Abstracts of Literature
Some Patients With Intracranial Aneurysms Have a Reduced Type III/Type I Collagen Ratio: A Case-Control Study—van den Berg JSP, Limburg M (Dept of Neurology, Academic Medical Center, PO Box 22660, 1100 DD Amsterdam, Netherlands), Pals G, Arwert F, Westerveld A, Hennekam RCM, Albrecht KW—Neurology. 1997;49:1546–1551.
A reduced production of type III collagen has been reported in previous studies to be associated with intracranial aneurysms. The purpose of this prospective case-control study was to assess the possible role of a reduced type III collagen production as a risk factor for having an intracranial aneurysm. The study group consisted of 41 consecutively admitted patients with intracranial aneurysms. Intracranial aneurysms were demonstrated by intraarterial digital subtraction cerebral angiography or during operation. The control group consisted of 41 healthy volunteers matched for age and sex. Fibroblasts were cultured from skin biopsies from patients and control subjects, and the type III/type I collagen ratios were determined. The type III/type I collagen ratios in the controls ranged from 5.5 to 19.8%, with a median ratio of 10%, and none had a ratio below 5.5%. The type III/type I collagen ratios in patients ranged from 1.1 to 25.1%, with a median ratio of 10.5%, and eight patients (19.5%) had a low (<5.5%) ratio (p=0.005, Fisher’s exact test). Our findings support the hypothesis that a reduced production of type III collagen may contribute to the formation of intracranial aneurysms in some patients.
Key Words: aneurysm, collagen
Intracranial Aneurysm: Anatomic Factors That Predict the Usefulness of Intraoperative Angiography—Derdeyn CP (Section of Neuroradiology, Mallinekrodt Institute of Radiology, Washington University School of Medicine, 510 S Kingshighway Blvd, St Louis, MO 63110), Moran CJ, Cross III DT, Sherburn EW, Dacey Jr RG—Radiology. 1997;205:335–339.
Purpose: To correlate the size and location of intracranial aneurysm with the need to reposition the aneurysm clip after intraoperative angiography.
Materials and Methods: In 199 consecutive patients with 234 clipped intracranial aneurysms, 273 intraoperative angiographic studies were retrospectively reviewed. Aneurysm size and location, determined with preoperative angiographic and surgical reports, were correlated with the frequency of clip repositioning because of parent- or branch-vessel compromise or unexpected residual aneurysm.
Results: Findings from intraoperative angiograms resulted in clip repositioning in 46 of 273 (16.8%) studies. Clip repositioning was statistically significantly less frequent with aneurysms of the posterior communicating (three of 52 [5.7%] studies) and anterior choroidal (none of 12 studies) arteries. High rates of clip repositioning were found in aneurysms of the superior hypophyseal artery (seven of 18 [38.9%] studies), superior cerebellar artery (three of five [60.0%] studies), and bifurcation of the internal carotid artery (three of nine [33.3%] aneurysms). In 98 conventional follow-up angiographic studies, seven (7%) false-negative cases with unsuspected aneurysm neck remnant were found.
Conclusion: The rate of clip repositioning in aneurysms of the posterior communicating or anterior choroidal arteries was less than that at other locations (P<.05). Intraoperative angiography may not be necessary when aneurysms are at these two locations.
Key Words: aneurysm, angiography, intraoperative
Remote Effect of Brain Retraction on Regional Cerebral Blood Flow and Cerebrovascular Reserve on Single Photon Emission Computed Tomography—Sloniewski P, Zieliñski P (Dept of Neurosurgery, Medical University of Gdansk, Debinki Str 7, 80-211 Gdansk, Poland)—Surg Neurol. 1997;48:511–513. ©1997 by Elsevier Science Publishing Co, Inc.
Background The purpose of this study is to evaluate the effect of brain retraction 1 year or more after intracranial aneurysm clipping, demonstrated by a regional cerebral blood flow (rCBF) imaging technique.
Methods and Results rCBF and cerebrovascular reserve (CV) were evaluated in 40 patients 12–25 months after operation, using single photon emission computed tomography (SPECT) with Tc-99m-hexamethylpropylene amine oxime (HMPAO) combined with acetazolamide test. The images were analysed semiquantitatively, focusing on regions of interest (ROIs) chosen for places retracted during the operation. The regions of hypoperfusion in the retracted tissue were clearly visible in 26 cases. Assymmetry of measured activity, expressed in the Assymmetry Index, reached 12% (SEM±8). After injection of acetazolamide during hypercapnia, the assymmetry decreased.
Conclusions The results confirm the negative role of brain retraction. However, these consequences seem to be diminished by good vasoreactivity. ©1997 by Elsevier Science Inc.
Key Words: surgery, cerebral blood flow
Early Carotid Atherosclerosis of the Internal and External Carotid Artery Related to Twenty-Four-Hour Blood Pressure Variability—Sander D, Klingelhöfer J (Dept of Neurology, Technical University of Munich, Möhlstrasse 28, D-81675 München, Germany)—Cerebrovasc Dis. 1997;7:338–344. Reprinted with permission of S. Karger AG, Basel.
We analyzed the relationship between 24-hour blood pressure variability and spatial distribution and extent of early carotid atherosclerosis in 208 hypertensive and 216 normotensive patients aged over 55 years. Circadian blood pressure patterns were evaluated noninvasively with a long-term blood pressure monitor. The extent of atherosclerosis was measured as the intima-to-media wall thickness (IMT) of the internal (ICA) and external carotid artery (ECA). No significant differences regarding age, sex, smoking, diabetes, cholesterol and triglycerides were found in either patient group. In both groups, a linear correlation between ICA and ECA IMT was observed. However, the slope of the regression line was clearly increased in hypertensive patients [0.563 (95% confidence interval 0.522, 0.604) vs. 0.436 (0.364, 0.509); p<0.01]. Multivariate regression analysis revealed the strongest correlation between the IMT of the ICA and the diurnal systolic blood pressure variability; this parameter was not significantly associated with the ECA IMT. The odds ratio of having ischemic heart disease was significantly raised in patients with early atherosclerosis of the ICA but not the ECA [4.7 (2.5, 8.8); p<0.001 vs. 1.6 (0.7, 3.6)]. Our results show that the diurnal systolic blood pressure variability is closely correlated with early carotid atherosclerosis of the ICA but not the ECA territory. The analysis of circadian blood pressure patterns is useful to explain the focal effects of blood pressure on the development of atherosclerosis.
