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for some degree of reorganization that corresponds to clinical recovery Speech and language therapy are particularly valuable in identifying the risk of aspiration as noted above Speci c therapy should be given in appropriate cases, and certainly improves the morale of the patient and family Further comments on the value of such therapy can be found in Chap 23, on language disturbances Preventive Measures Since the primary objective in the treatment of atherothrombotic disease is prevention, efforts to control the risk factors must continue The carotid vessels, being readily accessible, must always be examined for the presence of a bruit; the latter quite reliably indicates a stenosis, though not all stenoses cause a bruit and some bruits heard bilaterally are transmitted sounds from a stenotic aortic valve Ultrasound examination of the carotid is justi ed in almost all patients with TIAs and ischemic stroke While a self-audible bruit occasionally indicates carotid stenosis, dissection, or bromuscular dysplasia, it is usually benign and in some instances associated with an enlarged, superiorly displaced jugular bulb a benign anatomic variant that can be discerned on CT scan (Adler and Ropper) Other instances are attributable to raised intracranial pressure (pseudotumor cerebri) The management of patients with asymptomatic carotid bruits has been considered above For patients who have had a stroke from atherothrombotic disease and are functional, preventive measures consist of reducing the future occurrence of strokes Such measures include the following: (1) aspirin which has been shown to reduce the risk of second stroke slightly, but its effect, as already noted, should not be overestimated (see page 697); (2) any required antihypertensive agents whether given therapeutically or for diagnostic procedures, should be administered with caution; (3) cholesterol-lowering drugs should be administered unless the cholesterol level is already low or there is a contraindication; (4) smoking cessation is mandatory and the patient should be supported in such efforts; and (5) particular care should be taken to maintain the systemic blood pressure, oxygenation, and intracranial blood ow during general surgical procedures, especially in elderly patients The ultimate solution of the problems of ischemic infarction and TIAs lies in more fundamental elds namely, the prevention or alleviation of hypertension and atherosclerosis.

As already stated, this is the commonest cause of stroke The characteristic feature is the abrupt onset of a focal neurologic de cit In most cases of cerebral embolism, the embolic material consists of a fragment that has broken away from a thrombus within the heart Somewhat less frequently the source is intra-arterial, from the distal end of a thrombus within the lumen of an occluded or severely stenotic carotid or vertebral artery or the distal end of a carotid dissection, or possibly from an atheromatous plaque that has ulcerated into the lumen of the carotid sinus Single or sequential emboli may also arise from large atheromatous plaques in the ascending aorta Thrombotic or infected material (endocarditis) that adhere to the aortic or mitral heart valves and break away are also well appreciated sources of embolism Embolism due to fat, tumor cells (atrial myxoma), brocartilage, amniotic uid, or air seldom enters into the differential diagnosis of stroke except in special circumstances The embolus usually becomes arrested at a bifurcation or other

FIGURE 1-1

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site of natural narrowing of the lumen of an intracranial vessel, and ischemic infarction follows The infarction is pale, hemorrhagic, or mixed; hemorrhagic infarction nearly always indicates embolism, though most are pale Any region of the brain may be affected, the territory of the middle cerebral artery, particularly the superior division, being the most frequently involved The two cerebral hemispheres are approximately equally affected Large embolic clots can block large vessels (sometimes the carotids in the neck or at their termination intracranially), while tiny fragments may reach vessels as small as 02 mm in diameter usually with inconsequential effects The embolic material may remain arrested and plug the lumen solidly, but more often it breaks into fragments that enter smaller vessels and disappear, so that even careful pathologic examination fails to reveal their nal location In this instance, the clinical effects may clear in hours The anatomic diagnosis must then be made by inference, eg, absence of a vascular occlusion at the proper site to explain the infarct; absence of atherosclerosis or other cause of occlusion in the offending cerebral vessel; presence of a source of emboli, atrial brillation, or infarcts in other organs such as the kidneys and spleen; the occurrence of hemorrhagic infarction; and nally the clinical history, which is characterized by an absolutely abrupt onset, as described below Because of the rapidity with which embolic occlusion develops, there is not much time for collateral in ux to become established Thus, sparing of the territory distal to the site of occlusion is not as evident as in thrombosis However, the vascular anatomy and ischemia-modifying factors mentioned above, under The Ischemic Stroke, are still operative and in uence the size and magnitude of the infarct Brain embolism is predominantly a manifestation of heart disease, and fully 75 percent of cardiogenic emboli lodge in the brain The commonest identi able cause is chronic or recent atrial brillation, the source of the embolus being a mural thrombus within the atrial appendage (Table 34-7) Patients with chronic atrial brillation are about six times more liable to stroke than an agematched population with normal cardiac rhythm (Wolf et al) and the risk is considerably higher if there is also rheumatic valvular disease as mentioned earlier Furthermore, the risk conferred by the presence of atrial brillation varies with age, being 1 percent per year in persons younger than 65, and as high as 8 percent per year in those over 75 with additional risk factors These levels of risk are of prime importance in determining the advisability of anticoagulation, as discussed below Embolism may also occur during paroxysmal atrial brillation or utter Mural thrombus deposited on the damaged endocardium overlying a myocardial infarct in the left ventricle, particularly if there is an aneurysmal sac, is an important source of cerebral emboli, as is a thrombus associated with severe mitral stenosis without atrial brillation Emboli tend to occur in the rst few weeks after an acute myocardial infarction, but Loh and colleagues found that a lesser degree of risk persists for up to 5 years Cardiac catheterization or surgery, especially valvuloplasty, may disseminate fragments from a thrombus or a calci ed valve Mitral and aortic valve prostheses are additional important sources of embolism Another source of embolism is the carotid or vertebral artery, where clot forming on an ulcerated atheromatous plaque may be detached and carried to an intracranial branch (artery-to-artery embolism) A similar phenomenon may occur with arterial dissections and sometimes with bromuscular disease of the carotid or vertebral arteries Atheromatous plaques in the ascending aorta have been rec-.