View clinical trials related to Subarachnoid Hemorrhage.
Filter by:In this protocol, the investigators present methods and preliminary results from the PLATFORM-CVD Study, an EHR-based multicenter cohort. This study will focus on assessing the distribution of major cerebrovascular diseases, determining the risk factors associated with disease incidence and worse in-hospital outcomes, as well as describing the quality of care. Data from this cohort will be used to develop suitable prediction models for cerebrovascular diseases using real-world data and to understand how outcomes for cerebrovascular diseases would change with quality improvement interventions.
Theoretical Framework & Background Cortical spreading depressions (CSD) and seizures, are crucial in the development of delayed cerebral ischemia and poor functional outcome in patients suffering from acute brain injuries such as subarachnoid hemorrhage. Multimodal neuromonitoring (MMNM) provides the unique possibility in the sedated and mechanically ventilated patients to record these electrophysiological phenomena and relate them to measures of cerebral ischemia and malperfusion. MMNM combines invasive (e.g. electrocorticography, cerebral microdialysis, brain tissue oxygenation) and noninvasive (e.g. neuroimaging, continuous EEG) techniques. Additionally, cerebral microdialysis can measure the unbound extracellular drug concentrations of sedatives, which potentially inhibit CSD and seizures in various degrees, beyond the blood-brain barrier without further interventions. Hypotheses 1. Online multimodal neuromonitoring can accurately detect changes in neuronal metabolic demand and pathological neuronal bioelectrical changes in highly vulnerable brain tissue. 2. Online multimodal neuromonitoring can accurately detect the impact of pathological neuronal bioelectrical changes on metabolic demand in highly vulnerable brain tissue. 3. The occurrence and duration of pathological neuronal bioelectrical changes are dependent on sedatives and antiepileptic drug concentrations 4. The occurrence and duration of pathological neuronal bioelectrical changes have a negative impact on functional and neurological long-term patient outcome. 5. Simultaneous invasive and non-invasive multimodal neuromonitoring can identify a clear relationship of both methods regarding pathological neuronal bioelectrical changes and metabolic brain status. Methods Systematic analysis of MMNM measurements following standardized criteria and correlation of electrophysiological phenomena with cerebral metabolic changes in all included patients. In a second step neuroimaging, cerebral extracellular sedative drug concentrations and neurological functional outcome, will be correlated with both electrophysiologic and metabolic changes. Due to numerous high-resolution parameters, machine learning algorithms will be used to correlate comprehensive data on group and individual levels following a holistic approach. Level of originality Extensive, cutting edge diagnostic methods are used to get a better insight into the pathophysiology of electrophysiological and metabolic changes during the development of secondary brain damage. Due to the immense amount of high-resolution data, a computer-assisted evaluation will be applied to identify relationships in the development of secondary brain injury. For the first time systematic testing of several drug concentrations beyond the blood-brain barrier will be performed. With these combined methods, we will be able to develop new cerebroprotective treatment concepts on an individual basis.
Change and effect of cerebral autoregulation during targeted temperature management in neurocritical patients
An investigator-initiated clinical drug study Main Objective: To explore neuroprotective properties of xenon in patients after aneurysmal subarachnoid hemorrhage (SAH). Primary endpoint: Global fractional anisotropy of white matter of diffusion tensor imaging (DTI). Hypothesis: White matter damage is less severe in xenon treated patients, i.e. global fractional anisotropy is significantly higher in the xenon group than in the control group as assessed with the 1st magnetic resonance imaging (MRI). After confirmation of aSAH and obtaining a signed assent subjects will be randomized to the following groups: Control group: Standard of Care (SOC) group: Air/oxygen and Normothermia 36.5-37.5°C; Xenon group: Normothermia 36.5-37.5°C +Xenon inhalation in air/oxygen for 24 hours. Brain magnetic resonance imaging techniques will be undertaken to evaluate the effects of the intervention on white and grey matter damage and neuronal loss. Neurological outcome will be evaluated at 3, 12 and 24 months after onset of aSAH symptoms Investigational drug/treatment, dose and mode of administration: 50±2 % end tidal concentration of inhaled xenon in oxygen/air. Comparative drug(s)/placebo/treatment, dose and mode of administration: Standard of care treatment according to local and international consensus reports. Duration of treatment: 24 hours Assessments: Baseline data Information that characterizes the participant's condition prior to initiation of experimental treatment is obtained as soon as is clinically reasonable. These include participant demographics, medical history, vital signs, oxygen saturation, and concentration of oxygen administered. Acute data The collected information will contain quantitative and qualitative data of aSAH patients, as recommended by recent recommendations of the working group on subject characteristics, and including all relevant Common Data Elements (CDE) can be applied. Specific definitions, measurements tools, and references regarding each SAH CDE can be found on the weblink here: https://www.commondataelements.ninds.nih.gov/SAH.aspx#tab=Data_Standards.
