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...
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...
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...
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...
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...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...

You might also read

Related Articles

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

Sort by
Same author

Underweight is associated with increased risk of all-cause dementia in older adults with vascular risk factors, independent of brain atrophy and small vessel disease.

Journal of Alzheimer's disease : JAD·2026
Same author

Remote Ischemic Conditioning for Acute Ischemic Stroke: The RICAIS Randomized Clinical Trial.

Journal of atherosclerosis and thrombosis·2026
Same author

[Brain Dock for Maintaining Activities of Daily Living in the Elderly].

Brain and nerve = Shinkei kenkyu no shinpo·2026
Same author

Catheter Ablation and Oral Anticoagulation for Secondary Stroke Prevention in Atrial Fibrillation: The STABLED Randomized Clinical Trial.

JAMA neurology·2026
Same author

Viral load and pathophysiology-based framework in varicella-zoster virus meningitis: Focus on altered consciousness and outcomes.

Journal of the neurological sciences·2026
Same author

The Japanese Society of Hypertension Guidelines for blood pressure control using digital technologies.

Hypertension research : official journal of the Japanese Society of Hypertension·2026

Related Experiment Video

Updated: Jun 19, 2026

Protocol for Isolating the Mouse Circle of Willis
06:30

Protocol for Isolating the Mouse Circle of Willis

Published on: October 22, 2016

[Cerebral vessel disease and inflammatory process].

Kazuo Kitagawa1

  • 1Department of Neurology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka 565-0871, Japan.

Brain and Nerve = Shinkei Kenkyu No Shinpo
|October 7, 2009
PubMed
Summary
This summary is machine-generated.

Inflammation drives atherosclerosis, increasing risks for heart attack and stroke. Targeting inflammation may prevent cerebral infarction.

More Related Videos

A Visual Approach for Inducing Dolichoectasia in Mice to Model Large Vessel-Mediated Cerebrovascular Dysfunction
04:29

A Visual Approach for Inducing Dolichoectasia in Mice to Model Large Vessel-Mediated Cerebrovascular Dysfunction

Published on: May 17, 2024

Related Experiment Videos

Last Updated: Jun 19, 2026

Protocol for Isolating the Mouse Circle of Willis
06:30

Protocol for Isolating the Mouse Circle of Willis

Published on: October 22, 2016

A Visual Approach for Inducing Dolichoectasia in Mice to Model Large Vessel-Mediated Cerebrovascular Dysfunction
04:29

A Visual Approach for Inducing Dolichoectasia in Mice to Model Large Vessel-Mediated Cerebrovascular Dysfunction

Published on: May 17, 2024

Area of Science:

  • Cardiovascular Science
  • Neuroscience
  • Immunology

Context:

  • Atherosclerosis, characterized by atheromatous plaque, is a significant risk factor for cerebrovascular events.
  • Inflammation is a key driver in the development, progression, and rupture of atherosclerotic plaques.
  • Blood inflammatory markers, like high-sensitivity C-reactive protein (hs-CRP), are linked to myocardial and cerebral infarction.

Purpose:

  • To explore the role of inflammation in atheromatous plaque development and cerebrovascular disease.
  • To investigate the association between blood inflammatory markers, carotid plaque characteristics, and cerebral small vessel disease.
  • To evaluate the potential of anti-inflammatory therapies for cerebral infarction prevention.

Summary:

  • Inflammation is central to atheromatous plaque pathogenesis, influencing its progression and rupture.
  • Elevated blood inflammatory markers, including hs-CRP, correlate with increased risk of myocardial infarction and cerebral infarction.
  • Inflammatory cells within carotid plaques express various pro-inflammatory mediators, impacting plaque stability and echogenicity.
  • Blood inflammatory marker levels are associated with carotid plaque progression, echogenicity, and the severity of intracranial arterial diseases, including silent infarction and white matter lesions.

Impact:

  • Understanding inflammation's role in atherosclerosis can lead to novel diagnostic markers for stroke risk.
  • Identifying inflammatory pathways involved in plaque rupture offers targets for therapeutic interventions.
  • Anti-inflammatory strategies hold promise for both primary and secondary prevention of cerebral infarction, potentially reducing stroke burden.