Abstracts of Literature
Five-Year Experience in Using Coil Embolization for Ruptured Intracranial Aneurysms: Outcomes and Incidence of Late Rebleeding—Byrne JV (Dept of Radiology, The Radcliffe Infirmary NHS Trust, Woodstock Rd, Oxford, England, OX2 6HE, United Kingdom), Sohn, MJ, Molyneux AJ—J Neurosurg. 1999;90:656–663.
Object. During a 5-year period 317 patients presenting with aneurysmal subarachnoid hemorrhage were successfully treated by coil embolization within 30 days of hemorrhage. The authors followed patients to assess the stability of aneurysm occlusion and its longer-term efficacy in protecting patients against rebleeding.
Methods. Patients were followed for 6 to 65 months (median 22.3 months) by clinical review, angiography performed at 6 months posttreatment, and annual questionnaires. Stable angiographic occlusion was evident in 86.4% of small and 85.2% of large aneurysms with recurrent filling in 38 (14.7%) of 259 aneurysms. Rebleeding was caused by aneurysm recurrence in four patients (between 11 and 35 months posttreatment) and by rupture of a coincidental untreated aneurysm in one patient. Annual rebleeding rates were 0.8% in the 1st year, 0.6% in the 2nd year, and 2.4% in the 3rd year after aneurysm embolization, with no rebleeding in subsequent years. Rebleeding occurred in three (7.9%) of 38 recurrent aneurysms and in one (0.4%) of 221 aneurysms that appeared stable on angiography.
Conclusions. Periodic follow-up angiography after coil embolization is recommended to identify aneurysm recurrence and those patients at a high risk of late rebleeding.
Key Words: subarachnoid hemorrhage, aneurysm
Improved Survival After Aneurysmal Subarachnoid Hemorrhage: Review of Case Management During a 12-Year Period—Cesarini KG, Hårdemark H-G, Persson L (Dept of Neurosurgery, Univ Hospital, S-751 85 Uppsala, Sweden)—J Neurosurg. 1999;90:664–672.
Object. Based on the concept that unfavorable clinical outcome after aneurysmal subarachnoid hemorrhage (SAH), to a large extent, is a consequence of all ischemic insults sustained by the brain during the acute phase of the disease, management of patients with SAH changed at the authors’ institution in the mid-1980s. The new management principles affected referral guidelines, diagnostic and monitoring methods, and pharmacological and surgical treatment in a neurointensive care setting. The impact of such changes on the outcome of aneurysmal SAH over a longer period of time has not previously been studied in detail. This was the present undertaking.
Methods. The authors analyzed all patients with SAH admitted to the neurosurgery department between 1981 and 1992. This period was divided in two parts, Period A (1981–1986) and Period B (1987–1992), and different aspects of management and outcome were recorded for each period. In total, 1206 patients with SAH (mean age 52 years, 59% females) were admitted; an aneurysm presumably causing the SAH was found in 874 (72%).
The 30-day mortality rate decreased from 29% during the first 2 years (1981–1982) to 9% during the last 2 years (1991–1992) (Period A 22%; Period B 10%; p<0.0001) and the 6-month mortality rate decreased from 34 to 15% (Period A 26%; Period B 16%; p<0.001). At follow-up review conducted 2 to 9 years (mean 5.2 years) after SAH occurred, patients were evaluated according to the Glasgow Outcome Scale. Subarachnoid hemorrhage–related poor outcome (vegetative or dead) was reduced (Period A 30%; Period B 18%; p<0.001). There was an increase both in patients with favorable outcome (good recovery and moderate disability) (Period A 61%; Period B 66%) and in those with severe disability (Period A 9%; Period B 16%; p<0.01).
Conclusions. This study provides evidence that the prognosis for patients with aneurysmal SAH has improved during the last decades. The most striking results were a gradual reduction in mortality rates and improved clinical outcomes in patients with Hunt and Hess Grade I or II SAH and in those with intraventricular hemorrhage. The changes in mortality rates and the clinical outcomes of patients with Hunt and Hess Grades III to V SAH were less conspicuous, although reduced incidences of mortality were seen in some subgroups; however, few survivors subsequently appeared to attain a favorable outcome.
Key Words: subarachnoid hemorrhage, aneurysm
Oxidative Stress in the Human Brain After Subarachnoid Hemorrhage—Gaetani P (Dept of Neurosurgery, Istituto Clinico “Humanitas,” Via Manzoni 56, I-20089 Rozzano, Milan, Italy), Pasqualin A, Rodriguez-y-Baena R, Borasio E, Marzatico F—J Neurosurg. 1998;89:748–754.
Object. The aim of this study was to verify the patterns of antioxidant enzymatic activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the human brain after subarachnoid hemorrhage (SAH) to verify whether an “oxidative stress situation” characterizes the brain response to subarachnoid bleeding.
Methods. Forty samples of gyrus rectus or temporal operculum that were obtained during a surgical approach to anterior circulation aneurysms were used for this study. The activity of total SOD, GSH-Px, and the SOD/GSH/Px ratio (which expresses the balance between the production of hydrogen peroxides by dismutation of superoxide radicals and the scavenging potential) were calculated in each case. Twelve samples were obtained from patients who underwent surgery for unruptured aneurysms (control group); 13 samples were obtained during surgical procedures performed within 72 hours of SAH; and 15 samples were obtained during delayed surgical procedures (>10 days post-SAH). Ten patients presented with clinical deterioration caused by arterial vasospasm. In both SAH groups, the mean total SOD activity was significantly higher than in the control group (p=0.029). The mean activity of GSH-Px did not differ significantly between the SAH and control groups (p=0.731). There was a significant increase in the SOD/GSH-Px ratio in both SAH groups, as compared with controls (p<0.05). There was a significant correlation between the enzymatic activity and the clinical severity of the hemorrhage, with findings of lower values of SOD and, mainly, of the SOD/GSH-Px ratio in the poor-grade patients. The SOD/GSH-Px ratio was 2.14±0.44 in patients who presented with clinical vasospasm and 1.24±0.2 in cases without vasospasm.
Conclusions. The results of this study show an imbalance of the antioxidant enzymatic activities in the human brain after SAH, which is linked to the severity of the initial bleeding and possibly modified by the development of arterial vasospasm.
Key Words: subarachnoid hemorrhage, free radicals
Aneurysm Retreatment After Guglielmi Detachable Coil and Nondetachable Coil Embolization: Report of Nine Cases and Review of the Literature—Horowitz M (5323 Harry Hines Blvd, Dallas, TX 75235-8855), Purdy P, Kopitnik T, Dutton K, Samson D—Neurosurgery. 1999;44:712–720.
