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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...

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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...

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Hemorrhagic Stroke l: Introduction

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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: Jun 27, 2026

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Inflammation as therapeutic objective in stroke.

Joaquín Jordán¹, Tomás Segura, David Brea

¹Grupo de Neurofarmacologia, Departamento de Ciencias Médicas, Facultad de Medicina, Universidad Castilla-La Mancha. Centro Regional de Investigaciones Biomédicas, Avda Almansa, 14, 02006-Albacete, Spain. Joaquin.jordan@uclm.es

Current Pharmaceutical Design

|December 17, 2008

Summary

Inflammation plays a key role in acute ischemic stroke, involving immune cells like microglia. Understanding these inflammatory pathways is crucial for developing effective stroke therapies.

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Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

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Last Updated: Jun 27, 2026

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

Area of Science:

Neuroscience
Immunology
Pathology

Background:

Ischemic stroke is a leading cause of neurological disability.
Inflammation is increasingly recognized as a significant factor in acute neurodegenerative disorders, including stroke.
Microglia and other glial cells are key initiators of the inflammatory response in the central nervous system (CNS) following ischemic events.

Purpose of the Study:

To review the cellular and molecular mechanisms of the inflammatory response in the CNS after ischemic stroke.
To elucidate the roles of innate immune cells, particularly microglia and macrophages, in processing and transmitting inflammatory signals.
To explore therapeutic strategies targeting neuroinflammation in acute stroke.

Main Methods:

Review of cellular and molecular pathways involved in stroke-induced inflammation.
Focus on the function of CNS innate immune cells (microglia, macrophages).
Analysis of adhesion molecules, inflammatory mediators (cytokines, chemokines, MMPs), transcription factors, and immune system modulation.

Main Results:

Activated microglia and macrophages are central to propagating inflammatory signals.
Expression of adhesion molecules (selectins, immunoglobulin superfamily, integrins) is relevant post-ischemia.
Inflammatory mediators like cytokines, chemokines, and matrix metalloproteinases are key players.

Conclusions:

While anti-inflammatory treatments show promise in animal models, clinical translation for acute stroke remains challenging.
Further research into cellular and molecular inflammatory pathways is essential for developing effective stroke therapies.
Understanding neuroinflammation is critical for advancing therapeutic interventions for ischemic stroke.