Third occurrence of cerebral venous thrombosis in a 33-year-old woman.
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Adult↗
Biomedical subjects
M Weih
Publications and source records attributed to M Weih.
Risk and predictors of early epileptic seizures in acute cerebral venous and sinus thrombosis.
We assessed the risk and determined predictors of early epileptic seizures (ES) in patients with acute cerebral venous and sinus thrombosis (CVST). A prospective series of 194 consecutive patients with acute CVST admitted to neurological wards in two German university hospitals was analysed for frequency of ES and in-hospital mortality. Demographic, clinical and radiological characteristics during the acute stage were retrospectively analysed for significant association with ES in univariate and multivariate analyses. During the acute stage, 19 patients (9.8%) died. Early symptomatic seizures were found in 86 patients (44.3%). Status epilepticus occurred in 11 patients (12.8%) of whom four died. Amongst patients with epileptic seizures, mortality was three times higher in those with status than in those without (36.4% and 12%, respectively). In multivariate logistic regression analysis, motor deficit [odds ratio (OR) 5.8; 95% CI 2.98-11.42; P < 0.001], intracranial haemorrhage (OR 2.8; 95% CI 1.46-5.56; P = 0.002) and cortical vein thrombosis (OR 2.9; 95% CI 1.43-5.96; P = 0.003) were independent predictors of early epileptic seizures. Status epilepticus was an important source of morbidity and early mortality in patients with CVST in this study. Patients with focal motor deficits, cortical vein thrombosis and intracranial haemorrhage carried the highest risk for ES. Prophylactic antiepileptic treatment may be an option for these patients.
Adolescent↗
QTL analyses of drought tolerance and growth for a Salix dasyclados x Salix viminalis hybrid in contrasting water regimes.
Quantitative trait loci (QTL) for growth traits and water-use efficiency have been identified in two water regimes (normal and drought-treated) and for a treatment index. A tetraploid hybrid F2 population originating from a cross between a Salix dasyclados clone (SW901290) and a Salix viminalis clone ('Jorunn') was used in the study. The growth response of each individual including both above and below ground dry-matter production (i.e. shoot length, shoot diameter, aboveground and root dry weight, internode length, root dry weight/total dry weight, relative growth rate and leaf nitrogen content) was analysed in a replicated block experiment with two water treatments. A composite interval mapping approach was used to estimate number of QTL, the magnitude of the QTL and their position on genetic linkage maps. QTL specific for each treatment and for the treatment index were found, but QTL common across the treatments and the treatment index were also detected. Each QTL explained from 8% to 29% of the phenotypic variation, depending on trait and treatment. Clusters of QTL for different traits were mapped close to each other at several linkage groups, indicating either a common genetic base or tightly linked QTL. Common QTL identified between treatments and treatment index in the complex trait dry weight can be useful tools in the breeding and selection for drought stress tolerance in Salix.
Biomass↗
[Risk factors in ischemic stroke. Review of evidence in primary prevention].
Risk factors are traits which can increase disease risk. In the case of ischemic stroke, risk factors have important roles in primary prevention, clinical practice, and epidemiological research. However, the underlying models, methods, and suited study design are often unknown. Based on interventions, cohort studies, case control studies, and meta-analyses, we give an up-to-date overall survey of the most important established and modifiable risk factors in the primary prevention of ischemic stroke. Each risk factor was assessed using a uniform pattern and systematically analyzed according to intervention type, evidence level, risk reduction, and prevalence.
Causality↗
A negative personal and family history for venous thrombotic events is not sufficient to exclude thrombophilia in patients with cerebral venous thrombosis.
A hereditary thrombophilia is found in 20-30% of patients with cerebral venous thrombosis (CVT). These patients might have an increased rate of a positive personal or family history of venous thrombotic events. We investigated the diagnostic value of a structured personal and family history for venous thrombotic events in 56 consecutive cases of CVT. Fourteen of 56 patients (25%) had a hereditary thrombophilia, mostly factor V Leiden. Patients with both CVT and hereditary thrombophilia had more frequently a positive family and personal history than patients affected by CVT only but the difference was not strong enough to differ from the 42 CVT patients without thrombophilia (43% vs. 31%; P = 0.52 and 14% vs. 10 %; P = 0.63). We conclude that a negative personal and family history of venous thrombotic events is not sufficient to exclude thrombophilia and patients with CVT should be tested for inherited thrombophilia regardless of the patient's past personal and family history for venous thrombotic events.
