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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...
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Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

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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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Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

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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...
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Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

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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...
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Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

1
Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component...
1
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

2
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...
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Related Experiment Video

Updated: Apr 20, 2026

In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
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Fatal cerebral malaria: a venous efflux problem.

Ute Frevert1, Adéla Nacer2

  • 1Division of Medical Parasitology, Department of Microbiology, New York University School of Medicine New York, NY, USA.

Frontiers in Cellular and Infection Microbiology
|November 22, 2014
PubMed
Summary

Severe intracranial hypertension (IH) causes fatal respiratory arrest in cerebral malaria (CM). This study models CM, revealing how parasite sequestration or leukocyte adhesion increases intracranial pressure, leading to brainstem herniation and death.

Keywords:
CD8+ T cellPlasmodiumbrain edemacytoadherenceintracranial hypertensionmacrophagepostcapillary venulevascular leakage

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Area of Science:

  • Pathology
  • Immunology
  • Neuroscience

Background:

  • Cerebral malaria (CM) in children often results in fatal respiratory arrest, with unclear underlying pathology.
  • Existing hypotheses for CM pathogenesis lack a unifying mechanism applicable to both human and experimental models.

Purpose of the Study:

  • To propose and validate a unifying model for CM pathogenesis centered on intracranial hypertension (IH).
  • To elucidate the mechanisms leading to fatal outcomes in experimental and human CM.

Main Methods:

  • Dynamic imaging of mice infected with Plasmodium berghei ANKA to model experimental CM.
  • Analysis of leukocyte adhesion in postcapillary venules (PCV) and its effect on venous blood flow.
  • Correlation of increased intracranial pressure (ICP) with cerebral edema formation.

Main Results:

  • Leukocyte adhesion in PCV was shown to impair venous blood flow, leading to increased ICP.
  • Increased ICP exacerbates cerebral edema, a key feature of both murine and pediatric CM.
  • The study proposes that cytoadherence in human CM and leukocyte arrest in murine CM converge on IH.

Conclusions:

  • A unified model of intracranial hypertension (IH) explains fatal respiratory arrest in cerebral malaria (CM).
  • This IH model reconciles distinct pathogenetic mechanisms in human and experimental CM.
  • The model provides a framework for understanding parasite-induced neuronal dysfunction and fatal outcomes in CM.