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din, and also prostacyclin, a vasodilating prostaglandin In patients who cannot tolerate aspirin, the platelet aggregate inhibitor clopidogrel or a similar drug (such as ticlopidine or dipyridamole) can be substituted (see below) A number of controlled studies have attested to the therapeutic value of aspirin and ticlopidine, clopidogrel, or dipyridamole, but it is important not to exaggerate the magnitude of their effects These studies have been critically reviewed by Tijssen and by Algra and colleagues With few exceptions, it can be concluded that aspirin is bene cial in preventing stroke; whether low doses (50 to 100 mg) and high doses (1000 to 1500 mg) provide equivalent protection is still uncertain From a review of these studies, it appears that both dosages are effective and that the addition of dipyridamole further reduces the risk of stroke by a small amount Ticlopidine and clopidogrel are believed by some, on the basis of clinical trials, to be marginally more effective than aspirin for the prevention of stroke, but they are far more expensive, and ticlopidine is potentially toxic (neutropenia) Dipyridamole in high doses has not been as well tolerated by our patients because of induced dizziness The combined use of these drugs with aspirin has not been extensively examined, but recent data from the PROFESS trial (Prevention Regimen for Effectively Avoiding Second Strokes) has suggested that there may be an increased risk of cerebral hemorrhage when aspirin is combined with clopidogrel; our patients have not experienced such events, but perhaps the combination should be used with caution These studies notwithstanding, the therapeutic effectiveness of aspirin is still rather slight The cumulative evidence from trials with aspirin alone indicates that a dose of aspirin of at least 30 mg/ day reduces by 13 percent, at most, the progression or recurrence of stroke (Algra et al) Moreover, in each of the trials, a signi cant number of subsequent ischemic strokes occurred in patients while they were receiving aspirin The best course of treatment for patients who have lacunar or atherothrombotic strokes while already receiving antiplatelet medications is not clear Control of blood pressure and the administration of a lipid-lowering drug is advisable, even if lipid levels are normal Switching to warfarin from anti-platelet agents is sensible in some circumstances but should be done with caution Other Forms of Medical Treatment Treatment by hemodilution was popularized by the studies of Wood and Fleischer, who showed a high incidence of short-term improvement when the hematocrit was reduced to approximately 33 percent That lowering blood viscosity improves regional blood ow in the heart had been known for some time, and a similar effect on the brain has been demonstrated by CBF studies Earlier observations had shown a reduction in the overall neurologic de cit, but almost all larger randomized trials which included patients in many settings who were treated at various times up to 48 h after stroke failed to con rm any such bene t, and the use of this treatment has been virtually abandoned Nevertheless, we continue to see a few patients whose hemiparesis and aphasia have improved during and just after removal of a unit or more of blood and replacement with albumin and saline While this treatment cannot be recommended as a routine approach, it may have some merit in selected situations, such as uctuating stroke Therapies aimed at improving blood ow by enhancing cardiac output (aminophylline, pressor agents), by improving the microcirculation (mannitol, glycerol, dextran), or by use of a large number of vasodilating drugs (see below) have failed to show consistent bene ts, but several are still under study.

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Hyperbaric oxygen may reduce ischemic de cits temporarily but has no sustained effect Induced hypothermia limits the size of ischemic stroke, but it is technically dif cult to administer and often has serious side effects Calcium channel blockers of the types administered for cardiac disease have also been found to increase CBF and to reduce lactic acidosis in stroke patients However, several multicenter clinical trials that compared calcium channel blockers with placebo did not establish a difference in outcome in the two groups There has also been interest, as noted earlier in this chapter, in drugs that inhibit excitatory amino acid transmitters and free-radical scavengers such as dimethyl sulfoxide (DMSO) and growth factors, but so far none of these has been successfully applied to humans Despite some experimental evidence that certain vasodilators, such as CO2 and papaverine, increase CBF, none has proved bene cial in carefully studied human stroke cases at the stage of TIAs, thrombosis in evolution, or established stroke Vasodilators may actually be harmful, at least on theoretical grounds, since by lowering the systemic blood pressure or dilating vessels in normal brain tissue (the autoregulatory mechanisms are lost in vessels within the infarct), they may reduce the intracranial anastomotic ow Moreover, the vessels in the margin of the infarct (border zone) are already maximally dilated New discoveries regarding the role of nitric oxide in vascular control will probably give rise to new pharmacologic agents, which will have to be evaluated Surgery and Angioplasty for Symptomatic Carotid Stenosis Comments have already been made concerning the opening of an occluded carotid artery soon after a stroke Here we discuss the patient who has passed the acute period, when surgery is safer, or who has TIAs The region that most often lends itself to such therapy is the carotid sinus (the bulbous expansion of the internal carotid artery just above its origin from the common carotid) Other sites suitable for surgical management include the common carotid, innominate, and subclavian arteries Operation on the vertebral artery at its origin has proved successful only in exceptional circumstances In recent years balloon angioplasty and stenting of the carotid artery have become increasingly popular as an alternative to surgery (see below) Surgery and angioplasty, in our opinion, are as yet applicable mainly to the group of patients with symptomatic carotid artery stenosis (the asymptomatic ones are discussed below) who have substantial extracranial stenosis but not complete occlusion, and, in special instances, in those with nonstenotic ulcerated plaques Those with stenosis constitute less than 20 percent of all patients with TIAs (Marshall); but from the perspective of surgical therapy, the term symptomatic encompasses both TIAs and small strokes ipsilateral to the stenosis There is now convincing evidence that well-executed surgery in appropriately chosen cases arrests the TIAs and diminishes the risk of future strokes These views have received strong af rmation from two well-designed randomized studies the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST) The conclusion, reached in each of these studies, was that carotid endarterectomy for symptomatic lesions causing severe degrees of stenosis ( 70 to 80 percent reduction in diameter) is effective in reducing the incidence of ipsilateral hemispheral strokes These two trials differed in the method of estimating the degree of stenosis, but when adjustments are made, the results are comparable (Donnan et al) Patients in the European study with mild or moderate stenosis (up to 70 percent) did not bene t from endar-.

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