Adult↗
Risk of recurrence of cerebral venous and sinus thrombosis during subsequent pregnancy and puerperium.
OBJECTIVE: To assess the risk of recurrence of cerebral venous and sinus thrombosis (CVST) during subsequent pregnancy and puerperium in women with previous cerebral venous occlusive disease. METHODS: The authors retrospectively studied the relapse rate of CVST and the incidence of extracerebral venous thrombosis during subsequent pregnancies in 39 women (from 125 patients with CVST) who suffered a CVST at childbearing age. RESULTS: Mean follow up was 10.25 years (range 1 to 20). Twenty two pregnancies and 19 births were observed in 14 women without evidence of either recurrence of CVST or extracerebral venous thrombosis. One pregnancy occurred during oral anticoagulation and was interrupted and two pregnancies ended with spontaneous abortions. Low dose heparin had been given during five pregnancies. CONCLUSIONS: The risk of recurrence for CVST during pregnancy seems to be low and these data do not justify a negative advice on pregnancy in women with previous CVST. Further studies are needed to evaluate the need for a prophylactic anticoagulation during pregnancy and puerperium.
Adolescent↗
Neuroprotective effects of the antifungal drug clotrimazole.
Pretreatment with 10 microM of the antifungal drug clotrimazole potently reduced the death of cultured rat cerebellar granule cells induced by oxygen/glucose deprivation, and the excitotoxic effect of glutamate on cultured hippocampal neurons and cerebellar granule cells. In patch-clamped hippocampal pyramidal neurons, 10-50 microM clotrimazole caused a decrease in the amplitude of N-methyl-D-aspartate (NMDA) receptor-mediated currents. Glutamate induced intracellular Ca(2+) overload, as measured by Fluo-3 confocal fluorescence imaging, while clotrimazole reduced Ca(2+) overload and promoted the recovery of intracellular calcium homeostasis after glutamate treatment. Using tetramethylrhodamine ethyl ester fluorescence as a marker of mitochondrial membrane potential we found that clotrimazole prevented the glutamate-induced loss of mitochondrial membrane potential. Our data provide evidence that the protective effect of clotrimazole against oxygen/glucose deprivation and excitotoxicity is due to the ability of this drug to partially block NMDA receptor-gated channel, thus causing both reduced calcium overload and lower probability of the mitochondrial potential collapse.
Animals↗
[Ischemia tolerance; model for research, hope for clinical practice?].
A brief episode of ischemia renders the brain resistant against subsequent, longer ischemic events. This ischemic tolerance has been shown in numerous experimental models of cerebral ischemia. After global cerebral ischemia, ischemic tolerance may protect up to 90% of hippocampal CA1 neurons. In focal ischemia, this phenomenon reduces infarct volume by 20-60%. However, the basic molecular mechanisms of ischemic tolerance are largely unknown. During the induction phase, N-methyl-d-aspartate (NMDA) and adenosine receptors and, possibly, oxygen free radicals and conservation of energy metabolism are required. Protein kinases, transcription factors, and immediate early genes appear to transduce the signal into a tolerant response. Ischemic tolerance can be observed in different phases. The early phase lasts for several hours after the preconditioning stimulus and adenosine receptors and ATP-dependent potassium channels play a role similar to that in cardiac ischemic tolerance. The delayed protection, retained for a maximum of 2-4 days, currently is best explained by genetic remodeling with expression or repression of multiple genes. Several candidates have been identified to date, among them heat-shock proteins, cytokines, and antioxidant enzymes. Several studies have shown that angina pectoris before myocardial infarction represents a clinical correlate of experimental preconditioning protocols. Accordingly, evidence for a possible protective effect of transient ischemic attacks (TIAs) occurring before stroke are accumulating.
Animals↗
Evidence for increased sensitivity to nutrient and water stress in a fast-growing hybrid willow compared with a natural willow clone.