Key Words: blood pressure, carotid artery stenosis
Aortic Plaque Morphology and Vascular Events: A Follow-up Study in Patients With Ischemic Stroke—Cohen A (Service de Cardiologie, Saint-Antoine University and Medical School, Université Pierre et Marie Curie, 184 rue du faubourg St-Antoine, 75571 Paris Cedex 12, France), Tzourio C, Bertrand B, Chauvel C, Bousser M-G, Amarenco P—Circulation. 1997;96:3838–3841.
Background Atherosclerotic disease of the aortic arch has been found to be associated with the risk of ischemic stroke. We have shown that atherosclerotic plaques ≥4 mm in thickness in the ascending aorta and proximal arch detected by transesophageal echocardiography are a risk factor for ischemic stroke. The purpose of this study was to evaluate the impact, if any, of plaque morphology (ulceration, hypoechoic plaques or calcification) on the risk of subsequent vascular events.
Methods and Results We followed for a period of 2 to 4 years, a cohort of 334 patients 60 years or older who were consecutively admitted with brain infarction and who had transesophageal echocardiography. The risk of vascular events in patients with plaques in the aortic arch according to the presence of surface ulceration, calcifications, and sessile or mobile thrombus was estimated during a total of 788 person-years of follow-up. Hypoechoic plaques, calcifications, and ulceration were more frequently found in patients with plaques ≥4 mm as compared with those with plaques <4 mm. The presence of ulceration did not increase the relative risk of vascular events in patients with plaque ≥4 mm (the relative risk was 4.3 [P<.001] in those with ulceration and 5.7 [P<.001]) in those without ulceration. The lack of calcification did increase the risk of vascular events in patients with plaque ≥4 mm. The highest relative risk of events was found among the patients with noncalcified plaques (relative risk, 10.3; 95% confidence interval, 4.2 to 25.2; P<.001). The risk of events was systematically higher in patients without calcifications than in patients with calcifications regardless of what other morphological features were considered.
Conclusions In patients with brain infarction, the risk associated with aortic plaque thickness (≥4 mm) is markedly increased by the absence of plaque calcifications. These findings are important for the design of therapeutic trials in such patients.
Key Words: aortic arch, stroke, ischemic
Hypokalemia and Potassium Excretion in Stroke Patients—Gariballa SE, Robinson TG, Fotherby MD (University Dept of Medicine for the Elderly, The Glenfield Hospital, Leicester LE3 9QP, UK)—J Am Geriatr Soc. 1997;45:1454–1458.
Objectives: To determine (1) the prevalence of hypokalemia (plasma potassium ≤3.4 mmol/L) in a group of stroke patients in comparison with age- and sex-matched groups of patients having sustained a myocardial infarction or having mild hypertension and (2) the association between plasma potassium concentration and stroke outcome.
Design: Observational study.
Participants: A total of 421 consecutive stroke patients admitted to a teaching hospital, 150 consecutive patients 50 years or older with myocardial infarction admitted to the hospitals Coronary Care Unit, and 161 out-patients 60 years or older with borderline and established hypertension.
Measurements: All stroke and cardiac patients had plasma urea and electrolytes estimated within 2 hours of hospital admission; in the hypertensive group blood samples were taken in clinic. Stroke patients had blood pressure, stroke severity (Barthel score) and smoking status recorded. A sub-group of 61 stroke patients and all 79 hypertensive patients not taking antihypertensive medication had 24-hour urine electrolyte excretion measured. Outcome (independent, dependent, or dead) at 3 months post-stroke was established in 349 patients.
Results: Hypokalemia occurred more frequently in stroke patients than in patients with myocardial infarction (84 (20%) vs 15 (10%), P=.008) or patients with hypertension (84 (20%) vs 13 (8%), P<.001), even when patients taking diuretics were excluded from analysis (56 (19%) vs 12 (9%) of cardiac group, P=.014 and 56 (19%) vs 4 (5%) of hypertensive group, P=.005, respectively). 24-hour urine excretion of potassium and the potassium: creatinine ratio was lower in stroke patients than in hypertensive patients (41±21 vs 62±25 mmol/24 hour, P=.001, 5.5±2.2 vs 7.4±2.6 mmol/24 hour, P=.001, respectively). On survival analysis, a lower plasma potassium on admission to hospital was associated with an increased chance of death, independent of age, stroke severity, history of hypertension, blood pressure level, or smoking history (hazard ratio 1.73 (95% CI: 1.03–2.9) for a 1 mmol/L lower plasma potassium concentration).
Conclusions: Hypokalemia post stroke is common and may be associated with a poor outcome.
Key Words: potassium, stroke, acute
Stroke Mechanisms and Clinical Presentation in Large Subcortical Infarctions—Horowitz DR (Dept of Neurology, Box 1052, The Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029), Tuhrim S—Neurology. 1997;49:1538–1541.
Large subcortical infarctions may be due to cerebral embolism and cause cortical signs more frequently than small subcortical infarctions, which usually result from small-vessel disease and are not associated with cortical findings. We evaluated 51 consecutive patients with a subcortical infarct on CT that was 1.5 cm or larger for a potential carotid or cardiac source of embolism and determined how frequently aphasia, hemineglect, or gaze paresis occurred. A carotid or cardiac embolic source was identified in 63% of the total population with a carotid source occurring in 23% and a cardiac source occurring in 49%. More than one-half of the patients with hypertension or diabetes mellitus had an embolic source, whereas all patients without these risk factors had a possible carotid or cardiac source of embolism. Aphasia or hemineglect occurred in 39% of patients and gaze paresis occurred in 41%. Large subcortical strokes frequently result in a different clinical syndrome and from a different mechanism than small subcortical strokes.
Key Words: subcortical infarction, cerebral embolism
Dichotomizing Stroke Outcomes Based On Self-Reported Dependency—Kay R (Dept of Medicine, Prince of Wales Hospital, Shatin, Hong Kong), Wong KS, Perez G, Woo J—Neurology. 1997;49:1694–1696.
Patients participating in a clinical trial of stroke therapy were assessed 3 months after randomization using the Barthel Index, the Modified Rankin Scale, questions on activities of daily living, and extent of recovery. Those who needed help in performing the activities of daily living and had not recovered completely were classified as dependent. Self-reported dependency had a sensitivity of 94% and specificity of 80% against the Barthel Index dichotomized at 16 or below, or a sensitivity of 85% and specificity of 87% against the Modified Rankin Scale dichotomized at 2 or above.
Key Words: stroke outcome, activities of daily living
von Willebrand Factor and Risk of Ischemic Stroke—Qizilbash N (Memory Trials Research Group, Dept of Clinical Geratology, University of Oxford, Radcliffe Infirmary, Oxford OX2 6HE, UK), Duffy S, Prentice CRM, Boothby M, Warlow C—Neurology. 1997;49:1552–1556.
