The Nordic Cooling Stroke Study—NOCSS. A Multicenter Study of Induced Mild Hypothermia in Acute Stroke Patients. Ongoing Clinical Trial
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Neonatal hypoxic-ischaemic encephalopathy (HIE) is major cause of neonatal mortality and morbidity. Therapeutic hypothermia is standard clinical care for moderate hypoxic-ischaemic (HI) brain injury, however it reduces the risk of death and disability only by 11% and 40% of the treated infants still develop disabilities. Thus it is necessary to develop supplementary therapies to complement therapeutic hypothermia in the treatment of neonatal HIE. The modified Rice-Vannucci model of HI in the neonatal mouse is well developed and widely applied with different periods of hypothermia used as neuroprotective strategy in combination with other agents. However, different studies use different periods, time of initiation and duration of hypothermia following HI, with subsequent varying degrees of neuroprotection. So far most rodent data is obtained using exposure to 5-6h of therapeutic hypothermia. Our aim was to compare the effect of exposure to three different short periods of hypothermia (1h, 1.5h and 2h) following HI insult in the postnatal day 7 C57/Bl6 mouse, and to determine the shortest period providing neuroprotection. Our data suggests that 1h and 1.5h of hypothermia delayed by 20min following a 60min exposure to 8%O2 do not prove neuroprotective. However, 2h of hypothermia significantly reduced tissue loss, TUNEL+ cell death and microglia and astroglia activation. We also observed improved functional outcome 7 days after HI. We suggest that the minimal period of cooling necessary to provide moderate short term neuroprotection and appropriate for the development and testing of combined treatment is 2h.
Neonatal Encephalopathy
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Dizocilpine
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Hypothermia therapy is an old and important method of neuroprotection. Until now, many neurological diseases such as stroke, traumatic brain injury, intracranial pressure elevation, subarachnoid hemorrhage, spinal cord injury, hepatic encephalopathy, and neonatal peripartum encephalopathy have proven to be suppressed by therapeutic hypothermia. Beneficial effects of therapeutic hypothermia have also been discovered, and progress has been made towards improving the benefits of therapeutic hypothermia further through combinations with other neuroprotective treatments and by probing the mechanism of hypothermia neuroprotection. In this review, we compare different hypothermia induction methods and provide a summarized account of the synergistic effect of hypothermia therapy with other neuroprotective treatments along with an overview of hypothermia neuroprotection mechanisms and cold/hypothermia-induced proteins.
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Therapeutic window
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Introduction: Both the American Heart and American Stroke Associations recommend pre-notification of potential stroke patients to receiving facilities. Although Emergency Medical Services (EMS) may identify stroke symptoms in the field, initiation of the stroke code process is often postponed until after the patient arrives in the Emergency Department (ED). This could lead to unnecessary delays in assessment and intervention during an acute stroke. Hypothesis: We hypothesized that initiating a stroke code based on advanced notification of stroke symptoms via EMS and a Stroke Code Pit Stop (SCPS) would lead to decreased time of assessment, diagnosticssitics and IV tPA initiation. Methods: A pre- and post-intervention study of 733 patients presenting to 2 EDs in a 5 campus hospital system. Both EDs initiated a SCPS, with pre-notification of stroke symptoms via EMS and stroke code activation prior to patient arrival. Data were reviewed from January 2013-April 2014, comparing code stroke metrics pre- and post...
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Stroke
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Neuronal cells are extremely vulnerable and have a limited capacity for self-repair in response to injury. For those reasons, there is obvious interest in limiting neuronal damage. Mechanisms and strategies used in order to protect against neuronal injury, apoptosis, dysfunction, and degeneration in the central nervous system are recognized as neuroprotection. Neuroprotection could be achieved through several classes of natural and synthetic neuroprotective agents. However, considering the side effects of synthetic neuroprotective agents, the search for natural neuroprotective agents has received great attention. Recently, an increasing number of studies have identified neuroprotective properties of chitosan and its derivatives; however, there are some significant challenges that must be overcome for the success of this approach. Hence, the objective of this review is to discuss neuroprotective properties of chitosan and its derivatives.
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