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Related Concept Videos

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...
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.
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...
Inflammation01:38

Inflammation

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Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

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Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
12:14

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Published on: February 12, 2016

Ischaemic stroke: a thrombo-inflammatory disease?

Bernhard Nieswandt1, Christoph Kleinschnitz, Guido Stoll

  • 1University Hospital Würzburg, Rudolf Virchow Centre, DFG Research Centre for Experimental Biomedicine, Josef-Schneider-Strasse 2, 97080 Würzburg, Germany. bernhard.nieswandt@virchow.uni-wuerzburg.de

The Journal of Physiology
|July 20, 2011
PubMed
Summary

Platelet activation via specific receptors, not aggregation, drives progressive ischemic stroke. This highlights a novel thrombo-inflammatory cascade crucial for infarct growth after reperfusion injury.

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Area of Science:

  • Neuroscience
  • Hematology
  • Pathology

Background:

  • Ischemic stroke is a major global health issue with limited treatment options.
  • Progressive stroke can occur despite reperfusion, termed 'reperfusion injury'.
  • The role of platelets and coagulation in stroke progression was unclear.

Purpose of the Study:

  • To elucidate the specific mechanisms of platelet involvement in ischemic stroke progression.
  • To investigate the contribution of platelet adhesion and coagulation pathways to infarct maturation.
  • To understand the 'thrombo-inflammatory' cascade in acute stroke.

Main Methods:

  • Utilized the mouse model of transient middle cerebral artery occlusion (tMCAO).
  • Investigated platelet adhesion/activation via von Willebrand factor (vWF) receptor glycoprotein (GP) Ib, vWF, and collagen receptor GPVI.
  • Examined the role of platelet aggregation through GPIIb/IIIa.
  • Assessed the involvement of coagulation factor XII (FXII)-driven processes.

Main Results:

  • Early platelet adhesion/activation via GP Ib/vWF and GPVI are critical in infarct development.
  • Platelet aggregation via GPIIb/IIIa does not significantly contribute to infarct maturation.
  • FXII-driven coagulation pathways and platelet activation form a 'thrombo-inflammatory' cascade.
  • This cascade drives infarct growth following transient middle cerebral artery occlusion.

Conclusions:

  • Specific platelet adhesion pathways, not aggregation, are key drivers of ischemic stroke progression.
  • A thrombo-inflammatory cascade involving platelets and coagulation contributes to infarct expansion.
  • These findings offer potential therapeutic targets for managing progressive stroke and reperfusion injury.