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Hemorrhagic Stroke ll: Pathophysiology

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 ll: Pathophysiology

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: Introduction

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: Introduction

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...

Clot Retraction and Fibrinolysis

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.

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Updated: Jul 7, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

Fibrinogen gamma' in ischemic stroke: a case-control study.

Elim Y L Cheung, Shirley Uitte de Willige, Hans L Vos

|February 2, 2008

Summary

The fibrinogen gamma'/total fibrinogen ratio is linked to ischemic stroke, particularly during the acute phase. The FGG-H3 haplotype may offer protection against developing ischemic stroke.

Related Experiment Videos

Last Updated: Jul 7, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

Area of Science:

Biochemistry
Genetics
Neurology

Background:

Fibrinogen is a key protein in blood coagulation.
Alterations in fibrinogen structure and levels may influence thrombotic events.
Fibrinogen gamma' chain and its genetic variations (haplotypes) are implicated in various diseases.

Purpose of the Study:

To investigate the association between fibrinogen gamma' levels, the fibrinogen gamma'/total fibrinogen ratio, and FGG haplotypes with ischemic stroke risk.
To explore the role of these factors in different phases of ischemic stroke.

Main Methods:

Case-control study involving 124 ischemic stroke patients and 125 controls.
Measurement of fibrinogen gamma' levels and fibrinogen gamma'/total fibrinogen ratio.
Analysis of FGG haplotypes using genetic association methods.

Main Results:

The fibrinogen gamma'/total fibrinogen ratio was elevated in the acute phase of stroke and reduced in the convalescent phase (3 months post-stroke).
FGG haplotype 3 (H3) showed a significant association with reduced ischemic stroke risk (OR 0.60; 95% CI, 0.38-0.94).
FGG-H2 was linked to a decreased fibrinogen gamma'/total fibrinogen ratio but not directly to stroke risk.

Conclusions:

The fibrinogen gamma'/total fibrinogen ratio is a potential biomarker for ischemic stroke, especially in the acute phase.
The FGG-H3 haplotype may confer a protective effect against ischemic stroke.
Further research is warranted to elucidate the precise mechanisms linking fibrinogen gamma' and FGG haplotypes to stroke pathophysiology.