OBJECTIVE: Guglielmi detachable coil embolization of cerebral aneurysms is becoming increasingly used to manage certain intracranial lesions based on aneurysm geometry, patient condition, and patient and surgeon preferences. Aneurysm recurrences or incomplete initial treatments are not uncommon, making repeat treatment necessary using either surgical or endovascular techniques.
METHODS: Between January 1993 and June 1998, 1025 cerebral aneurysms were managed by the authors at a single hospital. One hundred twenty-four of these lesions were treated using Guglielmi detachable coils, and one was managed with nondetachable coils. During the follow-up period, eight patients who underwent embolization at our institution and one who underwent embolization elsewhere received repeat treatment. Five were approached surgically, and four underwent re-embolization. All charts and films were reviewed retrospectively to determine patient outcome and clinical success.
RESULTS: No patient in the subgroup of this clinical study suffered a permanent complication from initial aneurysm coiling, no episodes of subsequent bleeding occurred, and no complications resulted from any subsequent therapies. The anatomic results were excellent, and all aneurysms were totally or near totally obliterated.
CONCLUSION: Subtotal initial coil embolization of aneurysms can be managed safely using a variety of surgical and endovascular techniques. Our approach to this predicament, lessons we have learned, and a review of the literature are herein discussed.
Key Words: aneurysm, endovascular therapy
Current Results of the Surgical Management of Aneurysms of the Basilar Apex—Samson D (Dept of Neurological Surgery, The Univ of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, CS5. 104B, Dallas, TX 75235-8855), Batjer H, Kopitnik TA Jr. Neurosurgery. 1999;44:697–704.
OBJECTIVE: To provide current information regarding the expected clinical outcomes and sources of morbidity and mortality in the modern surgical management of basilar apex aneurysms.
METHOD: A retrospective review was conducted of 303 cases of such aneurysms that were treated surgically during 18 years at one institution. Postoperative angiography was performed in 81% of the cases. Clinical grading using the Glasgow Outcome Scale was conducted at the time of hospital discharge and for 91% of the surviving patients at 6 months after surgery. The preoperative parameters that were linked statistically to poor clinical outcome were identified through the use of single and multivariate analyses.
RESULTS: More than 80% of the patients were operated on using some modification of the trans-sylvian exposure, and temporary arterial occlusion was used routinely. Good outcomes (Glasgow Outcome Scale scores of 4 or 5) were achieved in 76% of the patients at the time of discharge and in 81% of the patients at 6 months after surgery. There was no incidence of postoperative subarachnoid hemorrhage. Residual aneurysm was revealed by postoperative angiography in 6% of the cases. Factors found to be statistically linked to poor outcome included poor admission grade (Hunt and Hess Grades IV and V), patient age older than 65 years, computed tomographic demonstration of thick basal cistern clot, aneurysm size greater than 20 mm, and symptoms attributable to brain stem compression.
CONCLUSION: Direct microsurgical repair of basilar apex aneurysms should result in good clinical outcomes in 80 to 85% of cases, with reliable prevention of subarachnoid bleeding and routine elimination/reduction of symptoms secondary to mass effect. Those patients who are at high risk for poor outcomes can be identified by the presence of certain clinical, radiographic, and demographic features before undergoing surgery and can be considered for alternative or adjunctive modes of therapy if long-term efficacy of such treatment is demonstrated.
Key Words: aneurysm, basilar artery
Lone Atrial Fibrillation: Prognostic Differences Between Paroxysmal and Chronic Forms After 10 Years of Follow-Up—Scardi S (Cardiovascular Center, Ospedale Maggiore, via Pieta 19, 34100 Trieste, Italy), Mazzone C, Pandullo C, Goldstein D, Poletti A, Humar F—Am Heart J. 1999;137:686–691. Copyright © 1999 by Mosby, Inc.
Background Lone atrial fibrillation (LAF) is defined by the presence of atrial fibrillation unassociated with other evidence of organic heart disease. There are conflicting data concerning the prognostic importance, rate of embolic complications, and survival in subjects affected by this arrhythmia.
Methods and Results One hundred forty-five patients younger than 50 years at the time of the first diagnosis were identified; 96 had paroxysmal and 49 had chronic LAF. They were followed up with clinical and echocardiographic controls, and we recorded every thromboembolic complication and death. During the follow-up (10±8 years) among patients with paroxysmal LAF, 1 (1%) had an ischemic stroke, 2 a transient ischemic attack, and 1 a myocardial infarction. In the group with chronic LAF, 1 patient had moderate heart failure, 2 myocardial infarction, and 1 transient ischemic attack. In this group, 8 embolic complications in 7 (16.3%) patients were observed. One patient with intestinal embolism died during surgery; 2 (6.1%) patients died suddenly.
Conclusions The prognosis of young patients with paroxysmal LAF appears to be excellent, whereas patients with chronic LAF are at increased risk of embolic complications and higher mortality rates. Our results suggest that LAF is not always a benign disorder, as suggested by previous studies. Subgroups with substantially increased risk for thromboembolic events caused by LAF should be better identified.
Key Words: atrial fibrillation, stroke outcome
Ischemic Stroke Risk and Passive Exposure to Spouses’ Cigarette Smoking—You RX (National Stroke Research Institute, Austin and Repatriation Medical Centre, Heidelberg West, Australia), Thrift AG, McNeil JJ, Davis SM, Donnan GA, for the Melbourne Stroke Risk Factor Study (MERFS) Group—Am J Public Health. 1999;89:572–575.
Objectives. This study investigated the association between ischemic stroke risk and passive exposure to cigarette smoking.
Methods. Risk factors among 452 hospitalized cases of first-episode ischemic stroke were compared with 452 age- and sex-matched “neighborhood” controls.
Results. The risk of stroke was twice as high for subjects whose spouses smoked as for those whose spouses did not smoke (95% confidence interval=1.3, 3.1), after adjustment for the subject’s own smoking, heart disease, hypertension, diabetes, and education level. These results were confirmed when analysis was limited to those who never smoked.
Conclusions. These findings provide evidence that spousal smoking may be a significant risk factor for ischemic stroke.
Key Words: risk factors, cerebral ischemia
Prevention of Poststroke Depression: 1 Year Randomised Placebo Controlled Double Blind Trial of Mianserin With 6 Month Follow Up After Therapy—Palomäki H (Dept of Neurology, Univ of Helsinki, Haartmaninkatu 4, 00290 Helsinki 29, Finland), Kaste M, Berg A, Lönnqvist R, Lönnqvist J, Lehtihalmes M, Hares J—J Neurol Neurosurg Psychiatry. 1999;66:490–494.
Objectives—(1) To test whether early prophylactic antidepressive treatment by mianserin is able to prevent poststroke depression, and (2) to discover whether mianserin as an antidepressant has any beneficial influence on the outcome of ischaemic stroke.