We carried out a case-control study to determine whether von Willebrand factor (vWF) antigen (and factor VII and tissue plasminogen activator [tPA] antigens) are associated with ischemic stroke. Ninety-five patients with transient ischemic attack or minor ischemic stroke recruited from the Oxfordshire Community Stroke Project and one neurology clinic were compared with 236 controls, group-matched for age and sex, from the same general practitioners as the incident cases. In crude analyses, concentrations of vWF antigen were significantly higher in cases than in controls (p=0.004). The age- and sex-adjusted odds ratios from lowest (referent) to highest quartile of vWF antigen were 1.00, 1.15, 2.34, and 2.36. (trend test, p=0.006). Factor VII antigen and tPA antigen were not significantly different between cases and controls. Although adjustment for other potential risk factors abolished the statistical significance of the association between vWF and disease, this was largely due to the influence of history of ischemic heart disease. We conclude that vWF is a potent and independent risk factor for transient ischemic attack, minor ischemic stroke, and, by extrapolation, ischemic stroke in general. The data also suggest that vWF may be a risk factor for both ischemic stroke and ischemic heart disease. We found no evidence to implicate factor VII and tPA as risk factors for ischemic stroke.
Key Words: von Willebrand factor, risk factors
Hemostatic Factors as Predictors of Ischemic Heart Disease and Stroke in the Edinburgh Artery Study—Smith FB (Wolfson Unit for Prevention of Peripheral Vascular Diseases, Dept of Public Health Sciences, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG, Scotland, UK), Lee AJ, Fowkes FGR, Price JF, Rumley A, Lowe GDO—Arterioscler Thromb Vasc Biol. 1997;17:3321–3325.
Plasma fibrinogen is a consistent predictor of ischemic heart disease (IHD) in prospective studies, but there are fewer data relating other hemostatic variables to IHD and also to stroke. We therefore studied the relationships of plasma fibrinogen, von Willebrand factor antigen, tissue plasminogen activator (TPA) antigen, factor VII, and fibrin D-dimer to incidence of IHD and stroke and determined whether any associations could be explained by conventional risk factors and baseline heart disease. In the Edinburgh Artery study, 1592 men and women aged 55 to 74 years, randomly sampled from the general population, were followed prospectively over 5 years to detect fatal and nonfatal IHD and stroke events. During the 5 years, 268 new vascular events were identified. Baseline plasma fibrinogen was independently related to risk of stroke in multivariate analysis that adjusted for cigarette smoking, LDL-cholesterol, systolic blood pressure, and preexisting IHD (relative risk [RR] 1.52, 95% confidence interval [CI] 1.17, 1.98). TPA antigen, and fibrin D-dimer were also independently associated with risk of stroke (RR 1.69, 95% CI 1.22, 2.35 and RR 1.96, 95% CI 1.12, 3.41, respectively). Significant relationships were found between TPA antigen and myocardial infarction (P≤.05). In older men and women, increased coagulation activity and disturbed fibrinolysis are predictors of future vascular events (both IHD and stroke).
Key Words: tissue plasminogen activator, cerebral ischemia
Body Iron Stores and the Risk of Carotid Atherosclerosis: Prospective Results From the Bruneck Study—Kiechl S (Dept of Neurology, Innsbruck University Hospital, Anichstr 35, A-6020 Innsbruck, Austria), Willeit J, Egger G, Poewe W, Oberhollenzer F—Circulation. 1997;96:3300–3307.
Background Fe2+ released from tissue iron stores may accelerate lipid peroxidation by virtue of its pro-oxidant properties and thus promote early atherogenesis.
Methods and Results The present prospective survey addresses the potential association between serum ferritin concentrations and the 5-year progression of carotid atherosclerosis as assessed by ultrasonographic follow-up evaluations. The study population comprises a random sample of 826 men and women 40 to 79 years old. Serum ferritin was one of the strongest risk predictors of overall progression of atherosclerosis. The main part of this association appeared to act through modification of the atherogenic potential of LDL cholesterol (OR [95% CI] for a 1-SD unit increase in ferritin at LDL levels of 2.5, 3.6, and 4.9 mmol/L: 1.55 [1.30 to 1.85], 1.77 [1.40 to 2.24], and 2.05 [1.50 to 2.80]: P=.0012 for effect modification). Changes in iron stores during the follow-up period modified atherosclerosis risk, in that a lowering was beneficial and further iron accumulation exerted unfavorable effects. All these findings applied equally to incident atherosclerosis and the extension of preexisting atherosclerotic lesions. The significance of prominent iron stores in the development of carotid stenosis was clearly less pronounced. Finally, ferritin and LDL cholesterol showed a synergistic association with incident cardiovascular disease and death (n=59).
Conclusions The present study provided strong epidemiological evidence for a role of iron stores in early atherogenesis and suggests promotion of lipid peroxidation as the main underlying pathomechanism. This hypothesis could in part explain the sex difference in atherosclerotic vascular disease.
Key Words: carotid artery diseases, iron
Atrial Fibrillation in Older Stroke Patients: Association With Recurrence and Mortality After First Ischemic Stroke—Kaarisalo MM (Rykmentintie 26, 20810 Turku, Finland), Immonen-Räihä P, Marttila RJ, Lehtonen A, Salomaa V, Sarti C, Sivenius J, Torppa J, Tuomilehto J—Am Geriatr Soc. 1997;45:1297–1301.
Objectives: The objective of this study was to determine the association of atrial fibrillation (AF) with stroke recurrence and mortality and with the causes of death in ischemic stroke patients aged 75 years and older.
Design: A population-based study.
Setting: The cities of Turku and Kuopio in Finland.
Participants: The study cohort consisted of 2635 consecutive patients aged 75 years and older, with a first ischemic stroke, registered in the FINMONICA Stroke Register.
Measurements: 28-day and 1-year stroke mortality, causes of death, and recurrence of stroke.
Results: There were 767 stroke patients with AF (mean age 82.2) and 1868 patients without AF (mean age 81.4). Mortality was higher in the AF group both 28 days (33.9% vs 28.1%, P=.003) and 1 year after the attack (52.7% vs 43.0%, P<.001). The age- and sex-adjusted relative risk of death at 28 days was 1.25 in the AF group (95% confidence interval (CI) 1.04–1.50, P=.018), and at 1 year it was 1.41 (95% CI 1.18–1.67, P<.001). In a Cox proportional hazards model, 1-year mortality risk comparing the AF-group with non-AF group was 1.24 (95% CI 1.10–1.39, P<.001). The strongest risk factor predicting 1-year mortality was recent myocardial infarction (MI) (RR 1.90, 95% CI 1.49–2.42). Myocardial infarction was more often the underlying cause of death in the AF group during the period of 28 days, but not from 28 days up to 1 year. The 1-year recurrence rate among those alive at day 28 was 11.5% in the AF group and 9.4% in the non-AF group (P=.240).
