Related Experiment Video

Updated: Aug 19, 2026

A Novel Strategy Combining Array-CGH, Whole-exome Sequencing and In Utero Electroporation in Rodents to Identify Causative Genes for Brain Malformations
08:22

A Novel Strategy Combining Array-CGH, Whole-exome Sequencing and In Utero Electroporation in Rodents to Identify Causative Genes for Brain Malformations

Published on: December 1, 2017

Congenital hydrocephalus secondary to intra-uterine germinal matrix/intraventricular haemorrhage

A Hill, B Rozdilsky

    Developmental Medicine and Child Neurology
    |August 1, 1984
    PubMed

    An infant with hydrocephalus which had been diagnosed at birth died at one month of age. Subsequent neuropathological studies demonstrated old germinal matrix haemorrhage and complete occlusion of the aqueduct of Sylvius by fibroglial tissue, both of which appeared to be older than four weeks, indicating that they had occurred in utero. These observations are consistent with the occurrence of intra-uterine intraventricular haemorrhage secondary to haemorrhage of the subependymal germinal matrix, leading to occlusion of the aqueduct of Sylvius and hydrocephalus prior to birth.

    More Related Videos

    Modeling Neonatal Intraventricular Hemorrhage Through Intraventricular Injection of Hemoglobin07:57

    Modeling Neonatal Intraventricular Hemorrhage Through Intraventricular Injection of Hemoglobin

    Published on: August 25, 2022

    Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats04:12

    Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

    Published on: March 28, 2025

    Related Concept Videos

    Hemorrhagic Stroke ll: Pathophysiology01:29

    Hemorrhagic Stroke ll: Pathophysiology

    A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
    Bacterial Meningitis II: Pathophysiology01:26

    Bacterial Meningitis II: Pathophysiology

    Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
    Increased Intracranial Pressure l: Introduction01:14

    Increased Intracranial Pressure l: Introduction

    Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
    Increased Intracranial Pressure ll: Pathophysiology01:29

    Increased Intracranial Pressure ll: Pathophysiology

    Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
    Cerebral Edema l: Introduction01:19

    Cerebral Edema l: Introduction

    Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
    Cerebral Edema ll: Pathophysiology01:22

    Cerebral Edema ll: Pathophysiology

    Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...