Methods—A randomised, double blind, placebo controlled study involved 100 consecutive patients under 71 years old admitted to hospital for an acute ischaemic stroke; they were enrolled to receive 60 mg/day mianserin or placebo for 1 year. They were examined on admission, and at 2, 6, 12, and 18 months with depression, stroke, and functional outcome scales.
Results—According to DSM-III-R, the prevalence of major depression was 6% at the initial stage, 11% at 1 year, and 16% at 18 months. At no time point did prevalences differ between the treatment groups, nor were differences found in depression scales, although at 2 months a greater improvement from initial assessment on the Hamilton depression scale was evident in patients on mianserin (p=0.05). Some beneficial changes on the Hamilton depression scale and Beck depression inventory were found in patients older than 56 (median age) and in men treated with mianserin, but not in other subgroups. Mianserin treatment did not affect stroke outcome as measured by neurological status, nor did it have any influence on functional outcome as measured by Rankin scale or Barthel index.
Conclusion—It was not possible to show that early initiation of antidepressant therapy can prevent poststroke depression, because the prevalence of poststroke depression remained low even in patients on placebo. In this stroke population with a low rate of depressive patients, antidepressive medical treatment failed to affect stroke outcome.
Key Words: stroke outcome, depression
Poststroke Seizures in Stroke Rehabilitation Patients—Teasell RW (London Health Sciences Centre, 339 Windermere Rd, London, Ontario N6A 5A5, Canada), McRae MP, Wiebe S—J Stroke Cerebrovasc Dis. 1999;8:84–87. Copyright © 1999 by National Stroke Association.
The incidence, seizure type, location and type of stroke, and anticonvulsant medications, including adverse effects, were studied in a stroke rehabilitation population. Of 563 consecutive stroke patients admitted to the rehabilitation unit, 14 had a history of a seizure and were excluded from the primary study group. Of the remaining 549 stroke rehabilitation patients, 43 (7.8%) suffered a poststroke seizure (PSS). When only hemispheric patients were studied, the incidence of poststroke seizures rose to 43 of 460 (9.3%) as no brainstem stroke patients suffered seizures. The average age of the PSS patients was 55.4 years. The incidence of PSS in all stroke infarction patients was significantly smaller (22 of 450, 4.9%) when compared with hemorrhagic strokes (21 of 99, 21.2%) (P<.001). The incidence of PSS among hemispheric infarcts was 22 of 379 (5.8%) versus 21 of 81 (25.9%) of hemispheric hemorrhagic strokes (P<.001). Twenty-six PSS patients had primarily cortical involvement, 13 had both cortical and subcortical involvement, and only 4 had primarily subcortical involvement. Seizures occurred within the first 24 hours in 23.8% of stroke patients, 52.4% within the first week, in 66.7% within the first month, in 83.3% within the first 6 months, and in 88.1% within the first year. In the 43 patients with PSS, 19 (44.2%) were reportedly focal in nature, 12 (27.2%) were generalized, and 6 (14.0%) were focal with secondary generalization. Three (7.0%) were complex-partial seizures and 3 (7.0%) were of an undetermined type. Of the 14 stroke rehabilitation patients excluded from the study group because of a prestroke seizure, 6 (42.9%) suffered a PSS in contrast to the 43 of 549 (7.8%) with no premorbid history of a seizure (P<.001).
Key Words: stroke outcome, seizures
Anticardiolipin Antibodies and Their Associations With Cerebrovascular Risk Factors—Tanne D, D’Olhaberriague L, Schultz LR, Salowich-Palm L, Sawaya KL, Levine SR (Director WSU/DMC Stroke Program, WSU School of Medicine, Univ Health Center 6-E, 4201 St Antoine, Detroit, MI 48201)—Neurology. 1999:52:1368–1373. Copyright © by the American Academy of Neurology.
Objective: To investigate associations between cerebrovascular risk factors and anticardiolipin (aCL) immunoreactivity. Background: High titers of aCL immunoreactivity, mainly the immunoglobulin (Ig) G isotype, were shown to predict aCL-related thrombo-occlusive complications. Methods: aCL antibodies, and IgG and IgM isotypes were measured by a validated assay in a single laboratory, run in duplicate, in 749 individuals with first ischemic stroke (n=300) and patients with other CNS disease or undergoing diagnostic procedures. Results: Age varied according to aCL categories, with a mean of 61.8 years among patients with negative aCL (<10 IgG phospholipid units [GPL]) to 62.3, 64.9, and 69.9 years in patients with immunoreactivity 10 to 20, 20 to 40, and >40 GPL respectively (p=0.02). History of atrial fibrillation, congestive heart failure, or valvular heart disease was associated with significantly higher rates of positive IgG aCL (>10 GPL) and with higher immunoreactivity. IgG aCL immunoreactivity increased significantly, in a dose-response manner, as a function of the number of cerebrovascular risk factors present. In patients with first ischemic stroke, rates of 10 to 20, 20 to 40, and >40 GPL were 14%, 7%, and 0% among those with no risk factors versus 20%, 12%, and 12% respectively among patients with four or more risk factors (p=0.007). No significant associations were identified, however, between IgM isotype aCL and any of the risk factors or increasing number of risk factors. Conclusion: The presence of multiple cerebrovascular risk factors is associated with substantially higher rates of positive IgG isotype aCL, and with higher immunoreactivity. These findings should caution against overdiagnosis of the antiphospholipid syndrome, and consequent changes in management among patients with multiple cerebrovascular risk factors.
Key Words: risk factors, antibodies, antiphospholipid
Factor V Arg506Gln Mutation Is Not Associated With Cardiovascular Mortality in Older Women—Roest M (Julius Center for Patient Oriented Research, Utrecht Univ Medical School, Utrecht, Netherlands), Banga JD, Tempelman MJ, de Groot PG, Grobbee DE, Sixma JJ, van der Schouw YT—Am J Epidemiol. 1999;149:665–670. Copyright © by The Johns Hopkins Univ School of Hygiene and Public Health.
Factor V Arg506Gln is the most common genetic risk factor for venous thrombosis and is associated with myocardial infarction in young women, especially among smokers. The authors studied the relation of factor V Arg506Gln to cardiovascular mortality in older women in a prospective cohort study of 12,239 women, living in the city of Utrecht, who were initially aged between 52 and 67 years. Women were followed on vital status between 1976 and 1995 (168,513 years). The factor V Arg506Gln mutation was determined in urine samples of 524 women who died of cardiovascular disease and in a reference group of 517 women who did not. Data were analyzed using a nested case-referent analysis. Factor V Arg506Gln heterozygosity was not associated with the risk of mortality by myocardial infarction, cerebrovascular disease, and other cardiovascular disease, with respective rate ratios and 95% confidence intervals being 1.1 (0.5–2.3), 1.2 (0.5–3.1), and 0.6 (0.2–1.7). No evidence of association was found in subgroups of smokers and age. Factor V Arg506Gln is not a risk factor for cardiovascular mortality in older women. Discrepancies with other studies may be explained by different study populations, as age and sex may modify both the frequency of cardiovascular disease and the effect of its risk factors.
