how to print barcode in asp.net c# Transient Ischemic Attacks in Microsoft Office

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Transient Ischemic Attacks
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As has already been emphasized, when brief transient ischemic attacks (TIAs) precede a stroke, they almost always stamp the underlying process as atherothrombotic There is little doubt that they are due to transient focal ischemia, but their precise mechanism is not fully understood (see further on); they might be thought of as temporary strokes that fortunately reverse themselves They belong, therefore, under the heading of atherosclerotic thrombotic disease but are discussed separately here because of their clinical importance Current opinion holds that TIAs are brief, reversible episodes of focal, nonconvulsive ischemic neurologic disturbance The consensus had been that their duration should be less than 24 h, an idea introduced 30 years ago by a committee assigned to study the problem It is more useful, however, to separate attacks that last only a few minutes (up to 1 h) and leave no permanent signs, from those of longer duration which are more likely to be due to embolism In any clinical analysis of TIAs, it is also important to separate a single transient episode from repeated ones tat are all of uniform type The latter are more often a warning sign of impending vascular occlusion, particularly of the internal carotid artery, while the former, especially when prolonged are often due to an embolus that leaves no lasting effect It should also be pointed out that blood diseases that cause excessive viscosity or sludging of blood (polycythemia vera, sickle-cell disease, thrombocytosis, leukemia, and hyperglobulinemic states) may also cause TIAs prior to a stroke In a prospective study of 390 patients with focal TIAs caused by atherosclerotic vascular disease, the 5-year cumulative rate of fatal or nonfatal cerebral infarction was 23 percent (Heyman et al) Interestingly, the rate of myocardial infarction in this group of patients, particularly in those with carotid lesions, was almost as high (21 percent) and in other series, it has exceeded the risk of stroke Thus the occurrence of carotid TIAs is a predictor not only of cerebral infarction but also of myocardial infarction About twothirds of all patients with TIAs are men with hypertension, re ecting the higher incidence of atherosclerosis in this group Occasionally, in younger adults, TIAs may occur as relatively benign phenomena, without recognizable features of atherosclerosis or risk factors for it Migraine is suspect in such patients (see page 151); other such instances are due to special hematologic disorders such as the antiphospholipid antibody discussed later in the chapter Clinical Picture Transient ischemic attacks can re ect the involvement of virtually any cerebral artery: common or internal carotid; middle, posterior, or anterior cerebral; ophthalmic; vertebral,
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MAJOR CATEGORIES OF NEUROLOGIC DISEASE
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basilar, or cerebellar; or a penetrating branch to the basal ganglia or brainstem (lacunar TIAs) If the posterior cerebral arteries are considered with the vertebrobasilar system, transient ischemic episodes are slightly more common in this system than in the eld of the carotid territory TIAs may precede, accompany, or infrequently follow the development of a stroke, or they can occur by themselves without leading to a stroke a fact that makes any form of therapy dif cult to evaluate As just noted, TIAs that presage stroke may last a few seconds or up to an hour, longer ones almost certainly being due to embolic infarction Most last 2 to 15 min There may be only a few attacks or several hundred Between attacks, the neurologic examination discloses no abnormalities A stroke may occur after the rst or second episode or only after numerous attacks have occurred over a period of weeks or months Not infrequently the attacks gradually cease and no important paralysis occurs So far it has not been possible to distinguish those individuals in whom a stroke will develop from those in whom it will not except in a general way Many attacks which appear over a long period of time tend to be less likely to lead to thrombosis Prolonged, uctuating TIAs are the most ominous About 20 percent of infarcts that follow TIAs occur within a month after the rst attack, and about 50 percent within a year (see Whisnant et al, 1973) Hemispheric Transient Ischemic Attacks (Carotid Artery Territory) The neurologic features of the transient episode indicate the territory or artery involved and are fragments of the stroke that may be approaching In the carotid system, TIAs indicate involvement of one cerebral hemisphere or eye The visual disturbance is ipsilateral; the sensorimotor disturbance is contralateral Individual attacks tend to involve either the eye or the brain; only rarely are the two involved simultaneously In the hemispheric attacks, ischemia occurs mainly in the distal territory of the middle cerebral artery or in an adjacent border zone, producing weakness or numbness of the opposite hand and arm However, many different combinations may be seen: face and lips, lips and ngers, ngers alone, hand and foot Rather than being paralyzed or weak, the arm may shake irregularly, simulating