The hypothesis that fast-growing breeds of willow (Salix spp.) are more sensitive to nutrient and water stress and less efficient in nutrient- and water-use than slower-growing natural willow clones was tested. Cuttings of a natural clone of S. viminalis L. collected in Sweden (L78183) and a hybrid clone of S. schwerinii E. Wolf. x S. viminalis L. ("Tora") were grown outdoors in pots under various experimental conditions in a full-factorial design. The experimental conditions included three fertilization, two irrigation and two temperature regimes. Classical growth analysis techniques, based on an initial and a final harvest, were used as a screening method, together with calculation of intrinsic water-use efficiency (foliar carbon isotope ratio; delta13C). In addition, nitrogen-use efficiency was calculated as the product of nitrogen productivity and mean residence time of nitrogen on an annual basis. There were significant differences in plant structural parameters (leaf area ratio, specific leaf area) and water-use efficiency between the clones. Furthermore, several clone x treatment interaction effects on various growth parameters indicated that the clones adapted to specific environments in different ways. "Tora" plants produced up to 25% more shoot biomass than plants of the natural clone in response to high rates of fertilization and irrigation, whereas clone ranking was reversed in most other treatments. The results support the hypothesis that fast-growing hybrids are more sensitive to nutrient and water stress than slower-growing natural clones. The hypothesis that natural clones have higher resource-use efficiency than fast-growing hybrids was supported with respect to water, but not nitrogen.
Biomass↗
Proteolysis of oxidized proteins after oxygen-glucose deprivation in rat cortical neurons is mediated by the proteasome.
Oxidative injury contributes to cellular damage during and after cerebral ischemia. However, the downstream catabolic pathways of damaged cellular components in neurons are largely unknown. In the current study, the authors examined the formation of oxidized proteins and their active degradation by the proteasome. In near-pure rat primary cortical neurons, it was found that protein-bound carbonyls as markers for oxidized proteins are increased after oxygen-glucose deprivation (OGD). During and after OGD, degradation of proteins metabolically radiolabeled before OGD increases two-to threefold compared with the normal protein turnover. Proteolysis after reoxygenation was attenuated by the presence of dimethylthiourea, a radical scavenger, and was blocked by lactacystin, a specific proteasome inhibitor. Lactacystin also increased the amount of protein carbonyls formed. In contrast, the activity of the proteasome complex itself after OGD was not different from sham-washed controls. The authors suggest that oxygen-glucose deprivation increases free radicals, which, in turn, oxidize proteins that are recognized and actively degraded by the proteasome complex. This protease itself is relatively resistant against oxidative injury. The authors conclude that the proteasome may be an active part of the cellular defense system against oxidative stress after cerebral ischemia.
Acetylcysteine↗
Coagulopathies in ischemic stroke.
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Blood Coagulation Disorders↗
Sulfonylurea drugs do not influence initial stroke severity and in-hospital outcome in stroke patients with diabetes.
BACKGROUND AND PURPOSE: Sulfonylurea drugs inhibit ATP-dependent potassium channels and may increase mortality after myocardial infarction. Sulfonylurea drugs also inhibit ischemic preconditioning in experimental models of brain ischemia and in clinical studies in the human heart. METHODS: In the present study we examined the impact of sulfonylurea drugs on in-hospital mortality and the immediate neurological deficit of diabetic stroke patients. From a larger stroke data bank, we studied 146 diabetic patients with acute hemispheric ischemic stroke. Sixty patients were using sulfonylurea drugs. RESULTS: Major baseline characteristics such as age, blood pressure, admission glucose level, HbA(1c), distribution of cardiovascular risk factors, and presumed stroke etiology (Trial of Org 10172 in Acute Stroke Treatment [TOAST] criteria) were not different. Mortality (15% versus 14%; P=0.86) and initial stroke severity (Canadian Neurological Scale score, 7.4 versus 7.5; P=0.79) were not significantly different between patients with and without sulfonylurea drugs. Further end points such as Rankin Scale score, deteriorating stroke, duration of hospital stay, type of infarcts on CT/MRI, requirement of intensive care, and complications were not different. In a stepwise logistic regression model, sulfonylurea drugs were not independent predictors for increased mortality, deteriorating stroke, or stroke severity. CONCLUSIONS: In the present hospital-based study, sulfonylurea drugs in patients with diabetes and stroke are not associated with increased stroke severity, mortality, or a worse in-hospital outcome.
Aged↗
Inhibition of Na(+),K(+)-ATPase activity in cultured rat cerebellar granule cells prevents the onset of apoptosis induced by low potassium.
