Abstracts of Literature
1999; Lippincott Williams & Wilkins; Volume: 30; Issue: 7 Linguagem: Inglês
10.1161/01.str.30.7.1494
ISSN1524-4628
AutoresAskiel Bruno, Engin Y. Yilmaz,
ResumoHomeStrokeVol. 30, No. 7Abstracts 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 and Engin Y. YilmazEngin Y. Yilmaz Originally published1 Jul 1999https://doi.org/10.1161/01.STR.30.7.1494Stroke. 1999;30:1494–1500Cerebral AneurysmsAB-14403-99 Resumption of Work After Aneurysmal Subarachnoid Hemorrhage in Middle-Aged Japanese Patients—Nishino A (Dept of Neurosurgery, Stroke Center, Sendai National Hospital, 2-8-8 Miyagino, Miyagino-ku, Sendai 983-8520, Japan), Sakurai Y, Tsuji I, Arai H, Uenohara H, Suzuki S, Li JH—J Neurosurg. 1999;90:59–64.Object. Previous reports on the results of treatment for aneurysmal subarachnoid hemorrhage (SAH) have been based only on activities of daily living after discharge, whereas resumption of work has received insufficient attention. Most Japanese work under a lifetime employment system, and it is best for those who have recovered from SAH to return to work for their previous employer. The present study was conducted to determine the extent to which discharged patients who have suffered an SAH resume their former occupations in Japan, focusing on those between 40 and 49 years of age, who usually have a strong desire to return to work.Methods. The participants consisted of 193 patients with SAH. Based on the results of telephone interviews or written questionnaires, their work status at 1 year after onset was analyzed.The work resumption rates for patients with Hunt and Kosnik neurological Grades 1 or 2 on admission were higher than for those with Grades 3 or 4 (p=0.015) and lower for patients with basilar artery aneurysms than for those with aneurysms at other sites (p=0.028). With regard to premorbid occupation, the work resumption rates were high (80%) for professionals and engineers, many of whom were public servants, or teachers at junior or senior high schools. The resumption rates were also high for primary industry workers (80%), but lowest (20%) for professional drivers (p=0.04–0.001). The work resumption rate was lower for women than for men (p=0.01).Conclusions. These findings indicate that resumption of work is determined not only by medical factors, but also by social factors including gender, type of occupation, employment system, and socioeconomic background.subarachnoid hemorrhage, stroke outcomeAB-14404-99Chronic Shunt-Dependent Hydrocephalus After Early Surgical and Early Endovascular Treatment of Ruptured Intracranial Aneurysms—Gruber A (Dept of Neurosurgery, Univ of Vienna Medical School, Waehringer Guertel 18-20, A-1090 Vienna, Austria), Reinprecht A, Bavinzski G, Czech T, Richling B—Neurosurgery. 1999;44:503–512.OBJECTIVE: The goal of this study was to document the influence of the treatment method (early surgery versus early endovascular treatment) on the development of chronic shunt-dependent hydrocephalus in a series of 242 patients treated within 7 days after aneurysmal subarachnoid hemorrhage (SAH).METHODS: The following parameters were prospectively recorded in a computerized database and retrospectively analyzed for association with chronic shunt-dependent hydrocephalus: 1) Hunt and Hess grade, 2) Fisher computed tomographic grade, 3) incidence of repeat SAH, 4) aneurysm location, and 5) treatment method (early surgery versus early endovascular treatment).RESULTS: Forty of 187 patients (21.4%) who survived the SAH and its neurological and/or medical sequelae underwent definitive shunting for treatment of chronic hydrocephalus. The rate of shunt dependency was positively correlated with a higher Hunt and Hess grade (P<0.001), a higher Fisher computed tomographic grade (P=0.003), the occurrence of intraventricular hemorrhage (P<0.001), repeat SAH (P=0.003), and aneurysms arising at the anterior communicating artery (P<0.001).CONCLUSION: The results of the present study indicate that the treatment method used does not affect the risk of the later development of chronic shunt-dependent hydrocephalus (early surgery, 23.2% [29 of 125]; early endovascular treatment, 17.7% [11 of 62]; P=0.45).subarachnoid