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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...

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...

Stroke: Introduction and Types

Stroke: Introduction and Types

A stroke is an acute neurological event caused by the sudden disruption of cerebral blood flow, leading to rapid loss of neuronal function. Neurons depend on continuous oxygen and glucose supply, so even brief interruptions can cause irreversible injury within minutes. Strokes are classified into ischemic and hemorrhagic types.Ischemic StrokeIschemic strokes are most common and occur due to arterial occlusion, depriving brain tissue of oxygen and nutrients. This leads to energy failure, ionic...

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Related Experiment Video

Updated: Jun 20, 2026

Photothrombotic Ischemia: A Minimally Invasive and Reproducible Photochemical Cortical Lesion Model for Mouse Stroke Studies

Photothrombotic Ischemia: A Minimally Invasive and Reproducible Photochemical Cortical Lesion Model for Mouse Stroke Studies

Published on: June 9, 2013

Histopathological changes in acute ischemic stroke.

Otilia Mărgăritescu¹, L Mogoantă, Ionica Pirici

¹Department of Neurosurgery, Emergency County Hospital, Craiova, Romania.

Romanian Journal of Morphology and Embryology = Revue Roumaine De Morphologie Et Embryologie

|August 20, 2009

Summary

This summary is machine-generated.

Histopathological changes in acute ischemic stroke reveal four evolving stages of brain injury. These stages detail neuronal damage, inflammation, and tissue repair over time, highlighting the heterogeneity of stroke pathology.

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Area of Science:

Neuropathology
Neuroscience
Stroke Research

Background:

Acute ischemic stroke causes significant brain damage.
Understanding the temporal evolution of these lesions is crucial for effective treatment.

Purpose of the Study:

To investigate the histopathological changes in acute ischemic stroke.
To classify the evolution of brain lesions into distinct stages.

Main Methods:

Analysis of brain tissue from 22 acute ischemic stroke cases.
Histopathological examination to identify cellular and tissue alterations.
Classification of lesions based on time from stroke onset to death (6 hours to 15 years).

Main Results:

Four distinct stages of brain lesion evolution were identified.
Stage 1 (1-2 days): Neuronal injury and spongiosis.
Stage 2 (3 days-53 years): Acute and chronic inflammation, coagulative necrosis, mononuclear infiltrate, astrogliosis, spongiosis, and neo-vascularization.
Stage 3 (26 days-23 years): Absence of inflammation, cavitation, astrogliosis, and macrophages.

Conclusions:

Brain injury in acute ischemic stroke is heterogeneous, involving all brain components.
The study establishes a chronological framework for the development and progression of ischemic stroke lesions.
Recognizing these stages aids in understanding stroke pathology and potential therapeutic targets.