View clinical trials related to Delayed Cerebral Ischemia.
Filter by:Aneurysmal subarachnoid haemorrhage is a complex pathology, the pathophysiology of which is still imperfectly understood. Its morbidity and mortality remain significant. In addition to the damage sustained by the brain in the immediate aftermath of aneurysmal rupture, which is inaccessible to life-saving treatment, a significant proportion of lesions occur at a distance from the initial event. Delayed cerebral ischaemia is one of the most morbid complications. It combines an inflammatory pattern with vascular dysfunction and neuronal excitotoxicity, leading to avoidable secondary neuronal loss. Vascular dysfunction is mediated by a loss of homeostasis between endothelial cells and figurative blood cells, including platelets. However, the interrelationship between these elements and the precise chronology of the dysfunction remain imperfectly described to date. It therefore seems appropriate to propose temporal monitoring of platelet activation kinetics over time, combined with concomitant collection of markers of endothelial damage, in order to clarify the vascular chronobiology of this pathology.
The goal of this clinical trial is to examine the effect of limb occlusion therapy (remote ischemic conditioning, RIC) in subjects with aneurysmal subarachnoid hemorrhage. The main question it aims to answer is whether RIC can improve long-term recovery in participants with aneurysmal subarachnoid hemorrhage. Researchers will compare levels of functional independence in participants in the RIC-group to participants in the sham-group.
Delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH) results from a complex combination of macro- and microvascular processes. Besides cerebral vasospasms (CVS), DCI is caused by microthrombosis, neuroinflammation, microvascular dysfunction and cortical spreading depolarization.The glycocalyx plays an essential role in regulation of inflammation, oxidative stress and thrombosis, and could be involved in the pathophysiology of DCI. This study is a single-center prospective observational pilot (phase 1) and correlation (phase 2) study recruiting patients with an aneurysmal subarachnoid hemorrhage. The primary aim of the study is to evaluate the feasibility of performing measurements of the glycocalyx using side-stream darkfield (SDF) imaging sublingually and on the conjunctiva, and by sampling blood for analysis of markers of glycocalyx shedding. Moreover, the objective is to determine characteristic Doppler waveform morphologies in DCI patients by means of thorough analysis of transcranial Doppler (TCD) measurements. The secondary objective is to determine whether changes in glycocalyx integrity correlate with the development of DCI and whether these changes are associated with increased inflammation and with variation in TCD signals. Finally, changes in glycocalyx integrity, in TCD waveform morphology and in levels of inflammatory markers will be correlated with patient outcome at 6 weeks and 6 months after ictus.
Nimodipine reduces the risk of poor outcome and delayed cerebral ischemia in patients suffering aneurysmal subarachnoid haemorrhage (SAH), but its mode of action is unknown. Its beneficial effect is assumed to be due its neuroprotective effects by reducing intracellular calcium and thereby cellular apoptosis, but higher concentrations might induce marked systemic hypotension, thereby inducing cerebral ischemia. Since several dosing regimes and routes of administration with inconclusive superiority exist and since the target site concentration of nimodipine - the unbound drug concentrations beyond the blood-brain barrier - is still not known, it is reasonable to measure nimodipine concentrations within the blood, cerebrospinal fluid (CSF) and interstitial brain tissue following oral, intra-venous and intra-arterial administration and correlate intra-arterial nimodipine administration to measures of cerebral metabolism and oxygenation. Therefore, the investigators propose to investigate in 30 patients suffering severe aneurysmal SAH and requiring cerebral microdialysis for cerebral neurochemical monitoring: - the ability of nimodipine to penetrate into the brain of neurointensive care patients by comparing exposure in brain, CSF and plasma, dependent on the route of administration (i.e. oral, intra-venous, and intra-arterial) and dosing intra-venously (0.5 - 2mg/h) - the impact of orally, intra-venously, and intra-arterially delivered nimodipine on cerebral metabolism, i.e. lactate/pyruvate ratio, pbtO2 and transcranial doppler flow velocities - the effect of oral and intra-venous nimodipine on systemic hemodynamic and cardiac parameters, using continuous Pulse Contour Cardiac Output (PiCCO) monitoring - the penetration properties of ethanol - as an excipient of nimodipine infusion - into the brain by comparing exposure in brain, CSF and plasma and quantifying the neuronal exposure to alcohol dependent on blood levels
Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) was long thought to be caused by subarachnoid blood-induced vasospasm. Experimental and clinical evidence suggest activation of several pathophysiological pathways, affecting the cerebral microcirculation. Recently, lower in-hospital mortality and less non-home discharge was reported in patients treated with therapeutic low-molecular weight heparin (LMWH), compared to patients with standard, prophylactic LMWH, pointing towards a potential benefit of higher doses of LMWH in the acute course after aSAH. Treatment with therapeutic LMWH might improve clinical outcome in endovascularly treated aSAH patients. The primary objective is to evaluate whether aSAH patients treated with therapeutic LMWH have a lower 30-day mortality rate compared to patients treated with prophylactic LMWH. Secondary objectives are to evaluate whether there are significant differences between patients treated with therapeutic and prophylactic LMWH in development of DCI, (hemorrhagic) complications during admission, hydrocephalus, non-home discharge location, quality of life, clinical outcome and cognitive functioning at three and six months, total health care costs. A single center, prospective, phase II randomized clinical trial in aneurysmal SAH patients ≥18 years old, in whom the causative aneurysm is treated with endovascular coiling less than 72 hours after initial SAH. Patients are randomized into 2 groups: (1) Therapeutic dose LMWH group: the standard prophylactic dose, administered upon hospital admission, will be replaced by nadroparin s.c. twice daily 5700 IE anti-Xa, starting within 24 hours after coiling and continued until 21 days after ictus of initial SAH. After 21 days, patients will continue with standard care prophylactic dose until discharge or when mobilized for more than 6 hours per day; (2) Control group: standard of care treatment with prophylactic dose of LMWH; nadroparin, s.c. once daily 2850 AxaIU until discharge or when mobilized for at least 6 hours a day. Primary outcome: 30-days' mortality. Secondary outcome: DCI, venous thrombo-embolic complications, occurrence of major and non-major bleeding, hemorrhagic complications after external ventricular/lumbar drain (EVD/ELD) placement and lumbar puncture (LP), other SAH-related complications, shunt-dependent hydrocephalus, discharge location, quality of life, total health care costs, cognitive functioning, clinical outcome.