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HomeStrokeVol. 30, No. 8Abstracts of Literature Free AccessOtherPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessOtherPDF/EPUBAbstracts of Literature Askiel Bruno and Engin Y. Yilmaz Askiel BrunoAskiel Bruno Search for more papers by this author and Engin Y. YilmazEngin Y. Yilmaz Search for more papers by this author Originally published1 Aug 1999https://doi.org/10.1161/01.STR.30.8.1738Stroke. 1999;30:1738–1744Cerebral AneurysmsAB-14428-99Five-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, aneurysmAB-14429-99Improved 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, aneurysmAB-14430-99Oxidative 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 radicalsAB-14431-99Aneurysm 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 therapyAB-14432-99Current 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 arteryClinicalAB-14433-99Lone 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 outcomeAB-14434-99Ischemic 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 ischemiaAB-14435-99Prevention 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, depressionAB-14436-99Poststroke 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, seizuresAB-14437-99Anticardiolipin 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, antiphospholipidEpidemiologyAB-14438-99Factor 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 factorsAB-14439-99Ethnic 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, incidenceAB-14440-99Cross-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 diseasesAB-14441-99Migraine 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, migraineExperimental PathologyAB-14442-99Dexamethasone 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 i