In a consecutive series of 1930 carotid endarterectomies there were eight cases of postoperative intracerebral hemorrhage. One of these patients was operated on 2 weeks following cerebral infarction and had severe uncontrollable hypertension after surgery. A second patient had an intraoperative embolus and bled while fully heparinized on the 3rd postoperative day. Only one patient in the series bled into an area of documented cerebral infarction. The remainder of the cases represented hemorrhage into essentially normal brain. Seven of the eight patients with intracerebral hemorrhage had high-grade internal carotid artery stenosis preoperatively. Although several factors have contributed to the brain hemorrhages in this series of patients, postoperative cerebral hyperperfusion which often follows endarterectomy may have played an important role. Defective cerebrovascular autoregulation in chronically ischemic brain regions may predispose patients to intracerebral hemorrhage after removal of a high-grade stenosis of the internal carotid artery.

We describe a 63-year-old man with severe bilateral internal carotid artery disease who presented with repeated, brief attacks of left limb shaking precipitated by his standing up. Cerebral blood flow measured by xenon-133 inhalation showed reduced resting flows and a focal perfusion deficit in the right dorsofrontal and upper rolandic regions. Blood flow velocity and pulsatility index of the right middle cerebral artery measured by transcranial Doppler ultrasonography were also reduced. With hypercapnic challenge, both hemispheric tissue perfusion and blood flow velocity showed impaired reactivity. With induced hypotension, the focal perfusion deficit in the right dorsofrontal region was accentuated. Following right internal carotid endartectomy, resting cerebral blood flow and blood flow velocity improved, as did hypercapnic vasoreactivity. These reversible deficits in cerebral blood flow and vasoregulation, which were maximal in the dorsofrontal region, are consistent with low perfusion in the border zone territory or the distal fields and demonstrate that hemodynamic failure is the likely mechanism for limb-shaking transient ischemic attacks from severe carotid artery disease. (Stroke 1990;21:341-347)A ttacks of limb-shaking are an uncommon manifestation of transient cerebral ischemia, L characterized by brief, repetitive jerking movements of the arm or leg, resembling simple partial motor seizures. 1 Since the first recognition of this phenomenon by Fisher, 2 subsequent observations 3 " 5 have firmly established its association with severe carotid occlusive disease. Attacks appear to cease following carotid endarterectomy. 5 Transient focal cerebral ischemia has been the presumed explanation for these attacks, although hemodynamic studies have not been previously reported to support the specific role of perfusion insufficiency in the border zone territory.We describe an unusual patient with limb-shaking transient ischemic attacks (TIAs) whose symptoms occurred repeatedly upon his standing up. Hemodynamic findings from xenon-133 cerebral blood flow Received July 10, 1989; accepted October 3, 1989. (CBF) and transcranial Doppler ultrasonography (TCD) studies obtained during hypercapnia and induced hypotension support the mechanism of distalfield ischemia in the pathogenesis of these attacks. Case ReportA 63-year-old right-handed man with hypertension (treated with o-methyldopa) and diet-controlled diabetes mellitus presented with recurrent, brief, stereotypical attacks of left limb shaking precipitated by his standing up. He described "buckling and jerking" of his left leg, without weakness, which interfered with ambulation; he was unable to grasp objects with his left hand because of clumsiness. Each attack occurred reliably on his standing up from either a supine or a sitting position, with a 5-second latency. Each attack usually lasted no longer than 10 seconds; a few attacks lasted as long as 1-2 minutes. He experienced as many as six attacks daily; during each attack he remained fully alert and was ca...

The intravenous injection of the surface-active agents Tween 80 and Triton A20 into rabbits fed a normal diet resulted in marked and sustained elevations of the cholesterol, phospholipid, and total lipid content of their blood. The increase in phospholipid in general paralleled that of the blood cholesterol. The implications of the findings are briefly discussed.

Tb investigate the association between carotid plaque hematoma and symptoms of cerebral ischemia a retrospective review of 200 consecutive carotid endarterectomies at the Neurological Institute of New York was carried out. Data analyzed included cerebral ischemic symptoms, angiographic findings, preoperative use of antithrombotic agents, and microscopic pathology of endarterectomy specimens. No association was found between ischemic symptoms ipsilateral to the endarterectomy and presence, size, or age of plaque hematomas. Plaque hematomas were less common among patients who took antithrombotic agents preoperatively than among those who did not. The presence of plaque hematoma was associated with angiographic carotid cross-sectional area stenosis of >75%. Patients with stenosis of <75% were more likely than those with stenosis of >75% to have ischemic symptoms ipsilateral to the endarterectomy, suggesting that criteria for surgical treatment of carotid atherosclerosis differ for those who are symptomatic vs. those who are asymptomatic. These results demonstrate the limitation of using a surgical series to extend causal inferences about the relation between plaque hematoma and cerebral ischemic symptoms to the general population of people with carotid atherosclerosis. (Stroke 1987;18:879-881) H emorrhage into atheromatous plaque is a common feature of large artery atherosclerosis. 1 " 3 Some investigators have reported that carotid plaque hematomas occur significantly more often in symptomatic patients undergoing endarterectomy compared with those who are asymptomatic and that there is a correlation between age of the hematoma and timing of the symptoms.4 "* They postulate that plaque hematoma is an important precipitator of transient ischemic attack (TIA) and stroke, either by causing acute severe stenosis or by producing intimal disruption leading to overlying thrombus formation and consequent embolism. This argument provides a rationale for the role of endarterectomy in the prevention of stroke in people with atherosclerotic plaques or stenosis, both symptomatic and asymptomatic. Furthermore, it is suggested that the use of antithrombotic agents may obscure warning symptoms and may increase the risk of plaque hematoma. 6 We conducted a study of all persons undergoing endarterectomy at the Neurological Institute of New York from October 1982 to May 1984 to further investigate the relation of carotid plaque hematoma to the occurrence of TIA and stroke in surgically treated patients and to determine if preoperative use of antithrombotic agents was associated with the presence of plaque hematoma. Subjects and MethodsDuring the period under study, 200 carotid endarterectomies were performed. The study included those 198 endarterectomies about which clinical information could be found. Ninety-three men and 84 women with a mean age of 66 years comprised the study population; 156 had unilateral and 21 had bilateral endarterectomies. Clinical information was obtained by chart review to determine whether symptoms of foc...