hemorrhage, hydrocephalusClinicalAB-14405-99 Migraine and Stroke in Young Women: Case-Control Study—Chang CL, Donaghy M, Poulter N (Cardiovascular Studies Unit, Dept of Clinical Pharmacology, Imperial College School of Medicine, London W2 1PG, England), and World Health Organisation Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception—BMJ.1999;318:13–18.Objective To investigate the association between migraine and ischaemic or haemorrhagic stroke in young women.Design Hospital based case-control study.Setting Five European centres participating in the World Health Organisation Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception.Subjects 291 women aged 20–44 years with ischaemic, haemorrhagic, or unclassified arterial stroke compared with 736 age and hospital matched controls.Intervention Questionnaire.Main outcome measure Self reported history of headaches.Results Adjusted odds ratios associated with a personal history of migraine were 1.78 (95% confidence intervals, 1.14 to 2.77), 3.54 (1.30 to 9.61), and 1.10 (0.63 to 1.94) for all stroke, ischaemic stroke, and haemorrhagic stroke respectively. Odds ratios for ischaemic stroke were similar for classical migraine (with aura) (3.81, 1.26 to 11.5) and simple migraine (without aura) (2.97, 0.66 to 13.5). A family history of migraine, irrespective of personal history, was also associated with increased odds ratios, not only for ischaemic stroke but also haemorrhagic stroke. In migrainous women, coexistent use of oral contraceptives or a history of high blood pressure or smoking had greater than multiplicative effects on the odds ratios for ischaemic stroke associated with migraine alone. Change in the frequency or type of migraine on using oral contraceptives did not predict subsequent stroke. Between 20% and 40% of strokes in women with migraine seemed to develop directly from a migraine attack.Conclusions Migraine in women of childbearing age significantly increases the risk of ischaemic but not haemorrhagic stroke. The coexistence of oral contraceptive use, high blood pressure, or smoking seems to exert a greater than multiplicative effect on the risk of ischaemic stroke associated with migraine.migraine, womenAB-14406-99Small Centrum Ovale Infarcts: A Pathological Study—Lammie GA (Dept of Neuropathology Alexander Donald Building, Western General Hospital, Crewe Rd, Edinburgh EH4 2XU, UK), Wardlaw JM—Cerebrovasc Dis. 1999;9:82–90. Copyright © 1999 S. Karger AG, Basel.There are limited data, mainly clinical and radiological, on small centrum ovale infarcts (SCOIs). From a consecutive series of 159 autopsy brains we identified 12 cases which on gross pathological examination harboured a total of 21 SCOIs. In the majority of lesions histology revealed a significant component of incompletely infarcted brain. Clinicopathological data suggested that the underlying mechanism was likely to have been cardioembolic in 3 cases, and possibly embolic from heart or aortic arch in a further 5. Two cases were due to ipsilateral carotid artery atheroma (i.e. 10 of 12 cases had possible embolic sources). The majority of lesions appeared to lie in arterial borderzones. The combined data suggest that SCOIs are pathologically and pathogenetically heterogeneous, and therefore that the term 'lacune' is inappropriate because this implies intrinsic small vessel disease as the underlying cause. Clinically, potentially treatable cardiac and large vessel pathology should be excluded.lacunar infarction, stroke classificationAB-14407-99Endogenous Nitric Oxide Synthase Inhibitor: A Novel Marker of Atherosclerosis—Miyazaki H, Matsuoka H (The Cardiovascular Research Institute, Dept of Internal Medicine III, Kurume Univ School of Medicine, 67 Asahi-machi, Kurume, Fukuoka, 830-0011 Japan), Cooke JP, Usui M, Ueda S, Okuda S, Imaizumi T—Circulation. 