ISSN:1015-9770    

DOI:10.1159/000108097

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Research into the causes of ischemic damage has evolved into an exploration of the brain's molecular responses. In attempting to discover the specific mechanisms by which ischemic cells die, a number of protective responses which are used by the cells to prolong or assure survival have also been understood, and some of these may become useful therapeutic tools. In this limited review, the mechanisms that are most likely to play a role in determining whether an ischemic cell survives or not are identified and examined. Particular emphasis is placed on the role of immediate early genes, heat shock proteins and trophic factors, and the more recent suspicion that cell cycle genes may be involved in the process of death by apoptosis. As well, the possibility that spreading depression may be a tool that may permit a better understanding of some of these mechanisms as well as offer new therapeutic avenues is examined.

ISSN:1015-9770    

DOI:10.1159/000108011

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

We report presumed mechanisms of recurrent stroke in a prospective study on patients with lacunar infarction. Eighty-one patients with clinical and magnetic resonance imaging (MRI) findings compatible with lacunar infarction were followed for a median time of 48 months. Patients with recurrent stroke were assessed clinically by computed tomography, contrast-enhanced MRI and with respect to large-artery disease and cardioembolic sources of embolism. During follow-up, 9 patients (11.1%) died and 20 patients (24.7%) had 27 recurrent strokes (3 hemorrhagic, 24 ischemic). The annual risk of recurrent stroke was 6.8% and approximately even with time. Univariate analysis revealed age as the only risk factor significantly associated with recurrent stroke. Out of 24 episodes of recurrent ischemic stroke, 16 had clinical and neuroimaging features compatible with small penetrating artery occlusion, 6 were due to cortical infarcts, 1 episode was caused by presumed cerebral amyloid angiopathy, and 1 by a retinal infarct. Relevant large-artery disease was diagnosed in 2 patients with recurrent, small brainstem infarcts and in 2 patients with recurrent cortical and retinal infarcts. Although presumed lacunar infarcts predominated, our series highlights the heterogeneity of recurrent strokes after lacunar infarcts.

ISSN:1015-9770    

DOI:10.1159/000108012

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Background and purpose: Pachymeningitis cranialis hypertrophica is a heterogeneous disorder with many different causes. We correlate clinical characteristics, CT or MRI scans with angiography or magnetic resonance venography (MRV) in three patients in whom the etiology was undetermined. Case descriptions: All three patients had neurologic deficits and abnormalities in the venous phase of angiography, in particular, findings consistent with venous sinus compromise. Conclusion: This finding draws attention to the possible effect of pachymeningitis in producing venous congestion, which may be related in some cases to the clinical manifestations of the disorder.

ISSN:1015-9770    

DOI:10.1159/000108013

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Sixty-eight rats were embolized in the right carotid territory with a 200-μl suspension of white clots made from autologous blood. The purpose was to investigate the effect of early treatment with tirilazad mesylate alone and in combination with thrombolytic therapy delayed 2 h. Twenty-six rats died spontaneously before the second postoperative day, and 42 animals were killed after 48 h of survival. The brains were removed, and the infarct volumes were measured in percent of the affected hemisphere. The animals that had died spontaneously were used for an estimation of an overall treatment effect in an analysis combining infarct size and mortality. Spontaneous death occurred in: 45% of the animals in the control group, 41% in the group treated with tirilazad alone, 38% of the animals treated with recombinant tissue plasminogen activator (rt-PA) and 25% of the animals receiving combined treatment. Among the surviving animals, the median infarct volume was 47% in the control group (n = 12). Tirilazad treatment (7.5 mg/kg over 5 h) initiated 10 min after embolization (n = 10) reduced median infarct volume to 15 % (p = 0.003). Human rt-PA, 20 mg/kg, was infused intravenously during 1 h starting 2 h after embolization (n = 8). This treatment reduced median infarct volume to 31% (p = 0.22). When the two treatment regimens were combined (n= 12), the median infarct volume was reduced to 17% (p = 0.007). In the analysis combining infarct size and mortality, the infarct size among the spontaneously dead rats was set to 68%, which was the largest infarct found in these animals. Following this procedure, the median infarct volume was 63% in the control group, 38% in the group treated with tirilazad alone, 44% in the rats treated with rt-PA alone and 22% in the combined treatment group (p = 0.01, compared to the control group). In conclusion, the primary data analysis of the surviving animals showed that early treatment with tirilazad significantly reduced infarct size in this stroke model, whereas the analysis combining mortality rates and infarct volume indicated that the combination of rt-PA and tirilazad was superior to either therapy alone.