In cerebellar granule cells in culture, lowering of extracellular [K(+)] results in apoptotic death (D'Mello, S.R., Galli, C., Ciotti, T. and Calissano, P., Induction of apoptosis in cerebellar granule neurons by low potassium: inhibition of death by insulin-like growth factor I and cAMP, Proc. Natl. Acad. Sci. USA, 90 (1993) 10989-10993). In this model, we studied the influence of Na(+), K(+)-ATPase inhibition on apoptosis. We demonstrate that cell death (93+/-2 vs. 46+/-1.6%) as well as fragmentation of nuclear DNA induced by low extracellular potassium were prevented by addition of ouabain (0.1 mM), a specific inhibitor of the Na(+),K(+)-ATPase. Blockade of glutamatergic N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors by 5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine hydrogen maleate (MK-801; 20 microM) and 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX; 50 microM) did not inhibit the protective effect of ouabain. 24 h treatment with ouabain also decreased cell death induced by Fe(2+)/ascorbic acid (74+/-2% to 49+/-3%). We speculate that ouabain pretreatment enhances the resistance against low [K(+)]-induced apoptosis independent of glutamate-receptor activation. Since this effect can be mimicked by a free-radical generating system, we suggest an antioxidative effect underlying ouabain-induced neuroprotection.
Adenosine Triphosphatases↗
[Hereditary thrombophilia with ischemiC stroke and sinus thrombosis. Diagnosis, therapy and meta-analysis].
Hereditary thrombophilias are a heterogenous group of genetic coagulation disorders which, particularly in combination with acquired prothrombotic factors, induce a predisposition to thrombosis. After characterization of frequent thrombophilic syndromes like factor V-Leiden or the prothrombin 20210GA mutation, a number of case-control studies screened for the prevalence of these mutations in ischemic stroke and cerebral venous thrombosis (CVT). Our meta-analysis shows that factor V-Leiden and prothrombin are frequent and significantly associated with CVT (16.4% vs. 4.9% or 4.3, P < 0.001, and 12.1% vs. 1.9% or 5.8, P < 0.001). In ischemic stroke, only factor V-Leiden and not prothrombin is a weak but significant risk factor (5.9% vs. 2.6% or 1.6, P < 0.001, and 4.1% vs. 3.3% or 1.4, P = 0.1). The C677T homozygous point mutation in the MTHFR, a homocysteine-degrading enzyme, was also associated with arterial stroke (16% vs. 15% or 1.5, P < 0.001). For CVT, sufficient data are lacking. We therefore recommend screening for thrombophilia in CVT. In ischemic stroke, atrial premature complex (APC) resistance should be considered. As long as controlled studies are lacking, individual anticoagulant therapy must take hereditary and precipitating factors into account to assess potential thrombotic risk.
Cerebral Infarction↗
Melatonin is protective in necrotic but not in caspase-dependent, free radical-independent apoptotic neuronal cell death in primary neuronal cultures.
To assess the neuroprotective potential of melatonin in apoptotic neuronal cell death, we investigated the efficacy of melatonin in serum-free primary neuronal cultures of rat cortex by using three different models of caspase-dependent apoptotic, excitotoxin-independent neurodegeneration and compared it to that in necrotic neuronal damage. Neuronal apoptosis was induced by either staurosporine or the neurotoxin ethylcholine aziridinium (AF64A) with a delayed occurrence of apoptotic cell death (within 72 h). The apoptotic component of oxygen-glucose deprivation (OGD) unmasked by glutamate antagonists served as a third model. As a model for necrotic cell death, OGD was applied. Neuronal injury was quantified by LDH release and loss of metabolic activity. Although melatonin (0.5 mM) partly protected cortical neurons from OGD-induced necrosis, as measured by a significant reduction in LDH release, it was not effective in all three models of apoptotic cell death. In contrast, exaggeration of neuronal damage by melatonin was observed in native cultures as well as after induction of apoptosis. The present data suggest that the neuroprotectiveness of melatonin strongly depends on the model of neuronal cell death applied. As demonstrated in three different models of neuronal apoptosis, the progression of the apoptotic type of neuronal cell death cannot be withhold or is even exaggerated by melatonin, in contrast to its beneficial effect in the necrotic type of cell death.
Animals↗
Assessment of blood flow velocity and diameter of the middle cerebral artery during the acetazolamide provocation test by use of transcranial Doppler sonography and MR imaging.
