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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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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...
68
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

52
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...
52
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

39
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...
39
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

34
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...
34
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

31
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...
31
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

31
Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous...
31

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Related Experiment Video

Updated: May 5, 2026

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
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Brain Swelling versus Infarct Size: A Problematizing Review.

J Marc Simard1,2,3, Bradley Wilhelmy1, Natalya Tsymbalyuk1

  • 1Department of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Brain Sciences
|March 28, 2024
PubMed
Summary
This summary is machine-generated.

Brain swelling after stroke is a key predictor of outcomes, but current treatments are limited. New research focuses on mechanisms independent of infarct size, offering hope for better therapies for brain swelling.

Keywords:
SUR1-TRPM4brain edemabrain swellingcerebral ischemiamiddle cerebral artery occlusionreviewstroke

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Brain Infarct Segmentation and Registration on MRI or CT for Lesion-symptom Mapping
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Measuring Post-Stroke Cerebral Edema, Infarct Zone and Blood-Brain Barrier Breakdown in a Single Set of Rodent Brain Samples
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Area of Science:

  • Neuroscience
  • Neurology
  • Pathology

Background:

  • Brain swelling is a critical factor influencing neurological outcomes and mortality in human stroke patients.
  • Existing treatments for brain swelling are scarce due to a limited understanding of its underlying mechanisms.
  • Preclinical stroke research has primarily focused on reducing infarct size, with limited translational value for managing post-stroke brain swelling.

Purpose of the Study:

  • To highlight brain swelling as a distinct pathological entity in stroke, separate from infarct size.
  • To review novel approaches for studying brain swelling mechanisms independent of infarct size reduction.
  • To identify potential therapeutic targets for treating post-ischemic brain swelling.

Main Methods:

  • Review of existing literature on cerebroprotection in stroke models.
  • Analysis of studies focusing on brain swelling mechanisms distinct from infarct size.
  • Evaluation of translational relevance of novel research approaches.

Main Results:

  • Brain swelling in humans often manifests days after infarct size stabilization, necessitating treatments independent of infarct size reduction.
  • Brain edema and swelling are distinct pathological processes with unique molecular and cellular drivers.
  • Advances in research methodologies allow for the study of brain swelling independent of infarct size.

Conclusions:

  • Targeting mechanisms of brain swelling independent of infarct size is crucial for developing effective stroke treatments.
  • Understanding brain swelling as a distinct pathological entity opens new avenues for therapeutic intervention.
  • Novel approaches reviewed offer significant translational potential for managing post-ischemic brain swelling.