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Biomedical subjects

R Stingele

Publications and source records attributed to R Stingele.

At least 19 recordsLinked to original sources
PubMed2006

30 day results from the SPACE trial of stent-protected angioplasty versus carotid endarterectomy in symptomatic patients: a randomised non-inferiority trial.

BACKGROUND: Carotid endarterectomy is effective in stroke prevention for patients with severe symptomatic carotid-artery stenosis, and carotid-artery stenting has been widely used as alternative treatment. Since equivalence or superiority has not been convincingly shown for either treatment, we aimed to compare the two. METHODS: 1200 patients with symptomatic carotid-artery stenosis were randomly assigned within 180 days of transient ischaemic attack or moderate stroke (modified Rankin scale score of < or =3) carotid-artery stenting (n=605) or carotid endarterectomy (n=595). The primary endpoint of this hospital-based study was ipsilateral ischaemic stroke or death from time of randomisation to 30 days after the procedure. The non-inferiority margin was defined as less than 2.5% on the basis of an expected event rate of 5%. Analyses were on an intention-to-treat basis. This trial is registered at Current Controlled Trials with the international standard randomised controlled trial number ISRCTN57874028. FINDINGS: 1183 patients were included in the analysis. The rate of death or ipsilateral ischaemic stroke from randomisation to 30 days after the procedure was 6.84% with carotid-artery stenting and 6.34% with carotid endarterectomy (absolute difference 0.51%, 90% CI -1.89% to 2.91%). The one-sided p value for non-inferiority is 0.09. INTERPRETATION: SPACE failed to prove non-inferiority of carotid-artery stenting compared with carotid endarterectomy for the periprocedural complication rate. The results of this trial do not justify the widespread use in the short-term of carotid-artery stenting for treatment of carotid-artery stenoses. Results at 6-24 months are awaited.

Aged↗
PubMed2006

Selective affection of hippocampal CA-1 neurons in patients with transient global amnesia without long-term sequelae.

The aetiology, pathomechanisms and anatomical correlates of transient global amnesia (TGA) still remain obscure. Recently, focal MR-signal diffusion-weighted imaging (DWI) changes in the hippocampus have been described in patients with TGA, but the exact localization, long term outcome and pathophysiological nature of these lesions still remain unknown. The topography and time course of hippocampal DWI lesions in 41 TGA patients was studied using serial 3 T high-resolution MR-imaging and correlated to clinical and neuropsychometric results. Of these, 29 patients showed 36 DWI lesions with corresponding T(2) lesions in the hippocampus within a time window of 48 h after onset. Almost all lesions (94%; 34/36) were selectively found in the CA-1 sector (Sommer sector) of the hippocampal cornu ammonis. Most DWI lesions (8/10) were already detectable in the peri-acute phase <6 h after onset of symptoms. A follow-up study 4-6 months after the episode did not show evidence for residual structural sequelae of these lesions (n = 20/20). A venous MR angiography of the intracranial dural sinus showed an asymmetric venous drainage in 21/24 (88%) patients. In 11/16 (69%) patients with unilateral lesions, the asymmetry corresponded to the side of the DWI lesion. Significant episodic verbal memory deficits in the acute phase (n = 14/18) were associated with lesions of the dominant hemisphere while impairment of visuospatial memory was associated with lesions of the non-dominant hemisphere. Persistent neuropsychological sequelae were not detected 4-6 months after the episode (n = 16). This is the first prospective study combining high-resolution imaging and neuropsychometry analysing the detailed functional anatomy and outcome of hippocampal DWI/T(2) lesions in TGA supporting the view the TGA being a benign transient disorder. The TGA can be considered a model for a focal transient perturbation of memory circuits in the temporo-mesial region.

Adult↗
PubMed2006

[Stroke: causes and classification].

