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Thrombus and encapsulated hematoma in cerebral cavernous malformations
Masamitsu Abe1, Kenji Fukudome, Yasuo Sugita
1Department of Neurosurgery, Faculty of Medicine, Saga University, Nabeshima 5-1-1, 849-8501, Saga, Japan. abem@post.saga-med.ac.jp
Acta Neuropathologica
|March 11, 2005
Summary
Repeated bleeding in cerebral cavernous malformations (CCMs) may stem from thrombosed vessels. These vessels can grow via internal capillary bleeding, forming hematomas and potentially leading to CCM development.
Area of Science:
- Neurology
- Vascular Biology
- Pathology
Background:
- Cerebral cavernous malformations (CCMs) often present with thrombi, hematomas, and granulation tissue.
- The histological basis for recurrent hemorrhages and CCM growth remains incompletely understood.
Purpose of the Study:
- To investigate the role of histological changes, specifically thrombosis and associated vascular proliferation, in CCM pathogenesis.
- To examine the expression of coagulation regulators thrombomodulin (TM) and endothelial cell protein C receptor (EPCR) in CCM lesions.
Main Methods:
- Histological examination of 20 surgically resected CCM specimens.
- Immunohistochemical staining for Factor VIII-related antigen, TM, and EPCR.
Main Results:
- Organizing thrombi were identified in 15/20 CCMs, often associated with numerous capillaries.
- Capillaries expressing TM and EPCR were abundant within and around thrombi and hematoma capsules.
- Encapsulated hematomas showed thick capsules with degradation products and surrounding sinusoidal vessels.
Conclusions:
- Thrombosis in cerebral venules may initiate CCMs.
- Repeated bleeding from intra-lesional capillaries contributes to CCM expansion and hematoma formation.
- The observed vascular changes suggest a mechanism for CCM growth and recurrence.