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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...
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...
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 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...
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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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Related Experiment Video

Updated: Jun 21, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

The complement cascade: new avenues in stroke therapy.

Ricardo J Komotar1, Robert M Starke, Eric J Arias

  • 1Department of Neurological Surgery, Columbia University, New York, NY 10011, USA. rjk2103@columbia.edu

Current Vascular Pharmacology
|July 16, 2009
PubMed
Summary
This summary is machine-generated.

Stroke reperfusion can cause inflammation-induced damage, potentially linked to the complement system. This review explores this secondary injury and identifies potential therapeutic targets for stroke treatment.

Related Experiment Videos

Last Updated: Jun 21, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

Area of Science:

  • Neuroscience
  • Immunology
  • Vascular Biology

Background:

  • Stroke patients often achieve reperfusion after initial occlusion.
  • Reperfusion may paradoxically exacerbate brain injury through inflammation.
  • The complement system is implicated in this secondary damage, but mechanisms are unclear.

Purpose of the Study:

  • To review the literature on reperfusion injury in stroke.
  • To elucidate the role of the complement system in stroke-related inflammation.
  • To identify potential clinical therapeutic targets for mitigating secondary stroke damage.

Main Methods:

  • Literature review of experimental and clinical studies.
  • Analysis of evidence linking complement activation to post-stroke inflammation.
  • Identification of therapeutic strategies targeting the complement cascade.

Main Results:

  • Reperfusion is common in stroke but can trigger significant inflammation.
  • The complement system plays a critical role in mediating this inflammation-induced secondary injury.
  • Specific complement components and pathways are associated with increased stroke pathology.

Conclusions:

  • Complement inhibition represents a promising therapeutic strategy for stroke.
  • Targeting the complement system could reduce inflammation and improve outcomes after reperfusion.
  • Further clinical investigation is warranted to validate complement-targeted therapies for stroke.