how to print barcode in c# CEREBROVASCULAR DISEASES in Microsoft Office


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ing occlusion of small distal vessels In contrast to an embolus, a thrombus generally does not occlude the lumen completely from the rst moment of its formation; total blockage may occur only after several hours Once the lumen of the artery has been completely occluded, the thrombus may propagate distally and proximally to the next branching points and block an anastomotic channel These several dynamic events in the atherosclerotic-thrombotic process probably account for the prodromal ischemic attacks described below intermittent blockage of the circulation and variable impairment of function in the vascular territory, before proceeding to permanent ischemia Not infrequently, several arteries are affected by stenosis and thrombosis over a period of months or years Then it becomes dif cult to decipher the interplay of factors that have led to either transitory or persistent symptoms Some of the possibilities have been outlined by Adams and colleagues (1961) The evolution of the thrombotic process may be suf ciently prolonged to explain the clinical state known as stroke in evolution; when the hemodynamic disturbance stabilizes, the stage of completed stroke is reached These different stages acquire signi cance in relation to therapy and prognosis Pathophysiology of Thrombosis The process of thrombus formation involves an interplay between three components: the endothelium, circulating platelets, and a series of biochemical events that constitute a coagulative cascade When atherosclerosis is the primary condition, thrombus formation usually begins with a localized injury to the endothelium As indicated earlier, the endothelium overlying a plaque suffers damage from hemorrhage or necrosis of the vessel wall secondary to an alteration of the vasa vasorum Thrombus forms from brin and platelets that adhere to the endothelial surface and lead to partial or complete occlusion of the lumen In the process, aggregates of platelets are attracted to the site, partly through the action of prostacyclin (derived from arachidonic acid) Also, a substance called vasomodulin on the surface of the endothelium which, with protein C, normally inhibits the formation of brin through its interaction with thrombin is reduced at the injured site and induces clotting Homocystine has a similar effect and is believed thereby to promote thrombosis Circulating platelets increase in number locally, enlarge, and become more adherent to one another and to the injured vessel As they aggregate, they discharge their granules The latter process is stimulated by thromboxane A2, which is synthesized in the injured vessel wall This substance also releases coagulation proteins (including thrombin and Willebrand factor and other elements of the coagulative cascade) The third component ie, of the coagulative cascade involves the complex interplay of the well known series of factors that results in the formation of thrombin and the conversion of brinogen to brin Involved in this process are changes in a number of natural anticoagulative factors such as heparin cofactor 2, antithrombin III, protein C, and protein S Some of these are extrinsic to the blood vessels and hence may result in thrombosis in one or in multiple sites even without prior vascular injury Protein C is a vitamin K dependent protease which, in combination with its cofactors protein S and antithrombin III, inhibits coagulation A de ciency of any of these factors may predispose to in situ thrombosis within either the arterial or venous systems For example, protein C de ciency (heterozygous in one of every 16,000 individuals) is a cause of thrombosis of both veins and arteries; a resistance
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to activated protein C has also been described (causing venous thrombosis almost exclusively) Antiphospholipid antibody is another cause of vascular occlusion that is not incited by damage to the vessel wall (see page 735) The metabolic disturbances in Fabry disease also favor clotting Persons with certain in ammatory bowel diseases (ulcerative colitis, Crohn disease) are prone to develop thrombotic strokes Whether in ammation elsewhere in the body also predisposes to cerebral vascular occlusions, as has been suggested, is an open question Curiously, the hypercoagulable state induced by certain adenocarcinomas, does not produce in situ arterial occlusion (although it may precipitate cerebral venous thrombosis) Nevertheless, it does cause platelet- brin aggregation on cardiac valves with subsequent cerebral embolism ( marantic endocarditis, as discussed further on) These factors should be sought when thrombotic disease in cerebral arteries or veins occurs in children or young adults with unexplained strokes, in families with strokes, in pregnant or parturient women, and in women who are migraineurs or taking birth control pills (see further on) According to Markus and Hambley, whose review of this subject is recommended, screening for lupus anticoagulant, anticardiolipin antibodies, de ciency of proteins C and S, and antithrombin III is probably justi ed only in these special circumstances These causes of vascular thrombosis are taken up in later sections Clinical Picture of Atherothrombotic Stroke In general, the evolution of clinical phenomena in relation to cerebral thrombosis is more variable than that of embolism and hemorrhage In more than half of our patients, the main part of the stroke (paralysis or other de cit) is preceded by minor signs or one or more transient attacks of focal neurologic dysfunction, or TIAs (Table 34-5) In a sense, these herald the oncoming vascular catastrophe A history of such prodromal episodes is of paramount importance in establishing the diagnosis of atherothrombotic stroke Only rarely and for unclear reasons are embolism and cerebral hemorrhage preceded by a transient neurologic disorder In carotid and middle cerebral artery disease, the transient attacks consist of monocular blindness or of hemiplegia, hemianesthesia, or disturbances of speech and language In the vertebrobasilar system, the prodromal spells most often take the form of Table 34-5 Development of the clinical picture in 125 cases of cerebral thrombosis (C M Fisher)
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