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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...

Cerebral Edema ll: Pathophysiology

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...

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...

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...

Increased Intracranial Pressure ll: Pathophysiology

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...

Vascular Spasm

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...

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Related Experiment Video

Updated: May 13, 2026

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

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Published on: June 18, 2021

Circulating soluble RAGE increase after a cerebrovascular event.

Teresita Menini, Hisato Ikeda, Satoshi Kimura

Clinical Chemistry and Laboratory Medicine

|March 16, 2013

Summary

This summary is machine-generated.

Serum levels of soluble receptor for AGE (sRAGE) increase following ischemic and hemorrhagic stroke. These changes in sRAGE correlate with patient recovery, suggesting potential as biomarkers.

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Last Updated: May 13, 2026

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

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Published on: June 18, 2021

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Published on: May 22, 2019

Area of Science:

Neuroscience
Biochemistry

Background:

The receptor for AGE (RAGE) plays a crucial role in cerebral ischemia.
Elevated high mobility group box 1 protein (HMGB1), a RAGE ligand, is observed in stroke patients.
This study investigates the role of soluble RAGE (sRAGE) in stroke pathophysiology.

Purpose of the Study:

To determine if serum levels of soluble RAGE (sRAGE) increase after ischemic and hemorrhagic stroke.
To assess the correlation between sRAGE levels and patient recovery.
To evaluate sRAGE as a potential biomarker for stroke prognosis.

Main Methods:

A longitudinal study was conducted on 15 patients with ischemic and hemorrhagic stroke.
Serum sRAGE levels were measured using an enzyme-linked immunosorbent assay (ELISA).
Measurements were taken at admission and longitudinally over several weeks.

Main Results:

Initial serum sRAGE levels did not differ significantly between stroke patients and healthy controls.
Following stroke, serum sRAGE levels significantly increased (26-296%, p>0.001).
sRAGE level changes mirrored patient recovery, with parallel increases during recovery and decreases upon recurrence or aggravation.

Conclusions:

Circulating sRAGE levels demonstrably increase after both ischemic and hemorrhagic stroke.
sRAGE shows potential as a biomarker for monitoring stroke progression and patient outcomes.
Further research with larger cohorts is warranted to explore the prognostic value of sRAGE.