Conclusion: Recent MI and AF are independent negative prognostic factors in older patients with stroke. Although the relative risk estimates attributable to AF are of the same magnitude in older as in middle-aged stroke patients, the much higher prevalence of AF in the older patients emphasizes its absolute impact on the mortality and recurrence after the first ischemic stroke in the age group 75 years and older. The treatment of coexisting cardiac disease also has the potential to prevent deaths and recurrent stroke events in older persons.
Key Words: atrial fibrillation, stroke outcome
Inverse Association of Dietary Fat With Development of Ischemic Stroke in Men—Gillman MW (Dept of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care, 126 Brookline Ave, Suite 200, Boston, MA 02215), Cupples LA, Millen BE, Ellison RC, Wolf PA—JAMA. 1997;278:2145–2150.
Context.—A few ecological and cohort studies in Asian populations suggest an inverse association of the intake of both fat and saturated fat with risk of stroke. However, data among western populations are scant.
Objective.—To examine the association of stroke incidence with intake of fat and type of fat among middle-aged US men during 20 years of follow-up.
Design and Setting.—The Framingham Heart Study, a population-based cohort study.
Participants.—A total of 832 men, aged 45 through 65 years, who were free of cardiovascular disease at baseline (1966–1969).
Measurements and Data Analysis.—The diet of each subject was assessed at baseline by a single 24-hour dietary recall, from which intakes of energy and macronutrients were estimated. In Kaplan-Meier analyses, we calculated age-adjusted cumulative incidence rates of stroke. Using Cox regression, we estimated stroke incidence relative risks during 20 years of follow-up.
Main Outcome Measure.—Incidence of ischemic stroke, which occurred in 61 subjects during the follow-up period.
Results.—Mean intakes were 10 975 kJ for energy; 114 g (39% of energy) for total fat; 44 g (15%) for saturated fat; 46 g (16%) for monounsaturated fat; and 16 g (5%) for polyunsaturated fat. Risk of ischemic stroke declined across the increasing quintile of total fat (log-rank trend P=.008), saturated fat (P=.002), and monounsaturated fat (P=.008) but not polyunsaturated fat (P=.33). The age- and energy-adjusted relative risk for each increment of 3% of energy from total fat was 0.85 (95% confidence interval [CI], 0.78–0.94); for an increment of 1% from saturated fat, 0.91 (95% CI, 0.85–0.98); and for 1% from monounsaturated fat, 0.89 (95% CI, 0.83–0.96). Adjustment for cigarette smoking, glucose intolerance, body mass index, blood pressure, blood cholesterol level, physical activity, and intake of vegetables and fruits and alcohol did not materially change the results. Too few cases of hemorrhagic stroke (n=14) occurred to draw inferences.
Conclusion.—Intakes of fat, saturated fat, and monounsaturated fat were associated with reduced risk of ischemic stroke in men.
Key Words: cerebral infarction, diet
Lifetime Smoking Exposure Affects the Association of C-Reactive Protein With Cardiovascular Disease Risk Factors and Subclinical Disease in Healthy Elderly Subjects—Tracy RP (University of Vermont, Aquatec Bldg T205, 55 A S Park Drive, Colchester, VT 05446), Psaty BM, Macy E, Bovill EG, Cushman M, Cornel ES, Kuller LH—Arterioscler Thromb Vasc Biol. 1997;17:2167–2176.
Blood levels of C-reactive protein (CRP), a marker of inflammation, are related to cardiovascular disease risk. To determine cross-sectional correlates in the elderly, we measured CRP in 400 men and women older than 65 years and free of clinical cardiovascular disease at baseline as part of the Cardiovascular Health Study. Only 2% of the values were greater than 10 mg/L, the cut-point usually used to identify inflammation. CRP levels appeared tightly regulated, since there were strong bivariate correlations between CRP and the following: inflammation-sensitive proteins such as fibrinogen (r=.52); measures of fibrinolysis such as plasmin-antiplasmin complex (r=.23); pack-years of smoking (r=.30); and body mass index (r=.24; all P values≤.001). The association with pack-years was independent of the length of time since cessation of smoking. CRP levels were also associated with coagulation factors VIIc, IXc, and Xc; HDL cholesterol (negative) and triglyceride; diabetes status; diuretic use; ECG abnormalities; and level of exercise. Because of effect modification, two multiple linear regression prediction models were developed for CRP, one each for never smokers and ever smokers. An a priori physiologic model was used to guide these analyses, which disallowed the use of other inflammation-sensitive variables such as fibrinogen. In never smokers, the independent predictors were body mass index (+), diabetes status (+), plasmin-antiplasmin complex (+), and the presence of ECG abnormalities (+): this model predicted 15% of the CRP population variance. In ever smokers, the predictors were body mass index (+), plasmin-antiplasmin complex (+), pack-years of smoking (+), HDL cholesterol (−), and ankle-arm blood pressure index (−): this model predicted 42% of the population variance. We conclude that levels of CRP in the healthy elderly are tightly regulated and reflect lifetime exposure to smoking as well as level of obesity, ongoing level of fibrinolysis, diabetes status, and level of subclinical atherothrombotic disease. Moreover, exposure to smoking affects the relation of CRP to these other factors.
Key Words: inflammation, cigarette smoking
Transient Middle Cerebral Artery Occlusion by Intraluminal Suture: I. Three-Dimensional Autoradiographic Image-Analysis of Local Cerebral Glucose Metabolism-Blood Flow Interrelationships During Ischemia and Early Recirculation—Belayev L, Zhao W, Busto R, Ginsberg MD (Dept of Neurology [D4–5], University of Miami School of Medicine, PO Box 016960, Miami, FL 33101)—J Cereb Blood Flow Metab. 1997;17:1266–1280.
