View clinical trials related to Subarachnoid Hemorrhage.
Filter by:After endovascular treatment of the intracranial aneurysm, recanalization may occur, with a risk of recurrent subarachnoid haemorrhage or long-term angiographic recurrences of aneurysms. Few data exist on patients' long-term follow-up after subarachnoid haemorrhage caused by ruptured intracranial aneurysms.
Autoimmune diseases are diseases in which inappropriate immune responses that have the capability of harming host cells play an important role. Evidence suggests that the presence of certain autoimmune diseases such as rheumatoid arthritis or systematic lupus erythematosus increase the risk of cardiovascular disease (CVD). However, this evidence is inconsistent for autoimmune disorders and no systematic approach has been previously used to study the relationship between a range of common autoimmune disorders and specific forms of cardiovascular diseases such as myocardial infarction, intracerebral and subarachnoid haemorrhage, or venous thrombosis. The investigators will use linked electronic health records to investigate whether commonly diagnosed autoimmune disorders are associated with increased risk of CVD development and whether effects differ in men and women and change with age.
Patients with brain hemorrhage resulting from a ruptured aneurysm (SAH) are at risk of developing a condition called vasospasm, one or two weeks after their hemorrhage. This is a major cause of stroke and death following SAH. A special type of CT scan, called CT perfusion, analyzes regional blood flow in the brain. We hypothesize that CT perfusion scans performed on admission and day 6 post-hemorrhage will enable us to predict which patients will go on to develop vasospasm.
Study of heterogeneity in associations between heart rate and the initial presentation of 12 cardiovascular diseases.
Study of heterogeneity in associations between social deprivation and the initial presentation of 12 cardiovascular diseases.
With evolving endovascular technologies there is a growing debate centered on the relative safety and efficacy of the currently accepted alternatives for the treatment of ruptured cerebral aneurysms in the face of acute subarachnoid hemorrhage (SAH). The purpose of this study is to compare the safety and efficacy of microsurgical clipping and endovascular coiling of acutely ruptured cerebral aneurysms in a prospective, randomized fashion.
Subarachnoid hemorrhage (SAH) is associated with a high mortality and frequently leads to severe disability in survivors caused by cerebral vasospasm and infarction. This study aims to elucidate the role of neuroinflammation (endocannabinoids and cortisol levels in cerebrospinal fluid) in the pathophysiology of cerebral vasospasm and the value of the bilateral bispectral index (BIS) for the early diagnosis of cerebral vasospasm.
The purpose of this study is to use transcranial Doppler (TCD) to predict intracranial pressure (ICP) and clinical outcome of neurocritical patients.
In this project we are collecting cerebrospinal fluid and blood from patients at Vanderbilt Medical Center who have a subarachnoid hemorrhage which has followed the rupture of a brain aneurysm. We then propose to study the cerebrospinal fluid using a novel microscopic laser directed mass spectrometric analysis (MALDI) available at Vanderbilt. The cerebrospinal fluid and blood will then be analysed for different biological markers, protein expression and gene expression. These markers will then be statistically correlated with clinical data including prediction of vasospasm, time to vasospasm and response to standard therapy.
Hypothesis: During severe brain trauma (injury, surgery) the ensuing inflammatory response in the central nervous system (CNS) results in a decrease in the expression of the transporter protein p-glycoprotein (PGP) in the blood brain barrier. This loss results in the penetration into the brain of certain drugs that are normally excluded by the transporter protein. In this study the working hypothesis is that the agitation observed in patients with CNS trauma treated with morphine is related to the inflammation evoked loss of PGP in the blood brain barrier and the accumulation of the morphine metabolite 3-morphine glucuronide.