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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...

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...

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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Related Experiment Video

Updated: May 10, 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

Microglia and ischemic stroke: a double-edged sword.

Anita R Patel¹, Rodney Ritzel, Louise D McCullough

¹Department of Neuroscience, University of Connecticut Health Center Farmington, Connecticut 06030.

International Journal of Physiology, Pathophysiology and Pharmacology

|June 11, 2013

Summary

This summary is machine-generated.

Microglia, the brain's immune cells, become activated during ischemic stroke, influencing injury or repair. Understanding their diverse roles is key to developing new stroke therapies targeting neuroinflammation.

Keywords:

CD45 chimera inflammatory response ischemic stroke macrophage microglia

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Last Updated: May 10, 2026

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

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Published on: June 20, 2025

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Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury

Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury

Published on: September 4, 2013

Area of Science:

Neuroscience
Immunology
Pathophysiology

Background:

Inflammatory processes are central to stroke pathophysiology.
Microglia, resident immune cells in the brain, are rapidly activated after ischemic stroke.
Microglial activation is normally regulated by neuronal-glial communication but is disrupted by stroke.

Purpose of the Study:

To investigate the role of microglia in ischemic stroke.
To explore therapeutic strategies targeting microglial activation.
To understand the mechanisms regulating microglial phenotypes and functions.

Main Methods:

Analysis of inflammatory signaling pathways in stroke models.
Identification of ligands and receptors involved in microglial activation.
Development of experimental tools to detect microglial inflammatory mediators.

Main Results:

Ischemic stroke triggers microglial activation by disabling endogenous inhibitory signals.
Activated microglia display diverse phenotypes, releasing both pro- and anti-inflammatory mediators.
Microglial function in stroke outcome (injury exacerbation or repair) depends on specific molecular signals received by their receptors.

Conclusions:

Microglia play a complex, dual role in ischemic stroke, potentially exacerbating injury or promoting repair.
Targeting microglial activation represents a promising therapeutic avenue for stroke.
Further research is needed to fine-tune immunomodulatory interventions based on the heterogeneous profiles of microglia for effective stroke treatment.