1999;99:1141–1146. Copyright © 1999 American Heart Association, Inc.Background—Exposure to risk factors such as hypertension or hypercholesterolemia decreases the bioavailability of endothelium-derived nitric oxide (NO) and impairs endothelium-dependent vasodilation. Recently, a circulating endogenous NO synthase inhibitor, asymmetric dimethylarginine (ADMA), has been detected in human plasma. The purpose of this study was to examine the relationship between plasma ADMA and atherosclerosis in humans.Methods and Results—Subjects (n=116; age, 52±1 years; male:female ratio, 100:16) underwent a complete history and physical examination, determination of serum chemistries and ADMA levels, and duplex scanning of the carotid arteries. These individuals had no symptoms of coronary or peripheral artery disease and were taking no medications. Univariate and multivariate analyses revealed that plasma levels of ADMA were positively correlated with age (P<0.0001), mean arterial pressure (P<0.0001), and Σ glucose (an index of glucose tolerance) (P=0.0006). Most intriguingly, stepwise regression analysis revealed that plasma ADMA levels were significantly correlated to the intima-media thickness of the carotid artery (as measured by high-resolution ultrasonography).Conclusions—This study reveals that plasma ADMA levels are positively correlated with risk factors for atherosclerosis. Furthermore, plasma ADMA level is significantly correlated with carotid intima-media thickness. Our results suggest that this endogenous antagonist of NO synthase may be a marker of atherosclerosis.atherosclerosis, nitric oxideAB-14408-99Diabetic Nephropathy Is Associated With an Increased Familial Risk of Stroke—Lindsay RS (Dept of Diabetes, Royal Infirmary of Edinburg NHS Trust, Lauriston Place, Edinburgh EH3 9YW, Scotland, UK), Little J, Jaap AJ, Padfield PL, Walker JD, Hardy KJ—Diabetes Care. 1999;22:422–425.OBJECTIVE—To test the hypothesis that genetic susceptibility to diabetic nephropathy is associated with an increased familial risk of vascular disease, we have examined the causes and rates of death of parents of individuals with type 1 diabetes complicated by diabetic nephropathy compared with the causes and rates of death of parents of control subjects with diabetes uncomplicated by nephropathy.RESEARCH DESIGN AND METHODS—Individuals with at least a 14-year duration of type 1 diabetes complicated by diabetic nephropathy were identified and matched for age, sex, and duration of diabetes to control subjects. A total of 118 patients and 118 matched control subjects were identified and approached to obtain information on parental age and cause of death. For parents who had died, the cause of death was ascertained from the death certificate.RESULTS—Kaplan-Meier curves showed that parents of subjects with nephropathy (PN) had reduced survival compared with parents of diabetic subjects without nephropathy (PC) (log rank test P<0.05). There was an excess of all vascular deaths and, in particular, strokes in the parents of subjects with nephropathy (PN: 20 of 103 deaths, 19% vs. PC: 3 of 66 deaths, 4%; Fisher's exact test P<0.01).CONCLUSIONS—Parents of diabetic patients with nephropathy have reduced survival. This seems to be largely explained by an increase in vascular deaths and, in particular, a four-fold increase in the number of strokes. This supports the hypothesis that a common hereditary risk factor predisposes to both vascular death and diabetic renal disease.diabetes mellitus, risk factorsEpidemiologyAB-14409-99 G20210A Mutation in Prothrombin Gene and Risk of Myocardial Infarction, Stroke, and Venous Thrombosis in a Large Cohort of US Men—Ridker PM (Cardiovascular Div, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115), Hennekens CH, Miletich JP—Circulation. 1999;99:999–1004. Copyright © 1999 American Heart Association, Inc.Background—A single base pair mutation in the prothrombin gene has recently been identified that is associated with increased prothrombin levels. Whether this mutation increases the risks of arterial and venous thrombosis among healthy individuals is controversial.Methods and Results—In a prospective cohort of 14 916 men, we determined the prevalence of the G20210A prothrombin gene variant in 833 men who subsequently developed myocardial infarction, stroke, or venous thrombosis (cases) and in 1774 age- and smoking status-matched men who remained free of thrombosis during a 10-year follow-up (control subjects). Gene sequencing was used to confirm mutation status in a subgroup