Cerebrovascular disease is caused by ischaemic stroke, intracerebral haemorrhage, subarachnoidal haemorrhage or cerebral vein and sinus thrombosis. Approximately 80% of all cerebrovascular accidents are caused by ischaemic stroke, whereas 20% are due to primary haemorrhage. This article summarizes the typical causes of each of the four main groups of cerebrovascular disease and points out clinical differences. Special attention is given to transitory ischemic attacks since new reports underline the necessity of early diagnostic and therapeutic intervention. Useful diagnostic and clinical scales are presented and discussed.

Brain Ischemia↗
PubMed2006

[Coagulation disorders and stroke].

Hereditary and acquired coagulation disorders may play an important role in the pathophysiology of acute ischaemic stroke. Because of the low prevalence of these disorders and the considerable costs of unmindful diagnostic effort, a custom-tailored approach is desirable. Suggestive in favour of a possible prothrombotic clotting disorder are young patients, repeated episodes of thrombosis in the patient's history, inappropriate atherosclerotic vascular changes, previous repeated miscarriages in stroke patients, or structural cardiac abnormalities as a patent foramen ovale. Disorders affecting antithrombin III, protein C und S, APC-resistance, the prothrombin mutation, homocysteinaemia, antiphospholipid antibodies, and procoagulatory cellular interaction are discussed.

Antibodies, Antiphospholipid↗
PubMed2006

[Therapy of acute stroke].

Current therapeutic concepts for acute cerebral ischaemia and cerebral haemorrhage are summarized. Patient selection for thrombolysis, the role of stroke MRI and the choice of recanalization techniques are discussed. The treatment of intracerebral haemorrhage with particular emphasis on evacuation of haematoma and acute haemostatic therapy are discussed.

Acute Disease↗
PubMed2004

Platelet-leukocyte interaction and platelet activation in migraine: a link to ischemic stroke?

OBJECTIVES: Migraine has been identified as an independent risk factor for ischemic stroke. Both neurogenic inflammation and platelet activation have been linked to the pathophysiology of migraine. Increased platelet activation results in up-regulation of specific binding to leukocytes which promotes pro-inflammatory leukocyte secretion and their tethering to endothelium, a mechanism that has been demonstrated in stroke and which could provide a link to migraine. We aimed to determine whether platelet-leukocyte aggregation is increased in migraine patients outside an acute attack. METHODS: Seventy two patients with migraine according to IHS criteria were compared to a control group (n = 72). Whole blood flow cytometry was used to quantify the activation dependent P selectin on the platelet, and to assess the fraction of platelets bound to the different leukocyte subsets. RESULTS: Migraine patients showed significantly more platelet-leukocyte aggregates compared to the control subjects (p = 0.003). This effect was driven by an increased polymorphonuclear cell-platelet aggregation (p = 0.003) whereas platelet aggregation with monocytes and lymphocytes was not. Platelet activation was also increased (p = 0.001). CONCLUSIONS: In migraine pro-inflammatory platelet adhesion to leukocytes occurs during the headache free interval similar to that seen in acute coronary and cerebrovascular syndromes. This may suggest a link between migraine and stroke on a cellular level.

Acute Disease↗
PubMed2003

Transcranial oximetry using fast near infrared spectroscopy can detect failure of collateral blood supply in humans.

We tested the hypothesis that transcranial oximetry by fast scanning near infrared spectroscopy can detect local desaturation of hemoglobin in arterial vessels of cerebral circulation with impaired blood supply. A total of 74 near infrared spectroscopy recordings were taken from the intact skull of humans. Perfusion of the hemisphere under the detector was assessed in one of four groups: (1) healthy volunteer; (2) patient, unaffected side; (3) patient, affected side with intact collateral blood supply; (4) patient, affected side, impaired collateral blood supply. Transcranial saturation was 0.90+/-0.01 (all values reported as mean+/-S.E.) in healthy volunteers (n=24), 0.92+/-0.008 in the unaffected hemisphere of patients (n=23), 0.92+/-0.001 in the affected side if collateral supply with blood was intact (n=16). There was no statistical significance between these groups. Saturation in affected hemispheres with impaired collateral blood supply (n=9) was 0.81+/-0.028, which was significantly different from all other groups (P<0.05, one way-ANOVA). We conclude, that transcranial pulse oximetry can detect local hypoxia if collateral blood supply fails.