Key Words: thrombosis, risk factors
Ethnic Differences in Incidence of Stroke: Prospective Study With Stroke Register—Stewart JA, Dundas R, Howard RS, Rudd AG, Wolfe CDA (Dept of Public Health Sciences, Guy’s King’s College, and St Thomas’s School of Medicine, 5th Floor, Capital House, London SE1 3QD)—BMJ. 1999;318:967–971.
Objective To identify ethnic differences in the incidence of first ever stroke.
Design A prospective community stroke register (1995–6) with multiple notification sources. Pathological classification of stroke in all cases was based on brain imaging or necropsy data. Rates were standardised to European and world populations and adjusted for age, sex, and social class in multivariate analysis.
Setting A multi-ethnic population of 234 533 in south London, of whom 21% are black.
Results 612 strokes were registered. The crude annual incidence rate was 1.3 strokes per 1000 population per year (95% confidence interval 1.20 to 1.41) and 1.25 per 1000 population per year (1.15 to 1.35) age adjusted to the standard European population. Incidence rates adjusted for age and sex were significantly higher in black compared with white people (P<0.0001), with an incidence rate ratio of 2.21 (1.77 to 2.76). In multivariable analysis increasing age (P<0.0001), male sex (P<0.003), black ethnic group (P<0.0001), and lower social class (P<0.0001) in people aged 35–64 were independently associated with an increased incidence of stroke.
Conclusions Incidence rates of stroke are higher in the black population; this is not explained by confounders such as social class, age, and sex. Ethnic differences in genetic, physiological, and behavioural risk factors for stroke require further elucidation to aid development of effective strategies for stroke prevention in multi-ethnic communities.
Key Words: cerebral ischemia, incidence
Cross-Sectionally Assessed Carotid Intima-Media Thickness Relates to Long-Term Risk of Stroke, Coronary Heart Disease and Death as Estimated by Available Risk Functions—Bots ML (Julius Centre for Patient Oriented Research, HP D.01.335, Univ Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands), Hoes AW, Hofman A, Witteman JCM, Grobbee DE—J Intern Med. 1999;245:269–276. Copyright © Blackwell Science Ltd.
Objective. To relate cross-sectionally assessed indicators of carotid atherosclerosis measured in participants of the Rotterdam Study to absolute 10–12 year risks of stroke, coronary heart disease and death estimated by risk functions available from other studies.
Setting. General population living in the suburb of Ommoord in Rotterdam, The Netherlands.
Subjects. A sample of men and women (n=1683), aged 55 years or over, drawn from participants from the Rotterdam Study (n=7983).
Main outcomes measures. Three risk scores were used to estimate for each individual the absolute risk of stroke, coronary heart disease and death within 10–12 years as a function of their cardiovascular risk factor profile. Cross-sectionally measured indicators of carotid atherosclerosis (presence of atherosclerotic lesions and common carotid intima–media thickness) were subsequently related to these risk scores.
Results. The 10-year absolute risk of stroke increased linearly from 4.8% (95% CI=3.8, 5.8) for subjects in the lowest quintile to 16.1% (12.3, 21.9) for subjects in the highest quintile of common carotid intima–media thickness distribution. Similarly, the 10-year absolute risk for coronary heart disease rose from 13.1% (95% CI=12.0, 14.2) to 23.4% (95% CI=21.4, 25.4), whereas the risk of death within 11.5 years rose from 15.0% (95% CI=12.8, 17.4) in the lowest quintile to 46.0% (42.8, 49.3) in the upper quintile. The absolute risks of stroke, coronary heart disease or death rose from 8.8, 15.8 and 26.9% to 14.3, 19.8 and 40.9%, respectively, when plaques in the common carotid artery were present. Similar findings were observed for plaques in the carotid bifurcation.
Conclusion. Common carotid intima–media thickness and carotid plaques are markers for increased risk of stroke, coronary heart disease and death within 10–12 years.
Key Words: risk factors, carotid artery diseases
Migraine History and Migraine-Induced Stroke in the Dijon Stroke Registry—Sochurkova D, Moreau T, Lemesle M, Menassa M, Giroud M (Neurology Unit, Univ Hospital 3, rue du Faubourg Raines, F-21000 Dijon, France), Dumas R—Neuroepidemiology. 1999;18:85–91. Copyright © 1999 S. Karger AG, Basel.
Two thousand three hundred and eighty-nine patients with first-ever stroke were registered in the population-based Dijon Stroke Registry over an 11-year period. There was a history of migraine in 49 cases (2%), with a majority of women (2.8% versus 1.1% men) with the following distribution: 27 cases among 1,380 large-artery cerebral infarctions (1.9%), 6 cases among 358 small-artery cerebral infarctions (1.6%), 6 cases among 412 cerebral infarctions due to cardiac embolism (1.4%), 7 cases among 191 cerebral hemorrhages (3.6%) and 3 cases among 47 subarachnoid hemorrhages (6.3%). The male/female ratio was 0.58 for the 49 strokes with a history of migraine versus 1.27 for the 2,340 strokes with no history of migraine. Twelve migraine-induced ischemic strokes occurred with an infarction of the posterior area of the brain in young patients. The annual incidence was 0.80/100,000/year (confidence interval, CI=0.37–1.57) with a predominance of women (1.02/100,000/year, CI=0.52–1.25; men: 0.57/100,000/year; CI=0.28–1.04). We conclude that a history of migraine is more frequent in women, in particular in those with hemorrhagic strokes, and that the incidence of migraine-induced stroke in our population-based study is higher in women, although it remains low.
Key Words: stroke classification, migraine
Dexamethasone Effects on Cerebral Protein Synthesis Prior to and Following Hypoxia-Ischemia in Immature Rat—Tuor UI (Biosystems, Institute for Biodiagnostics, NRCC, 435 Ellice Ave, Winnipeg, Manitoba R3B 1Y6, Canada), Manley JJ, Fyfe C, Bascaramurty S—Brain Res Bull. 1999;48:61–64. Copyright © 1999 Elsevier Science Inc.
