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Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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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...
14
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

20
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...
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Vascular Spasm01:16

Vascular Spasm

4.8K
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last...
4.8K
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

16
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...
16
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

17
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...
17
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

44
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...
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Related Experiment Video

Updated: Apr 27, 2026

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

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Cerebral vasospasm.

Christopher D Baggott1, Beverley Aagaard-Kienitz2

  • 1Department of Neurological Surgery, University of Wisconsin Hospital and Clinics, 600 Highland Avenue, Madison, WI 53792, USA.

Neurosurgery Clinics of North America
|July 5, 2014
PubMed
Summary
This summary is machine-generated.

Cerebral vasospasm, a complication of aneurysmal subarachnoid hemorrhage, leads to delayed ischemic neurologic deficits. Understanding its complex mechanisms, diagnosis, and treatment is crucial for improving patient outcomes.

Keywords:
Cerebral vasospasmDelayed ischemic neurologic injuryNeurologic deficitsSubarachnoid hemorrhage

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Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
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Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound

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A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
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Last Updated: Apr 27, 2026

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
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Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
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A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
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Area of Science:

  • Neurology
  • Neurosurgery
  • Critical Care Medicine

Background:

  • Aneurysmal subarachnoid hemorrhage frequently leads to cerebral vasospasm.
  • Cerebral vasospasm is a major cause of delayed ischemic neurologic deficits, contributing to significant morbidity and mortality.
  • The pathophysiology of cerebral vasospasm is complex and not fully understood, involving multiple factors.

Purpose of the Study:

  • To provide a literature-guided perspective on cerebral vasospasm.
  • To examine the underlying mechanisms of cerebral vasospasm.
  • To review the diagnostic approaches and treatment strategies for cerebral vasospasm.

Main Methods:

  • Literature review and synthesis of existing research on cerebral vasospasm.
  • Analysis of factors contributing to delayed neurologic deterioration post-subarachnoid hemorrhage.
  • Examination of current diagnostic modalities and therapeutic interventions.

Main Results:

  • Cerebral vasospasm involves intricate mechanisms including large-vessel spasm, impaired autoregulation, inflammation, and genetic factors.
  • Delayed neurologic deterioration is multifactorial, with spreading cortical depolarization also implicated.
  • Established diagnostic tools and emerging treatments aim to mitigate vasospasm's effects.

Conclusions:

  • Cerebral vasospasm remains a critical challenge after subarachnoid hemorrhage.
  • A comprehensive understanding of its pathophysiology is essential for effective management.
  • Continued research into diagnosis and treatment is vital to reduce associated neurological deficits.