Intracranial Atherosclerosis 2008
DOI: 10.1002/9781444300673.ch5
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Stroke Mechanisms

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Cited by 13 publications
(17 citation statements)
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References 50 publications
(57 reference statements)
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“…Even though atherosclerosis within intracranial arteries possesses distinct features by virtue of unique anatomy and hemodynamics in the intracranial vascular system, the course of atherogenesis may be based on the general mechanism (D'Armiento et al, ; Elkind, ; Kiechl & Willeit, ). Normally, atherogenesis in intracranial arteries engages with a series of systemic and local lipid‐driven inflammatory activities (Wong, Caplan, & Kim, ; Wu, Li, Hou, & Chu, ). Chronic systemic inflammation may exacerbate the progression of ICAS via the activation of endothelial injury and inflammatory cells within cerebral arteries (Chen & Fisher, ; Wong et al, ).…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Even though atherosclerosis within intracranial arteries possesses distinct features by virtue of unique anatomy and hemodynamics in the intracranial vascular system, the course of atherogenesis may be based on the general mechanism (D'Armiento et al, ; Elkind, ; Kiechl & Willeit, ). Normally, atherogenesis in intracranial arteries engages with a series of systemic and local lipid‐driven inflammatory activities (Wong, Caplan, & Kim, ; Wu, Li, Hou, & Chu, ). Chronic systemic inflammation may exacerbate the progression of ICAS via the activation of endothelial injury and inflammatory cells within cerebral arteries (Chen & Fisher, ; Wong et al, ).…”
Section: Introductionmentioning
confidence: 99%
“…Normally, atherogenesis in intracranial arteries engages with a series of systemic and local lipid‐driven inflammatory activities (Wong, Caplan, & Kim, ; Wu, Li, Hou, & Chu, ). Chronic systemic inflammation may exacerbate the progression of ICAS via the activation of endothelial injury and inflammatory cells within cerebral arteries (Chen & Fisher, ; Wong et al, ). Additionally, local inflammatory infiltration evolving a fate of macrophages may increase the vulnerability of atherosclerotic plaques, which results in the rupture of plaques and subsequent thrombotic events (Hilgendorf, Swirski, & Robbins, ; Moore, Sheedy, & Fisher, ; Wong et al, ).…”
Section: Introductionmentioning
confidence: 99%
“…3 Patients with thrombotic atherosclerotic plaques may develop progressive occlusion, and this may result in hypoperfusion and regional artery-to-artery embolism within the vascular territory. 4 Neurological status in such patients is usually dependent on both the degree of collateral blood supply to the occluded vascular territory and the amount of potentially salvageable ischemic brain tissue, ie, the ischemic penumbra. The amount can be judged clinically by a mismatch in diffusion-perfusion or diffusion-symptom in the ischemic tissue and appears to identify patients with stroke who are more likely to respond to delayed intra-arterial recanalization, that is, recanalization performed beyond the currently recommended 6-hour time limit.…”
mentioning
confidence: 99%
“…In addition, patients with MCA occlusion may have disabling cognitive impairment, especially for those with bilateral diseases. 5 For our two patients, the etiology of their recurrent TIAs was likely to be hemodynamic impairment from total MCA occlusion, arising from atherosclerotic stenosis and superimposed thrombosis based on angiographic findings. The optimal management of them was controversial.…”
Section: Discussionmentioning
confidence: 87%