We hypothesized that the neuroprotection against cerebral hypoxic-ischemic damage observed with dexamethasone treatment in immature rats is related to a change in cerebral protein synthesis. Six-day-old Wistar rats were injected with either vehicle (10 ml/kg) or dexamethasone (0.1 mg/kg) 24 h prior to cerebral hypoxia-ischemia. Local cerebral protein synthesis (incorporation of 14C-leucine into proteins) was measured in 7-day-old rats during normoxia, during hypoxia-ischemia, and after hypoxia-ischemia which was produced with right carotid artery ligation and 2-h exposure to 8% O2. In normoxic controls, cerebral protein synthesis was similar in dexamethasone and vehicle-treated animals. During hypoxia-ischemia, local cerebral protein synthesis decreased markedly (p<0.0001) in ischemic regions ipsilateral to the occlusion, irrespective of treatment. After hypoxia-ischemia, protein synthesis declined even further in vehicle-treated animals. Reductions in protein synthesis were substantially more severe in vehicle- than dexamethasone-treated animals, particularly after hypoxia-ischemia (p<0.0001). Thus, neuroprotection with dexamethasone is not related to a reduction in basal levels of cerebral protein synthesis, but is associated with an improved protein synthesis during and following hypoxia-ischemia.
Key Words: cerebral ischemia, dexamethasone
Changes in the Diffusion of Water and Intracellular Metabolites After Excitotoxic Injury and Global Ischemia in Neonatal Rat Brain—Dijkhuizen RM (MGH-NMR Center, 13th St, Bldg 149, Charlestown, MA 02129), de Graaf RA, Tulleken KAF, Nicolay K—J Cereb Blood Flow Metab. 1999;19:341–349. Copyright © 1999 The International Society of Cerebral Blood Flow and Metabolism.
The reduction of the apparent diffusion coefficient (ADC) of brain tissue water in acute cerebral ischemia, as measured by diffusion-weighted magnetic resonance imaging, is generally associated with the development of cytotoxic edema. However, the underlying mechanism is still unknown. Our aim was to elucidate diffusion changes in the intracellular environment in cytotoxic edematous tissue. The ADC of intracellular metabolites was measured by use of diffusion-weighted 1H-magnetic resonance spectroscopy after (1) unilateral N-methyl-d-aspartate (NMDA) injection and (2) cardiac arrest-induced global ischemia in neonatal rat brain. The distinct water ADC drop early after global ischemia was accompanied by a significant reduction of the ADC of all measured metabolites (P<0.01, n=8). In the first hours after excitotoxic injury, the ADC of water and the metabolites taurine and N-acetylaspartate dropped significantly (P<0.05, n=8). At 24 and 72 hours after NMDA injection brain metabolite levels were diminished and metabolite ADC approached contralateral values. Administration of the NMDA-antagonist MK-801 1.5 hours after NMDA injection completely normalized the water ADC but not the metabolite ADC after 1 to 2 hours (n=8). No damage was detected 72 hours later and, water and metabolite ADC had normal values (n=8). The contribution of brain temperature changes (calculated from the chemical shift between the water and N-acetylaspartate signals) and tissue deoxygenation to ischemia-induced intracellular ADC changes was minor. These data lend support to previous suggestions that the ischemia-induced brain water ADC drop may partly be caused by reduced diffusional displacement of intracellular water, possibly involving early alterations in intracellular tortuosity, cytoplasmic streaming, or intracellular molecular interactions.
Key Words: magnetic resonance imaging, cerebral ischemia
Blood-Brain Barrier Glutamine Transport During Normoglycemic and Hyperglycemic Focal Cerebral Ischemia—Kawai N, Stummer W, Ennis SR, Betz AL, Keep RF (Dept of Surgery, Univ of Michigan, R5605 Kresge I, Ann Arbor, MI 48109-0532) J Cereb Blood Flow Metab. 1999;19:79–86. Copyright © 1999 The International Society of Cerebral Blood Flow and Metabolism.
This study examines the effects of middle cerebral artery (MCA) occlusion in the rat on blood to brain glutamine transport, a potential marker of early endothelial cell dysfunction. It also examines whether the effects of ischemia on glutamine transport are exacerbated by hyperglycemia. In pentobarbital-anesthetized rats, 4 hours of MCA occlusion resulted in a marked decline in the influx rate constant for [14C]l-glutamine from 16.1±1.2 μL · g−1 · min−1 in the contralateral hemisphere to 7.3±2.5 μL · g−1 · min−1 in the ischemic core (P<0.001). This reduction was even greater in xylazine–ketamine-anesthetized rats in which the influx decreased to 2.6±1.1 μL · g−1 · min−1. This greater reduction appears related to the hyperglycemia induced by xylazine–ketamine anesthesia. Glucose injection in pentobarbital-anesthetized rats also resulted in a greater decline in [14C]l-glutamine influx in the ischemic core but had no effect on the contralateral tissue. The effects of hyperglycemia on glutamine transport in the ischemic tissue were associated with a decline in plasma volume, which may reflect either endothelial cell swelling or plugging of the microvasculature. The reduction in glutamine transport during ischemia was progressive, but even as early as 1 hour, there was a 60% and 40% decline in influx in hyperglycemic and normoglycemic rats, respectively. The fall in [14C]l-glutamine influx may reflect a dissipation of the endothelial cell [Na+] gradient. A decline in this gradient would affect many blood–brain barrier transporters with potentially deleterious effects on the ischemic brain.
Key Words: cerebral ischemia, blood-brain barrier
Tissue Plasminogen Activator Does not Increase Neuronal Damage in Rat Models of Global and Focal Ischemia—Klein GM, Li H, Sun P, Buchan AM (Rm 1162, Foothills Hospital, 1403 29th St NW, Calgary, Alberta T2N 2T9, Canada)—Neurology. 1999;52:1381–1384. Copyright © 1999 by the American Academy of Neurology.
Background: Intravenous tissue plasminogen activator (tPA) is the only approved treatment for acute ischemic stroke. Recent results from both in vitro and in vivo animal model experiments suggest the possibility that tPA is neurotoxic. Methods: The authors evaluated the putative neurotoxicity of tPA in both global and focal animal models of ischemic stroke. Global ischemia was induced in male Wistar rats using a modified four-vessel occlusion technique, with percentage neuronal injury assessed at 7 days through necrotic and normal cell count in the CA1 region. Transient focal ischemia was induced in male spontaneously hypertensive rats subjected to middle cerebral artery clipping, with measurement of cortical infarct volume at 24 hours. tPA was administered in 1, 5, or 10 mg/kg doses given intravenously as a 10% bolus, 90% over the following hour, analogous to current human treatment protocols. Results: In the global model, percent hippocampal injury was 60%±23%, 66%±26%, 55%±26%, and 52%±12% in the saline control, 1, 5, and 10 mg/kg tPA groups, respectively. In the focal model, after 120 minutes of ischemia, the control infarct size was 151±39 mm3, and for the group given 10 mg/kg of tPA, it was 158±28 mm3. Conclusions: Despite sublethal insults, with moderate injury induced by ischemia, there was no evidence that increasing doses of tPA exacerbated ischemic injury.
