Early deterioration of cerebrospinal fluid dynamics in a neonatal piglet model of intraventricular hemorrhage and posthemorrhagic ventricular dilation

Aquilina, Kristian; Chakkarapani, Ela; Thoresen, Marianne

doi:10.3171/2012.8.peds11386

Cited by 19 publications

(17 citation statements)

References 58 publications

(60 reference statements)

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“…Mice with transgenic TGF‐β overexpression developed hydrocephalus with higher expression of ECM proteins in the brain than wild types (Wyss‐Coray et al, ). In a clinical study, increased TGF‐β1 and ECM protein expression in the CSF were associated with PHH development in preterm infants (Aquilina, Chakkarapani, & Thoresen, ; Douglas‐Escobar & Weiss, ). The TGF‐β1 isoform is mostly associated with PHH after IVH in neonates and adults (Gomes, Sousa Vde, & Romao, ).…”

Section: Phh Pathophysiology and Potential Mechanismsmentioning

confidence: 99%

Posthemorrhagic hydrocephalus development after germinal matrix hemorrhage: Established mechanisms and proposed pathways

Klebe

McBride

Krafft

et al. 2019

J of Neuroscience Research

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In addition to being the leading cause of morbidity and mortality in premature infants, germinal matrix hemorrhage (GMH) is also the leading cause of acquired infantile hydrocephalus. The pathophysiology of posthemorrhagic hydrocephalus (PHH) development after GMH is complex and vaguely understood, although evidence suggests fibrosis and gliosis in the periventricular and subarachnoid spaces disrupts normal cerebrospinal fluid (CSF) dynamics. Theories explaining general hydrocephalus etiology have substantially evolved from the original bulk flow theory developed by Dr. Dandy over a century ago. Current clinical and experimental evidence supports a new hydrodynamic theory for hydrocephalus development involving redistribution of vascular pulsations and disruption of Starling forces in the brain microcirculation. In this review, we discuss CSF flow dynamics, history and development of theoretical hydrocephalus pathophysiology, and GMH epidemiology and etiology as it relates to PHH development. We highlight known mechanisms and propose new avenues that will further elucidate GMH pathophysiology, specifically related to hydrocephalus.

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Section: Phh Pathophysiology and Potential Mechanismsmentioning

confidence: 99%

Posthemorrhagic hydrocephalus development after germinal matrix hemorrhage: Established mechanisms and proposed pathways

Klebe

McBride

Krafft

et al. 2019

J of Neuroscience Research

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“…Another effect of an IVH is that it can block the CSF drainage pathway, at least transiently 9, 56 , either within the ventricular system or at the CSF outflow sites. This may lead to, or contribute to, PHH.…”

Section: Ivh-induced Brain Injurymentioning

confidence: 99%

Challenges for intraventricular hemorrhage research and emerging therapeutic targets

Garton

Hua

Xiang

et al. 2017

Expert Opinion on Therapeutic Targets

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Introduction – Intraventricular hemorrhage (IVH) affects both premature infants and adults. In both demographics, it has high mortality and morbidity. There is no FDA approved therapy that improves neurological outcome in either population highlighting the need for additional focus on therapeutic targets and treatments emerging from preclinical studies. Areas Covered – IVH induces both initial injury linked to the physical effects of the blood (mass effect) and secondary injury linked to the brain response to the hemorrhage. Preclinical studies have identified multiple secondary injury mechanisms following IVH, and particularly the role of blood components (e.g. hemoglobin, iron, thrombin). This review, with an emphasis on pre-clinical IVH research, highlights therapeutic targets and treatments that may be of use in prevention, acute care, or repair of damage. Expert Opinion – An IVH is a potentially devastating event. Progress has been made in elucidating injury mechanisms, but this has still to translate to the clinic. Some pathways involved in injury also have beneficial effects (coagulation cascade/inflammation). A greater understanding of the downstream pathways involved in those pathways may allow therapeutic development. Iron chelation (deferoxamine) is in clinical trial for intracerebral hemorrhage and preclinical data suggest it may be a potential treatment for IVH.

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“…GM-IVH has been modeled in several animal species including the dog, rabbit, sheep, rat, mouse and pig, either by directly injecting blood into the ventricles or by changing hemodynamic properties, such as blood pressure, the volume of blood circulating, serum glycerol, carbon dioxide, osmolarity or oxygenation levels (Goddard et al, 1980 ; Yoshioka et al, 1989 ; Balasubramaniam and Del Bigio, 2006 ; Georgiadis et al, 2008 ; Tosun et al, 2013 ). The two most-used animals models of IVH are the intracerebral injection of sterile collagenase, a hemorrhage-inducing agent (Krafft et al, 2012 ; Lekic et al, 2012 ), in mice, and the intracerebroventricular injection of fresh homologs blood in adult Sprague-Dawley rats or in piglets at 9–22 h of life (Aquilina et al, 2007 , 2012 ). The appropriate model is selected based on the pathophysiology of hemorrhage induction and injury progression.…”

Section: Principal Insults To the Developing Brain And Their Animal Mmentioning

confidence: 99%

Blood-brain barrier dysfunction in disorders of the developing brain

et al. 2015

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Disorders of the developing brain represent a major health problem. The neurological manifestations of brain lesions can range from severe clinical deficits to more subtle neurological signs or behavioral problems and learning disabilities, which often become evident many years after the initial damage. These long-term sequelae are due at least in part to central nervous system immaturity at the time of the insult. The blood-brain barrier (BBB) protects the brain and maintains homeostasis. BBB alterations are observed during both acute and chronic brain insults. After an insult, excitatory amino acid neurotransmitters are released, causing reactive oxygen species (ROS)-dependent changes in BBB permeability that allow immune cells to enter and stimulate an inflammatory response. The cytokines, chemokines and other molecules released as well as peripheral and local immune cells can activate an inflammatory cascade in the brain, leading to secondary neurodegeneration that can continue for months or even years and finally contribute to post-insult neuronal deficits. The role of the BBB in perinatal disorders is poorly understood. The inflammatory response, which can be either acute (e.g., perinatal stroke, traumatic brain injury) or chronic (e.g., perinatal infectious diseases) actively modulates the pathophysiological processes underlying brain injury. We present an overview of current knowledge about BBB dysfunction in the developing brain during acute and chronic insults, along with clinical and experimental data.

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Early deterioration of cerebrospinal fluid dynamics in a neonatal piglet model of intraventricular hemorrhage and posthemorrhagic ventricular dilation

Cited by 19 publications

References 58 publications

Posthemorrhagic hydrocephalus development after germinal matrix hemorrhage: Established mechanisms and proposed pathways

Posthemorrhagic hydrocephalus development after germinal matrix hemorrhage: Established mechanisms and proposed pathways

Challenges for intraventricular hemorrhage research and emerging therapeutic targets

Blood-brain barrier dysfunction in disorders of the developing brain

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