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• The phenomenon of shunting of blood in association with various intracranial lesions is well known; however, usually clinical symptoms are attributable to the lesion and not to the redistribution of regional cerebral blood flow (rCBF).We repprt three patients investigated by angiography and rCBF studies in whom symptoms appeared to be due to a hemodynamic steal within one cerebral hemisphere, between hemispheres, and from the brain into a tumor, respectively.

DESPITE an ever-growing literature on the subject, the basic pathological mechanisms concerned in the effect of oxygen lack on the brain remain largely unknown.1 One reason for confusion in this field has been the synonymous use of the terms anoxia and ischemia. For example, it is still widely held that "anoxia" will under certain conditions produce cerebral edema,2-5 this term implying, in some instances, deprivation of the organism's oxygen supply and, in others, diffuse cerebral ischemia which involves many other factors in addition to anoxia. The importance of this "anoxic edema" concept has immediate and obvious implication for the clinician, since it is recognized that an increase in brain volume may in itself prove fatal by compression of vital structures.6Much of the evidence supporting the anoxic edema hypothesis was based either on histopathological findings now believed to belargely artifactual7 or indirectly on measurements of

• Fifty-three patients with acute cerebral infarction were treated in a doubleblind study with either dexamethasone or placebo within 24 hours of the onset of stroke. Forty-one of these survived for longer than 28 days, and the patients treated with the steroid fared slightly worse than those treated with placebo at the end of this time. Two of the five patients who died in the placebo group died of cerebral edema, compared with three out of seven patients who died in the steroid group. Infectious complications, gastrointestinal hemorrhage, and occasional serious exacerbations of diabetes occurred more commonly in the steroid group.

TO THE EDITOR. —We found the hypothesis of carotid plaque disruption proposed by Fisher et al1 interesting but at variance with our clinicopathologic data in Toronto, Canada. The authors emphasize surface events in carotid plaques, but we believe that events within the body of the plaque may be equally, or even more, important.We evaluated 71 consecutive symptomatic carotid plaques, and found 85% had large hemorrhages, about half of which were massive and destructive to the plaque. The hemorrhages were mainly deeply situated, rarely connected to the lumen, but occurred mainly at the "shoulder" of the plaque, often the site of rich vascularity. Intraluminal clot was microscopic and infrequent except in one occluded case. Intraplaque hemorrhages were often older than the elapsed time, since symptoms, apparently preceding clinical events by weeks, were presumably not directly related. One patient underwent bilateral carotid surgery, and the pathologic findings of the symptomatic

TO THE EDITOR. —The commentaries by Drs Yatsu and Fields and by Drs Quiñones-Baldrich and Moore on the management of asymptomatic patients with carotid bruits and carotid stenosis provide two extreme perspectives.Drs Yatsu and Fields believe discovery of an asymptomatic neck bruit does not justify investigation since the risk of thromboembolic stroke is low. Drs Quiñones-Baldrich and Moore maintain that prophylactic endarterectomy is indicated for lesions of greater than or equal to 70% stenosis, assuming the patient is healthy, and that surgical morbidity and mortality is less than 3%.Our calculations indicate that surgery should be contemplated only for patients with a stroke risk of at least 5% per year.1 Assuming a mortality from causes other than stroke of 4% per year, a perioperative stroke or death rate of 3%, and a stroke risk reduction of two thirds (after uncomplicated surgery), the "break-even point" (after which a beneficial