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

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...
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 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...
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...
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...
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

The CSDH Grading Scheme for Middle Meningeal Artery Embolization: Stratified Risk of Surgical Rescue.

Neurosurgery·2026
Same author

Turnover Time in Neuroangiography Suites: Comparison Between Cases Performed at an Ambulatory Neurosurgery Center Versus a Tertiary Hospital.

Stroke (Hoboken, N.J.)·2026
Same author

Thrombectomy in Posterior Circulation Tandem Occlusions: Multicenter Comparative Analysis of Procedural Techniques and Predictors of Clinical Outcomes.

Radiology·2026
Same author

Stereotactic radiosurgery and dural arteriovenous fistulas: three decades of experience at the University of Pittsburgh.

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia·2026
Same author

Decreased Risk of Severe Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage in the Era of Intravenous Milrinone.

World neurosurgery·2026
Same author

Carotid Revascularization Protocol for Symptomatic Stenosis.

Seminars in neurology·2026

Related Experiment Video

Updated: May 11, 2026

Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations
14:58

Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations

Published on: October 20, 2017

Hydrocephalus after arteriovenous malformation rupture.

Bradley A Gross1, Pui Man Rosalind Lai, Rose Du

  • 1Department of Neurological Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.

Neurosurgical Focus
|May 3, 2013
PubMed
Summary

Ruptured arteriovenous malformations (AVMs) requiring external ventricular drains (EVDs) or permanent shunts were linked to lower initial Glasgow Coma Scale scores, intraventricular hemorrhage, and AVM-associated aneurysms.

More Related Videos

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

Related Experiment Videos

Last Updated: May 11, 2026

Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations
14:58

Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations

Published on: October 20, 2017

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

Area of Science:

  • Neurosurgery
  • Neurology
  • Radiology

Background:

  • Ruptured arteriovenous malformations (AVMs) can lead to hydrocephalus, necessitating interventions like external ventricular drains (EVDs) and permanent shunts.
  • The specific rates and risk factors for these interventions in AVM rupture patients are not well-established.

Purpose of the Study:

  • To determine the incidence of EVD placement and long-term shunt dependence in patients with ruptured AVMs.
  • To identify risk factors associated with the need for EVD placement and permanent shunting following AVM rupture.

Main Methods:

  • Retrospective review of 87 consecutive patients with ruptured AVMs.
  • Analysis of patient demographics, hemorrhage patterns, AVM features, and surgical treatments.
  • Univariate and multivariate logistic regression to identify risk factors for EVD placement and shunt dependence.

Main Results:

  • 44% of patients required EVD placement, and 18% needed a permanent shunt.
  • Univariate analysis identified initial Glasgow Coma Scale (GCS) score, intraventricular hemorrhage (IVH), AVM-associated aneurysms, and early surgery as risk factors for EVD placement.
  • Multivariate analysis indicated AVM-associated aneurysms as a significant risk factor for EVD placement. Initial GCS score and IVH were significant risk factors for shunt placement.

Conclusions:

  • Hydrocephalus following AVM rupture is associated with initial GCS score, IVH, and AVM-associated aneurysms.
  • AVMs with associated aneurysms present a higher risk of hemorrhage and subsequent hydrocephalus-related morbidity.