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Related Concept Videos

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 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...
Cerebral Edema l: Introduction01:19

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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...
Anatomy of the Brain: Ventricles01:18

Anatomy of the Brain: Ventricles

There are hollow fluid-filled cavities known as ventricles deep inside the human brain. There are two lateral ventricles, one in each cerebral hemisphere, and each has three different projections — the anterior, inferior, and posterior horns visible from the lateral side. A thin membrane called the septum pellucidum separates the two lateral ventricles. The slender third ventricle in the diencephalon is connected to each lateral ventricle via a channel called the interventricular foramen. The...
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Related Experiment Video

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Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
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Published on: March 28, 2025

Hydrocephalus and Chiari type I malformation.

Concezio Di Rocco1, Paolo Frassanito, Luca Massimi

  • 1Pediatric Neurosurgery, Catholic University Medical School, Policlinic A. Gemelli, Largo Agostino Gemelli, 8, 00168 Rome, Italy.

Child'S Nervous System : Chns : Official Journal of the International Society for Pediatric Neurosurgery
|September 20, 2011
PubMed
Summary
This summary is machine-generated.

Hydrocephalus and Chiari type I malformation (CIM) association has complex causes. Understanding these diverse pathogenetic mechanisms is key to effective treatment strategies for CIM and hydrocephalus.

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Last Updated: May 29, 2026

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
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Area of Science:

  • Neuroscience
  • Neurosurgery
  • Pediatric Neurology

Background:

  • The association between hydrocephalus and Chiari type I malformation (CIM) is long-recognized.
  • The underlying pathogenetic mechanisms linking these two conditions remain complex and debated.

Purpose of the Study:

  • To explore the heterogeneous pathogenetic mechanisms underlying the association of hydrocephalus and Chiari type I malformation.
  • To discuss the implications of these mechanisms for therapeutic approaches.

Main Methods:

  • Review of clinical and radiological data from patients with complex craniosynostosis.
  • Analysis of pathogenetic hypotheses including supratentorial pressure and cephalo-cranial disproportion.
  • Consideration of jugular foramen stenosis and venous hypertension.

Main Results:

  • Multiple pathogenetic pathways may lead to the radiological association of ventricular enlargement and hindbrain herniation.
  • Supratentorial hypertensive hydrocephalus can exert pressure causing CIM.
  • Cephalo-cranial disproportion in complex craniosynostosis can lead to secondary hydrocephalus and CIM.

Conclusions:

  • The diverse etiologies of hydrocephalus and CIM necessitate tailored therapeutic strategies.
  • Endoscopic third ventriculocisternostomy is an emerging treatment option for its physiological correction of CSF dynamics.
  • This endoscopic approach offers minimal interference with developmental processes involved in hydrocephalus and CIM.