Cerebral thrombus

Buchan A, Gates P, Pelz D, Barnett HJ. Intraluminal thrombus in the cerebral circulation. Implications for surgical management. Stroke 1988 19 681-687. 

Dissection of the internal carotid and vertebral arteries is a common cause of stroke, particularly in young patients. Although many occur due to trauma, it is estimated that over half occur spontaneously. The mechanism of stroke following arterial dissection is either by artery-to-artery embolism, by thrombosis in situ, or by dissection-induced lumenal stenosis with secondary cerebral hypoperfusion and low-flow watershed infarction. Occasionally, dissection may lead to the formation of a pseudoaneurysm as a source of thrombus formation. Vertebrobasilar dissections that extend intracranially have a higher risk of rupture leading to subarachnoid hemorrhage (SAH). ° ... 

Ischemic stroke is the abrupt development of a focal neurologic deficit that occurs due to inadequate blood supply to an area of the brain. Most often, this is due to a thrombotic or embolic arterial occlusion leading to cerebral infarction. A thrombotic occlusion occurs when a thrombus forms inside an artery in the brain. An embolism refers to a clot originating outside of the brain in which a piece of the clot breaks loose and is carried to the brain. 

Ischemic strokes account for 88% of all strokes and are due either to local thrombus formation or to emboli that occlude a cerebral artery. Cerebral atherosclerosis is a causative factor in most cases of ischemic stroke, although 30% are of unknown etiology. Emboli can arise either from intra- or extracranial arteries. Twenty percent of embolic strokes arise from the heart. 

In carotid atherosclerosis, plaques may rupture, resulting in collagen exposure, platelet aggregation, and thrombus formation. The clot may cause local occlusion or may dislodge and travel distally, eventually occluding a cerebral vessel. 

The final result of both thrombus formation and embolism is arterial occlusion, decreasing cerebral blood flow and causing ischemia and ultimately infarction distal to the occlusion. 

Platelet aggregation increases like an avalanche because, once activated, platelets can activate other platelets. On the injured endothelial cell, a platelet thrombus is formed, which obstructs blood flow. Ultimately, the vascular lumen is occluded by the thrombus as the latter is solidified by a vasoconstriction produced by the release of serotonin and thromboxane A2 from the aggregated platelets. When these events occur in a larger coronary artery, the consequence is a myocardial infarction involvement of a cerebral artery leads to stroke. 

Sasaki Y, Seki J, Giddings JC, Yamamoto J (1996) Effects of NO-donors on thrombus formation and microcirculation in cerebral vessels of the rat. Thromb Haemost 76(1) 111-117... 

As discussed previously, aspirin inhibits platelet-induced thrombus formation through its ability to inhibit thromboxane biosynthesis. Aspirin has therefore been used to help prevent the onset or recurrence of heart attacks in some individuals by inhibiting thrombus formation in the coronary arteries.97,109 Similarly, daily aspirin use may help prevent transient ischemic attacks and stroke by preventing cerebral infarction in certain patients.97,109 The role of aspirin in treating coagulation disorders is discussed in more detail in Chapter 25... 

Fig. 5. 9a,b. Subacute wall-adherent thrombus (a). After embolic infarction of the middle cerebral artery ultrasound has identified an echolucent structure within the ICA, highly suggestive of thrombus. Tl-weighted spin echo image with fat saturation confirms an intraluminal thrombus (a) with a mild stenosis (a, b), gradually resolving over weeks... 

If the MI patient cannot be transported to a cardiac center in time, fibrinolytic treatment of the coronary thrombus is instituted. For this purpose, fibrinolytics (streptokinase or recombinant tissue plasminogen activators) are given intravenously. Fibrinolysis is associated with an increased risk of bleeding cerebral hemorrhages are of particular concern. A coronary bypass operation is available as a third therapeutic option. 

Q1 A stroke involves significant reduction in blood flow to a part of the brain. It can be caused either (i) by an embolus or by intravascular clotting, which blocks blood flow to an area (approximately 85% of strokes), or (ii) by haemorrhage from a ruptured blood vessel, which compresses the brain tissue (approximately 15% of strokes). Patients with extensive atherosclerosis are at risk of intravascular coagulation and blockage of cerebral blood flow, but a vessel can be blocked by a thrombus originating in another part of the circulation. This cause of stroke is common in elderly patients >60 years of age. Aneurysms which rupture suddenly are a more common cause of stroke in younger patients. 

The venous anatomy is very variable. Venous blood flows centrally via the deep cerebral veins and peripherally via the superficial cerebral veins into the dural venous sinuses, which lie between the outer and meningeal inner layer of the dura and drain into the internal jugular veins (Stam 2005) (Fig. 4.4). The cerebral veins do not have valves and are thin walled, and the blood flow is often in the same direction as in neighboring arteries. There are numerous venous connections between the cerebral veins and the dural sinuses, the venous system of the meninges, skull, scalp, and nasal sinuses, allowing infection or thrombus to propagate between these vessels. 

Akins PT, Glen S, Nemeth PM et al. (i996). Carotid artery thrombus associated with severe iron-deficiency anemia and thrombocytosis. Stroke 27 i002-i005 Al-Hakim M, Katirji MB, Osorio I et al. (i993). Cerebral venous thrombosis in paroxysmal... 

Martin R, Bogousslavsky J, Miklossy J et al. (1992). Floating thrombus in the innominate artery as a cause of cerebral infarction in young adults. Cerebrovascular Diseases 2 177-181... 

Magnetic resonance imaging has greater sensitivity than CT for the changes of cerebral venous thrombosis (Bousser and Ross Russell 1997 Ferro et at 2007). In the acute phase, at less than three to five days, the thrombus is isointense on both Ti- and T2-weighted sequences. Subsequently, the thrombus becomes hyperintense (Fig. 29.3). After two to three weeks, findings depend on whether or not the sinus remains occluded or whether it is partly or completely recanalized. 

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