View clinical trials related to Cerebral Infarction.
Filter by:Autonomic modulation by transcutaneous vagal nerve stimulation in acute ischaemic stroke requiring mechanical thrombectomy: a phase IIa, sham controlled randomised trial.
Acute stroke afflicts nearly 700,000 patients in the US and is the number 3 cause of death. Only 2-9% of this large number is treated with t-PA if they arrive within 4.5 hours. An equally small percentage of patients with large vessel occlusion undergo thrombectomy. The thrombectomy patients may or may not receive t-PA. Some of these patients rarely receive intravenous GPIIB/IIIa inhibitors. Many lines of evidence suggest that GP IIb/IIIa inhibitors, a class of FDA approved potent platelet inhibitors that have been used extensively along with heparin for acute coronary syndromes (heart attacks) and unstable angina (chest pain), may be safe enough to give in these circumstances.
AISDTS is a prospective registry study, in which clinical information, examination and imaging data of patients with acute ischemic stroke receiving different treatment strategies were collected, grouped and statistically analyzed, and corresponding clinical prediction models were constructed to explore the role of clinical biological indicators in the occurrence and development of stroke.
This study is designed to evaluate the safety, efficacy, and pharmacokinetics of balovaptan compared with placebo in participants with acute ischemic stroke (AIS) at risk of developing Malignant Cerebral Edema (MCE)
This is a randomized open-label, with blinded outcome pilot study to evaluate the effect on inflammatory laboratory values and explore clinical outcomes in patients who present with ischemic strokes due to large vessel occlusions and are treated with either current accepted management, or accepted management in addition to transcutaneous auricular vagal nerve stimulation.
The study will be a prospective, randomized, double- blinded placebo, single center pilot clinical trial. Patients with acute ischemic stroke due to large vessel occlusion undergoing endovascular thrombectomy will be included. The treatment group will receive 200 mg intravenous/oral minocycline hydrochloride in addition to endovascular thrombectomy for a total of 21 days. The control group will receive standard medical and endovascular care along with a similar looking placebo. Patients will be randomized to the treatment or control group by the Pharmacy eliminating the selection bias. The patient and evaluator will be blind to the allocation of patients further minimizing the bias. Through randomization we expect to achieve two groups that are comparable in their baseline clinical characteristics.
Evaluating the collateral circulation of acute ischemic stroke (AIS) mainly depends on the imaging examination. At present, there is no effective and sensitive biomarker for collateral circulation. Thus, the research objective was to evaluate the predicting role of the CBP/P300-interacting transactivator with Glu/Asp-rich C-terminal domain 2 Ratio (CITED2) from peripheral blood mononuclear cells in the collateral circulation of AIS. We classified the AIS patients into two groups (the good collateral group and the poor collateral group) by DWI-ASPECTS score. The western blot was applied to test the protein expression of vascular endothelial growth factor (VEGF) and CITED2. Then, we collected other clinical data. Binary logistic regression analysis between collateral circulation and clinical data was performed. Finally, Receiver operating characteristic (ROC) curve analysis was used to explore the predictive value of the CITED2.
To examine the revascularization efficacy and safety of T-02 and its associated performance characteristics in treatment of appropriately selected subjects experiencing an acute ischemic stroke when the treatment is initiated within 24 hours after last seen well under the current guideline, and to generate hypotheses to be confirmed in subsequent confirmatory clinical investigations
In the Russian Federation, ischemic cerebral infarction is recorded annually in more than 450,000 people. It is the second most common cause of death after coronary heart disease. The 30-day mortality rate after an ischemic cerebral infarction is more than 25%, and during the following year about half of the patients die. To date, all candidate neuroprotective drugs tested in various clinical trials have demonstrated insufficient efficacy . Therefore, the development of new approaches to the treatment of severe brain injuries of various etiologies is one of the most important tasks of critical condition medicine. Brain damage due to stroke triggers a number of pathophysiological reactions, which are based on the accumulation of glutamate with the development of excitotoxicity. The effect of glutamate on NMDA receptors is one of the main factors of neurodegenerative disorders. Xenon is an anesthetic whose neuroprotective properties have been shown in many experimental studies. Хenon inhalation after ischemia and reperfusion suppresses ischemic brain damage and tPA-induced cerebral hemorrhages, and damage to the blood-brain barrier. The most interesting is a randomized controlled trial performed by R. Laitio et al. (2016), in which the use of xenon in combination with hypothermia in clinical practice was studied for the first time. In patients who have undergone community-acquired cardiac arrest, xenon inhalation at a concentration of 40 vol.% within 24 hours in combination with hypothermia, led to less damage to the white matter of the brain than with patients using hypothermia alone. The 6-month mortality rate was 27% in the xenon and hypothermia group and 35% in the hypothermia group. It is important to note that today, despite a large pool of convincing preclinical studies proving the neuroprotective properties of xenon, there is not a single clinical study of its use in ischemic stroke. Therefore, the research objectives is to determine whether the strategy of using xenon-oxygen mixture inhalation is better than oxygen-air mixture inhalation with respect to the change in scores on the NIHSS, Rankin and Glasgow coma scales on day 7, the duration of stay in the ICU and the frequency of nosocomial pneumonia.
In this prospective, single-arm, open-label, imaging and treatment study, the investigator will test the hypothesis that crizanlizumab will prevent the progression of silent cerebral infarcts in patients with sickle cell disease. Study participants will undergo brain MRI before initiation of crizanlizumab and at 6 and 30 months after starting crizanlizumab infusions. The crizanlizumab cohort will be compared to a matched, observational cohort of patients not receiving crizanlizumab.