of participants. Overall, carrier rates for the G20210A mutation were similar among case and control subjects; the relative risk of developing any thrombotic event in association with the 20210A allele was 1.05 (95% CI, 0.7 to 1.6; P=0.8). We observed no evidence of association between mutation and myocardial infarction (RR=0.8, P=0.4) or stroke (RR=1.1, P=0.8). For venous thrombosis, a modest nonsignificant increase in risk was observed (RR=1.7, P=0.08) that was smaller in magnitude than that associated with factor V Leiden (RR=3.0, P<0.001). Nine individuals carried both the prothrombin mutation and factor V Leiden (5 controls and 4 cases). One individual, a control subject, was homozygous for the prothrombin mutation.Conclusions—In a large cohort of US men, the G20210A prothrombin gene variant was not associated with increased risk of myocardial infarction or stroke. For venous thrombosis, risk estimates associated with the G20210A mutation were smaller in magnitude than risk estimates associated with factor V Leiden.thrombosis, risk factorsAB-14410-99Seasonal Variation in Stroke Mortality Rates—Lanska DJ (VA Medical Center, 500 E Veterans St, Tomah, WI 54660), Hoffmann RG—Neurology. 1999;52:984–990. Copyright © 1999 by the American Academy of Neurology.Objective: To identify possible contributors to the seasonal variation in stroke mortality. Background: Stroke and respiratory disease mortality rates were calculated from vital statistics and census data for the United States from 1938 to 1988. State-specific average temperatures by month were derived from data obtained from the National Climatic Data Center for 1938 to 1987. Methods: Each time series was decomposed into a trend, a seasonal effect, and a residual effect. Multiple regression was used to fit both a trend and a seasonal harmonic series. Cross-correlation was used to assess the relationship between the residual time series. Results: There is a strong and consistent seasonal pattern of high stroke and respiratory disease mortality in the colder winter months. Stroke mortality was significantly and independently both positively associated with respiratory disease mortality and inversely associated with temperature. The sharp initial increases in both respiratory disease and stroke mortality in the late fall and early winter are synchronous, and the amplitudes are strongly associated, except for a saturation effect with extreme respiratory disease amplitudes. Conclusions: Seasonal change in stroke mortality is associated with seasonal variation in both respiratory disease and temperature. Respiratory disease and temperature may influence stroke mortality nonspuriously by affecting stroke case fatality, incidence, or both.stroke outcome, epidemiologyExperimental PathologyAB-14411-99 Nitric Oxide Mediates Neurologic Injury After Hypothermic Circulatory Arrest—Tseng EE, Brock MV, Lange MS, Troncoso JC, Lowenstein CJ, Blue ME, Johnston MV, Baumgartner WA (Div of Cardiac Surgery, Johns Hopkins Hospital, Blalock 618, 600 N Wolfe St, Baltimore, MD 21287)—Ann Thorac Surg. 1999;67:65–71. Copyright © 1999 by The Society of Thoracic Surgeons.Background. Prolonged hypothermic circulatory arrest (HCA) causes neurologic injury. However, the mechanism of this injury is unknown. We hypothesized that HCA causes nitric oxide production to result in neuronal necrosis. This study was undertaken to determine whether the neuronal nitric oxide synthase inhibitor 17477AR reduces necrosis after HCA.Methods. Thirty-two dogs underwent 2 hours of HCA at 18°C. Nitric oxide synthase catalytic assay and intracerebral microdialysis for nitric oxide production were performed in acute nonsurvival experiments (n=16). Sixteen animals survived for 72 hours after HCA: Group 1 (n=9) was treated with 17477AR (Astra Arcus), and group 2 (n=7) received vehicle only. Animals were scored from 0 (normal) to 500 (coma) for neurologic function and from 0 (normal) to 100 (severe) for neuronal necrosis.Results. Administration of 17477AR reduced nitric oxide production in the striatum by 94% (HCA alone), 3.65±2.42 μmol/L; HCA and 17477AR, 0.20±0.14 μmol/L citrulline). Dogs treated with 17477AR after HCA had superior