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CEREBROVASCULAR DISEASES
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ple, weakness or numbness may involve the ngers and face in some episodes and only the ngers in others; or dizziness and ataxia may occur in some attacks, while in others diplopia is added to the picture In basilar artery disease, each side of the body may be affected alternately All the involved parts may be affected simultaneously, or a march or spread from one region to another may occur over a period of 10 s to a minute or a few minutes much slower than the spread of a seizure The individual attack may cease abruptly or fade gradually Lacunar Transient Ischemic Attacks It has been recognized that strokes due to occlusion of small penetrating vessels of the brain have a proclivity to be intermittent ( stuttering ) at their onset and occasionally to allow virtually complete restitution of function between discrete episodes Whether this constitutes a lacunar TIA has been debated, but it seems to us that the problem is our inability to distinguish a transitory occlusion of a small vessel from that of a larger vessel Donnan and colleagues speak of a capsular warning syndrome, which we have seen a number of times, consisting of escalating episodes of weakness in the face, arm, and leg and culminating in a capsular lacunar lesion These lacunar TIAs may stutter or remit, and there is no doubt that one or many of them may precede a lacunar stroke Mechanism of Transient Ischemic Attacks The question here, so far not satisfactarily answered, is whether low ow or embolic particles are responsible for TIAs Whatever the exact cause of the attacks, they are in most cases intimately related to vascular stenosis and, usually, to ulceration due to atherosclerosis and to thrombus formation Embolization of brin-platelet material from atherosclerotic sites may indeed be the cause of attacks in some cases, but it is dif cult to understand, in attacks of identical pattern, how successive emboli from a distance would enter the same arterial branch each time Moreover, one would expect the involved cerebral tissue to be at least partially damaged, leaving some residual signs When a single transient episode has occurred, the factor of recurrence does not enter into the diagnosis, and cerebral embolism must then be strongly considered In some cases of documented embolism, the neurologic state uctuates from normal to abnormal repeatedly for as long as 36 h, giving the appearance of TIAs ( accelerated TIAs ); in others, a de cit of several hours duration occurs, ful lling the traditional (now largely discarded) criterion of TIAs As already noted, the same sequence of events can precede lacunar infarction and seem most likely to be due to locally reduced blood ow Again, a single transitory episode, especially if it lasts longer than 1 h, and multiple episodes of different pattern, suggest embolism and must be distinguished from brief (2- to 10min) recurrent attacks of the same pattern, which suggest atherosclerosis and thrombosis in a large cerebral or feeding vessel Ophthalmoscopic observations of the retinal vessels made during episodes of transient monocular blindness show either an arrest of blood ow in the retinal arteries and breaking up of the venous columns to form a boxcar pattern or scattered bits of white material temporarily blocking the retinal arteries These observations indicate that in some cases of ischemic attacks involving the retinal vessels, a temporary, complete, or relatively complete cessation of blood ow occurs locally and that the cause is sometimes microembolism TIAs have in the past been attributed to cerebral vasospasm or to transient episodes of systemic arterial hypotension with resulting compromise of the intracranial circulation, but neither of
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these mechanisms is likely in the typical case Although hypotension may cause focal EEG changes, it has not, in the authors experience, reproduced the attacks in either the carotid or basilar territory In the majority of cases, the attacks bear no strict relation to position or activity, although they are likely to occur when the patient is up and around rather than lying down Nevertheless, a small proportion of patients with carotid or basilar artery stenosis clearly relate the onset of their attacks to standing up after lying or sitting Transient symptoms present on awakening from sleep usually indicate that a stroke is impending Rarely, TIAs are experienced in relation to exercise, outbursts of anger or joy, and bouts of coughing On the other hand, exercise and postural TIAs are particularly suggestive of stenosis of aortic branches, as occurs in Takayasu disease (see further on) and dissection of the aortic arch and occasionally in a xed carotid stenosis TIAs induced by hyperventilation are said to be characteristic of moyamoya disease, a progressive stenosis of intracranial vessels discussed in a later section In states of anemia, polycythemia, thrombocythemia, extreme hyperlipidemia, hyperviscosity from macroglobulinemia, sickle cell anemia, and hypoglycemia, there may be transient neurologic de cits related to rheologic changes in blood, as already mentioned In some of these cases, stenosis in a large or small vessel appears to have accounted for a restricted neurologic de cit, but just as often the vasculature is normal Patients with antiphospholipid antibodies may have TIAs, the mechanism of which is unde ned In some instances the TIAs begin after the artery has already been occluded by thrombus As shown by Barnett, emboli may arise from the distal end of the thrombus or enter the upper part of the occluded vessel through a collateral artery However, almost one- fth of carotid TIAs in the series of Pessin and colleagues and a somewhat larger proportion of cases reported by Ueda and coworkers had neither stenosis nor ulceration of the carotid arteries In most of the cases with normal carotids, the ischemic attacks exceeded 1 h in duration, suggesting embolism from the heart or great vessels including the aortic arch; but there were also a small number of brief ischemic attacks that were unexplained even after arteriography In general, hemodynamic changes in the retinal or cerebral circulation make their appearance when the lumen of the internal carotid artery is reduced to 15 mm or less (normal diameter, 70 mm; range, 5 to 10 mm, smaller part of this range in women) This corresponds to a reduction in cross-sectional area of more than 95 percent The exact degree of stenosis that may cause TIAs and the risk of stroke with mild and moderate degrees of stenosis is controversial and is addressed further on Differential Diagnosis of Transient Ischemic Attacks Transient focal neurologic symptoms are ubiquitous in neurologic practice They may be due to seizures, migraine, or unusual conditions such as transient global amnesia (page 379), and they occur occasionally in patients with multiple sclerosis Almost always the clinical setting in which they occur indicates the nature of the attack Transient episodes, indistinguishable from TIAs, are also known to occur in patients with meningioma, glioblastoma, metastatic brain tumors situated in or near the cortex, and even with subdural hematoma Although infrequent, these attacks are important mainly because the use of anticoagulants is relatively contraindicated in some of these circumstances The episodes that we have seen with meningiomas and subdural hematomas have consisted mainly of transient aphasia or speech arrest lasting from 2
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