Active clinical trials for "Subarachnoid Hemorrhage"

This pilot study will compare the two hypertonic solutions currently used for subarachnoid hemorrhage (SAH) - related complications and to determine if the reduction of chloride load is safer, and as efficacious as the classic hypertonic solution.

This is a Safety, Tolerability, Pharmacokinetic and Pharmacodynamic Study of SFX-01 in Subarachnoid Haemorrhage, with exploratory evaluations of efficacy.

This is a multicenter, prospective, randomized, open-label trial with blinded endpoint (PROBE) assessment. Adult patients with the diagnosis of non-traumatic SAH, as proven by computed tomography (CT) within 24 hours after the onset of headache, will be randomly assigned to the treatment group or the control group. Patients in the treatment group will receive standard treatment with the addition of a bolus of TXA (1 g intravenously) immediately after randomization, followed by continuous infusion of 1 g per 8 hours until the start of aneurysm treatment, or a maximum of 24 hours after the start of medication. Patients in the control group will receive standard treatment without TXA. The primary outcome measure is favorable functional outcome, defined as a score of 0 to 3 on the modified Rankin Scale (mRS), at 6 months after SAH. Primary outcome will be determined by a trial nurse blinded for treatment allocation.

Many people who have undergone subarachnoid hemorrhage from an aneurysm (an artery of a vein in the brain) struggle with a pronounced fatigue as well as a number of other sequelae such as impaired concentration, memory deficits and emotional problems. Exhaustion is often permanent and can lead to a significant worsening of quality of life and be the cause of disability. This condition does not only have major consequences for the individual who is affected, but also for their families and for society. So far no effective treatment for fatigue has been found. The drug OSU6162 has shown a beneficial effect on fatigue and other impairments after stroke and after traumatic brain injury. There is good reason to believe that OSU6162 can also improve fatigue and other impairments after aneurysm bleeding and thus increase the chance of returning to the level of daily function they had before the bleeding. The study is double blinded and measures the effect of OSU6162 and placebo on fatigue and neuropsychological function.

Phase 1/2a Multicenter, Controlled, Randomized, Open Label, Dose Escalation, Safety, Tolerability, and Pharmacokinetic Study Comparing EG-1962 and Nimodipine in Patients with Aneurysmal Subarachnoid Hemorrhage

All patients with acute aneurysmal hemorrhage are treated in accordance with our institutional protocol. After securing of the aneurysm, some smokers with acute aneurysmal hemorrhage are randomly assigned to transdermal nicotine replacement (NRT). The short- and long-term effect of NRT will be studied comparing non-smokers, smokers without NRT and smokers with NRT.

Purpose: - Vasospasm and secondary ischemia following subarachnoidal hemorrhage considerably affect the clinical outcome. The purpose of this study is to determine whether crystalloid (Lactated Ringer's solution) or colloid (hydroxyethyl starch) intravenous infusion is more effective in the treatment of subarachnoid hemorrhage (SAH) Treatment: - Patients are randomly divided into two groups. Depending on the blood pressure of the patients the members of the first group receive 15-50 ml/kg Lactated-Ringer's solution daily as part of the treatment, while the others 15 ml/kg Lactated-Ringer's and 15-50 ml/kg hydroxyethyl starch solution daily. Measurements: Neurological status of patients will be determined by the NIH Stoke Scale Score and the Glasgow Coma Scale (GCS) on a daily basis. The mid-term survival and quality of life are evaluated with Barthel Index and Glasgow Outcome Scale (GOS) 14 and 30 days following admission to our clinic. Hypothesis: -The prevalence of vasospasms, the mortality rate and the medium-term quality of life following subarachnoid hemorrhage is improved if patients are treated with intravenous colloid (hydroxyethyl starch) infusion compared to intravenous crystalloid infusion.

Background: Although glucose is essential to cerebral function, abundant experimental and clinical evidence demonstrates that endogenously released lactate, rather than glucose, is the preferential energy substrate for the brain in conditions of stress and acute injury. In patients with severe Traumatic Brain Injury (TBI) and aneurysmal subarachnoid hemorrhage (SAH) monitored with cerebral microdialysis and brain tissue oxygen (PbtO2), our preliminary data show that increased brain extracellular lactate is frequently observed. Our findings indicate that elevated brain lactate more often occurs in the absence of brain hypoxia/ischemia and is mainly the consequence of increased cerebral glycolysis, i.e. it occurs in association with high extracellular pyruvate. These data suggest that the primary source of elevated lactate is activated glycolysis and strongly support the concept that endogenously released lactate can be utilized by the injured human brain as energy substrate. They prompt further investigation to examine whether exogenous lactate supplementation can be a valuable neuroprotective strategy after TBI or SAH. Indeed, in animal models of brain injury, administration of exogenous lactate improves neuronal and cognitive recovery. Hypothesis: The investigators test the hypothesis that lactate therapy, administered during the acute phase of TBI or SAH, might exercise neuroprotective actions by restoring brain energetics and improving brain tissue PO2 and cerebral blood flow (CBF). Aim of the study: The aim of this single-center study is to examine the effect of sodium lactate infusion on cerebral extracellular metabolites, brain tissue PO2 and cerebral blood flow, measured with CT perfusion and transcranial doppler (TCD). Design: Prospective phase II interventional study examining the effect of a continuous 3-6 hours infusion of sodium lactate (20-40 µmol/kg/min), administered within 48 hours from TBI or SAH, on cerebral extracellular glucose, pyruvate, glutamate, glycerol, PbtO2 and CBF.

Rupture of brain aneurysms is a common cause of death and disability, accounting for as many as 10% of stroke cases in the United States. While much of the resulting injury to the nervous system is caused by the initial bleeding from the aneurysm, many of these patients develop cerebral vasospasm, pathological constriction of the blood vessels supplying the brain, several days following hemorrhage. As many as a third of patients can suffer a resulting neurological deficit and stroke, presumably caused by the decreased blood flow to the brain (ischemia). This delayed brain injury accounts for a significant percentage of poor outcomes following aneurysm rupture. Studies have shown that remote ischemia to many organs can precondition other tissues (including the brain) to be more tolerant to decreases in blood flow. This "remote ischemic preconditioning" has the promise of protecting the brain from ischemic injury. Whereas in other forms of stroke the onset of ischemia cannot be predicted in the general population, following aneurysm rupture the investigators know which patients are likely to develop vasospasm and when. Therefore, ischemic preconditioning following aneurysm rupture may help prevent some of the ischemic injury caused by vasospasm. Remote ischemic preconditioning by transient limb ischemia (produced by inflation of a blood pressure cuff on the arm or leg) has been shown to minimize injury to other organs, most notably the heart. Remote ischemic preconditioning of the brain following aneurysm rupture has not yet been investigated.

Delayed cerebral vasospasm and secondary ischemic infarction are feared complications after aneurysmal subarachnoid hemorrhage (aSAH). To date, there is no effective therapy to prevent these ischemic complications. The arterial partial pressure of carbon dioxide (PaCO2) is one of the main determinants of cerebral blood flow (CBF) in healthy subjects. It is yet largely unknown, if and to what extent modulations of PaCO2 can influence CBF in patients after aSAH. The trial is a phase 1 study in which the feasibility of hypercapnia in SAH patients is tested. PaCO2 is gradually raised to 60 mmHg in 10 mechanically ventilated aSAH patients. Cerebral oxygen saturation measured by NIRS and CBF determined by an intracerebral thermodilution probe are the primary end points. If the feasibility is confirmed, this trial will be followed by a phase 2 dose finding study.