Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Cerebral Edema ll: Pathophysiology

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...

Hemorrhagic Stroke ll: Pathophysiology

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...

Ischemic Stroke ll: Pathophysiology

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...

Hemorrhagic Stroke l: Introduction

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...

Ischemic Stroke l: Introduction

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.

Transient Ischemic Attack l: Introduction

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

You might also read

Related Articles

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

Sort by

Same author

Vertebral artery hypoplasia and hemodynamic impairment in transient global amnesia: a case control study.

Frontiers in neurology·2024

Same author

<i>Lentzea sokolovensis</i> sp. nov., <i>Lentzea kristufekii</i> sp. nov. and <i>Lentzea miocenica</i> sp. nov., rare actinobacteria from Miocene lacustrine sediment of the Sokolov Coal Basin, Czech Republic.

International journal of systematic and evolutionary microbiology·2024

Same author

Orolingual Angioedema in Stroke Without r-tPA Treatment: Evidence for Insular and Opercular Contribution.

Stroke·2024

Same author

The structured ambulatory post-stroke care program for outpatient aftercare in patients with ischaemic stroke in Germany (SANO): an open-label, cluster-randomised controlled trial.

The Lancet. Neurology·2023

Same author

Visual Evoked Potentials in Acute Retinal Migraine.

JAMA neurology·2023

Same author

Autoimmune basal ganglia encephalitis with hemolytic anemia.

Annals of hematology·2022

Search research articles

Related Experiment Video

Updated: Apr 23, 2026

A Rat Model of Middle Cerebral Artery Occlusion/Reperfusion Without Damaging the Anatomical Structure of Cerebral Vessels

A Rat Model of Middle Cerebral Artery Occlusion/Reperfusion Without Damaging the Anatomical Structure of Cerebral Vessels

Published on: May 17, 2024

Facial angioedema and stroke.

Ralph Werner¹, Moritz Keller, Johannes C Woehrle

¹Department of Neurology/Stroke Unit, Katholisches Klinikum Koblenz-Montabaur, Koblenz, Germany.

Cerebrovascular Diseases (Basel, Switzerland)

|October 4, 2014

Summary

Recombinant tissue-type plasminogen activator (rtPA) significantly increases angioedema risk in stroke patients. Insular and peri-insular cortex involvement is key in stroke-related angioedema, even without rtPA.

Area of Science:

Neurology
Neuroscience
Vascular Neurology

Background:

Angioedema (AE) in stroke is primarily linked to recombinant tissue-type plasminogen activator (rtPA) treatment.
Previous research suggests a role for the insular cortex in AE development post-stroke.

Purpose of the Study:

To determine the incidence of AE in acute stroke patients.
To identify specific brain structures predominantly involved in AE development.

Main Methods:

Retrospective analysis of a stroke database for AE cases.
MRI data analysis involving image standardization and infarction superimposition.
Identification of overlapping areas to pinpoint regions of interest.

Main Results:

More Related Videos

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice

Published on: June 22, 2022

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

Published on: May 22, 2019

Related Experiment Videos

Last Updated: Apr 23, 2026

A Rat Model of Middle Cerebral Artery Occlusion/Reperfusion Without Damaging the Anatomical Structure of Cerebral Vessels

A Rat Model of Middle Cerebral Artery Occlusion/Reperfusion Without Damaging the Anatomical Structure of Cerebral Vessels

Published on: May 17, 2024

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice

Published on: June 22, 2022

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

Published on: May 22, 2019

2.3% of rtPA-treated stroke patients (20/865) developed AE; one case occurred without thrombolysis.
rtPA was a major risk factor (OR 93), with ACE-inhibitor treatment and diabetes also identified as risk factors.
AE was predominantly lateralized contralateral to the ischemic side (90%), with insular/peri-insular involvement in 81% of cases.

Conclusions:

Stroke-associated AE exhibits unique cerebral pathology, differing from AE in other conditions.
The insular and peri-insular cortex are critically involved in the pathophysiology of AE in stroke.
While rtPA is a major risk factor, AE can occur independently, suggesting complex underlying mechanisms.