Fever in acute stroke worsens prognosis

Azzimondi, G; Bassein, Leona; Nonino, Francesco; Fiorani, L; Vignatelli, Luca; Re, Giuseppe; D’Alessandro, R

doi:10.1097/00008506-199604000-00012

Cited by 65 publications

(88 citation statements)

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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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“…In animal models of cerebral ischaemia [4][5][6][7] and trauma [8,9] a rise in body core temperature in excess of 38°C is associated with increased neuronal damage. In stroke patients a rise in body temperature independently predicts poor outcome [10] and increased mortality [11][12][13][14] but when the human brain is injured by trauma, the evidence for a relationship between raised body temperature and worse neurological outcome is not as clear [15,16]. However, it is assumed that the deleterious metabolic, inflammatory and biochemical mechanisms associated with raised body temperature in animal models of stroke and trauma may operate similarly in the brain injured human [17].…”

mentioning

confidence: 99%

Differences between brain and rectal temperatures during routine critical care of patients with severe traumatic brain injury*

Childs

Vail

Protheroe³

et al. 2005

Anaesthesia

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SummaryTheoretical models suggest that small differences only exist between brain and body temperature in health. Once the brain is injured, brain temperature is generally regarded to rise above body temperature. However, since reports of the magnitude of the temperature gradient between brain and body vary, it is still not clear whether conventional body temperature monitoring accurately predicts brain temperature at all times. In this prospective, descriptive study, 20 adults with severe primary brain trauma were studied during their stay in the neurointensive care unit. Brain temperature ranged from 33.4 to 39.9°C. Comparisons between paired brain and rectal temperature measurements revealed no evidence of a systematic difference [mean difference )0.04°C (range )0.13 to 0.05°C, 95% CI), p = 0.39]. Contrary to popular belief, brain temperature did not exceed systemic temperature in this relatively homogeneous patient series. The mean values masked inconsistent and unpredictable individual brain-rectal temperature differences (range 1.8 to )2.9°C) and reversal of the brain-body temperature gradient occurred in some patients. Brain temperature could not be predicted from body temperature at all times. Brain temperature is seldom measured during routine neurointensive care but there is a long-held assumption that since the temperatures of healthy internal organs differ only slightly [1], temperature measurements of the rectum, bladder, pulmonary artery and tympanum can be used as surrogates for brain temperature. Using these conventional body sites, temperatures greater than 38.5°C are commonly encountered during neurocritical care [2,3] and cause concern. In animal models of cerebral ischaemia [4][5][6][7] and trauma [8,9] a rise in body core temperature in excess of 38°C is associated with increased neuronal damage. In stroke patients a rise in body temperature independently predicts poor outcome [10] and increased mortality [11][12][13][14] but when the human brain is injured by trauma, the evidence for a relationship between raised body temperature and worse neurological outcome is not as clear [15,16]. However, it is assumed that the deleterious metabolic, inflammatory and biochemical mechanisms associated with raised body temperature in animal models of stroke and trauma may operate similarly in the brain injured human [17]. This assumption underpins current opinion that even a small increase in body temperature (1-2°C) above normal (37°C) accelerates ischaemic damage and increases the size of the primary brain lesion [9,18] and should therefore be prevented [13].Little is known about human brain temperature, but theoretical models suggest that during normothermia the temperature of the brain is close to that of internal carotid arterial blood before the blood enters the circle of Willis [19]. In man, direct measurement of brain temperature Anaesthesia, 2005, 60, pages 759-765

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“…A temperature greater than >37.9ᵒC within the first week after the stroke was an independent predictor of a poor outcome (101,102). Lowering an acutely elevated temperature greatly influences outcome and prognosis (103).…”

Section: Temperaturementioning

confidence: 99%