View clinical trials related to Subarachnoid Hemorrhage.
Filter by:Despite the advances in neurosurgical and -radiological techniques and intensive care, the mortality and morbidity rates in SAH have not changed in recent years. There is still only a limited understanding of the mechanisms of secondary insults causing brain injury after SAH, also called delayed cerebral ischemia (DCI). In this study, the investigators are exploring the use of quantifiable biomarkers from blood and continuous EEG monitoring as tools for the diagnostics of DCI. Additionally, the investigators are looking into other clinical variables (eg. pain, heart function) as factors of DCI.
The investigators are planning that can these markers be used a predictive marker at SAH and for this aim we will study both patiens' blood sample and their CT image.
Searching a dysfunction of corticotropic and thyrotropin axis during the acute phase ( ≤48h ) of a subarachnoid hemorrhage secondary to spontaneous rupture of cerebral aneurysm. Impact on the incidence of complications and recovery are evaluated at 1 month. Blood sample are made within 48 hours of the onset of bleeding with assay of total plasma cortisol, plasma ACTH at 8 am and thyroid hormones (T3, free T4 , and TSH). Dynamic test ACTH stimulation (test Synacthene) with renewal of serum cortisol to H + 1 (60min). Evaluation in the first 30 days of the incidence of rebleeding, hydrocephalus, of vasospasm, infection and epilepsy. GOS to 1 month.
The purpose of this study is to determine the relationship between the Neuroinflammatory response and headache pain after subarachnoid hemorrhage.
Vitamin D has been promoted to vascular regeneration in non-cerebral arteries because of its anti-inflammatory properties. Cerebral vasospasm (CVS) as the most feared complication after subarachnoid hemorrhage (SAH), correlated with higher mortality and poor outcome, is the result of a multifactorial mechanism with inflammation as one of the main role players. The investigators therefore hypothesized that vitamin D attenuates cerebral vasospasm and increases the chance for favorable outcome after SAH.
Serum uric acid level is a commonly measured biomarker. The association between serum uric acid level and the risk of developing cardiovascular diseases has been observed in some studies, while others showed controversial results. Estimation of this association may help to predict cardiovascular outcomes and may guide new treatment strategies. The hypothesis is that increased serum uric acid level is associated with a range of cardiovascular diseases.
The SAHaRA trial will clarify the role of treating anemia with Red Blood Cell (RBC) transfusion in a unique and vulnerable patient population, and determine whether that impacts on functional outcomes and mortality. It will guide best practice standards and clarify the optimal RBC transfusion strategy in patients with aSAH.
This phase III trial will establish whether IL-1Ra, with sub-cutaneous (SC) administration twice daily for up to 21 days post aneurysmal subarachnoid haemorrhage (aSAH), improves clinical outcome as measured by ordinal shift in mRS at 6 months. Patients with SAH transferred to a neurosurgical centre will be identified and approached for study participation. Following consent, patients will be randomised to receive either IL-1Ra or placebo for a maximum of 21 days from onset of symptoms. Patients who are found to be non-aneurysmal following randomisation will be withdrawn from the study treatment. Blood samples for plasma IL-6 will be obtained prior to randomisation and at day 3-5 post randomisation for IL-6 & IL-1 measurement. Safety will be measured at 30 days post randomisation and outcome assessed at 6 months post randomisation.
Each year, approximately 30,000 people in the United States suffer an intra-cranial hemorrhage due to aneurysmal rupture. Of those surviving the initial event, up to 40% will go on to have further neurological injury secondary to stroke (delayed cerebral ischemia) caused by constriction of blood vessels (i.e. vasospasm). Previous studies have shown that the medication sildenafil, given intravenously, improves vasospasm, but has an associated degree of hypotension. The degree of hypotension was well within safety thresholds for these patients. Sildenafil is a medication that strongly inhibits the protein phosphodiesterase-V (PDE-V). The hypothesis for this study is that oral sildenafil will also improve vasospasm, but does not result in as much hypotension. Specifically, the investigators look to show that comparable doses of oral sildenafil produces the same degree of PDE-V inhibition as an intravenous dose while the degree of hypotension is reduced. Additionally, using measurements of cerebral blood flow regulation acquired using transcranial Doppler ultrasound, the investigators look to show that oral sildenafil produces the same degree of improvement in vasospasm and blood flow regulation.
Sub Arachnoid Hemorrhage (SAH) is a public health concern because of its high incidence (7/100 000 inhab.), its mortality rate (25%), and its morbidity rate (50%).