BACKGROUND AND PURPOSE: Our purpose was to show changes in the diameter of the M1 segment of the middle cerebral artery (MCA) by using high-resolution MR imaging in patients with chronic internal carotid artery occlusion after IV administered acetazolamide challenge. Changes in blood flow velocity of the basal cerebral arteries are thought to correlate with changes of cerebral blood flow. Changes in the diameter of the basal cerebral arteries, however, might influence the validity of transcranial Doppler measurements. METHODS: Eight patients with internal carotid artery occlusion who were undergoing acetazolamide testing for assessment of cerebrovascular vasomotor reactivity were included in the study. Blood flow velocities of both MCAs were measured with transcranial Doppler sonography before and 25 minutes after the administration of acetazolamide. Before and 15 minutes after the administration of medication, MR imaging was performed contralateral to the occlusion side. A T2-weighted turbo-gradient spin-echo sequence was chosen to show a cross section of the M1 segment in high resolution (pixels, 0.27 x 0.29 mm). Based on interpolated data, the smallest and greatest MCA diameters were determined. RESULTS: We did not find changes in the diameter of the MCA after acetazolamide provocation testing with high-resolution MR imaging in patients with occlusive extracranial carotid artery disease. CONCLUSION: The results of our study support the hypothesis that changes in MCA flow velocity measured by transcranial Doppler sonography reflect relative changes in cerebral blood flow after acetazolamide provocation testing.
Acetazolamide↗
Cerebral endothelial cells release TNF-alpha after stimulation with cell walls of Streptococcus pneumoniae and regulate inducible nitric oxide synthase and ICAM-1 expression via autocrine loops.
TNF-alpha, inducible NO synthase (iNOS), and ICAM-1 are considered to be key proteins in the inflammatory response of most tissues. We tested the hypothesis that cell walls of Streptococcus pneumoniae (PCW), the most common cause of adult bacterial meningitis, induce TNF-alpha, iNOS, and ICAM-1 expression in rat primary brain microvascular endothelial cell cultures. We detected TNF-alpha mRNA by RT-PCR already 1 h after stimulation with PCW, while TNF-alpha protein peaked at 4 h (9.4 +/- 3.6 vs 0.1 +/- 0.1 pg/microgram protein). PCW induced iNOS mRNA 2 h after stimulation, followed by an increase of the NO degradation product nitrite (18.1 +/- 4 vs 5.8 +/- 1.8 at 12 h; 18.1 +/- 4 vs 5.8 +/- 1.8 pmol/microgram protein at 72 h). The addition of TNF-alpha Ab significantly reduced nitrite production to 62.2 +/- 14.4% compared with PCW-stimulated brain microvascular endothelial cells (100%). PCW induced the expression of ICAM-1 (measured by FACS), which was completely blocked by TNF-alpha Ab (142 +/- 18.6 vs 97.5 +/- 12.4%; 100% unstimulated brain microvascular endothelial cells). Cerebral endothelial cells express TNF-alpha mRNA as well as iNOS mRNA and release the bioactive proteins in response to PCW. PCW-induced NO production is mediated in part by an autocrine pathway involving TNF-alpha, whereas ICAM-1 expression is completely mediated by this autocrine loop. By these mechanisms, cerebral endothelial cells may regulate critical steps in inflammatory blood-brain-barrier disruption of bacterial meningitis.
Animals↗
Induction of ischemic tolerance in rat cortical neurons by 3-nitropropionic acid: chemical preconditioning.
Sublethal ischemia leads to increased tolerance against subsequent ischemia. We investigated whether tolerance could also be elicited by mild respiratory-chain inhibition (chemical hypoxia) in a rat neuronal-cell enriched culture system. 3-Nitropropionic acid (3-NPA) caused a concentration-dependent inhibition of succinate-dehydrogenase. Two hours preconditioning with 3-NPA 24-48 h before oxygen-glucose deprivation (OGD) reduced neuronal damage morphologically and reduced lactate deydrogenase (LDH) release up to 72% compared to sham-treated sister cultures without 3-NPA. In an attempt to elucidate transcriptional mechanisms, we found no rapid translocation of the hypoxia-sensitive transcription factors N F-KB or hypoxia-inducible factor-I (HIF-I) at 3-NPA concentrations sufficient to trigger tolerance against OGD. In accordance to previous in vivo and brain slice data, we conclude that 3-NPA chemically induces tolerance against oxygen-glucose deprivation in vitro. However, the underlying mechanisms remain elusive.
Animals↗