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derstood The explanation most consistent with our observations is that embolic material, after occluding an artery and causing ischemic necrosis of brain tissue, then fragments and migrates distally from its original site This allows partial restoration of the circulation to the infarcted zone, and blood seeps through the damaged small vessels (Fisher and Adams) In such cases, one often cannot nd the embolus by arteriography or postmortem examination, or one nds only a few fragments proximal to the pale ischemic zones Cerebral hemorrhage is one of two types In the intracerebral variety, blood leaks from the vessel (usually a small artery) directly into the brain, forming a hematoma in the brain substance and sometimes spreading into the ventricles and then to the subarachnoid space Once the leakage is arrested, the blood slowly disintegrates and is absorbed over a period of weeks and months The mass of clotted blood causes physical disruption of the tissue and pressure on the surrounding brain The second type of bleeding originates from an aneurysmal dilation at branching points of the large arteries of the circle of Willis; the bleeding is almost exclusively contained within the subarachnoid spaces and therefore, causes little immediate focal effect on the brain In this way, subarachnoid hemorrhage differs from other stroke syndromes However, blood within the subarachnoid space, if large in quantity, may cause a delayed cerebral ischemia through a mechanism of constriction of the vessels of the circle of Willis and their primary branches (vasospasm) In addition to these two main types of hemorrhage, a bland infarction in many instances has areas of leakage of blood into the brain, so-called hemorrhagic infarction
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So distinctive is the clinical presentation of cerebrovascular disease that the diagnosis is seldom in doubt The common mode of expression is the stroke, de ned as the sudden occurrence of a nonconvulsive, focal neurologic de cit In its most severe form the patient becomes hemiplegic or even comatose an event so dramatic that it had been given its own designations, namely apoplexy, cerebrovascular accident (CVA), or shock (colloquial) However, stroke is the currently preferred term In its mildest form it may consist of a trivial neurologic disorder insuf cient for the patient even to seek medical attention There are all gradations of severity between these two extremes, but in all forms of stroke the denotative feature is the temporal pro le of neurologic events It is the abruptness with which the neurologic de cit develops a matter of seconds or minutes that stamps the disorder as vascular Embolic strokes characteristically occur suddenly, and the de cit reaches its peak almost at once Thrombotic strokes may have a similarly abrupt onset, but they evolve somewhat more slowly over a period of several minutes or hours and occasionally days; in the latter case, the stroke usually progresses in a saltatory fashion, ie, in a series of steps rather than smoothly In hypertensive cerebral hemorrhage, also abrupt in onset, the de cit may be virtually static or steadily progressive over a period of minutes or hours, while subarachnoid hemorrhage is almost instantaneous The other important aspect of the temporal pro le is the arrest and then regression of the neurologic de cit in almost all except the fatal strokes At one extreme of rapid regression is a focal syndrome that reverses itself entirely and dramatically over a period of minutes or up to an hour; this de nes the transient ischemic attack (TIA) Not infrequently, an extensive de cit from embolism reverses itself within a few hours or days More often, and this is the case in most thrombotic strokes, improvement occurs gradually
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over weeks and months, and the residual disability is considerable A gradual downhill course over a period of several days or weeks will usually be traced to a nonvascular disease The only exceptions are the additive effects of multiple vascular occlusions (platelet thrombosis, lupus erythematosus, and other arteritides; see Table 34-1) and the progressive brain edema surrounding large infarctions and cerebral hemorrhages The neurologic de cit re ects both the location and the size of the infarct or hemorrhage Hemiplegia stands as the classic sign of all cerebrovascular diseases, whether in the cerebral hemisphere or brainstem, but there are many other manifestations, occurring in large but highly recognizable combinations These include mental confusion, numbness and sensory de cits of many types, aphasia, visual eld defects, diplopia, dizziness, dysarthria, and so forth The neurovascular syndromes that they form enable the physician to localize the lesion sometimes so precisely that even the affected arterial branch can be speci ed and to indicate whether the lesion is an infarct or a hemorrhage These neurovascular syndromes are described in the section that follows It would be incorrect to assume that every cerebrovascular illness expresses itself as a clearly delineated stroke Some lesions are clinically silent or cause disorders of function so mild as to concern the patient little if at all Neither the patient nor the family can then date the onset of the illness Other small incidents may become sources of complaint only when their cumulative effects become manifest Sometimes, stenosis of the common or internal carotid results in a chronic marginally low blood ow, which, by uctuating during physical activity, may diminish vision or induce a defect in sensory or motor function or an abnormality of movement Another problem is that certain dominant hemispheric lesions cause aphasic disturbances, which hamper history taking, and nondominant ones cause anosognosia, in which the patient is unaware of his de cits or denies them hence his descriptions are close to useless Imaging techniques, as already alluded to, continue to enhance the clinical study of stroke patients; they allow the demonstration of both the cerebral lesion and the affected blood vessel CT scanning demonstrates and accurately localizes even small hemorrhages, hemorrhagic infarcts, subarachnoid blood, clots in and around aneurysms, regions of infarct necrosis and arteriovenous malformations Magnetic resonance imaging (MRI) also demonstrates these lesions and, in addition, reveals ow voids in vessels, hemosiderin and iron pigment, and the alterations resulting from ischemic necrosis and gliosis Of the two procedures, MRI is particularly advantageous in demonstrating small lacunar lesions deep in the hemispheres and abnormalities in the brainstem (a region obscured by adjacent bone in CT scans) One of the diagnostic advances in the last decade has been the introduction of the diffusion-weighted technique, which allows the early detection of an infarctive lesion within minutes of the stroke, ie, considerably earlier than CT and MRI scan (Fig 34-1) The various MRI imaging sequences used in the diagnosis and dating of stroke are discussed below and in Chap 2 Other ancillary procedures for the investigation of cerebrovascular disease include Doppler ultrasound ow studies, which demonstrate atheromatous plaques and stenoses of large vessels, particularly of the carotid but also the vertebrobasilar arteries The transcranial Doppler technique has reached a degree of precision whereby occlusion or spasm of the main vessels of the circle of Willis can be seen Arteriography, now enhanced by digital processing of images, most accurately demonstrates stenoses and oc-
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