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Transient Ischemic Attack l: Introduction

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...

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 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...

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.

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...

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Updated: Jul 8, 2026

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

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Published on: August 18, 2015

Persistent hyperfibrinogenemia in acute ischemic stroke / transient ischemic attack (TIA).

Shani Shenhar-Tsarfaty¹, Einor Ben Assayag, Irena Bova

¹Department of Neurology, Tel Aviv Sourasky Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Thrombosis and Haemostasis

|January 25, 2008

Summary

Persistent hyperfibrinogenemia is common after acute ischemic stroke. This elevated fibrinogen (a blood clotting protein) remains consistently high, suggesting long-term management is crucial for stroke patients.

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Area of Science:

Neurology
Hematology
Cardiovascular Medicine

Background:

Elevated fibrinogen is a known response to acute ischemic stroke.
The long-term behavior of this hyperfibrinogenemia remains unclear.
Atherothrombo-inflammation may underlie persistent hyperfibrinogenemia in stroke patients.

Purpose of the Study:

To determine if hyperfibrinogenemia following acute ischemic stroke is transient or persistent.
To investigate the time course of fibrinogen concentration in stroke patients.
To assess the role of atherothrombo-inflammation in stroke-related hyperfibrinogenemia.

Main Methods:

Fibrinogen levels were measured in stroke patients on admission and at 12 months post-event.
A control group was included for comparison.
Analysis of variance (ANOVA) was used to compare fibrinogen concentrations across different time points and groups.

Main Results:

Stroke patients exhibited significantly higher fibrinogen concentrations on admission compared to controls (p < 0.001).
Fibrinogen levels were already elevated early after stroke onset and did not significantly change over time (p = 0.268).
The increase in fibrinogen concentration over time was minimal in stroke patients compared to controls.

Conclusions:

Persistent hyperfibrinogenemia is a characteristic feature of acute ischemic stroke.
Elevated fibrinogen levels may be present from the early stages of the disease.
Long-term interventions targeting fibrinogen reduction may be beneficial for stroke patients.