Cerebrovascular Circulation↗
PubMed2001

Independent HIV replication in paired CSF and blood viral isolates during antiretroviral therapy.

BACKGROUND: The goal of highly active antiretroviral therapy in HIV-infected patients is to reduce plasma viral load (VL) below quantifiable levels. Mutations associated with drug resistance within the HIV-1 genome can limit therapeutic success. Low VL implicates a low risk of emergence of resistant mutants. Whether there is divergent development of HIV strains in different biologic compartments is not understood. METHODS: The authors studied VL and the occurrence of mutations conferring resistance in viral genomes isolated from blood and CSF samples of 23 HIV-infected patients. They determined sequences of HIV-1 RNA by reverse transcriptase PCR amplification and direct sequencing. They measured resistance to antiretroviral drugs genotypically by detection of drug-related point mutations and VL by a branched-DNA assay. RESULTS: Amplification of HIV was successful even in patients with plasma or CSF VL below detection limit. VL was considerably lower in CSF as compared with blood (p < 0.0001). There was no correlation between CSF and plasma VL. The mutational pattern in viral copies derived from blood and CSF was not identical. Ten (9%) of the total number of 118 mutations associated with drug resistance occurred in blood isolates only; 14 (11%) were detected exclusively in CSF strains. CONCLUSION: There is evidence for viral replication at HIV RNA levels less than 50/mL. The results suggest divergent evolution of HIV-1 in different biologic compartments. The presence of resistant mutants in the CSF may escape regular diagnostic in blood. Therapeutic success may fail after adapting therapy to genotypic resistance patterns detected in one compartment only.

Adult↗
PubMed2001

Bootstrap statistics of ECASS II data: just another post hoc analysis of a negative stroke trial?

UNLABELLED: The results of the Second European-Australasian Acute Stroke Study (ECASS II) were negative with respect to the primary endpoint. This post hoc analysis of ECASS II data was designed to make the least number of a priori assumptions. This is accomplished by a bootstrap-based hypothesis test on a non-parametric test statistic. No assumptions are made on shape or variance of population distributions and the method does not suffer from the disadvantages of dichotomization. By reducing the number of a priori assumptions, the possibilities to modify the test result by adjusting the test procedure are minimized. RESULTS: If rt-PA does not improve the outcome (null hypothesis), the probability of observing a difference of modified ranking scale equal or larger than the one observed in ECASS II is 0.047. We therefore rejected the null hypothesis.

Controlled Clinical Trials as Topic↗
PubMed2000

Bedside monitoring of cerebral blood flow in patients with acute hemispheric stroke.

