Spontaneous Dissection of Carotid and Vertebral Arteries
The first case of spontaneous dissection of the internal carotid artery (ICA) was reported in 1954 by Jentzer. Since then, other cases have been described (Bostrom and Liliequist 1967; Ehrenfeld and Wylie 1976; Fisher et al. 1978; Mokri et al. 1979; Ander
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16.1
Introduction
The first case of spontaneous dissection of the internal carotid artery (ICA) was reported in 1954 by Jentzer. Since then, other cases have been described (Bostrom and Liliequist 1967; Ehrenfeld and Wylie 1976; Fisher et al. 1978; Mokri et al. 1979; Anderson et al. 1980; Friedmann et al. 1980; Bradac et al. 1981a), and these have helped widen our understanding of the clinical and angiographic aspects of this disease. Spontaneous dissection is today a wellrecognized pathology that is responsible for stroke in many cases. Its incidence is reported to be three to four cases per 100,000 persons yearly (Schievink 2001; Menon and Norris 2008; Redekop 2008). Young and middle-aged patients are predominantly affected.
16.2
Pathology and Pathogenesis
From a pathological point of view, the lesion is characterized by a subintimal hemorrhage, leading to stenosis or occlusion of the artery. The hemorrhage can involve the outer media or the sub-adventitial layer, resulting in the formation of pseudoaneurysms. Dissection occurs because of a primary intimal tear, allowing the blood to pass into the arterial wall. Primary intramural hemorrhage can also occur through rupture of the vasa vasorum. The pathogenesis of dissection can be traumatic, but in the spontaneous form, the pathogenesis is
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not completely clear. Structural changes of the arterial wall, associated with mechanical factors, are probably involved. Indeed, it is well known that dissection occurs frequently in patients with fibromuscular dysplasia (FMD), Ehlers–Danlos syndrome, Marfan syndrome, and lupus erythematosus (Anderson et al. 1980; Mitsias and Levine 1994; Schievink et al. 1994a; North et al. 1995). Association with cystic medial necrosis has also been demonstrated in some cases (Schievink et al. 1994a). Such cases are more frequent in patients with migraine and in women using oral contraceptives (Mokri et al. 1986; D’Anglejan-Chatillon et al. 1989). A family history has also been reported (Schievink and Mokri 1995). Trauma, even minor, and neck manipulation (Hufnagel et al. 1999; Nadgir et al. 2003) are present in the clinical history of some patients. In this context, the association of trauma, even minor, and raised blood alcohol as a cause of dissection, particularly in the vertebrobasilar sector, have been emphasized (Hiraiwa et al. 2005). Some authors (Konrad et al. 2003; Vila et al. 2003) have reported in cases of dissection a deficiency of alpha 1-antitrypsin. This is a proteinase that has a protective action on collagen and elastin— important components of the connective tissue of the arterial wall. The same deficiency has been identified in cases of FMD, which shows a high tendency for dissection (Schievink et al. 1998).
G.B. Bradac, Cerebral Angiography, DOI 10.1007/978-3-642-54404-0_16, © Springer-Verlag Berlin Heidelberg 2014
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16.3
Location
Extracranial ICA: 2–3 cm distal to the bifurcation is the most frequent site of dissection. This commonly ends abruptly, with rare exceptions, where the artery enters
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