neurologic function (62.22±29.82 for group 1 versus 141.86±61.53 for group 2, p=0.019) and significantly reduced neuronal necrosis (9.33±4.67 for group 1 versus 38.14±2.23 for group 2, p<0.00001) compared with untreated HCA dogs.Conclusions. Our results provide evidence that neuronal nitric oxide synthase mediates neuronal necrosis after HCA and plays a significant role in HCA-induced neurotoxicity. Pharmacologic strategies to inhibit neuronal nitric oxide synthase after the ischemic period of HCA may be clinically beneficial.nitric oxide, cerebral ischemiaAB-14412-99Pretreatment With Intravenous FGF-13 Reduces Infarct Volume and Ameliorates Neurological Deficits Following Focal Cerebral Ischemia in Rats—Yao DL (Dept of Pharmacology, Human Genome Sciences, 9410 Key West Ave, Rockville, MD 20850), Masonic K, Petullo D, Li YL, Lincoln C, Wibberley L, Alderson RF, Antonaccio M—Brain Res. 1999;818:140–146. Copyright © 1999 Elsevier Science B.V.Fibroblast growth factor-13 (FGF-13), novel member of FGF family has recently been molecularly cloned as a result of high throughput sequencing of a ovarian cancer cell, hippocampal, and kidney cDNA libraries. The human gene encodes for a protein with a molecular weight of 22 kDa that is most homologous to FGF-8 (70% similarity). In the current study, we tested the effects of intravenously administered FGF-13 in a model of permanent focal cerebral ischemia in Sprague–Dawley rats. FGF-13 or the vehicle was administered systematically via the tail vein 30 min prior, and 30 min and 24 h after the occlusion of the left middle cerebral artery (MCAo). Animals were weighted and evaluated behaviorally prior to and at 24 and 48 h after MCAo. The volume of cerebral infarct and swelling were determined using an image analysis system (BioQuant) and cresyl violet stained sequential sections from the forebrain region. Histopathology was evaluated to compare the therapeutic effects. We found a 63% reduction in infarct volume in FGF-13- vs. vehicle-treated animals (infarct volume was 21.9±3.8% in vehicle- and 8.1±1.6% in FGF-13-treated rats, p=0.0016) and a moderate inhibition of brain swelling by FGF-13. The reduction in infarct volume and brain swelling were associated with improvement of clinical deficits in FGF-13 treated animals (p<0.001). Histopathological examination determined that nervous tissue was better preserved in FGF-13 treated rats than those of controls. These data show that pretreatment with intravenous FGF-13 reduces infarct size and ameliorates neurological deficits following permanent focal cerebral ischemia in rats.cerebral ischemia, stroke, experimentalAB-14413-99A Comparative Study of the Effects of Two Nitric Oxide Synthase Inhibitors and Two Nitric Oxide Donors on Temporary Focal Cerebral Ischemia in the Wistar Rat—Coert BA, Anderson RE, Meyer FB (Dept of Neurosurgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905)—J Neurosurg. 1999;90:332–338.Object. A critical review of the literature indicates that the effects of nitric oxide synthase (NOS) inhibitors on focal cerebral ischemia are contradictory. In this experiment the authors methodically examined the dose-dependent effects of two NOS inhibitors and two NO donors on cortical infarction volume in an animal model of temporary focal cerebral ischemia simulating potential ischemia during neurovascular interventions.Methods. Ninety-two Wistar rats underwent 3 hours of combined left middle cerebral artery and bilateral common carotid artery occlusion after having been anesthetized with 1% halothane. A nonselective NOS inhibitor, NG-nitro-l-arginine-methyl-ester (l-NAME), and two NO donors, 3-morpholinosydnonimine hydrochloride and NOC-18, DETA/NO, (Z)-l-[2(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate, were administered intravenously 30 minutes before ischemia was induced. A selective neuronal NOS inhibitor, 7-nitroindazole (7-NI), was administered intraperitoneally in dimethyl sulfoxide (DMSO) 60 minutes before ischemia was induced. Two ischemic control groups, to which either saline or DMSO was administered, were also included in this study. Seventy-two hours after flow restoration, the animals were perfused with tetrazolium