OBJECTIVE: To test the practicability of a new double indicator dilution method for bedside monitoring of cerebral blood flow (CBF) and to assess the clinical value of CBF monitoring as a prognostic tool for outcome and in therapy of elevated intracranial pressure (ICP) in patients with acute hemispheric stroke. DESIGN: Prospective study. Clinical evaluation of a new method. SETTING: Neurological intensive care unit of a university hospital. PATIENTS: Ten patients with acute complete middle cerebral artery territory- or hemispheric infarctions. INTERVENTIONS: Two combined fiberoptic thermistor catheters were placed in the right jugular bulb and in the thoracic aorta. Central venous injections of ice-cold indocyanine green dye were performed. CBF was estimated by calculating the mean transit times of the cold bolus and dye. MEASUREMENTS AND MAIN RESULTS: A total of 104 reproducible CBF measurements were obtained. No complications associated with the method were observed. Twelve pairs of measurements were performed within 30 mins with unchanged clinical conditions. The standard deviation of repeated measurements was 2.7 mL/100 g/min; the interrater reliability was between 0.95 and 0.99. The median CBF in patients who died (n = 4) was lower (27 mL/100g/min) than in those who survived (n = 6) (45 mL/100g/ min). Patients who died more frequently had low CBF values of <30 mL/100g/min (22 of 38; 58%) than patients who survived (10 of 54; 19%). A total of 37 CBF measurements were done during ICP elevation of >20 mm Hg. In patients who survived, ICP elevations were only associated with low CBF values in 5 of 26 events; whereas in patients who died, ICP elevations were associated with low CBF values in 8 of 11 events. CONCLUSIONS: The new double indicator dilution technique may be suitable for serial bedside CBF measurement. It is easy to perform and can be rapidly repeated in the ICU environment. Validation of the method by comparison with standard methods is needed. The preliminary data indicate that bedside monitoring of CBF may give prognostic information for outcome and may guide therapy of elevated ICP in patients with malignant hemispheric infarction.

Acute Disease↗
PubMed1999

Update in thrombolytic therapy.

Several studies have proven the usefulness of thrombolytic agents in the therapy of ischemic stroke. Data from open and small placebo-controlled trials show a relationship between recanalization and an improved clinical outcome. Three large scaled studies have examine the effect of streptokinase treatment. Because of an increasing mortality the results of these studies were negative, and so streptokinase should not be used to treat acute ischemic stroke. In contrast, three rt-PA studies with together more than 2000 patients showed a significant benefit. Recent meta-analyses including data of all these trials show an odds ratio for death and disability of 0.67 (95 p. 100 CI 0.56; 0.8). The number needed to treat to prevent one death or disability is 11 in a 6 hour time window and 7 in a 3 hour time window. These are impressive numbers that are rarely found in other areas of internal or neurological medicine. The most important risk of thrombolytic therapy is the occurrence of intracerebral hemorrhage, which is reported as between 0-18 p. 100, but which is not associated with increased morbidity or mortality. At present, thrombolytic therapy cannot be recommended for all patients with acute stroke. Careful selection and experiences with this therapy and its risks are necessary.

Clinical Trials as Topic↗
PubMed1998

Tyrosine confounds oxidative electrochemical detection of nitric oxide.

We report evidence that a porphyrinic microsensor for detection of nitric oxide (NO) also detects biologically relevant concentrations of tyrosine (Tyr) in dog brain. Tyr is oxidized by this sensor at the same potential as NO, and the sensitivity for NO and Tyr are of the same order of magnitude. The interference from Tyr is of importance because 1) Tyr is abundant and 2) there is a concentration gradient of Tyr across the blood-brain barrier that can lead to unpredictable results if disturbed by ischemia or hypoxia. The knowledge of this interference is important for the interpretation of results obtained with this sensor and for the design of future studies.

Animals↗
PubMed1997

NO contributes to neurohypophysial but not other regional cerebral fluorocarbon-induced hyperemia in cats.

