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Watershed infarcts in a multiple microembolic model of monkey
Takakuni Maki1, Hideaki Wakita, Mitsuhito Mase
1Department of Neurology, Graduate School of Medicine, Kyoto University, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
Neuroscience Letters
|June 7, 2011
Summary
Embolic mechanisms, not just hemodynamic ones, can cause watershed infarcts. This study in macaque monkeys demonstrated microembolic roles in both cortical and internal watershed infarcts, suggesting a new understanding of stroke pathogenesis.
Area of Science:
- Neurology
- Vascular Biology
- Neuroimaging
Background:
- Watershed infarcts are brain lesions occurring in areas supplied by major cerebral arteries.
- The exact cause of watershed infarcts, whether hemodynamic or embolic, remains a subject of debate.
- Understanding the pathogenesis is crucial for developing effective stroke treatments.
Purpose of the Study:
- To investigate the role of microemboli in the development of watershed infarcts.
- To examine the acute and chronic changes associated with microembolic stroke in a primate model.
- To differentiate between hemodynamic and embolic causes of watershed infarcts.
Main Methods:
- A macaque monkey model was used to study multiple microinfarcts.
- 50 μm microbeads were injected into the internal carotid arteries.
- Magnetic Resonance Imaging (MRI) was employed to examine infarcts and associated changes.
Main Results:
- Monkeys developed both cortical and internal watershed infarcts in the acute phase after microbead injection.
- Chronic phase observations included atrophic changes and microbleeds in the affected brain regions.
- The study successfully modeled microembolic events leading to watershed infarcts.
Conclusions:
- Embolic pathogenesis is a significant contributor to the genesis of both cortical and internal watershed infarcts in primates.
- This finding challenges the traditional view solely focusing on hemodynamic factors.
- The macaque model provides valuable insights into stroke mechanisms and potential therapeutic targets.