Using autoradiographic image-averaging strategies, we studied the relationship between local glucose utilization (LCMRglc) and blood flow (LCBF) in a highly reproducible model of transient (2-hour) middle cerebral artery occlusion (MCAO) produced in Sprague-Dawley rats by insertion of an intraluminal suture coated with poly-L-lysine. Neurobehavioral examination at 60 minutes after occlusion substantiated a high-grade deficit in all animals. In two subgroups, LCBF was measured with 14C-iodoantipyrine at either 1.5 hours of MCAO, or at 1 hour of recirculation after suture removal. In two other matched subgroups, LCMRglc was measured with 14C-2-deoxyglucose at 1.5 to 2.25 hours of MCAO, and at 0.75 to 1.5 hours of recirculation after 2 hours of MCAO. Average image data sets were generated for LCBF, LCMRglc, and the LCMRglc/LCBF ratio for each study time. Middle cerebral artery occlusion for 2 hours induced graded LCBF decrements affecting ipsilateral cortical and basal ganglionic regions. After 1 hour of recirculation, LCBF in previously ischemic neocortical regions increased by 40% to 200% above ischemic levels, but remained depressed, on average, at about 40% of control. By contrast, frank hyperemia was noted in the previously ischemic caudoputamen. Mean cortical LCBF values during MCAO correlated highly with their respective LCBF values after 1 hour of recirculation (R=0.93), suggesting that postischemic LCBF recovery is related to the depth of ischemia. Despite focal ischemia, LCMRglc during ∼2 hours of MCAO was preserved, on average, at near-normal levels; but following ∼1 h of recirculation, LCMRglc became markedly depressed (on average, 55% of control in previously densely ischemic cortical regions). Regression analysis indicated that this depressed glucose utilization was determined largely by the intensity of antecedent ischemia. By pixel analysis, the ischemic core (defined as LCBF 0% to 20% of control) comprised 33% of the ischemic hemisphere, and the penumbra (LCBF 20% to 40%) accounted for 26%. The penumbra was concentrated at the coronal poles of the ischemic lesion and formed a thin shell around the central ischemic core. During 2 hours of MCAO, the LCMRglc/LCBF ratio within the ischemic penumbra was increased four-fold above normal (average, 179 umol/100 mL). In marked contrast, after ∼1 h recirculation, this uncoupling had almost completely subsided. The companion study (Zhao et al., 1997) further analyzes these findings in relation to patterns of infarctive histopathology.
Key Words: cerebral ischemia, cerebral metabolism
Transient Middle Cerebral Artery Occlusion by Intraluminal Suture: II. Neurological Deficits, and Pixel-Based Correlation of Histopathology With Local Blood Flow and Glucose Utilization—Zhao W, Belayev L, Ginsberg MD (Dept of Neurology [D4–5], University of Miami School of Medicine, PO Box 016960, Miami, FL 33101)—J Cereb Blood Flow Metab. 1997;17:1281–1290.
We conducted a pixel-based analysis of the acute hemodynamic and metabolic determinants of infarctive histopathology in a reproducible model of temporary (2-hour) middle cerebral artery occlusion (MCAO) produced in rats by an intraluminal suture. Three-dimensional averaged image data sets of local cerebral blood flow (LCBF) and glucose utilization (LCMRglc) acquired in the companion study (Belayev et al., 1997) either at the end of a 2-hour period of MCAO or after 1 hour of recirculation were comapped (using digitized atlas-templates) with data sets depicting the frequency of histological infarction in a matched animal group (n=8) in which 2 hours of MCAO was followed by 3-day survival, sequential neurobehavioral examinations, and perfusion-fixation and paraffin-embedding of brains for light-microscopic analysis. All rats developed marked postural-reflex and forelimb-placing deficits at 60 minutes of MCAO, signifying high-grade ischemia. Tactile placing deficits persisted during the 72-hour observation period while visual placing and postural-reflex abnormalities variably improved. Comapping of LCBF and histopathology showed that in those pixels destined to undergo infarction, LCBF measured at 2 hours of MCAO showed a sharp distributional peak centered at 0.14 mL/g/min. In 70% of pixels destined to infarct, LCBF at 2 hours of MCAO was 0.24 mL/g/min or below, and in 89% LCBF was below 0.47 mL/g/min (the upper limits of the ischemic core and penumbra, respectively, as defined in the companion study [Belayev et al., 1997]). Local cerebral glucose utilization measured at ∼1 hour after 2 hours of MCAO was distributed bimodally in the previously ischemic hemisphere. The major peak, at 22 μmol/100 g/min, coincided exactly with the distribution peak of pixels destined to undergo infarction, while in pixels with a zero probability of infarction, LCMRglc was higher by 12 to 13 μmol/100 g/min. These results indicate that local blood flow at 2 hours of MCAO is a robust predictor of eventual infarction. Pixels with ischemic-core levels of LCBF (0% to 20% of control) have a 96% probability of infarction, while the fate of the penumbra is more heterogeneous: below LCBF of 0.35 mL/g/min, the probability of infarction is 92%, while approximately 20% pixels in the upper-penumbral LCBF range (30% to 40% of control) escape infarction. Our data strongly support the view that the likelihood of infarction within the ischemic penumbra is highly influenced by very subtle differences in early perfusion.
Key Words: cerebral ischemia, histology
Delayed Reduction of Ischemic Brain Injury and Neurological Deficits in Mice Lacking the Inducible Nitric Oxide Synthase Gene—Iadecola C (Dept of Neurology, University of Minnesota, Box 295 UM HC, 420 Delaware St SE, Minneapolis, MN 55455), Zhang F, Casey R, Nagayama M, Ross ME—J Neurosci. 1997;17:9157–9164.
Inducible nitric oxide synthase (iNOS), an enzyme that produces toxic amounts of nitric oxide, is expressed in a number of brain pathologies, including cerebral ischemia. We used mice with a null mutation of the iNOS gene to study the role of iNOS in ischemic brain damage. Focal cerebral ischemia was produced by occlusion of the middle cerebral artery (MCA). In wild-type mice, iNOS mRNA expression in the post-ischemic brain begun between 24 and 48 hr peaked at 96 hr and subsided 7 d after MCA occlusion. iNOS mRNA induction was associated with expression of iNOS protein and enzymatic activity. In contrast, mice lacking the iNOS gene did not express iNOS message or protein after MCA occlusion. The infarct and the motor deficits produced by MCA occlusion were smaller in iNOS knockouts than in wild-type mice (p<0.05). Such reduction in ischemic damage and neurological deficits was observed 96 hr after ischemia but not at 24 hr, when iNOS is not yet expressed in wild-type mice. The decreased susceptibility to cerebral ischemia in iNOS knockouts could not be attributed to differences in the degree of ischemia or vascular reactivity between wild-type and knockout mice. These findings indicate that iNOS expression is one of the factors contributing to the expansion of the brain damage that occurs in the post-ischemic period. iNOS inhibition may provide a novel therapeutic strategy targeted specifically at the secondary progression of ischemic brain injury.