Key Words: cerebral ischemia, thrombolysis
Correlation of Regional Cerebral Blood Flow Measured by Stable Xenon CT and Perfusion MRI—Hagen T (Dept of Neuroradiology, Saarland Univ Medical School, D-66421 Homburg/Saar, Germany), Bartylla K, Piepgras U—J Comput Assist Tomogr. 1999;23:257–264. Copyright © 1999 Lippincott Williams & Wilkins, Inc. Philadelphia.
Purpose: The purpose of this work was to investigate the validity of perfusion MRI in comparison with stable xenon CT for evaluating regional cerebral blood flow (rCBF).
Method: The rCBF was measured by xenon CT and perfusion MRI within a 24 h interval in 10 patients (mean±SD age 63±10 years). For perfusion MRI, absolute values of rCBF were calculated based on the indicator dilution theory after injection of 0.1 mmol/kg of Gd-DTPA. Eight to 10 regions of interest (37 mm2) were located in the white and gray matter on the rCBF images for each of the 10 patients.
Results: The mean±SD values of rCBF in gray matter were 48.5±14.1 ml/100 g/min measured by xenon CT and 52.2±16.4 ml/100 g/min measured by perfusion MRI. In the white matter, the rCBF was 22.6±9.1 ml/100 g/min by xenon CT and 27.4±6.8 ml/100 g/min by perfusion MRI. There was a good correlation of rCBF values between perfusion MRI and xenon CT (Pearson correlation coefficient 0.83; p<0.0001).
Conclusion: Comparable to xenon CT, perfusion MRI provides relatively high resolution, quantitative local rCBF information coupled to MR anatomy.
Key Words: cerebral blood flow, magnetic resonance imaging
Absent Middle Cerebral Artery Flow Predicts the Presence and Evolution of the Ischemic Penumbra—Barber PA, Davis SM (Royal Melbourne Hospital, Parkville, Vic 3050, Australia), Darby DG, Desmond PM, Gerraty RP, Yang Q, Jolley D, Donnan GA, Tress BM—Neurology. 1999;52:1125–1132. Copyright © 1999 by the American Academy of Neurology.
Objectives: In acute ischemic stroke the pattern of a perfusion-imaging (PI) lesion larger than the diffusion-weighted imaging (DWI) lesion may be a marker of the ischemic penumbra. We hypothesized that acute middle cerebral artery (MCA) occlusion would predict the presence of presumed “penumbral” patterns (PI>DWI), ischemic core evolution, and stroke outcome. Methods: Echoplanar PI, DWI, and magnetic resonance angiography (MRA) were performed in 26 patients with MCA territory stroke. Imaging and clinical studies (Canadian Neurological Scale, Barthel Index, and Rankin Scale) were performed within 24 hours of onset and repeated at days 4 and 90. Results: MCA flow was absent in 9 of 26 patients. This was associated with larger acute PI and DWI lesions, greater PI/DWI mismatch, early DWI lesion expansion, larger final infarct size, worse clinical outcome (p<0.01) and provided independent prognostic information (multiple linear regression analysis, p<0.05). Acute penumbral patterns were present in 14 of 26 patients. Most of these patients (9 of 14) had no MCA flow, whereas all nonpenumbral patients (PI≤DWI lesion) had MCA flow (p<0.001). Penumbral-pattern patients with absent MCA flow had greater DWI lesion expansion (p<0.05) and worse clinical outcome (Rankin Scale score, p<0.05). Conclusions: Absent MCA flow on MRA predicts the presence of a presumed penumbral pattern on acute PI and DWI and worse stroke outcome. Combined MRA, PI, and DWI can identify individual patients at risk of ischemic core progression and the potential to respond to thrombolytic therapy beyond 3 hours.
Key Words: cerebral ischemia, angiography , magnetic resonance
Diagnostic Benefit of Echocontrast Enhancement for the Insufficient Transtemporal Bone Window—Nabavi DG (Dept of Neurology, Univ of Münster, Albert Schweitzer-Str 33, 48129 Münster, Germany), Droste DW, Schulte-Altedorneburg G, Kemény V, Panzica M, Weber S, Ringelstein EB—J Neuroimaging. 1999;9:102–107. Copyright © 1999 by the American Society of Neuroimaging.
Echocontrast agents (ECA) are known to improve transcranial color-coded duplex (TCCD) imaging, but its diagnostic benefit in the routine clinical setting has not clearly been defined. The authors investigated the diagnostic benefit of ECA application in 54 patients with insufficient transtemporal bone window, consecutively referred to their ultrasound laboratory. According to the precontrast imaging quality, patients were assigned to three categories: A, no intracranial structures or vessel segments visible on B-mode imaging and TCCD (n=5); and intracranial structures visible on B-mode imaging and vessel segments less than 5 mm in length (B, n=21), or larger than 5 mm in length (C, n=28) visible on TCCD. The effect of the echocontrast enhancement was assessed with respect to signal enhancement, imaging quality, and diagnostic confidence. In 49 out of 54 patients (91%), a significant improvement of the imaging quality was noted, enabling 43 (80%) neurovascular diagnoses of sufficient diagnostic confidence. The diagnostic ECA effect was strongly dependent on the precontrast imaging quality: upon echoenhancement, a satisfactory image quality was obtained in none of the patients of category A, as opposed to 16 (76%) and 27 (96%) patients of categories B and C, respectively. In summary, in 80% of our consecutive patient series with insufficient transtemporal bone window, application of ECA allowed for a conclusive TCCD study. Properties of the transtemporal precontrast scans are strongly predictive of the diagnostic benefit and should be taken into the decisive consideration.
Key Words: ultrasonography, contrast media
Contrast-Enhanced Transcranial Color-Coded Duplex Sonography: Efficiency and Validity—Gerriets T, Seidel G, Fiss I, Modrau B, Kaps M (Ratzeburger Allee 160, D-23538 Lübeck, Germany)—Neurology. 1999;52:1133–1137. Copyright © 1999 by the American Academy of Neurology.