chloride for histological evaluation.Cortical infarction volume was significantly reduced by 71% in the group treated with 1 mg/kg l-NAME when compared with the saline-treated ischemic control group (27.1±37 mm3 compared with 92.5±26 mm3, p<0.05). The NOS inhibitor 7-NI significantly reduced cortical infarction volume by 70% and by 92% at doses of 10 and 100 mg/kg: 35.2±32 mm3 (p<0.05) and 9±13 mm3 (p<0.005), respectively, when compared with the DMSO-treated ischemic control group (119±43 mm3). There was no significant difference between the saline-treated and DMSO-treated ischemic control groups. Treatment with NO donors did not significantly alter cortical infarction volume.Conclusions. These results support an important role for NO in ischemic neurotoxicity and indicate that neuronal NOS inhibition may be valuable in reducing cortical injury in patients suffering temporary focal cerebral ischemia during neurovascular procedures.nitric oxide, stroke, experimentalAB-14414-99Ultra-Early Clot Aspiration After Lysis With Tissue Plasminogen Activator in a Porcine Model of Intracerebral Hemorrhage: Edema Reduction and Blood-Brain Barrier Protection—Wagner KR (Research Service 151, Dept of Veterans Affairs Medical Center, 3200 Vine St, Cincinnati, OH 45220), Xi G, Hua Y, Zuccarello M, de Courten-Myers GM, Broderick JP, Brott TG—J Neurosurg. 1999;90:491–498.Object. Ultra-early hematoma evacuation (<4 hours) after intracerebral hemorrhage (ICH) may reduce mass effect and edema development and improve outcome. To test this hypothesis, the authors induced lobar hematomas in pigs.Methods. The authors infused 2.5 ml of blood into the frontal cerebral white matter in pigs weighing 8 to 10 kg. In the treatment group, clots were lysed with tissue plasminogen activator ([tPA], 0.3 mg) and aspirated at 3.5 hours after hematoma induction. Brains were frozen in situ at 24 hours post-ICH and hematomal and perihematomal edema volumes were determined on coronal sections by using computer-assisted morphometry.Hematoma evacuation rapidly reduced elevated cerebral tissue pressure from 12.2±1.3 to 2.8±0.8 mm Hg. At 24 hours, prior clot removal markedly reduced hematoma volumes (0.40±0.10 compared with 1.26±0.13 cm3, p<0.005) and perihematomal edema volumes (0.28±0.05 compared with 1.46±0.24 cm3, p 70%), markedly reduced perihematomal edema, and prevented the development of vasogenic edema. These findings in a large-animal model of ICH provide support for clinical trials that include the use of fibrinolytic agents and ultra-early stereotactically guided clot aspiration for treating ICH.thrombolysis, hemorrhagic strokeAB-14415-99Effect of Cigarette Smoke on Endothelial Regeneration in Vivo and Nitric Oxide Levels—Sarkar R (Sec of Vascular Surgery, UCLA Medical Center, Los Angeles, CA 90095), Gelabert HA, Mohiuddin KR, Thakor DK, Santibanez-Gallerani AS—J Surg Res. 1999;82:43–47. Copyright © 1999 by Academic Press.Background. Cigarette smoking accelerates atherosclerosis and restenosis after vascular reconstruction. The mechanisms by which smoking alters vessel structure after injury are unclear. This study examined the effects of cigarette smoking on endothelial regeneration, an important component of arterial remodeling.Materials and methods. Adult male rats were subjected to balloon injury of the thoracic aorta and exposed to mainstream cigarette smoke via a Griffith-type smoking machine for 2 weeks. Control groups included rats which were restrained in the machine but not smoked and a group not utilizing the machine. Aortic reendothelialization was determined using Evan's blue staining of the arterial surface. Serum levels of nitric oxide were measured to determine if smoke exposure altered this potential endothelial cell mitogen.Results. Cigarette smoking increased aortic endothelial regeneration (78.4±4.6% vs 59.2±2.1%, P<0.05) and was associated with an increase in serum nitric oxide level (59.9±7.1 μM vs 28.5±1.8 μM, P<0.05). Daily restraint alone in the smoking machine had no effect on endothelial regeneration.Conclusions. This is the first report on the effects of smoking on endothelial regeneration and demonstrates that smoking increases reendothelialization after large vessel injury and serum levels of nitric oxide, an EC mitogen.cigarette smoking, endotheliumImagingAB-14416-99 Correlation Between Symptomatic, Radiological and Etiological Diagnosis in Acute Ischemic Stroke—Tei H (Dept of Neurology, Toda Central General Hospital, 1-19-3 Honcho, Toda City, Saitama 3350023, Japan), Uchiyama S, Koshimizu M, Kobayashi M, Ohara K—Acta Neurol Scand. 