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Related Concept Videos

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...
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.
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...
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: May 24, 2026

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection
08:22

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection

Published on: July 21, 2013

Lenticulostriate infarction.

Pierre Decavel1, Fabrice Vuillier, Thierry Moulin

  • 1Service de Neurologie, CHU Besançon, Besançon, France.

Frontiers of Neurology and Neuroscience
|March 2, 2012
PubMed
Summary
This summary is machine-generated.

Lenticulostriate infarcts, caused by blockages in deep brain arteries, often stem from cardiac embolisms. Prognosis hinges on damage severity in the internal capsule, with these arteries being prone to necrosis.

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Last Updated: May 24, 2026

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Circumscribed Capsular Infarct Modeling Using a Photothrombotic Technique
08:25

Circumscribed Capsular Infarct Modeling Using a Photothrombotic Technique

Published on: June 2, 2016

Area of Science:

  • Neurology
  • Vascular Neurology
  • Cerebrovascular Disease

Background:

  • Lenticulostriate infarcts arise from ischemia in the middle cerebral artery's deep perforating branches.
  • These infarcts are frequently linked to internal carotid artery deep perforator branch infarctions.
  • Lenticulostriate arteries typically originate from the main middle cerebral artery trunk but can arise from cortical branches.

Purpose of the Study:

  • To differentiate the clinical presentation of lenticulostriate infarction from other anterior circulation infarcts.
  • To explore the primary mechanisms and prognostic factors associated with lenticulostriate infarction.

Main Methods:

  • Clinical case review and analysis of neuroimaging findings.
  • Review of etiological factors, focusing on embolic sources.
  • Assessment of neurological deficits and long-term outcomes.

Main Results:

  • Clinical signs encompass motor deficits, sensory deficits, and cognitive dysfunction.
  • Cardiac embolism is identified as the principal mechanism.
  • Prognosis is strongly correlated with the extent of damage in the posterior limb of the internal capsule.

Conclusions:

  • Lenticulostriate infarcts require distinct clinical differentiation from other anterior circulation strokes.
  • Cardiac embolism is a key etiology, challenging the frequent but often unproven association with lipohyalinosis.
  • The terminal, non-anastomosing nature of these arteries increases susceptibility to ischemia, necrosis, and hemorrhagic transformation.