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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...

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...

Atomic Nuclei: Types of Nuclear Relaxation

Atomic Nuclei: Types of Nuclear Relaxation

Nuclear relaxation restores the equilibrium population imbalance and can occur via spin–lattice or spin–spin mechanisms, which are first-order exponential decay processes.
In spin–lattice or longitudinal relaxation, the excited spins exchange energy with the surrounding lattice as they return to the lower energy level. Among several mechanisms that contribute to spin–lattice relaxation, magnetic dipolar interactions are significant. Here, the excited nucleus transfers energy to a nearby...

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.

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Related Experiment Video

Updated: May 22, 2026

A Magnetic Resonance Imaging Protocol for Stroke Onset Time Estimation in Permanent Cerebral Ischemia

A Magnetic Resonance Imaging Protocol for Stroke Onset Time Estimation in Permanent Cerebral Ischemia

Published on: September 16, 2017

Changes in T2 relaxation time after stroke reflect clearing processes.

Daniel-Christoph Wagner¹, Alexander Deten, Wolfgang Härtig

¹Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany. daniel-christoph.wagner@izi.fraunhofer.de

|April 27, 2012

Summary

This summary is machine-generated.

The imaging "fogging phenomenon" after ischemic stroke in rats reflects necrotic tissue clearance, not lesion volume changes. This finding is crucial for accurate stroke assessment using MRI and CT scans.

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Published on: September 25, 2019

Area of Science:

Neuroscience
Medical Imaging
Pathophysiology

Background:

Computed tomography (CT) and magnetic resonance (MR) imaging are vital for diagnosing and monitoring ischemic stroke.
A transient pseudo-normalized signal, known as the fogging phenomenon, is observed in both imaging methods post-stroke.

Purpose of the Study:

To investigate the pathophysiological changes linked to the fogging phenomenon.
To assess the impact of fogging on accurately determining ischemic lesion volume in a rat stroke model.

Main Methods:

Male spontaneously hypertensive rats underwent permanent middle cerebral artery occlusion.
T2-weighted MR sequences were used to measure ischemic lesion volume, brain edema, and signal changes at multiple time points.
Immunohistochemistry was employed to evaluate astrogliosis, microglia/macrophage infiltration, and angiogenesis.

Main Results:

MR fogging was observed in all rats at days 4, 8, and 11 post-stroke.
The T2 signal normalization during fogging was independent of infarct volume development.
Fogging coincided with necrosis, angiogenesis, and microglia/macrophage infiltration within the lesion.

Conclusions:

The fogging effect in ischemic stroke imaging is associated with the clearance of necrotic tissue.
Fogging does not influence the accurate determination of the ischemic lesion volume.
Understanding fogging is essential for precise stroke lesion assessment.