosis, prognosis, and management of IVH, and its complications will be reviewed. The prominent position of this lesion in neonatal medicine has been accompanied by a large increase in work from several disciplines. This chapter attempts to integrate this information in a meaningful way without oversimplifying a clearly complex problem.
Prolonged hydrocephalus induced by intraventricular hemorrhage in rats is reduced by curcumin therapy
2017, Neuroscience Letters
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In the early stage of IVH, the peri-ventricular microglia and blood-derived macrophages were rapidly activated to swallow the intraventricular hematoma, and hereby exert a protective effect around the lesion [20]. On the other hand, the reactive gliosis was formed following swelling and proliferation of astrocytes, which released plenty of pro-inflammatory factors; and thus it could accelerate the formation of glial scar and prevented the repair of BBB in the peri-ventricular and hippocampus at the chronic stage [9]. Though decreasing the deposition of chondroitin sulfate proteogly, the intracellular and extracellular components of glial scar formed in the long term of spinal cord injury were jointly inhabited by curcumin administration [6].
Prolonged hydrocephalus is a major cause of severe disability and death of intraventricular hemorrhage (IVH) patients. However, the therapeutic options to minimize the detrimental effects of post-hemorrhagic hydrocephalus are limited. Curcumin has been reported to confer neuroprotective effects in numerous neurological diseases and injuries, but its role in IVH-induced hydrocephalus has not been determined. The aim of present study was to determine whether curcumin treatment ameliorates blood brain barrier (BBB) damage and reduces the incidence of post-hemorrhagic hydrocephalus in IVH rat model. Autologous blood intraventricular injection was used to establish the IVH model. Our results revealed that repeated intraperitoneal injection of curcumin ameliorated IVH-induced learning and memory deficits as determined by Morris water maze and reduced the incidence of post-hemorrhagic hydrocephalus in a dose-dependent manner at 28 d post-IVH induction. Further, the increased BBB permeability and brain edema induced by IVH were significantly reduced by curcumin administration. In summary, these findings highlighted the important role of curcumin in improving neurological function deficits and protecting against BBB disruption via promoting the neurovascular unit restoration, and thus it reduced the severity of post-hemorrhagic hydrocephalus in the long term. It is believed that curcumin might prove to be an effective therapeutic component in prevent the post-IVH hydrocephalus in the near future.
Pathogenesis of Germinal Matrix Hemorrhage
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Ectopic ependymal cells in striatum accompany neurogenesis in a rat model of stroke
2012, Neuroscience
Citation Excerpt :
Ependymal cells outside the lateral ventricular wall have been described in intact human and rat SVZ as displaced ependymal cells (Quinones-Hinojosa et al., 2006; Danilov et al., 2009), in circumventricular organs (Matsui and Kobayashi, 1968; Rudert et al., 1968; Dellmann and Linner, 1979) and in the aqueductal wall as cyst cells (Fukuda and Hashimoto, 1987). They have also been found in brain tumors (Luse, 1961; Goebel and Cravioto, 1972), in the striatum of children with periventricular leucomalacia (Shortland et al., 1988; Fukumizu et al., 1995, 1996; Sarnat, 1995), in hydrocephalus (Clark and Milhorat, 1970) and in temporal lobe white matter in epileptic children (Sarnat, 1992). The origin and the function of these cells in mammalian brain are not known, while ependymal cell migration is crucial for spinal cord regeneration in fish and lizards (Allebardi and Zala, 1989; Anderson et al., 1986; Simpson, 1968).
Stroke-induced neurogenesis originates from a neural stem cell (NSC) niche in subventricular zone (SVZ). In mice, NSCs are concentrated in a so-called “neurogenic spot” in the lateral angle area of SVZ. We aimed to identify the “neurogenic spot” in the rat SVZ and to characterize the cellular changes in the ependymal cell compartment in this area at different time points after middle cerebral artery occlusion. The majority of ependymal cells outlining the ventricular wall did not proliferate, and their numbers in the “neurogenic spot” declined at 6 and 16 weeks after stroke. Cells with the ultrastructural properties of ependymal cells were detected in the adjacent striatum. The number of these ectopic ependymal cells (EE cells) correlated positively with the magnitude of lateral ventricular enlargement and negatively with the ependymal cell number in the “neurogenic spot”. EE cells were found along blood vessels, accumulated in the pericyst regions, and participated in scar formation but did not incorporate BrdU. We provide the first evidence for the occurrence of EE cells in the ischemic striatum following stroke.
Intraventricular Hemorrhage in the Neonate
2011, Fetal and Neonatal Physiology E-Book, Fourth Edition

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Glial reaction in periventricular areas of the brainstem in fetal and neonatal posthemorrhagic hydrocephalus and congenital hydrocephalus

Abstract

Brain Dev (Tokyo)

Brain Dev (Tokyo)

Pediatr Neurol

J Neurol Sci

J Neuroimmunol

Brain Res

Toxicology

Neuropathologic findings in short-term survivors of intraventricular hemorrhage

Am J Dis Child

Frequency and prognostic significance of germinal matrix hemorrhage, periventricular leukomalacia and pontosubicular necrosis in preterm neonates

Acta Neuropathol

Periventricular intraparenchymal cerebral haemorrhage in preterm infants: the role of venous infarction

J Pathol

Intraventricular hemorrhage in the premature infant-current concepts. Part 1

Ann Neurol

Perinatal brain damage

Histologic evolution of reactions to hemorrhage in the premature human infant's brain. A combined ultrasound and autopsy study and a comparison with the reaction in adults

Am J Pathol