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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...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

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...
Stroke: Introduction and Types01:29

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...
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: May 21, 2026

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

Pathophysiologic cascades in ischemic stroke.

Changhong Xing1, Ken Arai, Eng H Lo

  • 1Department of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

International Journal of Stroke : Official Journal of the International Stroke Society
|June 21, 2012
PubMed
Summary
This summary is machine-generated.

Despite advances in understanding ischemic stroke mechanisms, effective neuroprotectants are still lacking. Future stroke drug development requires an integrative approach to address complex signaling pathways involved in neuronal death and inflammation.

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Area of Science:

  • Neuroscience
  • Pathophysiology
  • Pharmacology

Background:

  • Significant progress has been made in elucidating the molecular and cellular underpinnings of ischemic stroke.
  • However, the translation of this knowledge into clinically effective neuroprotective therapies has remained a significant challenge.

Purpose of the Study:

  • To review the fundamental ischemic cascades following stroke.
  • To highlight key mechanisms including neuronal death, white matter damage, and neuroinflammation, with a specific focus on microglia.
  • To discuss the difficulties in developing clinically viable stroke drugs from mechanistic insights.

Main Methods:

  • Literature review and synthesis of current research on ischemic stroke.
  • Focus on molecular and cellular mechanisms.
  • Emphasis on neuroinflammation and microglia.

Main Results:

  • Ischemic stroke involves complex cascades affecting neurons and white matter.
  • Microglia play a crucial role in the inflammatory response post-stroke.
  • Current neuroprotective strategies derived from mechanistic studies have shown limited clinical success.

Conclusions:

  • Developing effective neuroprotective drugs for ischemic stroke is challenging.
  • An integrative approach is necessary, considering the multimodal and multicellular signaling involved in stroke.
  • Future research should focus on holistic therapeutic strategies to improve clinical outcomes.