Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
➤ Gửi thông báo lỗi ⚠️ Báo cáo tài liệu vi phạmNội dung chi tiết: Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
Vascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2y which he called “vascular brain tumor in pial tissue” (Rokitansky 1846). It was Virchow (1862-1863) who first differentiated tumors from brain angiomas, which were identified as vascular malformations of congenital derivation. The concept that brain arteriovenous matformation (BAVM) is an anomaly Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2caused by errors during vascular development in the embryo was suggested by Cushing and Bailey (1928) and Dandy (1928). However, some difficulties inEbook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
the differential diagnosis between BAVMs and tumors remained, as noted by Ziilch (1957) and Russell et al. (1959). An accurate description of this patVascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2halla et al. 1995: Ya§argyl 1987. 1999: Chaloupka and Huddle 1998; Valavanis et al. 2004), is still valid today.12.2Classification•Arteriovenous malformation (AVM)•Vein of Galen AVM•Cavernous malformations (cavernomas)•Capillary malformations (telangiectasia*)•Developmental venous anomaly (DVA), ven Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2ous angiomas•Transition forms•Vascular malformations part of well-defined congenital-hereditary' syndromes•Rendu-Osler syndrome•Sturge-Weber syndrome•Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
Wyburn-Mason syndrome•KI ippel-Trenaunay-Weber syndrome12.3Arteriovenous Malformations12.3.1 Pathogenesis and PathologyThe certain pathogenesis of AVMVascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2esis and angiogenesis. In the vasculogenesis, angioblasts differentiate into endothelial cells to form the primary' vascular plexus. Later, angiogenesis follows, in which the primary plexus undergoes remodeling and organization, leading to the formation of the final cerebral vessels (Streeter 1918; Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2Risau and Flamme 1995; Risau 1997). The causes of an aberrant vasculo-angiogenesis leading to AVMs are unknown. Many factors are probably involved; amEbook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
ong them, some endothelial growth factors (VEGFR1-VEGFR2) and their binding receptors (FLt-1; FLk-1) have been identified as important for the normal Vascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2by et al. 1995; Fong et al. 1995;G.B. Bradac. Cerebral Angiography,DOI 10.1007 /978-3-642-54404-0- 12. Ề Springer-Verlag Berlin Heidelberg 201416716312 Vascular Malformations of the Central Nervous SystemSonstein et al. 1996: Uranishi et al. 2001; Hashimoto et al. 2001).When considering the embryolo Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2gical development of the cerebral arteries and veins, some authors (Mullan et al. 1996a. b) have suggested that AVMs could already be present before tEbook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
he third month of gestation. In some cases, an AVM may be relatively small at birth and grow later. There are. however. reports describing the appearaVascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2ese patients, cerebral AVMs occurred in the pathologically altered brain as a result of different causes, such as vascular pathology (Schmit et al. 1996; Song et al. 2007), heterotopia (Stevens et al. 2009). and changes after radiosurgery (Rodríguez-Arias et al. 2000); in others, the brain parenchym Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2a was completely normal (Gonzalez et al. 2005; Bulsara et al. 2002). These observations raise doubts about the congenital nature of cerebral AVMs, whiEbook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
ch—at least in some cases—seem to be acquired lesions caused by different nonspecific insults on the brain.The main angioarchitectural characteristic Vascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2vascular flow leads to changes of the vessels. Histology' shows the nidus to be composed basically of dilated arteries and veins. In some vessels, the wall structure is still recognizable. characterized by the presence of a media with smooth muscle cells and an elastic lamina in the arteries and an Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2absence of muscle cells in the veins. In other arteries, prominent changes, characterized by areas of wall thickening caused by proliferation of fibroEbook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
blasts, muscle cells, and an increase in connective tissue, are present. Segments with a thinning of the wall also occur, which potentially can lead tVascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2 particularly due to fibroblast proliferation, not smooth muscle cells. The interposed parenchyma shows gliosis, hemosiderin pigmentation, and calcifications. resulting from ischemia or previoushemorrhages. The surrounding parenchyma may appear normal or show similar changes (Challa et al. 1995; Kal Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2imo et al. 1997; Brocheriou and Capron 2004).12.3.2IncidenceThe incidence of AVMs is not completely known. In general autopsy, they are discovered witEbook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
h a frequency of 0.15-0.8 % (McCormick 1984; Jellinger 1986). Multifocal lesions can occur with a frequency of 1-10 % (Perret and Nischioka 1966; RodeVascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2s (Rodesch et al. 1988; Lasjaunias 1997).12.3.3Clinical RelevanceOf AVMs, 5-10 % remain asymptomatic and are diagnosed incidentally by CT or MR investigations performed for other reasons. Some 40-50 % present with intracranial hemorrhage. 30 % with seizures. 10-15 % with headaches, and 5-10 % with n Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2eurological deficits (Perini et al. 1995; Stapf et al. 2002; Hofmeister et al. 2000; Valavanis et al. 2004); the incidence of symptomatic cerebral malEbook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
formation in the adult population is reported to be one-tenth the frequency' of intracranial aneurysm (Berenstein and Lasjaunias 1992; Valavanis et alVascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2orbidity of 1.7 % (Graf et al. 1983; Crawford et al. 1986; Ondra et al. 1990; Mast et al. 1997). The risk of a repeated hemorrhage after an initial episode is reported to increase in the first year, later decreasing until it reaches the level of the initial risk (Graf et al. 1983; Mast et al. 1997). Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2 It is the most frequent initial symptom in children (Berenstein and Lasjaunias 1992; Rodesch et al. 1995; Lasjaunias 1997).Cases of spontaneous thromEbook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2
bosis of AVMs (Sukoffet al. 1972; Levine et al. 1973; Mabe and Furuse 1977; Pascual-Castroviejo et al. 1977; Sartor 1978; Nehls and Pittman 1982; OmojVascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathology Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2 Yonekawa 1994; Abdulrauf et al. 1999) as well as its possible recanalization occurring even a few years later (Mizutani et al. 1995) have been reported. A long follow-up of these patients is mandatory.12.3.4Location Ebook Cerebral angiography normal anatomy and vascular pathology (2nd edition): Part 2Vascular Malformations of the Central Nervous System1212.1IntroductionRokitansky- is reported to be the first to have described this kind of pathologyGọi ngay
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