Objective: To evaluate the diagnostic efficiency and accuracy of contrast-enhanced transcranial color-coded sonography (CE-TCCS). Background: TCCS is hampered by insufficient ultrasonic penetration in 20% of cerebrovascular patients. Methods: In 47 patients whose basal arteries could not be assessed adequately, 59 TCCS examinations were performed before and after administration of the ultrasonic contrast agent (CA) Levovist. The assessability of different basal cerebral arteries after CA administration was evaluated off-line. Angiographic records were available from 11 patients. Results: Satisfactory investigation of the middle cerebral artery, the anterior cerebral artery, the P1 and P2 segments of the posterior cerebral artery, and the supraclinoid portion of the internal carotid artery siphon was possible in 5.1%, 28.8%, 35.6%, 55.9%, and 47.5% of patients before, and in 84.7%, 91.5%, 93.2%, 94.5%, and 93.2% of patients after contrast enhancement. Stenoses or occlusions of basal cerebral arteries were registered in 28 patients (60%). CE-TCCS diagnosis was confirmed by digital subtraction angiography or magnetic resonance angiography in 10 of the 11 patients, leading to positive and negative predictive values of 0.86 and 1.00. Conclusion: Contrast enhancement improves the diagnostic potential of TCCS significantly in patients with temporal bone window failure, and proved to be a reliable method for detecting middle cerebral artery and siphon occlusion.
Key Words: ultrasonography, contrast media
Local Inhibition of Tissue Factor Reduces the Thrombogenicity of Disrupted Human Atherosclerotic Plaques: Effects of Tissue Factor Pathway Inhibitor on Plaque Thrombogenicity Under Flow Conditions—Badimon JJ (Cardiovascular Biology Research Laboratory, The Zena and Michael A. Wiener Cardiovascular Institute Box 1030, Mount Sinai School of Medicine, New York, NY 10029), Lettino M, Toschi V, Fuster V, Berrozpe M, Chesebro JH, Badimon L—Circulation. 1999;99:1780–1787. Copyright © 1999 American Heart Association.
Background—Plaque disruption and subsequent thrombus formation lead to acute coronary syndromes and progression of atherosclerotic disease. Tissue factor (TF) appears to mediate plaque thrombogenicity. Tissue factor pathway inhibitor (TFPI) is the major physiological inhibitor of TF. This study analyzes the role of TF on thrombogenicity of disrupted human atherosclerotic plaques and the therapeutic possibilities of its specific inhibition.
Methods and Results—Human atherosclerotic and normal arterial segments were exposed to heparinized blood at flow conditions modeling medium-grade coronary stenosis in the Badimon perfusion chamber. The antithrombotic effects of the specific inhibition of plaque TF was assessed by reduction in the deposition of radiolabeled platelets and fibrin(ogen) and immunohistochemical analysis of perfused arteries. TF activity was inhibited by both recombinant TFPI and a polyclonal antibody against human TF. Human lipid-rich plaques were more thrombogenic than less advanced atherosclerotic plaques. Specific inhibition of TF activity reduced plaque thrombogenicity, inhibiting both platelet and fibrin(ogen) deposition (580 versus 194 platelets×106/cm2; P<0.01, and 652 versus 172×1012 molecules of Fg/cm2; P<0.05, respectively) and thrombosis (immunohistochemistry).
Conclusions—This study documents the key role of TF activity in acute arterial thrombosis after atherosclerotic plaque disruption and provides evidence of the benefit of blocking plaque TF activity. Therefore the inhibition of the TF pathway opens a new therapeutic strategy in the prevention of acute coronary thrombosis after plaque disruption.
Key Words: thrombosis, atherosclerosis
Low-Dose Vitamin K1 versus Short-Term Withholding of Acenocoumarol in the Treatment of Excessive Anticoagulation Episodes Induced by Acenocoumarol—Ortin M (Servicio de Hamatologia, Hospital Sierrallana, B0 de Ganzo s/n E-39300 Torrelavega, Cantabria, Spain), Olalla J-I, Marco F, Velasco N—Haemostasis. 1998;28:57–61. Copyright © 1999 S. Karger AG, Basel.
Background: No consensus exists about the management of iatrogenically induced excessive hypocoagulability episodes. Objective: To compare the two most common therapeutic approaches in such situations (discontinuation of the oral anticoagulant vs. low-dose subcutaneous vitamin K1) when acenocoumarol is the normally used anticoagulant. Patients and Methods: The study was retrospective and comparative. Patients received antithrombotic therapy using acenocoumarol. Anticoagulant plasmatic activity was assessed through the international normalized ratio (INR) recorded from December 1994 to December 1997 at two medical centers. Results: INR is brought faster to a safe range in patients treated with low-dose vitamin K1 (p=0.01). Their long-term behavior is also more stable and predictable and no resistance to the oral anticoagulant was found. Conclusion: Low-dose vitamin K1 is a safer therapeutic option compared to simply withholding the oral anticoagulant. Its best scheme of administration, however, has yet to be defined.
Key Words: anticoagulants, complications
Percutaneous Transluminal Angioplasty and Stent Placement for Recurrent Carotid Artery Stenosis—Lanzino G (Dept of Neurosurgery, State Univ of New York at Buffalo, 3 Gates Circle, Buffalo, NY 14209-1194), Mericle RA, Lopes DK, Wakhloo AK, Guterman LR, Hopkins LN—J Neurosurg. 1999;90:688–694.
Object. Treatment consisting of percutaneous transluminal angioplasty (PTA) and stent placement has recently been proposed as an alternative to surgical reexploration in patients with recurrent carotid artery stenosis following endarterectomy. The authors retrospectively reviewed their experience after performing 25 procedures in 21 patients to assess the safety and efficacy of PTA with or without stent placement for carotid artery restenosis.
Methods. The mean interval between endarterectomy and the endovascular procedures was 57 months (range 8–220 months). Seven arteries in five patients were treated by PTA alone (including bilateral procedures in one patient and repeated angioplasty in the same vessel in another). Early suboptimum results and recurrent stenosis in some of these initial cases prompted the authors to combine PTA with stent placement in the treatment of 18 arteries over the past 3 years. No major periprocedural deficits (neurological or cardiac complications) or death occurred. There was one periprocedural transient neurological event, and in one patient a pseudoaneurysm of the femoral artery (at the access site) required surgical repair. In the 16 patients who each underwent at least 6 months of follow-up review, no neurological events ipsilateral to the treated artery had occurred after a mean follow-up period of 27 months (range 6–57 months). Three of five patients who underwent PTA alone developed significant (>50%) asymptomatic restenoses that required repeated angioplasty in one and PTA with stent placement in two patients. Significant restenosis (55%) was observed in only one of the vessels treated by combined angioplasty and stent placement.
Conclusions. Endovascular PTA and stenting of recurrent carotid artery stenosis is both technically feasible and safe and has a satisfactory midterm patency. This procedure can be considered a viable alternative to surgical reexploration in patients with recurrent carotid artery stenosis.
Key Words: carotid artery diseases, angioplasty
Extracorporeal Circulation Before and After Ultrasonographic Evaluation of the Ascending Aorta—Ura M, Sakata R (96 Tainoshima, Tamukaemachi, Kumamotoshi, Japan, 862-0965), Nakayama Y, Miyamoto TA, Goto T—Ann Thorac Surg. 1999;67:478–483. Copyright © 1999 by The Society of Thoracic Surgeons.