ISSN:1015-9770    

DOI:10.1159/000108014

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Seven patients with presumed amphetamine-associated stroke are reported. Ischaemic stroke occurred in four patients, a transient ischaemic attack in one patient and a haemorrhagic stroke in two patients. All patients had used amphetamines within hours of the onset of focal neurological symptoms, but drug abuse was not admitted by three patients until 4, 5 and 8 weeks, respectively, after the admission. Other predisposing factors, besides concurrent alcohol abuse (n = 6), were present in only one patient (pro-coagulant state and protein-S deficiency). Amphetamine-associated stroke is heterogeneous clinically, pathologically and aetiologically. Drug abuse should always be considered in young patients with stroke, even if the patient denies the use of recreational drugs and if other stroke risk factors are present.

ISSN:1015-9770    

DOI:10.1159/000108015

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

Background and Purpose: Lifarizine is a novel ion channel modulator which is neuroprotective in experimental global and focal ischemia, at doses that have minimal systemic vascular effects. This was a preliminary efficacy and safety study of lifarizine in human stroke. Methods: In a multicenter, randomized, double-blind, parallel-group study, subjects with symptoms and signs of first ischemic stroke were randomized to receive lifarizine (250 μg/kg, i.v. stat. plus 60 mg b.d. orally for 5 days) or matching placebo, after stratification for age (21–74 or ≥: 75 years) and for time since stroke onset (<6 or 6–12 h). Primary end points were safety of lifarizine and functional outcome at 13 weeks, using the modified Barthel Index and the Rankin Scale. Secondary measures included the National Institutes of Health and Canadian Neurological scales. Results: Of 147 patients recruited, 117 were evaluated for efficacy analysis. Lifarizine was well tolerated; a single seizure was attributed to active treatment. Biochemical and hematological indices were unchanged. Blood pressure fell over the study period, particularly in the lifarizine group. All-patient mortality during the 3-month study was 12/75 (16%) for lifarizine and 17/72 (24%) for placebo; amongst evaluable patients, mortality was 9/63 (14%) for lifarizine and 13/54 (24%) for placebo. At 13 weeks, the improvement in functional independence in the lifarizine group versus the placebo group was 16% greater by the Rankin Scale, p = 0.52, and 11% greater by the Barthel score, p = 0.55. Conclusions: Lifarizine was well tolerated. Mortality and functional assessment data showed favorable trends. Further studies are justified to examine the efficacy of lifarizine in acute stroke.

ISSN:1015-9770    

DOI:10.1159/000108016

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

The aim of this study was to determine predictors of in-hospital mortality in 986 consecutive first-ever stroke patients by means of a multivariate analysis. In a first predictive model based on 13 demographic, anamnestic and clinical variables, age, previous or concomitant pathologic conditions (atrial dysrhythmia, chronic obstructive pulmonary disease, congestive heart failure, cirrhosis or chronic liver disease), deteriorated level of consciousness, vomiting, cranial nerve palsy, seizures and limb weakness appeared to be independent prognostic factors of in-hospital mortality. In addition to these 7 variables, intraventricular haemorrhage and middle cerebral topography were selected in a second predictive model based on clinical and neuroimaging variables. In both models, setting a cutoff point of 0.50 for predicting vital status at hospital discharge resulted in a sensitivity of 52%, specificity of 96% and total correct classification of 88%. Clinical factors indicative of the severity of stroke available at the time of initial diagnosis have a predominant influence upon in-hospital mortality irrespective of the stroke subtype, and may help clinicians to establish prognosis more accurately.

ISSN:1015-9770    

DOI:10.1159/000108017

出版商:S. Karger AG    

年代:1996

数据来源: Karger

ISSN:1015-9770    

DOI:10.1159/000108018

出版商:S. Karger AG    

年代:1996

数据来源: Karger

摘要:

We asked experts to offer their opinions on the subject: 'Carotid bruits without symptoms'. Who should be evaluated and how? Are there asymptomatic people without bruits who should be evaluated? How should we be dealing with this problem? The subject is important and timely because of published results of recent carotid endarterectomy trials [1, 2]. We informed each one that we do not expect new data, detailed analyses, or an authoritative review. Rather, we wanted their concise views on the subject. Their opinions follow.

ISSN:1015-9770    

DOI:10.1159/000108019

出版商:S. Karger AG    

年代:1996

数据来源: Karger