Key Words: cerebral ischemia, nitric oxide synthase
Brief Episodes of Ventricular Fibrillation Do Not Influence Postischemic Cerebral Perfusion Assessed by Positron Emission Tomography—Runsiö M (Dept of Cardiothoracic Surgery, Karolinska Hospital, 171 76 Stockholm, Sweden) Brodin L-Å, Eriksson L, Rosenqvist M, Samuelsson S, Stone-Elander S, Öwall A, Ingvar M—Crit Care Med. 1997;25:1827–1830.
Objectives: To establish the defibrillation threshold in patients receiving an implantable cardioverter defibrillator, at least three episodes of ventricular fibrillation are induced and converted back to regular rhythm, using direct current countershocks. The aim of this study was to examine the influence of repeated short episodes of ventricular fibrillation on global and regional cerebral perfusion.
Design: A prospective, descriptive study.
Setting: A positron emission tomography laboratory at a university hospital.
Patients: Four patients, admitted for defibrillation threshold tests 2 yrs after the implantation of a cardioverter defibrillator, were included in the study. Global and regional cerebral blood flow was measured by cerebral positron emission tomography, using an 15O-labeled tracer under propofol-induced general anesthesia. Electroencephalograms (EEGs) were concomitantly recorded.
Interventions: Induction and conversion of ventricular fibrillation.
Measurements and Main Results: No effect on global cerebral perfusion was observed after induced ventricular fibrillation lasting 21±3 secs. The average global cerebral perfusion was 23±1 mL/100 g/min after induction of anesthesia and 31±8 mL/100 g/min and 24±2 mL/100 g/min immediately after the termination of the first and second ventricular fibrillation episodes, respectively. Ten minutes after the second and the third threshold tests, global cerebral perfusion was 21±1 mL/100 g/min and 21±2 mL/100 g/min, respectively. Regional cerebral perfusion and EEGs were not influenced.
Conclusion: Short episodes of ventricular fibrillation did not induce any measurable effects on global and regional cerebral perfusion detectable by positron emission tomography 30 secs and 10 mins after restitution of sinus rhythm.
Key Words: tomography, emission computed, ventricular fibrillation
Cerebral White Matter Changes (Leukoaraiosis), Stroke, and Gait Disturbance—Briley DP (Stoke Mandeville Hospital NHS Trust, Mandeville Rd, Aylesbury, Bucks, HP21 8AL, UK), Wasay M, Sergent S, Thomas S—J Am Geriatr Soc. 1997;45:1434–1438.
Objectives: Leukoaraiosis, a radiological change of cerebral white matter thought to be caused by ischemia, is associated with gait disturbance. However, because of concomitant stroke and cerebral atrophy, the clinical relevance of leukoaraiosis is uncertain. We, therefore, sought to determine if leukoaraiosis is a predictor of gait disturbance after accounting for cerebral atrophy and stroke in patients with a high prevalence of cerebrovascular disease.
Design: Cross-sectional observational study.
Setting: Neurology service (inpatient and outpatient) of a Department of Veterans Affairs Hospital.
Participants: Consecutive sample of 130 patients, 127 men and three women.
Measurements: The findings of a gait scale were correlated to vascular risk factors, neurological examination as quantified by the NIH stroke scale and supplemental motor scale, and to brain CT findings. Brain CT scans were rated for leukoaraiosis, cerebral infarction, and cerebral atrophy.
Results: Gait disturbance was more frequent and more severe in subjects with leukoaraiosis, of whom 31% had mild and 49% moderate/severe gait disturbance compared with 27% with mild and 12% with moderate/severe gait disturbance in subjects without leukoaraiosis (P<.001). Leukoaraiosis, cerebral atrophy, a history of multiple strokes, and weakness and ataxia of the legs were independent predictors of gait disturbance. The proportion and severity of leukoaraiosis increased with increasing gait disturbance in subgroups without leg deficit (P<.001) and without multiple strokes (P<.001), but no association with leukoaraiosis was shown in patients with leg deficit or a history of multiple strokes (P=.037 and P=.186, respectively). Gait disturbance was more severe when both leukoaraiosis and cerebral atrophy were present (P=.019).
Conclusion: In our Veteran population, leukoaraiosis is an independent predictor of gait disturbance after accounting for stroke and cerebral atrophy. Although leukoaraiosis is a form of cerebrovascular disease, it appears to be most closely associated to gait disturbance in the absence of symptomatic stroke or leg deficit.
Key Words: leukoaraiosis, gait
Changes In Cerebral Blood Flow and Vasoreactivity in Response to Acetazolamide in Patients With Transient Global Amnesia—Sakashita Y (Dept of Neurology, Tonami General Hospital, 1-61 Shintomi-cho, Tonami, Toyama 939-13, Japan), Kanai M, Sugimoto T, Taki S, Takamori M—J Neurol Neurosurg Psychiatry. 1997;63:605–610.
Objective—Previous reports about changes in cerebral blood flow (CBF) in transient global amnesia disclosed decreased flow in some parts of the brain. However, CBF analyses in most reports were qualitative but not quantitative. The purpose of this study was to determine changes in CBF in transient global amnesia.
Methods—The CBF was measured and the vasoreactive response to acetazolamide was evaluated in six patients with transient global amnesia using technetium-99m hexamethylpropylene amine oxime single-photon emission computed tomography (SPECT). The CBF was measured during an attack in two patients and soon after an attack in the other four. About one month later, CBF was re-evaluated in each patient.
Results—Two patients examined during an attack and one patient examined five hours after an attack had increased blood flow in the occipital cortex and cerebellum. Three patients examined at six to 10 hours after an attack had decreased blood flow in the thalamus, cerebellum, or putamen. These abnormalities of blood flow almost disappeared in all patients one month after onset. The vasodilatory response to acetazolamide, which was evaluated initially using SPECT, was poor in areas of increased blood flow. By the second evaluation of CBF with acetazolamide, the vasodilatory response had returned to normal.
Conclusions—In a patient with transient global amnesia, CBF increased in the vertebrobasilar territory during the attack and decreased afterwards. The vasodilatory response to acetazolamide may be impaired in the parts of the brain with increased blood flow. It is suggested that transient global amnesia is distinct from migraine but may share the same underlying mechanism.
Key Words: cerebral blood flow, amnesia
Cerebral Microembolism in Patients With Stroke or Transient Ischaemic Attack as a Risk Factor for Early Recurrence—Valton L, Larrue V (Service de Neurologie, Hôpital de Rangueil, CHU de Toulouse, 31403 Toulouse Cedex 04, France), Pavy Le Traon A, Géraud G—J Neurol Neurosurg Psychiatry. 1997;63:784–787.