Background. To further gain insight into atheroembolization mechanisms epiaortic two-dimensional echocardiographic evaluation before extracorporeal circulation and after decannulation may be helpful.
Methods. Epiaortic two-dimensional echocardiography was performed before cannulation and after decannulation in 188 (124 men) patients (mean age, 67.7 years; range, 43 to 86 years) undergoing operation with extracorporeal circulation for ischemic heart disease during 1996.
Results. After decannulation, a new intimal lesion was recognized in 10 of 188 patients (5.3%): mobile type in 5 patients (3 ending with a stroke [60%], 2 having brain computed tomographic scans compatible with embolism), intimal tear in 2, and intimal irregularity in 3 patients. Stroke occurred in a significantly smaller number of patients (2 of 178 [1.1%]; p<0.001) without new lesions.
Conclusions. Clamp- or cannula-induced new lesions, especially of mobile type, are often complicated by postoperative stroke. Aggressive surgical technique modifications may need to be considered to avoid creating new lesions, particularly of the mobile type.
Key Words: ultrasonography, aortic arch
Carotid Endarterectomy With Patch Closure Versus Carotid Eversion Endarterectomy and Reimplantation: A Prospective Randomized Study—Ballota E, (Vascular Surgery Section, 1st Institute of General Surgery, Univ of Padua, School of Medicine, Policlinico Universitario, Via N Giustiniani 2, 35128 Padova, Italy), Da Giau G, Saladini M, Abbruzzese E, Renon L, Toniato A—Surgery. 1999;125:271–279. Copyright © 1999 by Mosby.
Background. Although carotid eversion endarterectomy (CEE) has obtained consensus providing excellent early and late results, conventional carotid endarterectomy (CEA) with or without patching continues to be considered the gold standard surgical procedure. The few studies published to date comparing CEE with CEA in a small series of patients have failed to show substantial advantages of one technique over the other, and further randomized comparative studies are still required. The purpose of this study was to compare the outcome of CEA with routine patch closure (CEAP) with that of CEE and reimplantation (CEER) of the internal carotid artery in the common carotid artery.
Methods. Three hundred thirty-six primary CEAs performed in 310 patients were randomized into 2 groups, 167 CEAPs and 169 CEERs. Surviving patients underwent duplex ultrasound scan control at 30 days, 6 months, 12 months, and every postoperative year thereafter. The mean follow-up was 34 months (range, 1 to 69 months). Demographic characteristics, risk factors, associated diseases, and indications for surgery were comparable in the 2 groups.
Results. Although the rate of intraoperative electroencephalogram changes was comparable in the 2 groups, the incidence of shunting was statistically higher in the CEAP group (28.1% vs 1.2%, P<.00001). The carotid cross-clamping time was significantly lower in the CEER group (P=.01). Although all deaths were in the CEAP group, the overall perioperative death and stroke-related death rates were comparable in the 2 groups. The perioperative stroke rate was statistically higher in the CEAP group (2.9% vs 0%, P=.03). Although the recurrent stenosis rate was comparable in the 2 groups (1.2% vs 0%), the CEAP group had a statistically higher rate of combined recurrent stenoses and occlusions (4.9% vs 0%, P=.003). The late mortality rate was similar in both groups.
Conclusions. Although the outcome of CEAP in this series is consistent with that of the main reported trials, the CEER procedure is less likely than CEAP to cause perioperative stroke and death and seems superior in reducing the incidence of recurrent stenosis and late occlusive events.
Key Words: carotid endarterectomy, surgical treatment
Items of Interest
Differential Capacity of Left and Right Hemispheric Areas for Compensation of Poststroke Aphasia
—Heiss W-D (Max-Planck-Institut für Neurologische Forschung, Gleueler Str 50, D-50931 Köln, Germany), Kessler J, Thiel A, Ghaemi M, Karbe H—
Ann Neurol. 1999;45:430–438. Copyright © 1999 by the American Neurological Association.
Biochemical and Molecular Characteristics of the Brain With Developing Cerebral Infarction—Kato H (Dept of Neurology, Washington Univ School of Medicine, Box 8111, 660 S Euclid Ave, St Louis, MO 63110), Kogure K—Cell Mol Neurobiol. 1999;19:93–108. Copyright © 1999 Plenum Publishing Corporation.
Intracranial Arteries of Human Fetuses Are More Resistant to Hypercholesterolemia-Induced Fatty Streak Formation Than Extracranial Arteries—Napoli C, Witztum JL, de Nigris F, Palumbo G, D’Armiento FP, Palinski W (Dept of Medicine, 0682, Univ of California, San Diego, 9500 Gilman Dr, MTF 110, La Jolla, CA 92093)—Circulation. 1999;99:2003–2010. Copyright © 1999 American Heart Association.
Prevention of a First Stroke—Gorelick PB (Center for Stroke Research, Rush Medical College, 1645 W Jackson Blvd, Suite 400, Chicago, IL 60612), Sacco RL, Smith DB, Alberts M, Mustone-Alexander L, Rader D, Ross JL, Raps E, Ozer MN, Brass LM, Malone ME, Goldberg S, Booss J, Hanley DF, Toole JF, Greengold NL, Rhew DC—JAMA. 1999;281:1112–1120.
Isolated Dysarthria Due to Extracerebellar Lacunar Stroke: A Central Monoparesis of the Tongue—Urban PP (Dept of Neurology, Univ of Mainz, Langenbeckstrasse 1, D 55101 Mainz, Germany), Wicht S, Hopf HC, Fleischer S, Nickel O—J Neurol Neurosurg Psychiatry. 1999;66:495–501.
Thrombotic Thrombocytopenic Purpura: Brain CT and MRI Findings in 12 Patients—Bakshi R (Lucy Dent Imaging Center, 3 Gates Circle, Buffalo, NY 14209), Shaikh ZA, Bates VE, Kinkel PR—Neurology. 1999;52:1285–1288. Copyright © 1999 by the American Academy of Neurology.
Focal Neurological Deficits in Children With β-Thalssemia Major—Incorpora G, Di Gregorio F, Romeo MA, Pavone P, Trifiletti RR, Parano E (Div di Neurologia Pediatrica Clinica Pediatrica, Univ di Catania, Viale Andrea Doria 6, I-95125 Catania, Italy)—Neuropediatrics. 1999;30:45–48. Copyright © Hippokrates Verlag Stuttgart.
The abstracts in this section have been typeset for consistency with journal format but otherwise appear as in the original articles.
- Copyright © 1999 by American Heart Association