By Alejandro Berenstein M.D., Pierre Lasjaunias M.D., Ph.D., Karel G. ter Brugge M.D. (auth.)
From the reviews:
"The presentation of the booklet is admirable with such a lot chapters starting with dialogue of simple pathophysiology and carrying on with with scientific points and functional suggestion. … The authors are cautious to not current easily the newest technological advances, yet to underpin the ebook with clinicopathological facets of vascular ailment which they regard as basic for the winning administration of those tough circumstances. … It services top as a reference textual content and has an available and simple to take advantage of index which is helping during this regard." (Justin pass, Acta Neurochirurgica, 2005)
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Additional resources for Surgical Neuroangiography: Vol. 2: Clinical and Endovascular Treatment Aspects in Adults
Upper limbs are less frequently involved than lower limbs. Fatty streaks (the earliest lesion of atherosclerosis) may be seen in the aorta in infancy and early childhood. Lesions in the vertebral and intracranial arteries appear much later in life. What makes certain segments of the vascular tree more prone to developing atherosclerosis than others is not entirely known. Local hemodynamic factors and rheological factors have been thought to be responsible. Atherosclerotic plaques tend to form at areas of low sheer stress, with bifurcations being particularly vulnerable (Strong 1992).
In the zone of flow separation), in relation to complex flow patterns associated with whirlpools, which form near the lateral wall of the bifurcation and extend into the carotid sinus. With time, the lesions progress, thicken, and often become complicated plaques, leading to severe stenosis, with or without ulceration. As the stenosis increases, the plaque becomes ulcerated and as thrombi form, the possibility of distal thromboembolic migration or obliteration of the carotid lumen increases, with potentially serious clinical consequences (Stebens 1995; Glasgov et al.
The histopathological appearance of the fully developed infarct is defined as coagulative necrosis affecting all cell types. At the margins of the infarct, there is a transition zone containing irreversibly injured neurons but preserved glial and endothelial cells that separates the central area of pan-necrosis from normal brain. Since neuronal injury in this border zone involves all neurons and not only those identified to be selectively vulnerable, the term "generalized neuronal necrosis" is given.