The incidence of early recurrence in 32 patients who had had a transient ischaemic attack or stroke in the anterior circulation was studied. Patients with a potential cardiac source of embolism were excluded from the study. All patients had transcranial Doppler (TCD) monitoring of the symptomatic middle cerebral artery for microembolic signal detection within seven days from the onset of symptoms. Four patients had early recurrence during a mean follow up of 15 (SD11) days. All early recurrences occurred in the same arterial territory as the initial ischaemic event. Three of the four patients with early recurrence had prior microembolic signals. The incidence of early recurrence was 50% (3/6) in patients with microembolic signals and 3.8% (1/26) in patients without microembolic signals (P=0.02). The findings suggest that TCD monitoring of patients with recent cerebral ischaemia of presumed arterial origin allows recognition of a subset of patients at high risk for early recurrence.
Key Words: cerebral embolism, ultrasonography, Doppler
Carotid Artery Stents: Early and Intermediate Follow-up With Doppler US—Robbin ML (Dept of Radiology, The University of Alabama at Birmingham, 619 S 19th St, New Hillman Bldg 623, Birmingham, AL 35233-1924), Lockhart ME, Weber TM, Vitek JJ, Smith JK, Yadav J, Mathur A, Iyer SS, Roubin GS—Radiology. 1997;205:749–756.
Purpose: To determine whether ultrasound (US) is a sensitive follow-up method after placement of a carotid artery stent for the detection of significant stenosis, occlusion, and other complications at early and intermediate follow-up.
Materials and Methods: Doppler US examinations were performed after stent placement in 170 carotid arteries in 119 patients with angiographic correlation. Prospective diagnostic US criteria for stenosis were peak-systolic velocity greater than 1.25 m/sec, internal carotid artery (ICA) to common carotid artery (CCA) peak-systolic velocity ratio of greater than or equal to 3:1, and intrastent doubling of peak-systolic velocity. Retrospective criteria for stenosis were also applied: peak-systolic velocity greater than 1.7 m/sec, ICA end-diastolic velocity greater than 0.4 m/sec, ICA/CCA peak-systolic velocity ratio greater than 2.0, and ICA/CCA end-diastolic velocity ratio greater than 2.4.
Results: Eighty-seven immediate and 83 intermediate (average, 7.3 months) follow-up US examinations were performed. Two stent occlusions were detected. One or more prospective US criteria were abnormal in 26 arteries with a stent. One or more retrospective criteria were positive in 47 arteries. Angiography showed corresponding findings, with only one significant stenosis (63%) in the ICA stents. Moderate collapse of a CCA stent was depicted at US.
Conclusion: Only one significant recurrent stenosis was detected, and no significant stenoses were missed at US. US successfully depicted carotid artery stent occlusion and a moderate stent collapse. Sensitivity in the detection of intrastent stenosis is promising. Further study to refine US criteria in a study with longer term follow-up is needed owing to the lack of significant recurrent stenosis in the intermediate follow-up group.
Key Words: stents, carotid artery stenosis
Evolving Indications For and Early Results of Carotid Artery Stenting—Criado FJ (Johnston Professional Building, Suite 570, 3333 N Calvert St, Baltimore, MD 21218), Wellons E, Clark NS—Am J Surg. 1997;174:111–114.
BACKGROUND: While carotid endarterectomy continues to be the gold standard of treatment for most patients with significant carotid artery disease, there are cases where lesion or anatomy-related factors create situations less than ideal for conventional surgery. Other therapeutic modalities, such as endoluminal stenting, may represent reasonable options for such patients.
METHODS: Thirty-three patients with 70% or greater internal carotid artery lesions were treated by endovascular stent placement from July 1994 through June 1996. Indications included transient ischemic attacks in 20 and previous stroke in 4; and 9 were asymptomatic.
RESULT: Stents were placed successfully in all instances. Mortality and stroke rates were zero. All patients remained asymptomatic during follow-up (mean 8 months), and stent patency by duplex ultrasound has been 100%. A single instance of intrastent restenosis has been observed.
CONCLUSIONS: Endoluminal stenting is an investigational technique of unproven efficacy and long-term durability. Yet it appears technically feasible, and possibly reasonable, as an alternate option for cases unfavorable for standard surgery.
Key Words: stents, carotid artery stenosis
Intra-arterial Thrombolysis in Acute Basilar Artery Thromboembolism: The Intial Mayo Clinic Experience—Wijdicks EFM (Dept of Neurology, Mayo Clinic Rochester, 200 First St SW, Rochester, MN 55905), Nichols DA, Thielen KR, Fulgham JR, Brown RD, Meissner I, Meyer FB, Piepgras DG—Mayo Clin Proc. 1997;72:1005–1013.
Objective: To investigate the feasibility of intra-arterial thrombolysis in acute basilar artery thrombosis.
Design: We reviewed a consecutive series of patients in whom intra-arterial thrombolysis was performed during the period from 1994 to 1996.
Material and Methods: Intra-arterial thrombolysis with urokinase was done in an attempt to recanalize the basilar artery in a series of nine patients with basilar artery thrombosis admitted to the neurologic intensive-care unit. At the time of initial assessment, all nine patients had major neurologic deficits attributable to brain-stem ischemia, including two patients with locked-in syndrome.
Results: Recanalization of the basilar artery system was successful in seven of the nine patients (a range of 2 to 13 hours after the ictus). Failure to recanalize the basilar artery occurred in two patients, who died after progressing to coma. Complete recovery or only minimal neurologic deficits were demonstrated in five of the nine patients. Despite recanalization of the basilar artery, two patients had no major change in their neurologic function, and both ultimately had severe ataxia and were fully dependent on others. A cerebellar hemorrhage occurred in one patient but without clinical worsening. Two patients had a retroperitoneal hematoma.
Conclusion: Intra-arterial thrombolysis with urokinase in acute basilar artery occlusion resulted in recanalization in seven of the nine patients (78%). Five of the nine patients recovered fully, including two patients who had had locked-in syndrome. In light of the devastating natural course of acute basilar artery occlusion, these initial results are encouraging and indicate that intra-arterial thrombolysis may be a useful emergency treatment, even in patients with prolonged symptoms of ischemia (up to 12 hours).
Key Words: thrombolytic therapy, basilar artery
Carotid Endarterectomy in the U.K. and Ireland: Audit of 30-day Outcome—McCollum PT (Consultant Vascular Surgeon, Vascular Unit, Ninewells Hospital, Dundee DD1 9SY, UK), da Silva A, Ridler BDM, de Cossart L—Eur J Vasc Endovasc Surg. 1997;14:386–391.
