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NCT ID: NCT04988932 Completed - Cerebral Ischemia Clinical Trials

Inhaled Nitric Oxide Treatment for Aneurysmal SAH Patients With Intractable Cerebral Vasospasm

Start date: July 31, 2012
Phase: N/A
Study type: Interventional

Aneurysmal subarachnoid haemorrhage (aSAH) is a rare but severe subtype of stroke with high mortality and morbidity. Besides rebleeding, delayed cerebral ischaemia and cerebral vasospasm (CVS) are thought to be major reasons for the poor outcome in survivors of aSAH. Despite advances in the detection and treatment of CVS 20-40% of CVS patients experience cerebral Ischaemia. Experimental animal studies for ischaemic stroke, traumatic brain injury, and SAH showed that inhaled nitric oxide (iNO) selectively dilates cerebral arteries and arterioles in hypoperfused brain tissue. The investigators therefore performed this prospective pilot study to evaluate the effects of iNO on cerebral perfusion in patients with refractory vasospasm after aSAH.

NCT ID: NCT03754725 Active, not recruiting - Dementia Clinical Trials

Ferritin and Iron Burden in SAH sIRB

Start date: October 1, 2020
Phase: Phase 1/Phase 2
Study type: Interventional

Ruptured cerebral aneurysms lead to subarachnoid hemorrhage (SAH),that has a high morbidity and mortality rate, the severity of which is predicted by the "Hunt-Hess grade" (HHG). SAH leads to iron (Fe) and hemoglobin (Hb) accumulation in the brain, which is toxic for neurons. Ferritin (iron reported in the brian) and iron overload leads to brain atrophy, specifically in the mesial temporal lobe (hippocampus, impairing patients' cognition. It is estimated that 50% of survivors have cognitive deficits. Most of the survivors of SAH could not return to work. Iron chelation therapy has been recently gaining ground as a therapeutic intervention in intraparenchymal hemorrhage and in SAH. However, there has not been any study that assess the iron deposition in the brain and the level of ferritin in the cerebrospinal fluid of SAH patients. The investigators propose to conduct a randomized trial using Deferiprone (oral chelating agent, "De") + standard of care versus standard of care in patient with SAH to: 1. assess the level of ferritin (Ft) in CSF (CSF withdrawn from ventriculostomy tube), 2. assess functional outcomes measured by the Montreal Cognitive Assessment (MoCA) score, a score used to assess the level of dementia, mainly in Alzheimer disease patients. 3. quantify the the total iron deposition in the brain based on MRI

NCT ID: NCT01832389 Completed - SAH Clinical Trials

Goal Directed Therapy After Aneurysmal Subarachnoid Haemorrhage

PiSAH
Start date: March 2013
Phase: N/A
Study type: Interventional

The objective of this study is to determine whether a goal-directed therapy can reduce the incidence of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage.

NCT ID: NCT01656317 Completed - SAH Clinical Trials

Rehabilitation of Patients After Subarachnoid Hemorrhage

SAH
Start date: January 1, 2012
Phase: N/A
Study type: Interventional

The study's main objective will be to assess which effect early initiated rehabilitation has on the frequency of complications and the level of physical and cognitive functioning after aneurysmal subarachnoid hemorrhage (SAH). To this end the following aspects will be investigated: The frequency of complications (with special emphasis on pulmonary complications,thromboembolic events, cerebral vasospasm, unintended discontinuation of drains and lines) - Length of stay in hospitals and socio-economic impact - Physical and cognitive function in the early and chronic phase after SAH - Health-related quality of life and participation in society in the chronic phase

NCT ID: NCT01569100 Completed - SAH Clinical Trials

Atorvastatin After Aneurysmal Subarachnoid Hemorrhage

Start date: December 2005
Phase: N/A
Study type: Observational

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, known as statins, have recently been demonstrated to improve endothelial function. Additionally, numerous studies have shown statins as having antiinflammatory and cell-signaling effects together with a selective up-regulation of the eNOS activity. These findings are of potential benefit for the prevention of cerebral vasospasm after a aneurysmal subarachnoid hemorrhage. Indeed, one of the possible mechanisms for this vasospasm is the eNOS depletion or even increase of eNOS expression after the hemorrhage. The purpose of this study is to observe the immediate effect of statins after aneurysmal subarachnoid hemorrhage (aSAH) in cerebral vasospasm and outcome at one year.

NCT ID: NCT01556620 Completed - Brain Trauma Clinical Trials

Is NIRS Able to Detect Ischemia Following Brain Insult

NIRS
Start date: November 2011
Phase: N/A
Study type: Observational

We hypothesize that newly developped NIRS sensor (EQUANOX Advanceā„¢, 8004CA, NONIN Medical, USA)is able to detect ischemic events recorded by brain tissue oxygen probe (Licox, Integra Neurosciences, USA) and that values are correlated.

NCT ID: NCT01343537 Terminated - Aneurysm Clinical Trials

Continuous Neurophysiological Monitoring Detection of Cerebral Vasospasm in Aneurysmal Subarachnoid Hemorrhage Subjects

Start date: December 2010
Phase: Phase 0
Study type: Interventional

Aneurysmal subarachnoid hemorrhage (bleeding on the brain due to a ruptured aneurysm) is a serious condition with a high morbidity (incidence of having ill health) and mortality (death). There are approximately 11 cases per 100,000 in the population per year, and approximately 40% of these cases are fatal. (Ingall) Among the fortunate subjects who survive the initial bleed, vasospasm and subsequent stroke are a major cause of morbidity. Vasospasm is defined as a prolonged severe, although reversible cause of arterial narrowing that occurs after bleeding into the subarachnoid space, most commonly after aneurysmal rupture. (Youman) The reduced arterial diameter inhibits blood flow and deprives the brain of oxygen, which often results in a stroke. Vasospasm is a major problem when treating subjects with aneurysmal subarachnoid hemorrhage. For these reasons, it is essential to diagnose cerebral vasospasm early, before permanent deficits develop. There may be another option to solve this dilemma. The field of neuro-monitoring (neurological monitoring) has the technology available to continuously monitor brain activity of these sedated ICU subjects. This may allow for early diagnosis and possibly identify changes in neurologic function before they become symptomatic. In the past, neuro-monitoring was primarily used in the operating room to monitor neurologic function during surgery in and around the spinal cord. Surgery to the spine or spinal cord also carries its own form of risk, either from mechanical trauma to the spinal cord or its nerve roots, or from interruption of the blood supply to these structures. Should damage to nerve fibers occur, the end result could be paralysis, loss of sensation, and onset of severe burning (i.e. neuropathic) pain. The field of intraoperative neuro-monitoring (IOM) was developed to address these risks during spine surgery, whereby nerves rostral (toward the head) or caudal (toward the feet) to the site of surgery are stimulated (usually via electrical pulses) and signals are recorded from the side opposite to the site of stimulation. Thus, the signals carried by nerve fibers are forced to pass through the region at risk from the surgery. In the event that changes in nerve responses are seen, the surgical team is notified, and they can change what they're doing to try and restore signals, thereby preserving function in the nerve fibers. This same technology has been used in the neurosurgical ICU to monitor subjects with severe brain injury from trauma, stroke, intracranial hemorrhage and subarachnoid hemorrhage. Using continuous electroencephalogram (EEG) monitoring combined with somatosensory evoked potentials (SSEPs) (a type of neuro monitoring) has been used to determine prognosis, identify subjects in subclinical status epilepticus (state of brain being in a constant seizure), predict elevations in the intracranial pressure Increased pressure within the skull), and diagnose cerebral hypoxia (not enough oxygen in the brain) (Amantini)