a seizure ( limb-shaking TIA ) or rarely display other transient movement disorders (Yanagihara et al) Less common manifestations include confusion, aphasia and dif culty in calculation (when the dominant hemisphere is involved), apractagnosia (nondominant hemisphere), and other temporoparietal disturbances Headache is not a feature of TIAs In ocular attacks, transient monocular blindness (also called amaurosis fugax) is the usual symptom Most of these episodes evolve swiftly, over 5 to 30 s, and are described as a horizontal shade falling (or rising) smoothly over the visual eld until the eye is completely but painlessly blind The attack clears slowly and uniformly Sometimes the attack takes the form of a wedge of visual loss, sudden generalized blurring, or, rarely, a gray or bright light Transient attacks of monocular blindness are usually more stereotyped than hemispheric attacks TIAs consisting of a homonymous hemianopia and paresthesias of the hand and arm should suggest a stenosis of the posterior cerebral artery The implications of amaurosis fugax have been evaluated by several investigators and found not to be quite as ominous as those of hemispheral TIAs, particularly in younger patients Poole and Ross Russell observed a group of 110 patients for periods of 6 to 19 years following an episode of amaurosis fugax (exclusive of the type caused by cholesterol emboli) At the end of 6 years, the mor-
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tality rate (due mainly to heart disease) had risen to 21 percent and the incidence of stroke to 13 percent (compared to expected gures of 15 and 3 percent, respectively, in an age-matched population) Of the patients who were alive at the end of the observation period, 43 percent had had no further attacks of amaurosis fugax following the initial episode Noteworthy also was the nding that among patients with normal carotid arteriograms, only 1 of 35 had had a stroke during the follow-up period, whereas stroke had occurred in 8 of 21 patients in whom the internal carotid artery was occluded or stenotic These gures are in keeping with those of Ackerman; in his series of 139 patients with amaurosis fugax and normal lumens of the common and internal carotid arteries, only 3 had a subsequent hemispheric stroke (personal communication) As pointed out by Benavente and colleagues, the risk of stroke over the 3 years following an attack is as low as 2 percent if there are no other issues such as diabetes, but it may be as high as 24 percent in older patients with risk factors for atherosclerosis The age of the patient with amaurosis fugax is of particular signi cance In the series of Poole and Ross Russell, the youngest patient to have a stroke after amaurosis fugax was 57 years old Tippin and coworkers reviewed the records of 83 patients with onset of amaurosis fugax before the age of 45 years and found evidence of stroke in none; moreover, 42 of these patients were examined after a mean period of 58 years during which no stroke had occurred It is evident that in this early-onset, good-prognosis group, a mechanism other than atherosclerosis was operative, such as migraine or an antiphospholipid antibody (discussed further on) Brainstem Transient Ischemic Attacks (Vertebrobasilar Circulation) Recurrent TIAs referable to vertebrobasilar disease tend to be less stereotyped and more prolonged than those related to the carotid circulation They are also more likely to culminate in a stroke The clinical picture of TIAs in the vertebrobasilar territory is diverse, since this circulation sustains such a varied sensorimotor traf c Vertigo, diplopia (vertical or horizontal), dysarthria, bifacial numbness, ataxia, and weakness or numbness of part or all of one or both sides of the body (ie, a disturbance of the long motor or sensory tracts bilaterally) are the hallmarks of vertebrobasilar involvement Transient vertigo, diplopia, or headache occurring as solitary symptoms should not be interpreted as a TIA Also, in some patients, the complaint of dizziness will prove, however infrequently, to be part of a carotid TIA; hence this symptom, in our experience and that of Ueda et al, is not a totally reliable indicator of the vascular territory involved Other manifestations of vertebrobasilar TIAs, in their approximate order of frequency, include staggering, veering to one side, a feeling of cross-eyedness, dark vision, blurred vision, tunnel vision, partial or complete blindness, pupillary change, ptosis, paralysis of gaze, dysarthria, and dysphagia Less common symptoms include hemiplegia, noise or pounding in the ear or in the head, pain in the head or face or other peculiar head sensations, vomiting, hiccups, sense of tilting, lapse of memory, confused behavior, drowsiness, transient unconsciousness (rare), impaired hearing, deafness, hemiballismus, hallucinosis, and forced deviation of the eyes So-called drop attacks (page 329), according to Ross Russell, have been recorded in 10 to 15 percent of patients with vertebrobasilar insuf ciency, but we have never observed such attacks as a recurrent ischemic phenomenon or a manifestation of other forms of cerebrovascular disease Vertebrobasilar TIAs may be identical from one episode to another, or they may vary in detail while maintaining the same basic pattern, the latter occurrence being more typical For exam-
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