Objectives and Design: A prospective study of 709 patients undergoing carotid surgery in the U.K. and Ireland was performed to evaluate the performance of vascular surgeons.
Materials and Methods: Fifty-nine surgeons (range 2–39 cases each) were sampled and all patients undergoing surgery over a 6-month period (1 March 1994–31 August 1994) were included in the study. Indications for surgery were TIA (35.9%), AF (23.3%), CVA (21.4%) and “others” (19.6%).
Results: Mean ipsilateral stenosis was 82% (30%–99%). Thirty-one percent of patients had preoperative neurological consults. Shunts were used in 67.6%, tacking sutures in 40.1%, drains in 71.9% and patches in 54.4% of cases. At 30 days there were nine (1.3%) deaths (four cardiac, three neurological). There were 15 ipsilateral postoperative CVAs (2.1%); 19% of patients had one or more complication, usually minor. Statistical analysis showed no independent risk factor for CVA other than seniority of the surgeon.
Conclusions: A combined stroke/death rate of 3% for the series was obtained at 30 days for all cases. This large, validated study suggests that members of the Vascular Society of G.B. and Ireland currently have a very low morbidity/mortality rate for performing carotid surgery. Continued audit is required to ensure that this quality of service does not deteriorate.
Key Words: outcome, carotid endarterectomy
Middle Cerebral Artery Blood Velocity, Embolisation, and Neurological Outcome During Carotid Endarterectomy: A Prospective Comparison of the Javid and the Pruitt-Inahara Shunts—Wilkinson JM, Rochester JR, Slvaguru A, Cameron IC, Fisher R, Beard JD (Sheffield Vascular Institute, Northern General Hospital, Herries Road, Sheffield, S5 7AU)—Eur J Vasc Endovasc Surg. 1997;14:399–402.
Objectives: To investigate the in vivo haemodynamic performance and neurological outcome of two types of carotid shunt.
Design: Randomised single surgeon study of consecutive symptomatic patients.
Setting: 163 consecutive patients undergoing carotid endarterectomy for symptomatic carotid disease were randomised to the Javid or Pruitt shunt.
Chief outcome measures: Middle cerebral artery velocity (MCAV), preoperatively, during clamping, during shunting and post-restoration of flow, embolic episodes, neurological outcome.
Main results: The MCAV preoperatively, at carotid clamping, and postoperatively was the same for both groups (p>0.15). During shunting the MCAV was significantly lower in the Pruitt group, p<0.005, 59% of the Javid and 34% of the Pruitt shunts maintained MCAV at preoperative levels p<0.005, χ2=8.92. The Javid shunt produced significantly more emboli (73% of cases) at declamping than the Pruitt (41%), p<0.0002, χ2=14.7. Four Javid patients and one Pruitt had disabling thromboembolic strokes; overall thromboembolic stroke rate 3.7%. The difference in stroke rates was not statistically significant (p=0.14).
Conclusions: The Pruitt shunt was unable to maintain preoperative MCAV in 66% of cases, the Javid shunt had a higher incidence of emboli on declamping. These factors may lead to an increased risk of stroke; however, the numbers required for statistical confirmation would be large.
Key Words: carotid endarterectomy, shunt
Items of Interest
Emergency Identification and Treatment of Acute Ischemic Stroke
—Kasner SE (Dept of Neurology, University of Pennsylvania Medical Center, 3400 Spruce St, Philadelphia, PA 19104), Grotta JC—
Ann Emerg Med. 1997;30:642–653.
Total Quality Improvement Method for Reduction of Delays Between Emergency Department Admission and Treatment of Acute Ischemic Stroke—Tilley BC (Division of Biostatistics and Research Epidemiology, Henry Ford Health Sciences Center, 1 Ford Pl, Suite 3 E, Detroit, MI 48202), Lyden PD, Brott TG, Lu M, Levine SR, Welch KMA—Arch Neurol. 1997;54:1466–1474.
Rational Approach to Combined Carotid and Ischaemic Heart Disease—Renton S, Hornick P, Taylor KM, Grace PA (University of Limerick, Regional General Hospital, Dooradoyle, Limerick, Ireland)—Br J Surg. 1997;84:1503–1510.
Ticlopidine and Clopidogrel in Secondary Stroke Prevention—Bousser MG (Service de Neurologie, Hôpital Saint-Antoine 184, rue du Faubourg Saint-Antoine, F-75571 Paris Cedex 12, France), Roberts RS, Gent M—Cerebrovasc Dis. 1997;7:17–23.
Aspirin With and Without Dipyridamole—Dyken ML (Indiana University Medical Center, Neurology, 545 Barnhill Dr, Indianapolis, IN 46202-5124)—Cerebrovasc Dis. 1997;7:10–16.
The Role of Chronic Brain Edema in the Formation of Lacunes in Binswanger’s Encephalopathy: Histopathological and Immunohistochemical Observations—Ma K-C (Laboratory of Neuropathology, University Hospital, S-751 85 Uppsala, Sweden), Olsson Y—Cerebrovasc Dis. 1997;7:324–331.
Platelet Function and Pharmacology of Antiplatelet Drugs—Nurden AT (Director, UMR 5533 CNRS, Hôpital Cardiologique, Ave de Magellan, F-33604 Pessac, France), Duperat VG, Nurden P—Cerebrovasc Dis. 1997;7:2–9.
Status of Patent Foramen Ovale, Atrial Septal Aneurysm, Atrial Septal Defect and Aortic Arch Atheroma as Risk Factors for Stroke—Devuyst G (Hôpital de Jolimont, Dept of Neurology, rue Ferrer 159, B-7100 Haine-St-Paul, Belgium), Bogousslavsky J—Neuroepidemiology. 1997;16:217–223.
Patterns of Sensory Dysfunction in Lateral Medullary Infarction: Clinical-MRI Correlation—Kim JS (Dept of Neurology, Asan Medical Center, Song-Pa PO Box 145, Seoul 138-600, South Korea), Lee JH, Lee MC—Neurology. 1997;49:1557–1563.
Treatment of Cerebral Vasospasm Due to Aneurysmal Subarachnoid Hemorrhage: Past, Present, and Future of Hyperdynamic Therapy—Pritz MB (Section of Neurological Surgery, Indiana University School of Medicine, 545 Barnhill Dr, Emerson 139, Indianapolis, IN 46202-5124)—Neurosurg Q. 1997;7:273–285.
The abstracts in this section have been typeset for consistency with journal format but otherwise appear as in the original articles.
- Copyright © 1998 by American Heart Association