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Related Concept Videos

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...
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...
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...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...

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A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
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[Ischemic stroke with antiphospholipid antibody].

Yasuhisa Kitagawa1, Hirohisa Ohkuma, Kentaro Tokuoka

  • 1Department of Neurology, Hachioji Hospital, Tokai University School of Medicine, 1838 Ishikawa cho, Hachioji-shi, Tokyo 192-0032, Japan.

Brain and Nerve = Shinkei Kenkyu No Shinpo
|November 4, 2008
PubMed
Summary
This summary is machine-generated.

Antiphospholipid syndrome (APS) increases stroke risk due to a hypercoagulable state. Diagnosis uses modified Sapporo criteria, and treatment involves antiplatelet or anticoagulant therapies for stroke prevention in affected patients.

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Area of Science:

  • Immunology
  • Hematology
  • Neurology

Context:

  • Antiphospholipid syndrome (APS) is linked to a hypercoagulable state, increasing the risk of stroke and ischemic events.
  • Diagnosis relies on the 2006 modified Sapporo criteria, assessing antiphospholipid antibodies (aPL) like lupus anticoagulant (LA) and beta2-glycoprotein I-dependent anticardiolipin antibodies.
  • Recent research suggests phosphatidylserine-dependent anti-prothrombin antibodies are closely associated with LA.

Purpose:

  • To review the role of antiphospholipid antibodies (aPL) in ischemic stroke.
  • To discuss diagnostic criteria and risk factors for stroke in APS.
  • To explore the mechanisms underlying thrombosis in APS and available therapeutic strategies.

Summary:

  • Antiphospholipid antibodies (aPL) are independent risk factors for first-time ischemic stroke, particularly in young women.
  • Stroke risk is elevated by beta2-GPI-dependent aCL, aGPL, and LA, with impaired protein C activation and potential endothelial cell activation contributing to thrombosis.
  • Therapeutic options include antiplatelet therapy for cryptogenic stroke with positive aPL and oral anticoagulation for established APS with occlusive disease.

Impact:

  • This review clarifies the association between aPL and stroke, aiding in risk stratification and diagnosis.
  • Understanding the mechanisms of thrombosis in APS can lead to improved preventative strategies.
  • Evidence-based therapeutic recommendations are provided for managing ischemic stroke risk in patients with aPL and APS.