At present, cerebral vasospasm (cVS) is the main cause of delayed cerebral infarction (DCI), which leads to high disability and mortality rate after aneurysmal subarachnoid hemorrhage. As a consequence, the key of reducing DCI is to prevent cVS. But unfortunately, despite years of efforts, the prevention and treatment of cVS is still a major clinical dilemma and various ways of treatment are still being explored. Recent studies have shown that stellate ganglion block (SGB) can dilate cerebral vessels and alleviate the impact of existing cVS. However, there is no study to evaluate the effect of early application of SGB on the improvement and prevention of cVS after aSAH.
Temporary hypercapnia leads to a reproducible increase of cerebral blood flow (CBF) and brain tissue oxygenation (StiO2) as shown in a previous study (Trial-Identification: NCT01799525). The aim of this study now was to measure the course of carbon dioxide partial pressure (pCO2) reactivity after prolonged hypercapnia, and to evaluate the therapeutic effect of graded hypercapnia.
Nimodipine reduces the risk of poor outcome and delayed cerebral ischemia in patients suffering aneurysmal subarachnoid haemorrhage (SAH), but its mode of action is unknown. Its beneficial effect is assumed to be due its neuroprotective effects by reducing intracellular calcium and thereby cellular apoptosis, but higher concentrations might induce marked systemic hypotension, thereby inducing cerebral ischemia. Since several dosing regimes and routes of administration with inconclusive superiority exist and since the target site concentration of nimodipine - the unbound drug concentrations beyond the blood-brain barrier - is still not known, it is reasonable to measure nimodipine concentrations within the blood, cerebrospinal fluid (CSF) and interstitial brain tissue following oral, intra-venous and intra-arterial administration and correlate intra-arterial nimodipine administration to measures of cerebral metabolism and oxygenation. Therefore, the investigators propose to investigate in 30 patients suffering severe aneurysmal SAH and requiring cerebral microdialysis for cerebral neurochemical monitoring: - the ability of nimodipine to penetrate into the brain of neurointensive care patients by comparing exposure in brain, CSF and plasma, dependent on the route of administration (i.e. oral, intra-venous, and intra-arterial) and dosing intra-venously (0.5 - 2mg/h) - the impact of orally, intra-venously, and intra-arterially delivered nimodipine on cerebral metabolism, i.e. lactate/pyruvate ratio, pbtO2 and transcranial doppler flow velocities - the effect of oral and intra-venous nimodipine on systemic hemodynamic and cardiac parameters, using continuous Pulse Contour Cardiac Output (PiCCO) monitoring - the penetration properties of ethanol - as an excipient of nimodipine infusion - into the brain by comparing exposure in brain, CSF and plasma and quantifying the neuronal exposure to alcohol dependent on blood levels
A randomized clinical trial investigating magnesium sulphate ability to reduce risk of cerebral vasospasm after acute subarachnoid hemorrhage hence improving outcome particularly in haptoglobin 2-2 patients who are highly susceptible for severe complications after subarachnoid hemorrhage.
Patients admitted to Haukeland University Hospital with either UIA or aSAH underwent a measurement of bioelectrical impedance and body mass composition using InBody 10. Lipids and lipoproteins were collected from plasma. 60 patients in total were included in the study.
The progression of brain lesions after severe head trauma or subarachnoid hemorrhage results from extra cranial aggression which is well controlled in intensive care and intracranial aggression which is less well known and therefore less well managed. The detection of events that can generate new lesions from intracranial monitoring is limited and late once the lesions are irreversible. Invasive cortical depolarizations (SD) can be observed using cortical electrodes and an acquisition system having access to the usually filtered DC signal (0 to 1 Hz). SD are observed at the onset of a new attack of the cortex and spread widely away from the site of aggression. During their propagation, SD generate a significant metabolic demand, and can cause ischemic injury, particularly after meningeal or post-traumatic hemorrhage. SDs are therefore both a marker of new lesion and a mechanism of progression of primary lesions. Yet this type of monitoring is only performed in some expert centers around the world. The analysis of the feasibility and safety of the placement of cortical electrodes in this indication is therefore an essential step to study the clinical benefit of individualized management on the basis of this monitoring.