Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
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

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...
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...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

ON COMPLEMENT-FIXATION IN MALIGNANT DISEASE.

The Journal of experimental medicine·2009
Same author

There is a limited critical period for dopamine's effects on D1 receptor expression in the developing rat neostriatum.

Brain research. Developmental brain research·1998
Same author

Agrin gene expression in ciliary ganglion neurons following preganglionic denervation and postganglionic axotomy.

Developmental biology·1995
Same author

Polymorphonuclear leukocyte behavior in a nonhuman primate focal ischemia model.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·1994
Same author

Computed tomography scanning findings associated with rapid expansion of abdominal aortic aneurysms.

Journal of vascular surgery·1994
Same author

Uptake of C5a by polymorphonuclear leukocytes (PMNs) after focal cerebral ischemia. I. Effect of tirilazad mesylate intervention on C5a uptake by PMNs.

Immunopharmacology·1994
Same journal

Retraction: In vivo NCL targeting affects breast cancer aggressiveness through miRNA regulation.

The Journal of experimental medicine·2026
Same journal

Intravesical mesothelin-based CAR T cells targeting MUC16 effectively control bladder cancer in preclinical models.

The Journal of experimental medicine·2026
Same journal

Flawed translation triggers oncogenic B-T cell communication.

The Journal of experimental medicine·2026
Same journal

Correction: LCK'ed in: Inborn errors of immunity in LCK reveal how TCR signaling is calibrated.

The Journal of experimental medicine·2026
Same journal

Mechanobiology of inflammation: Pulling the strings of innate immunity.

The Journal of experimental medicine·2026
Same journal

Bile acid retention in efferocytic macrophages shapes their inflammatory status during cholangitis.

The Journal of experimental medicine·2026
See all related articles

Related Experiment Video

Updated: Jun 19, 2026

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

EXPERIMENTAL HYDROCEPHALUS.

W S Thomas1

  • 1Department of Pathology of the Washington University Medical School, St. Louis.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary
This summary is machine-generated.

Experimental hydrocephalus in dogs, induced by injecting foreign substances like aleuronat into brain ventricles, causes inflammation and cerebrospinal fluid obstruction. This leads to ventricle dilation and increased intracranial pressure symptoms.

More Related Videos

Neuronavigation and Laparoscopy Guided Ventriculoperitoneal Shunt Insertion for the Treatment of Hydrocephalus
14:59

Neuronavigation and Laparoscopy Guided Ventriculoperitoneal Shunt Insertion for the Treatment of Hydrocephalus

Published on: October 14, 2022

Related Experiment Videos

Last Updated: Jun 19, 2026

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

Neuronavigation and Laparoscopy Guided Ventriculoperitoneal Shunt Insertion for the Treatment of Hydrocephalus
14:59

Neuronavigation and Laparoscopy Guided Ventriculoperitoneal Shunt Insertion for the Treatment of Hydrocephalus

Published on: October 14, 2022

Area of Science:

  • Neurology
  • Experimental Pathology

Background:

  • Internal hydrocephalus can be experimentally induced.
  • Aleuronat injection into ventricles causes acute and chronic inflammatory reactions.

Purpose of the Study:

  • To investigate the pathological changes and mechanisms of experimental internal hydrocephalus.
  • To identify the sites of cerebrospinal fluid outflow obstruction.

Main Methods:

  • Injection of aleuronat into ventricles of experimental animals.
  • Histological examination of brain tissue.
  • India ink injection to demonstrate cerebrospinal fluid pathway obstruction.

Main Results:

  • Aleuronat induced inflammatory responses, including cellular exudates and tissue proliferation.
  • Ventricle dilation occurred during the chronic stage, associated with obstruction.
  • India ink confirmed cerebrospinal fluid circulation blockage at various points.

Conclusions:

  • Experimental hydrocephalus involves inflammatory processes leading to cerebrospinal fluid outflow obstruction.
  • Obstruction can occur at multiple sites within the cerebrospinal fluid pathways.
  • This model provides insights into the pathogenesis of hydrocephalus and increased intracranial pressure.