title: Thrombus and encapsulated hematoma in cerebral cavernous malformations.
abstract: Thrombi, encapsulated hematomas, and granulation tissue are frequently seen in cerebral cavernous malformations (CCMs). We investigated the role that these histological changes play in repeated hemorrhages in CCMs as well as lesion growth, examining specimens of CCMs surgically harvested from 20 patients. The immunohistochemical study included thrombomodulin (TM) and endothelial cell protein C receptor (EPCR), which are important regulators of blood coagulation. Thick capsules, which contained blood degradation product, were seen in cases with encapsulated hematomas. Clusters of sinusoidal vessels were found outside of these thick capsules. Granulation tissue with inflammatory infiltrates and capillaries was seen in 4 cases with non-capsulated hematomas. Organizing thrombi were seen in sinusoidal vessels in 15 out of 20 cases. Factor VIII-related antigen staining demonstrated numerous capillaries in and around organizing thrombi and within the thickened vessel walls as well as in both the inner and outer sides of the hematoma capsule. TM and EPCR were positive in the endothelial cells of these capillaries, whereas they were negative in those of capillaries in the brain surrounding the lesions. Our study suggests that thrombosed sinusoidal blood vessels could gradually expand by repeated bleeding from numerous capillaries inside the wall and become encapsulated hematomas, and capillaries outside the thickened vessel wall could become sinusoidal blood vessels. Thrombosis within cerebral venules could be one of the causal factors of CCMs.
authors.affiliation: Department of Neurosurgery, Faculty of Medicine, Saga University, Nabeshima 5-1-1, 849-8501, Saga, Japan. abem@post.saga-med.ac.jp
authors.forename: Masamitsu
authors.initials: M
authors.lastname: Abe
authors.forename: Kenji
authors.initials: K
authors.lastname: Fukudome
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Sugita
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Oishi
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tabuchi
authors.forename: Teruaki
authors.initials: T
authors.lastname: Kawano
mesh_terms: D000199:Actins / Q000378:metabolism; D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD; D002543:Cerebral Hemorrhage / Q000378:metabolism / Q000473:pathology*; D002648:Child; D000074283:Endothelial Protein C Receptor; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D051272:Glucose Transporter Type 1; D006023:Glycoproteins / Q000378:metabolism; D006406:Hematoma / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007223:Infant; D002538:Intracranial Arteriovenous Malformations / Q000378:metabolism / Q000473:pathology*; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D011956:Receptors, Cell Surface; D013917:Thrombin / Q000378:metabolism; D013927:Thrombosis / Q000378:metabolism / Q000473:pathology*
chemical_list: D000199:Actins; D015703:Antigens, CD; D000074283:Endothelial Protein C Receptor; D005904:Glial Fibrillary Acidic Protein; D051272:Glucose Transporter Type 1; D006023:Glycoproteins; D019394:Ki-67 Antigen; D009004:Monosaccharide Transport Proteins; C478370:PROCR protein, human; D011956:Receptors, Cell Surface; C495677:SLC2A1 protein, human; D005169:Factor VIII; D013917:Thrombin