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Related Concept Videos

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...
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...
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...

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Related Experiment Video

Updated: Jun 6, 2026

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
10:34

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

Early micro vascular changes after subarachnoid hemorrhage.

Fatima A Sehba1, Victor Friedrich

  • 1Department of Neurosurgery, Mount Sinai School of Medicine, New York, NY 10029, USA. fatima.sehba@mssm.edu

Acta Neurochirurgica. Supplement
|December 1, 2010
PubMed
Summary

Subarachnoid hemorrhage (SAH) causes early brain injury and delayed vasospasm. Early SAH affects cerebral microvasculature, explaining ischemia even without large vessel constriction.

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The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects
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The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects

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

Published on: July 28, 2018

Related Experiment Videos

Last Updated: Jun 6, 2026

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
10:34

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects
09:00

The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects

Published on: October 2, 2014

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

Area of Science:

  • Neuroscience
  • Cerebrovascular Medicine
  • Pathophysiology

Background:

  • Subarachnoid hemorrhage (SAH) is linked to early ischemic injury and delayed vasospasm.
  • Early cerebral ischemia post-SAH is established, but the source remains unclear due to lack of early vasoconstriction evidence.

Purpose of the Study:

  • To summarize alterations in cerebral microvasculature within 48 hours after SAH.
  • To elucidate the role of microvasculature in early ischemic injury following SAH.

Main Methods:

  • Review of experimental SAH studies.
  • Analysis of human autopsy findings.
  • Examination of cerebral microvessel structure and function post-SAH.

Main Results:

  • Cerebral microvasculature is an early target of SAH.
  • Anatomical changes in microvessels occur early after experimental SAH.
  • These microvascular changes can cause functional deficits and explain cerebral ischemia.

Conclusions:

  • Microvascular alterations are key to early ischemic injury after SAH.
  • Changes in cerebral microvasculature may explain ischemia in the absence of large vessel vasoconstriction.
  • Understanding these early microvascular events is crucial for SAH pathogenesis.