The large increase in cerebral blood flow (CBF) after fluorocarbon (FC)-exchange transfusion is thought to be caused by low oxygen content, decreased viscosity, or direct vasodilatory effect of the FC perfusate. The aim of this study was to determine whether nitric oxide (NO)-mediated vasorelaxation is increased in FC-perfused hemoglobin (Hb)-free cats because NO is not scavenged by Hb. We measured regional CBF with radiolabeled microspheres in three groups of anesthetized mechanically ventilated cats. The first group [FC + N(omega)-nitro-L-arginine methyl ester (L-NAME), n = 7] underwent a complete FC-exchange transfusion with FC-43 and subsequent nitric oxide synthase (NOS) inhibition with L-NAME (10 mg/kg i.v.) followed by L-arginine (100 mg/kg i.v.). A second group (FC + saline; n = 6) underwent an identical protocol, but NOS was not antagonized (saline i.v.). In a third group (blood + L-NAME; n = 7), cats were not FC exchanged but NOS was inhibited. In a separate cohort of four FC-perfused cats, NOS activity in brain tissue samples was reduced to 26% of control after NOS inhibition. FC-exchange transfusion nearly doubled hemispheric blood flow in both FC-exchanged groups, whereas it was constant in the blood + L-NAME group. These increases in regional CBF (hemispheres, brain stem, cerebellum, thalamus, and white matter) were not reversed by inhibition of NOS, except in the neurohypophysis, where L-NAME reduced blood flow to levels comparable to values in the blood + L-NAME group. In summary, increases in regional CBF after total FC-exchange transfusion are not caused by a lack of NO scavenging, with the exception of neurohypophysis. These findings suggest an increased vasorelaxation in neurohypophysis of FC-perfused and Hb-free cats caused by unscavenged NO, but this mechanism does not play a major role in FC-related CBF increases in the rest of the cerebral circulation.

Animals↗
PubMed1996

Reduction of cytochrome-c oxidase copper precedes failing cerebral O2 utilization in fluorocarbon-perfused cats.

We determined the relationship of the low-potential copper (CuA) redox state of cytochrome-c oxidase to the brain tissue PO2 (PtiO2) and global cerebral O2 consumption (CMRO2) in vivo. The redox state of cytochrome-c oxidase copper was monitored in perfluorocarbon-exchanged cats under normoxic and graded hypoxic conditions with use of near-infrared spectroscopy. Continuous spectra ranging from 730 to 960 nm were acquired, and the change in copper redox state was assessed by the absorption changes at 830 nm. PtiO2 was measured with O2-sensitive electrodes implanted into the cortex, and CMRO2 was determined by sampling arterial and superior sagittal sinus perfusate and by measuring blood flow with radiolabeled microspheres. As PtiO2 decreased with hypoxia, the CuA of cytochrome-c oxidase became progressively reduced, whereas the CMRO2 was unchanged during the initial stages of hypoxia. Only with severe hypoxia, did CMRO2 and the amplitude of somatosensory evoked potentials decrease. We conclude that the CuA site of cytochrome-c oxidase is involved in a regulatory adjustment that helps maintain CMRO2 constant.

Animals↗
PubMed1994

Laser Doppler flowmetry of focal ischaemia and reperfusion in deep brain structures in rats.

Monitoring cerebral blood flow during focal ischaemia and reperfusion with established techniques such as hydrogen clearance and autoradiography is difficult. Laser Doppler flowmetry is a new technique, it allows one to continuously measure blood flow in small tissue samples. The objective of this study was to compare laser Doppler flowmetry with hydrogen clearance using a new single fiber probe to obtain measurements in deep brain structures and then to show the temporal profile of cerebral blood flow during focal ischaemia and after reperfusion. First, the single fiber laser Doppler method was compared with the hydrogen clearance method in ten Wistar rats. Second, focal cerebral ischaemia was induced in fifteen Wistar rats using a model of middle cerebral artery occlusion based on the intravascular insertion of a nylon suture; reperfusion occurred after withdrawal of the suture. The laser Doppler probe was placed in the lateral caudatoputamen, and local cerebral blood flow was measured continuously before and during occlusion as well as after reperfusion. The relative blood flow values obtained by the laser Doppler method and the hydrogen clearance method showed a good correlation (r = 0.76) and a linear relationship. A rapid decrease in laser Doppler flowmetry to 42 +/- 16% of former baseline values was seen with occlusion of the middle cerebral artery; during occlusion cerebral blood flow remained at this level. Reperfusion resulted in a heterogeneous pattern of cerebral blood flow as laser Doppler flowmetry values ranged from 25% to 134% of baseline values. The effects of middle cerebral artery occlusion and reperfusion on cerebral blood flow can be monitored on-line with laser Doppler flowmetry.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