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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...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Regulation of Stroke Volume01:27

Regulation of Stroke Volume

The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...

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Using Zebrafish Larvae to Study the Pathological Consequences of Hemorrhagic Stroke
06:36

Using Zebrafish Larvae to Study the Pathological Consequences of Hemorrhagic Stroke

Published on: June 5, 2019

Combinatorial interaction between CCM pathway genes precipitates hemorrhagic stroke.

Aniket V Gore1, Maria Grazia Lampugnani, Louis Dye

  • 1Laboratory of Molecular Genetics, Program in Genomics of Development, National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892, USA.

Disease Models & Mechanisms
|December 19, 2008
PubMed
Summary

Minor genetic deficits in cerebral cavernous malformation (CCM) pathway genes can synergize to cause intracranial hemorrhage (ICH). This study reveals rap1b

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Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
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Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

Published on: September 4, 2017

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Last Updated: Jun 27, 2026

Using Zebrafish Larvae to Study the Pathological Consequences of Hemorrhagic Stroke
06:36

Using Zebrafish Larvae to Study the Pathological Consequences of Hemorrhagic Stroke

Published on: June 5, 2019

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
05:12

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

Published on: September 4, 2017

Area of Science:

  • Genetics
  • Neurology
  • Vascular Biology

Background:

  • Intracranial hemorrhage (ICH) is a severe stroke with poorly understood causes.
  • Mutations in three CCM genes cause autosomal dominant genetic ICH, leading to cerebral cavernous malformations (CCM).
  • Interactions between CCM proteins and endothelial junction regulators suggest roles in ICH variability.

Purpose of the Study:

  • To investigate if minor genetic deficits in CCM pathway genes can initiate ICH.
  • To test the hypothesis that combined deficits in CCM and interacting proteins explain ICH variability.

Main Methods:

  • Combined knockdown of CCM pathway genes in zebrafish.
  • Assessed the role of rap1b, a Ras GTPase effector protein for CCM1/Krit1, in endothelial junctions.
  • Evaluated the incidence of ICH following combined gene function reduction.

Main Results:

  • Rap1b knockdown disrupts endothelial junctions in vivo and in vitro, confirming its role in the CCM pathway.
  • Minor reductions in Rap1b combined with reduced products of other CCM pathway genes led to a high incidence of ICH.
  • Demonstrated synergistic effects of minor polygenic deficits in initiating ICH.

Conclusions:

  • Supports the hypothesis that combined minor genetic deficits in the CCM pathway can initiate ICH.
  • Highlights the potential for polygenic interactions to explain ICH variability and penetrance.
  • Identifies rap1b as a crucial player in the CCM pathway and ICH development.