View clinical trials related to Cerebral Infarct.
Filter by:Ischemic stroke is a major public health issue, likely to cause functional disability. It is well known that sleep has an impact on brain plasticity, and after an ischemic stroke, studies have shown subjective sleep quality alterations and sleep architecture abnormalities. Furthermore, there is no clear guideline showing the usefulness of a systematic sleep investigation following an ischemic stroke. The aim of the study is to identify retrospectively correlation between polysomnographic abnormalities (sleep apnea, periodic limb movements, disturbed sleep architecture…) and functional recovery after an ischemic stroke. The study also assesses the impact of sleep abnormalities on survival, and the risk of new cardiovascular event.
Cerebral infarcts represent a major cause of morbidity/mortality in spite of therapeutics for a premature recanalisation (intravenous recombinant tissue plasminogen activator (rt-PA) and thrombectomy). Thrombolysis failure by the administration of rt-PA is frequent, in particular in proximal occlusion. Experimental studies suggest that neutrophils could play an important role in the thrombus development via the organization of a network (NET) within the thrombus. Targeting this network of NET could, in addition to the fibrinolysis, increase the rate of recanalisation and thus improve the neurological prognostic after a cerebral infarct. The aim of the research is to Study of the biochemical and histological composition of the stemming thrombi of cerebral thrombectomies with in vitro analysis of the sensibility in the thrombolysis induced by rt-PA +/- Desoxyribonuclease I (DNase I).
Traumatic brain injury (TBI) affects 1.5 million patients per year in the United States, resulting in more than 50,000 deaths and more than 230,000 hospitalizations annually. Approximately 90,000 of these patients will suffer permanent impairment and more than half will experience short-term disability. Secondary injury processes play a critical role in the development of ischemia after trauma to the central nervous system and occur hours-to-days after the primary insult. Ischemia can lead to cerebral infarction or stroke. Ischemia has been described as the single most important secondary insult and has been identified histologically in approximately 90% of patients who die following closed head injury. Several factors resulting in post-traumatic cerebral ischemia have been identified: increased intracranial pressure (ICP), systemic arterial hypotension, and cerebral vasospasm. Cerebral vasospasm has been described as a sustained arterial narrowing. Clinically, the onset of new or worsening neurological symptoms is the most reliable indicator of cerebral vasospasm following a ruptured cerebral aneurysm. However, cerebral vasospasm is often unrecognized in patients suffering from moderate to severe TBI. These patients frequently have altered mental status due to the primary brain injury. In addition, they require narcotics for their pain and paralytics and/or sedatives while on a mechanical ventilator for airway protection. Thus, relying on the neurological exam to observe deteriorating neurological signs consistent with post-traumatic vasospasm (PTV) is reliable. While the etiology and outcome of patients with vasospasm secondary to ruptured aneurysm is well documented, the clinical significance of PTV after TBI is unknown. A better understanding of the role of cerebral autoregulation in the development of cerebral vasospasm could provide the answer. This proposal is for a pilot observational study describing the association of the impairment of cerebral autoregulation as measured by near infrared spectroscopy (NIRS) with the development of clinically significant vasospasm in patients with moderate to severe TBI. The information will serve as preliminary data for further study.