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Related Concept Videos

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...
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...
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...
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...

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Related Experiment Video

Updated: May 28, 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

Bleeding source identification and treatment in brain arteriovenous malformations.

N Mjoli1, D Le Feuvre, A Taylor

  • 1Department Neurosurgery, University of Cape Town, Cape Town, South Africa.

Interventional Neuroradiology : Journal of Peritherapeutic Neuroradiology, Surgical Procedures and Related Neurosciences
|October 19, 2011
PubMed
Summary

Identifying bleeding sources in brain arteriovenous malformation (AVM) patients presenting with hemorrhage is crucial. Targeted endovascular treatment of these weak points, often intranidal aneurysms, can potentially reduce re-bleeding rates.

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Endovascular Perforation Model for Subarachnoid Hemorrhage Combined with Magnetic Resonance Imaging (MRI)
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Endovascular Perforation Model for Subarachnoid Hemorrhage Combined with Magnetic Resonance Imaging (MRI)

Published on: December 16, 2021

Area of Science:

  • Neurology
  • Interventional Radiology
  • Neurosurgery

Background:

  • Intracerebral hemorrhage in patients with brain arteriovenous malformation (AVM) can be life-threatening.
  • Identifying the specific bleeding source is critical for effective treatment and reducing re-bleed risk.
  • Previous research suggests eliminating weak points in AVMs may lower re-hemorrhage rates.

Purpose of the Study:

  • To determine the frequency and types of identifiable bleeding sources in patients with ruptured brain AVM.
  • To assess the correlation between hemorrhage location and the identified bleeding source.
  • To evaluate the efficacy and safety of targeted endovascular embolization for these sources.

Main Methods:

  • Retrospective cohort study of patients with bled brain AVM over a six-year period.
  • Correlation of CT/MRI hematoma location with digital subtraction angiography (DSA) findings to identify bleeding sources.
  • Review of neuroendovascular treatment notes for targeted embolization procedures.

Main Results:

  • Hemorrhage source identified in 18 of 41 (43.9%) patients presenting with bled AVM.
  • Intranidal false aneurysms were the most common source (11/18), followed by flow-related aneurysms (5/18).
  • Successful targeted embolization achieved in 90% of cases with a 9% complication rate, and a low annual hemorrhage rate of 0.7% during follow-up.

Conclusions:

  • A significant proportion of ruptured brain AVMs have an identifiable bleeding source on DSA, frequently an intranidal false aneurysm.
  • Targeted endovascular embolization of these vascular weak points is effective and safe.
  • Eliminating these sources may reduce the risk of future hemorrhages in AVM patients.