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Cerebral Infarction clinical trials

View clinical trials related to Cerebral Infarction.

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NCT ID: NCT03629275 Terminated - Ischemic Stroke Clinical Trials

Investigation of Neural Stem Cells in Ischemic Stroke

PISCES III
Start date: August 31, 2018
Phase: Phase 2
Study type: Interventional

A study of stereotactic, intracerebral injection of CTX0E03 neural stem cells into patients with moderate to moderately severe disability as a result of an ischemic stroke.

NCT ID: NCT03608904 Recruiting - Ischemic Stroke Clinical Trials

Stroke Recovery and Music or No Music

Start date: July 21, 2017
Phase: N/A
Study type: Interventional

The primary outcome of this study is to determine the quantitative increase in connectivity, as measured by fMRI brain and calculated as a percent increase from baseline in patients with ischemic stroke. Eligible patients will receive a listening session of music or spoken word listening, 30 days to 5 years following ischemic stroke. Assessments will include modified Rankin Scale, National Institute of Health Stroke Scale, functional Magnetic Resonance Imaging, motor function tests, and neuropsychological evaluations. Assessments occur at baseline, day 45, and day 90 after starting listening sessions.

NCT ID: NCT03608644 Not yet recruiting - Clinical trials for Acute Ischemic Stroke

Predictive Factors of Outcome of Mechanical Thrombectomy After Acute Ischemic Stroke

Start date: October 30, 2018
Phase:
Study type: Observational

Predictive factors of outcome of mechanical thrombectomy after acute ischemic stroke

NCT ID: NCT03607565 Recruiting - Cerebral Ischemia Clinical Trials

A New Parameter Derived From DSA to Evaluate Cerebral Perfusion

Start date: July 15, 2018
Phase:
Study type: Observational

This observational study focus on a new parameter of cerebral perfusion derived form digital substraction angiography.

NCT ID: NCT03605381 Recruiting - Stroke Clinical Trials

MORbidity PRevalence Estimate In StrokE

MORe PREcISE
Start date: September 30, 2018
Phase:
Study type: Observational

Information regarding the likely progress of post-stroke symptoms is vitally important to stroke survivors to allow them to plan for the future and to adjust to life after stroke. Moreover, the prevalence of morbidity secondary to stroke is of central importance to Health Professionals to understand the prognosis of the disease in the patients under their care. Additionally, it will also allow commissioners of care, planners and third sector organisations to adapt to and answer the needs of a post-stroke population. Currently, the data collected by national audit programmes are concentrated on what can be termed 'process or process of care' data. The utility of these data are in the ability to audit the care received by stroke survivors on stroke units against evidenced standards for care, thus ensuring evidence based practice. Nevertheless, process of care is only one form of measuring stroke unit care and the audit programmes collect some limited functional status data, data relating to risk-factor co-morbidities and treatment received data. Therefore, the scope of this study is to build on the minimum data set currently collected and to collect post-stroke data in domains not currently collected. The International Consortium for Health Outcomes Measurement (ICHOM) takes important steps to collect data outside of process of care data such as a Patient Reported outcome data in their minimum outcome data set for stroke [currently under review].. Nevertheless, the ICHOM doesn't currently advocate the specific collection of data relating to cognitive impairment or emotional problems secondary to stroke. It is in these important aspects that this study will augment the data set currently advocated by ICHOM to collect data in the areas of cognitive impairment and emotional problems secondary to stroke. Therefore, the aim of this study is to quantify the prevalence of morbidity at six months post-stroke.

NCT ID: NCT03601702 Recruiting - Clinical trials for Acute Ischemic Stroke

EmboTrap ® II Revascularization Device (Neuravi) in Acute Ischemic Stroke

Start date: January 1, 2022
Phase:
Study type: Observational [Patient Registry]

The primary aim of Registrap study is to assess the safety and effectiveness of the EmboTrap®II Clot Retriever device (Neuravi) in patients with acute ischemic stroke from large vessel occlusion.

NCT ID: NCT03578822 Completed - Clinical trials for Acute Ischaemic Stroke

Thrombolysis With rhPro-UK in 4.5-6 Hours After Acute Ischemic Stroke in a Double-blinded,Controlled Trial

PROUD
Start date: August 10, 2018
Phase: Phase 3
Study type: Interventional

This is a randomized,controlled, double-blinded, phase 3 clinical study to evaluate the efficacy and safety of recombinant human urokinase(rhPro-UK) versus basic treatment for patients with acute ischaemic stroke in 4.5-6 hours after stroke onset.

