Active clinical trials for "Subarachnoid Hemorrhage"

Extensive research has shown that the big event that leads to the initiation of vasospasm is the release of oxyhemoglobin (blood breakdown product).Depletion of NO synthase (19,20,21) was also noted after SAH.CSF is produced from choroid plexus in the ventricle. If the SAH is too dense, the blood in the subarachnoid space will not easy to be washed out.

According to Morgan et. al. (J Neurosurg 101:1026-1029, 2004): bilirubin as a cerebrospinal fluid marker of sentinel subarachnoid hemorrhage: a preliminary report in pigs, we're going to test the hypothesis in the cerebrospinal fluid of spontaneous subarachnoid hemorrhage patients.

A technique of MRI infusion -l'Arterial Spin Labeling-, non-invasive and non-irradiating, repeatable over time, appears promising in the field. This sequence allows for routine, generate perfusion maps relating to the entire brain volume

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.

Dysregulation of autonomic nervous system is evident in patients with spontaneous intracranial hemorrhage. In this study, we utilize a non-invasive method (heart rate and blood pressure variability analysis to analyze the autonomic activities in this group of neurosurgical patients. Our aim is to determine the utility of this modality in risk stratification and outcome prediction in these patients.

This study will provide novel information to the literature base for the pathophysiology of aneurysmal subarachnoid hemorrhage. The association of breakdown products in the serum of aSAH patients were reported in a very small case series of 3 patients, as mentioned above. However, while their results are intriguing and encouraging, our study will provide more definitive information about the GC in aSAH. If there is a positive correlation, the results of this study will guide future investigations into new therapies for this devastating disease such as MMP inhibition with doxycycline.

This study evaluates the pharmacokinetic profile of levetiracetam in critically ill patients who have suffered a subarachnoid hemorrhage. The patients will be evaluated for development of augmented renal clearance and the effects and duration of effects this may have on levetiracetam clearance.

Deficits in memory, executive function, and language are common cognitive sequelae of aneurysmal subarachnoid hemorrhage (aSAH). Previous study demonstrated that post-treatment antiplatelet therapy reduced risk for delayed cerebral ischemia caused by aSAH. However, the effect of antiplatelet therapy on cognition after aSAH is unclear. The aim of this study was to assess the effect of antiplatelet therapy on cognition after aSAH.

The outcome of brain injury (physical or stroke) may be related to a brain electrical phenomenon known as Cortical Spreading Depression (CSD). This is a brief cessation of function in a local region of brain tissue. It has been hypothesized that CSD may occur after brain injury and may expand the damage to adjacent brain areas. Our aim is to detect CSD by means of intracranial electrodes in patients with brain injuries and asses how these events alter the outcome of the patients.

The purpose of this study is to use transcranial Doppler (TCD) to predict intracranial pressure (ICP) and clinical outcome of neurocritical patients.