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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

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: Introduction01:15

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: Pathophysiology01:29

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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Related Experiment Video

Updated: Jun 1, 2026

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique
07:34

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique

Published on: December 15, 2023

Neuroprotection in acute ischemic stroke.

A Reza Noorian1, R Nogueira, R Gupta

  • 1Department of Neurology, Emory University School of Medicine, Marcus Stroke and Neuroscience Center, Grady Memorial Hospital, Atlanta, GA, USA.

Journal of Neurosurgical Sciences
|May 31, 2011
PubMed
Summary

Neuroprotective strategies for acute ischemic stroke aim to improve outcomes by extending treatment windows and protecting the brain post-reperfusion. Clinical trials need better patient selection and linkage to reperfusion for success.

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The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse
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The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse

Published on: July 25, 2011

Related Experiment Videos

Last Updated: Jun 1, 2026

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique
07:34

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique

Published on: December 15, 2023

The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse
08:27

The Application Of Permanent Middle Cerebral Artery Ligation in the Mouse

Published on: July 25, 2011

Area of Science:

  • Neurology
  • Cerebrovascular Diseases
  • Neuroprotection

Background:

  • Acute ischemic stroke is a leading cause of death and disability globally.
  • Reperfusion therapies improve outcomes but have limited time windows.
  • Neuroprotective strategies show promise in preclinical models but have failed in clinical trials.

Purpose of the Study:

  • To explore the potential of neuroprotective strategies in acute ischemic stroke.
  • To investigate methods for prolonging therapeutic time windows for reperfusion.
  • To identify reasons for the clinical failure of previous neuroprotection studies.

Main Methods:

  • Review of existing literature on acute ischemic stroke pathophysiology and treatment.
  • Analysis of factors contributing to the success or failure of neuroprotective agents.
  • Examination of patient selection criteria and timing in clinical trials.

Main Results:

  • Reperfusion treatments are effective but limited by time constraints.
  • Neuroprotective agents have not translated successfully to clinical benefit.
  • Clinical trial failures may stem from poor patient selection and trial design.

Conclusions:

  • Neuroprotection could extend reperfusion time windows, increasing patient eligibility.
  • Strategies to protect the brain post-reperfusion may prevent complications like edema and hemorrhage.
  • Future clinical success requires improved patient selection and integration with reperfusion therapies.