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Related Concept Videos

Formation of the Platelet Plug01:22

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The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
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Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
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Structure and Function of Platelets01:18

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The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
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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...
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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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Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
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Related Experiment Video

Updated: Apr 30, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
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Platelets and migraine.

Elisa Danese1, Martina Montagnana1, Giuseppe Lippi2

  • 1Laboratory of Clinical Chemistry and Hematology, University of Verona, Verona, Italy.

Thrombosis Research
|April 29, 2014
PubMed
Summary

Migraine is a complex neurovascular disorder involving reduced cerebral blood flow, inflammation, and pain pathway hypersensitization. Platelet biology, particularly serotonin metabolism and inflammation, plays a significant role in migraine pathogenesis.

Keywords:
HeadacheMigraineNitric OxidePathogenesisPlateletsSerotonin

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Area of Science:

  • Neuroscience
  • Vascular Biology
  • Pathophysiology

Background:

  • Migraine is a prevalent neurovascular disorder with complex pathogenesis.
  • Current understanding points to reduced cerebral blood flow, reactive hyperemia, sterile inflammation, and pain pathway hypersensitization.

Purpose of the Study:

  • To explore the intricate relationship between platelet biology and migraine pathogenesis.
  • To investigate the role of serotonin and nitric oxide metabolism in migraine.

Main Methods:

  • Review of existing literature on migraine pathogenesis.
  • Analysis of studies investigating platelet count, serotonin metabolism, and nitric oxide in migraine patients.

Main Results:

  • While platelet count showed no significant association, serotonin metabolism is notably impaired in migraine patients.
  • Evidence suggests nitric oxide may amplify reactive vasodilation post-ischemia.
  • Platelet-leukocyte aggregates contribute to sterile inflammation and pain signaling via cytokine release.

Conclusions:

  • Migraine pathogenesis involves neurovascular dysfunction, with platelet-derived factors like serotonin and inflammatory mediators playing a crucial role.
  • Further research is needed to confirm the role of nitric oxide abnormalities.