Body temperature in acute stroke: relation to stroke severity, infarct size, mortality, and outcome

Reith, Jakob; Jørgensen, Henrik; Pedersen, Palle; Nakamaya, H.; Jeppesen, Lise Leth; Olsen, Tom Skyhøj; Raaschou, Hans Otto

doi:10.1016/s0140-6736(96)90008-2

Cited by 829 publications

(508 citation statements)

References 23 publications

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“…Firstly, induction of an aseptic systemic inflammatory response after stroke is associated with increased morbidity and mortality (Enlimomab Acute Stroke Trial Investigators, 2001). Secondly, fever, a cardinal feature of the immune response in infection, is associated with worse neurologic outcome after stroke (Azzimondi et al, 1995;Reith et al, 1996). Thirdly, the cytokines secreted by leukocytes during the effector phase of an immune response might be toxic to neurons and glia (Barone et al, 1997;Hanisch et al, 1996;Touzani et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Sensitization to Brain Antigens after Stroke is Augmented by Lipopolysaccharide

Becker

Kindrick

Lester

et al. 2005

J Cereb Blood Flow Metab

113

158

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After stroke, the blood-brain barrier is transiently disrupted, allowing leukocytes to enter the brain and brain antigens to enter the peripheral circulation. This encounter of normally sequestered brain antigens by the systemic immune system could therefore present an opportunity for an autoimmune response to brain to occur after stroke. In this study, we assessed the immune response to myelin basic protein (MBP) in animals subjected to middle cerebral artery occlusion (MCAO). Some animals received an intraperitoneal injection of lipopolysaccharide (LPS; 1 mg/kg) at reperfusion to stimulate a systemic inflammatory response. At 1 month after MCAO, animals exposed to LPS were more likely to be sensitized to MBP (66.7% versus 22.2%; P ¼ 0.007) and had more profound and persistent neurologic deficits than non-LPS-treated animals. Exposure to LPS was associated with increased expression of the costimulatory molecule B7.1 early after stroke onset (P ¼ 0.009) and increased brain atrophy 1 month after MCAO (P ¼ 0.03). These data suggest that animals subjected to a systemic inflammatory insult at the time of stroke are predisposed to develop an autoimmune response to brain, and that this response is associated with worse outcome. These data may partially explain why patients who become infected after stroke experience increased morbidity.

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Section: Discussionmentioning

confidence: 99%

Sensitization to Brain Antigens after Stroke is Augmented by Lipopolysaccharide

Becker

Kindrick

Lester

et al. 2005

J Cereb Blood Flow Metab

113

158

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“…Clinical and experimental observational studies show the association between hyperthermia and a worse stroke prognosis. Possible reasons for this include increased metabolic demand in a context of brain ischemia, excitotoxicity and increased local inflammatory response [82][83][84][85] . Recommendations 1.…”

Section: Stroke In the Emergency Departmentmentioning

confidence: 99%

Guidelines for acute ischemic stroke treatment: part I

Oliveira‐Filho

Martins

Pontes-Neto

et al. 2012

Arq. Neuro-Psiquiatr.

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These guidelines are a result of several meetings from the Brazilian Stroke Society (Sociedade Brasileira de Doenças Cerebrovasculares -SBDCV, website www.sbdcv.org.br), which represents the Scientific Department in cerebrovascular diseases of the Brazilian Academy of Neurology, responsible for technical opinions and educational projects related to cerebrovascular diseases. Members from SBDCV participated in web-based discussion forum with pre-defined themes, followed by a formal onsite meeting in which controversies and final position statements were discussed. Finally, a writing group was created to revise and translate the final document, which was approved by all members of the SBDCV. The final text aims to guide specialists and non-specialists in stroke care in managing patients with acute ischemic stroke. The hemorrhagic stroke guideline has been previously published by the same group 1 . In the final recommendations, Oxford classification for evidence level and recommendation grade was used: EVIDENCE LEVELS1. Randomized controlled clinical trial (RCT) or systematic review (SR) of RCT with clinical endpoints. 2. RCT or SR of lower quality: with substitute, validated endpoints; with subgroup analysis or with a posteriori hypotheses; with clinical endpoints, but with methodological flaws.3. RCT with substitute, non-validated endpoints case-control studies. 4. Study with clinical endpoint, but with a higher potential bias (as in experiment without comparison group and other observational studies). 5. Representative forum or expert opinion without abovementioned evidence. RECOMMENDATION GRADESA Systematic review (homogeneous) of RCT; or single RCT with narrow confidence interval; or therapeutic results of "all or nothing" type. B Systematic review (homogeneous) of cohort studies; or cohort study and RCT of lower quality; or outcomes research or ecological study; or systematic review (homogeneous) of case-control studies; or case-control study. C Case reports (including cohort or case-control study of lower quality). D Expert opinion without critical evaluation, based on physiological or animal studies.In this first part of the guidelines, specific topics included were: epidemiology, stroke as a medical emergency, education, pre-hospital management, emergency management, neuroimaging and laboratory evaluation. A translated version of these guidelines in Portuguese is available in the Society's webpage (www.sbdcv.org.br).

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“…2 Though euthermia and euglycemia have not been shown to improve outcomes in acute stroke, studies have shown that hyperthermia and hyperglycemia are associated with worsened outcomes for patients with acute strokes. [3][4][5] autoregulate is diminished or absent in regions of and surrounding an acute ischemic stroke; as the area becomes ischemic, autoregulation opens the local vasculature maximally in an effort to drawn in as much blood as possible. Maximally dilated arterioles are perfused in direct correlation with systemic blood pressure, thus any drop in the systemic blood pressure leads to direct decreases in blood flow specifically in the area of ischemia; if there is a penumbra of marginally perfused tissue, such systemic blood pressure drops risk extending the area of fatal ischemia (increasing the size of the ischemic stroke).…”

Section: Inpatient Carementioning

confidence: 99%

Management of ischemic stroke: Part 2. The inpatient stay

Lu-Emerson

Likosky

Amin

et al. 2010

Journal of Hospital Medicine

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BACKGROUND:Acute ischemic stroke is commonly encountered by the hospitalist. There have been dramatic changes in our ability to care for these patients both acutely and in secondary prevention. The Joint Commission on Accreditation of Healthcare Organizations (JCAHO) primary stroke center certification has become progressively more important to institutions nationally and emphasizes many elements of the inpatient stay and discharge process.PURPOSE:After admission, the focus changes to avoidance of complications and the appropriate initiation of allied therapies and secondary prevention.DATA SOURCES:Primary trials, current guidelines.CONCLUSIONS:The hospitalist is well‐positioned to play a major role in the treatment of stroke patients as well as the systems work that aids in the management of this population. Journal of Hospital Medicine 2010;5:88–93. © 2010 Society of Hospital Medicine.

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Body temperature in acute stroke: relation to stroke severity, infarct size, mortality, and outcome

Cited by 829 publications

References 23 publications

Sensitization to Brain Antigens after Stroke is Augmented by Lipopolysaccharide

Sensitization to Brain Antigens after Stroke is Augmented by Lipopolysaccharide

Guidelines for acute ischemic stroke treatment: part I

Management of ischemic stroke: Part 2. The inpatient stay

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