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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.
Acute Coronary Syndrome IV: Interprofessional Care01:28

Acute Coronary Syndrome IV: Interprofessional Care

IntroductionThe management of Acute Coronary Syndrome (ACS) aims to minimize myocardial damage, preserve myocardial function, and prevent complications.Initial ManagementInpatient management involves continuous cardiac monitoring, preferably in an ICU, focusing on blood pressure, serum sodium, potassium, and creatinine levels, and urine output. Ongoing pharmacologic management is crucial for stabilizing the patient.Supplemental Oxygen: Administer supplemental oxygen if oxygen saturation is...
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...
Hemorrhagic Stroke l: Introduction01:17

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...
Transient Ischemic Attack l: Introduction01:26

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...

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Updated: Jul 19, 2026

Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
09:21

Optimized Management of Endovascular Treatment for Acute Ischemic Stroke

Published on: January 18, 2018

Evolving therapeutic approaches to treating acute ischemic stroke.

Jesse M Weinberger1

  • 1Mt. Sinai School of Medicine, One Gustave L. Levy Place, Box 1139, New York, NY 10029, United States. jesse.weinberger@mssm.edu

Journal of the Neurological Sciences
|September 29, 2006
PubMed
Summary

Acute ischemic stroke treatments are limited. This review explores neuroprotective strategies targeting excitotoxicity, free radicals, and apoptosis to improve outcomes beyond current recombinant tissue plasminogen activator (rt-PA) therapy.

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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
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Setting Up a Stroke Team Algorithm and Conducting Simulation-based Training in the Emergency Department - A Practical Guide
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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Area of Science:

  • Neuroscience
  • Neurology
  • Biomedical Research

Background:

  • Stroke is a leading cause of death and disability, with limited therapeutic options beyond recombinant tissue plasminogen activator (rt-PA).
  • The ischemic penumbra represents viable brain tissue at risk during stroke, offering a target for neuroprotective interventions.
  • Understanding mechanisms of neuronal death, including excitotoxicity, free radicals, and apoptosis, is crucial for developing new stroke therapies.

Purpose of the Study:

  • To review the causes and consequences of stroke.
  • To examine current and future neuroprotective treatment options for acute ischemic stroke.
  • To identify promising therapeutic targets for stroke neuroprotection.

Main Methods:

  • Review of existing literature on stroke pathophysiology and neuroprotection.
  • Analysis of mechanisms underlying neuronal death in ischemic stroke.
  • Evaluation of preclinical and clinical trial data for neuroprotective agents.

Main Results:

  • Recombinant tissue plasminogen activator (rt-PA) remains the sole approved thrombolytic therapy for acute ischemic stroke.
  • Many neuroprotective compounds effective in animal models have failed in human clinical trials.
  • The ischemic penumbra can be identified using MRI perfusion and diffusion imaging.

Conclusions:

  • Developing effective neuroprotective therapies for stroke remains a significant challenge.
  • Promising therapeutic avenues include targeting free radicals, modulating glutamatergic transmission, and stabilizing cell membranes.
  • Further research into stroke mechanisms and novel therapeutic targets is essential for improving patient outcomes.