1999;99:192–195. Copyright © Munksgaard 1999.Objectives—The aim of this study was to correlate with the symptomatic, radiological and etiological diagnosis in acute ischemic stroke. Subjects and methods—Two hundred and fifty patients with first-ever ischemic stroke within 24 h of onset were prospectively studied with 3-step diagnoses: 1) symptomatic diagnosis based on the Oxfordshire Community Stroke Project criteria (OCSP), 2) radiological diagnosis (CT or MRI) and 3) etiological diagnosis based on the Lausanne Stroke Registry criteria. Results—Most of the patients with symptoms of total anterior circulation infarcts (TACI), partial anterior circulation infarcts (PACI) and posterior circulation infarcts (POCI) had corresponding lesions on CT or MRI, while only 68% of lacunar infarcts (LACI) patients had small subcortical infarction (SSI). More than 60% of patients with TACI were classified into cardioembolism in the third diagnosis, while the etiology of PACI was either CE or large-artery atherosclerosis (LAA) in equal numbers. Only 58% of LACI patients were classified into small-artery disease (SAD) and 29% of them (30 cases) into LAA, of which 23 patients had lesions other than SSI. The positive predictive value of SAD in the combination of LACI and SSI was 0.78. The etiology of POCI was variable. Conclusion—Except for LACI, the symptomatic classification by OCSP corresponds well to the radiological diagnosis. The etiological diagnosis can be predicted by OCSP in TACI and PACI, but it is hard in POCI, and a number of LACI are due to LAA.cerebral infarction, stroke classificationAB-14417-99The Relationship Between Cerebral Infarction and Angiographic Characteristics in Childhood Moyamoya Disease—Mugikura S (Dept of Radiology, Hiraka General Hospital, 1-30 Ekimaemachi, Yokote, Akita 013-0036, Japan), Takahashi S, Higano S, Shirane R, Kurihara N, Furuta S, Ezura M, Takahashi A—Am J Neuroradiol. 1999;20:336–343. Copyright © American Society of Neuroradiology.BACKGROUND AND PURPOSE: In childhood-onset moyamoya disease, the angiographic disease process of stenoocclusive lesions is progressive, and cerebral infarctions often develop as a result of ischemia. Our purpose was to determine how the severity of stenoocclusive lesions in the anterior and posterior circulations affects the distribution of cerebral infarction in patients with childhood-onset moyamoya disease.METHODS: In 69 patients with childhood-onset moyamoya disease, angiograms were reviewed for stenoocclusive lesions, and CT scans, MR images, or both were reviewed for the sites and extent of cerebral infarction. The relationship between the angiographic and CT/MR findings were examined.RESULTS: The prevalence and degree of stenoocclusive lesions of the posterior cerebral artery (PCA) significantly correlated with the extent of lesions around the terminal portion of the internal carotid artery (ICA). The prevalence of infarction significantly correlated with the degree of stenoocclusive changes of both the ICA and PCA. Infarctions tended to be distributed in the anterior borderzone in less-advanced cases, while in more advanced cases lesions were additionally found posteriorly in the territory of the middle cerebral artery, the posterior borderzone, and the PCA territory.CONCLUSION: Our results indicate that progressive changes of the anterior and posterior circulations are associated with the distribution of cerebral infarction, culminating in a patchily disseminated or honeycomb pattern of infarction on CT and MR studies in late stages of the disease.stroke classification, angiographyAB-14418-99MRI Evidence of Past Cerebral Microbleeds in a Health Elderly Population—Roob G, Schmidt R, Kapeller P, Lechner A, Hartung H-P
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