NCT ID: NCT03577093 Recruiting - Ischemic Stroke Clinical Trials

Molecular Mechanisms of microRNA-494 Involving in Cerebral Ischemia

Start date: June 6, 2018
Phase:
Study type: Observational

We and other investigations suggested that the activation of nerve cell cycle following cerebral ischemia led to neuronal apoptosis, glial cell proliferation and the formation of glial scar.The cyclin-dependent kinases (CDKs) and cyclins jointly promoted the cell cycle progression. Our preliminary clinical trial found a new microRNA-miR-494, which involved in the occurrence of acute ischemic stroke. In our animal experiment, miR-494 could relieve cerebral ischemia injury through inhibiting cyclin-dependent kinase 6(CDK6), ubiquitin-conjugating enzyme E2L6 (UBE2L6) and histone deacetylase 3 (HDAC3), which suggested that miR-494 might play an important role in the regulation of cell cycle following cerebral ischemia. This project intends to verify the following hypothesis:①miR-494 suppresses CDK6, and/or fibroblast growth factor16(FGF16)-Ras-extracellular signal-regulated kinase(ERK)--v-myc avian myelocytomatosis viral oncogene homolog(MYC) pathway, and/or phosphatase and tensin homolog(PTEN)-/protein kinase B(AKT)-mechanistic target of rapamycin(mTOR)-S6k pathway;②miR-494 inhibits UBE2L6, upregulates the hypoxia-inducible factor 1 α(HIF-1α) expression in nerve cells, thereby increases the p21 and p27 protein levels and inhibits cyclin-dependent kinase2(CDK2)activity;③miR-494 represses HDAC3 and downregulates the cyclin-dependent kinase1(CDK1)protein level. These all mediate the cell cycle arrest of neurons and astrocytes, reduce the neuronal apoptosis and glial scar formation,promote the recovery of neurological function and provide new targets for the treatment of ischemic stroke.

NCT ID: NCT03571763 Recruiting - Ischemic Stroke Clinical Trials

The Impact of Anti-thrombosis on Cerebral Microbleeds and Intracranial Hemorrhage in Ischemic Stroke Patients

Start date: August 1, 2018
Phase:
Study type: Observational

The purpose of this prospective cohort study is to investigate whether antithrombotic therapy in the secondary prevention of ischemic stroke increases the risk of the emerging CMBs and whether the change is associated with an increased risk of intracranial hemorrhage, providing an imaging evidence for individualized antithrombotic therapy in such patients.

NCT ID: NCT03555643 Completed - Stroke Clinical Trials

Evaluation of the HARM for the Detection of a Cerebral Ischemia in TIA/TNA Patients

Start date: November 1, 2017
Phase:
Study type: Observational

The research project investigates the incidence of the hyperintense acute reperfusion marker (HARM) in patients with transient ischemic attack (TIA) or transient neurological attack (TNA). Initially, HARM was described after acute ischemic stroke and is caused by a blood-brain barrier disorder after recanalization of an acute vessel occlusion and consecutive reperfusion. These result in a contrast agent extravasation into the subarachnoid space, which can be easily detected on fluid attenuated inversion recovery (FLAIR) images. TIA is defined as a transient focal neurological deficit with a probably cerebrovascular cause. In contrast, TNA is defined as a transient non-focal neurological deficit with multiple causes, including cerebrovascular. The clinical diagnosis of TIA is often flawed and the delineation of TIA and TNA can be difficult. MRI is the most important diagnostic method for the detection or exclusion of cerebral ischemia in patients with TIA/TNA in daily clinical practice. However, on diffusion-weighted imaging (DWI) approximately two-thirds of TIA cases and only one-fifth of TNA cases demonstrate acute cerebral ischemia. Supplementary perfusion-weighted imaging (PWI) scans can only slightly increase this percentage. The well-known HARM could prove to be complementary to DWI and PWI and close or at least reduce the existing gap. In the case of TNA in particular, this could be of clinical relevance in order to avoid mistreatment or even dismissal without further clarification after supposedly inconspicuous imaging. Therefore, the aim of this study is to record the incidence of HARM in a statistically significant number of cases of patients with TIA and TNA and to investigate relationships with symptom duration and anatomical localization. In addition, the dynamics of contrast enhancement in the subarachnoid space in TIA and TNA cases with HARM will be analyzed in detail.