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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...

Secondary Spinal Cord Injury llI: Pathophysiology

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Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

Neurogenesis and Regeneration of Nervous Tissue

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In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...

Cytotoxic Edema: Pathophysiology

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Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...

Ischemic Stroke l: Introduction

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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.

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Related Experiment Video

Updated: Jul 7, 2026

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia

Published on: November 14, 2020

Neuroprotection and the ischemic cascade.

R A Felberg¹, W S Burgin, J C Grotta

¹Stroke Team, Department of Neurology, University of Texas-Houston Medical School, Houston, TX, USA.

|February 16, 2008

Summary

This summary is machine-generated.

Neuroprotection aims to halt delayed brain cell death after ischemia. While animal studies show promise, human trials need better strategies, possibly combining therapies.

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The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse

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Published on: July 25, 2011

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Last Updated: Jul 7, 2026

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia

Published on: November 14, 2020

The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse

The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse

Published on: July 25, 2011

Area of Science:

Neurology
Neuroscience
Cerebrovascular Medicine

Background:

Brain ischemia triggers a cascade of neuronal cell death, not immediate.
The ischemic cascade spreads from a core, offering a therapeutic window.
Salvaging the ischemic penumbra is a key goal in neuroprotection.

Purpose of the Study:

To review the principles and progress of neuroprotection in brain ischemia.
To evaluate the efficacy of various neuroprotective strategies in preclinical and clinical settings.
To propose future directions for effective neuroprotection therapies.

Main Methods:

Review of laboratory and clinical data on neuroprotective agents and hypothermia.
Analysis of animal stroke models investigating thrombolysis, calcium channel blockade, and receptor antagonism.
Examination of outcomes from human trials of neuroprotective therapies.

Main Results:

Hypothermia and various agents reduced infarct size in animal models.
Pharmacological interventions showed promise in animal cortical stroke models.
Human trials yielded disappointing results, with limited benefit beyond thrombolytics.

Conclusions:

Neuroprotection is based on the delayed nature of ischemic cell death.
Translating animal model success to human trials remains challenging.
Future neuroprotection may involve combination therapies with thrombolytics.