Active clinical trials for "Cerebral Infarction"

Non-fasting triglyceride levels are thought to play a role in stroke. The investigators hypothesise that the results of a standardised oral triglyceride tolerance test in the subacute setting (3-7 days) after the first ischaemic stroke are associated with the risk of recurrent stroke within 12 months after the index event.

Specific objectives: Evaluation of morbidity and mortality associated with the severity of pharyngeal residue in patients admitted to Hotêl-Dieu de France university hospital for Stroke based on the "The Yale pharyngeal residue scale" Evaluation of the accuracy of screening protocol of Dysphagia at the Emergency Department in patients admitted for stoke based on the "Emergency Department Dysphagia Screening Tool"

Anticoagulants are generally recognized as a necessary therapy to prevent the recurrence of ischemic stroke in patients with non-valvular atrial fibrillation (NVAF), but in some patients they also cause bleedings, particularly intracranial hemorrhage. One of the independent predictors of intracerebral hemorrhage is the presence of cerebral microbleeds (CMBs); a high incidence of intracerebral hemorrhage is reported in patients with multiple CMBs. Recent study suggested that patients who had CMBs at baseline developed more new CMBs after 2 years (26%), compared with patients (12%) who did not have CMBs at baseline. However, there has been no study on the progression of CMBs in patients receiving so-called novel oral anticoagulants (NOACs). This study tests the hypothesis that the incidence of hemorrhagic stroke is lower in patients receiving NOACs (dabigatran, rivaroxaban, apixaban, and edoxaban) than in those receiving warfarin, and this difference reflects the difference in the effects of warfarin and NOACs on the progression of CMBs. Towards this goal, we enroll 200 patients with at least one CMB detected by 1.5 T MRI (T2*WI) at baseline, who treated with NOACs or warfarin for 12 months. Primary endpoint is the proportion of subjects with an increased number of CMBs at Month 12 of treatment with NOACs or warfarin. If the results of this study support the efficacy of NOACs in preventing increase of CMBs, this would be of great interest to domestic and overseas clinicians, in view of the potential therapeutic impact, including that for primary prevention of ischemic stroke.

The purpose of this study is to determine whether levels of circulating endothelial progenitor cells (cEPC) are increased in the acute phase of ischemic stroke.

Adiponectin (Ad) is an abundant protein in human body, and reports have shown that it act as a novel risk factor for brain and heart ischemia injury. This 5 years follow-up study will focus on serum adiponectin concentration, activity and isoforms in Chinese population and its correlation to these diseases.

The aims of this project are to: investigate the adherence and persistence to anticoagulation (and in specific, to VKAs and NOACs) in AF patients with previous ischemic stroke; identify predictors of poor adherence and persistence and assess whether the SAMe-TT2R2 score predicts adherence and persistence to anticoagulation

Negligence or contempt of the etiology and pathogenesis of minor ischaemic stroke in the early diagnosis and effective treatment leads to more than 40-50% of patient with recurrent episodes, and 10% patient died. Therefore, diagnosis and treatment of minor ischaemic stroke according to the etiology and pathogenesis is important. The 2007 Korean modified TOAST type got some progress, but there exists two major disadvantages: imperfect diagnosis and pathogenesis of perforator artery infarction etiology; lack of typing according to the pathogenesis of large atherosclerotic infarction and taking measures of treatment according to the new types. Recently, domestic professor Gaoshan proposes new approach to diagnose and treat minor ischaemic stroke according to the etiology and pathogenesis of CISS typing, but the pathogenesis of hypoperfusion infarction with severe stenosis of large artery is unclear. Is it low perfusion? Or artery-artery embolization? Or both? How to distinguish the pathogenesis of branch artery disease: by atherosclerosis? Or hyalinosis? Or both? How to check the validity of clinical types? This study take different interventions according to different types and observation of the long term clinical results of intervention( mortality, recurrence rate, disability rate and rate of cerebral hemorrhage and subarachnoid hemorrhage), in order to clarify the new types can indeed solve the current problem of minor ischaemic stroke with high mortality, recurrence rate, disability rate and rate of cerebral hemorrhage and subarachnoid hemorrhage.

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 focuses on the relationship between obesity and stroke, which are both characterized by increasing incidence and prevalence with epidemic proportions worldwide and tremendous socio-economic consequences. Furthermore, obesity is an established risk factor for stroke and affects especially younger people, which increases the stroke incidence in younger patients. Unfortunately, the relationship between overweight and acute ischemic stroke including treatment by thrombolysis has not yet been evaluated thoroughly.

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.