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...
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...

You might also read

Related Articles

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

Sort by
Same author

Mechanisms and impact of long COVID: pathophysiology, neuropsychiatric effects and vaccination.

Frontiers in immunology·2026
Same author

GIP contributes to postprandial regulation of splanchnic blood supply in humans with type 2 diabetes: a randomised, single-blinded, placebo-controlled, crossover study.

Diabetologia·2026
Same author

Reproducibility of Splanchnic Blood Flow Measured Using Phase-Contrast MRI.

NMR in biomedicine·2026
Same author

Pitaya‑inspired compartmentalized microspheres with natural tannic acid-copper coating orchestrate smart release of ions and multi-drugs for synergistic treatment of infected bone defects.

Regenerative biomaterials·2026
Same author

Cerebral physiology following general anaesthesia with sevoflurane or propofol in healthy volunteers - a randomised, single-blind cross-over trial.

Journal of applied physiology (Bethesda, Md. : 1985)·2026
Same author

Study on the Mechanism of Hearing Loss Induced by USH2A Gene Knockout.

Human mutation·2026
Same journal

Brain barriers as checkpoints in endocrine regulation of body homeostasis.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2026
Same journal

Ferroptosis of microvascular pericytes contributes to ischemia-reperfusion injury in mice.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2026
Same journal

EXPRESS: Post-Ischemic Sodium Glucose Cotransporter Inhibition Attenuates Ischemia-Reperfusion Injury via Regulation of Mitochondrial Membrane Potential.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2026
Same journal

EXPRESS: Glymphatic System Dysfunction and Neurological Disorders: From Mechanisms to Therapeutic Strategies.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2026
Same journal

EXPRESS: Toll Like Receptor 4 (TLR4) in Neuroinflammation: From Acute Hemorrhagic Stroke to Chronic Neurodegeneration.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2026
Same journal

EXPRESS: Ventricular CSF-to-blood water transport kinetics in adult hydrocephalus.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2026
See all related articles

Related Experiment Video

Updated: Jul 2, 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

10.4K

Vascular permeability in cerebral cavernous malformations.

Abdul G Mikati1, Omaditya Khanna1, Lingjiao Zhang1

  • 1Neurovascular Surgery Program, Section of Neurosurgery, Department of Surgery, The University of Chicago Medicine and Biological Sciences, Chicago, Illinois, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|May 14, 2015
PubMed
Summary
This summary is machine-generated.

Familial cerebral cavernous malformations (CCMs) show increased brain vascular hyperpermeability. This finding in human subjects suggests brain permeability may indicate disease activity and guide therapy.

More Related Videos

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
05:12

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

Published on: September 4, 2017

11.4K
A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
08:12

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage

Published on: July 28, 2018

8.5K

Related Experiment Videos

Last Updated: Jul 2, 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

10.4K
Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
05:12

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

Published on: September 4, 2017

11.4K
A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
08:12

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage

Published on: July 28, 2018

8.5K

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Genetics

Background:

  • Familial cerebral cavernous malformations (CCMs) result from genetic mutations (CCM1, CCM2, CCM3), leading to protein haploinsufficiency.
  • Loss of CCM proteins elevates RhoA kinase-mediated endothelial permeability in vitro and in mouse models.
  • Previous research predicted increased vascular permeability in human familial CCM.

Purpose of the Study:

  • To investigate vascular hyperpermeability in the brains of human subjects with familial CCM.
  • To compare permeability between familial CCM, sporadic CCM, and control groups.
  • To assess the correlation between vascular permeability and CCM disease activity.

Main Methods:

  • A prospective, case-controlled observational study.
  • Dynamic contrast-enhanced quantitative perfusion magnetic resonance imaging (MRI) was used to measure brain vascular permeability.
  • Permeability was assessed in white matter far (WMF) from lesions and within CCM lesions.

Main Results:

  • Significantly greater WMF permeability was observed in familial CCM patients compared to sporadic CCM cases.
  • CCM lesion permeability was similar between familial and sporadic cases.
  • WMF permeability increased with age in sporadic patients but not in familial cases.
  • More aggressive familial CCM disease correlated with higher WMF permeability, unlike lesion permeability.
  • Statins showed a trend towards reducing WMF permeability.

Conclusions:

  • This study provides the first human evidence of brain vascular hyperpermeability in autosomal dominant CCM disease.
  • Brain vascular permeability, particularly in WMF, may serve as a biomarker for CCM disease activity.
  • Measuring brain permeability could aid in calibrating potential therapeutic interventions for CCM.