An early rise in body temperature is related to unfavorable outcome after stroke: data from the PAIS study

Hertog, Heleen M. den; Worp, H. Bart van der; Gemert, H. Maarten A. van; Algra, Ale; Kappelle, L. Jaap; Gijn, J. van; Koudstaal, Peter J.; Dippel, Diederik W.J.

doi:10.1007/s00415-010-5756-4

Cited by 40 publications

(48 citation statements)

References 23 publications

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“…Other studies have indicated that it is not admissional body temperature that is associated with adverse outcomes of stroke, but the temperature peak occurring a few days after the stroke (18)(19)(20). The present study revealed that the more serious the stroke and the higher the NIHSS score, the more the body temperature increased.…”

Section: A B Csupporting

confidence: 49%

Reduction of the systemic inflammatory induced by acute cerebral infarction through ultra-early thrombolytic therapy

Ruowei

Yang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Acute ischemic stroke induces systemic inflammation, exhibited as changes in body temperature, white blood cell counts and C-reactive protein (CRP) levels. The aim of the present study was to observe the effects of intravenous thrombolytic therapy on inflammatory indices in order to investigate the hypothesis that post-stroke systemic inflammatory response occurs in response to the necrosis of brain tissues. In this study, 62 patients with acute cerebral infarction and indications for intravenous thrombolysis were divided into three groups on the basis of their treatment and response: Successful thrombolysis (n=36), failed thrombolysis (n=12) and control (n=14) groups. The body temperature, white blood cell counts and highsensitivity (hs)-CRP levels were recorded pre-treatment and on post-stroke days 1, 3, 5 and 7. Spearman's correlation analysis showed that the pre-treatment National Institutes of Health Stroke Scale (NIHSS) score positively correlated with body temperature, white blood cell count and hs-CRP levels. On day 3 of effective intravenous thrombolysis, the body temperature and white blood cell were decreased and on days 3 and 5, the serum levels of hs-CRP were reduced compared with those in the failed thrombolysis and control groups. The results indicate that the systemic inflammatory response following acute cerebral infarction was mainly caused by ischemic injury of local brain tissue; the more serious the stroke, the stronger the inflammatory response. Ultra-early thrombolytic therapy may inhibit the necrosis of brain tissue and thereby reduce the inflammatory response.

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Section: A B Csupporting

confidence: 49%

Reduction of the systemic inflammatory induced by acute cerebral infarction through ultra-early thrombolytic therapy

Ruowei

Yang

et al. 2015

Experimental and Therapeutic Medicine

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“…In both ischemic stroke and intracerebral hemorrhage, hyperthermia is a common complication that occurs in up to 30% to 40% of patients, and it is independently associated with poor outcome and increased mortality (32,70,71,77,125). Although intracerebral hemorrhage has been less studied than IS, and the underlying mechanisms may differ, the adverse outcome of hyperthermia (defined in this context as an average core temperature within the first 24 h of >37.5 • C) is similar with IS or intracerebral hemorrhage.…”

Section: Stroke and Heat Stressmentioning

confidence: 84%

“…Thus, recommendations highlight the importance of directly monitoring brain temperature (where possible and if needed) in patients with traumatic and ischemic injury, effectively managing fever and maintaining body temperature in a safe normothermic range (e.g., 36.7-37.0 • C [98.0-98.6 • F]) for at least the first several days after acute stroke or head injury (32,70,71,125).…”

Section: Stroke and Heat Stressmentioning

confidence: 99%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…Recent clinical studies demonstrate that low body temperature within 6 hours of symptom onset is associated with severe ischemic stroke [2,20] and severe stroke subjects have relatively low body temperatures at admission within 12 hours of symptom onset in human subjects [21]. In animal models of experimental stroke, it is well known that controlledhypothermia is a neuroprotectant and a potential treatment in cerebral ischemia via reduction of energy requirements in the brain and protect the brain from infarct formation [22,23].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Impairment in Cerebrovascular Endothelial Cells is Involved in the Correlation between Body Temperature and Stroke Severity

Hu¹,

Doll²,

Sun³

et al. 2016

Aging and disease

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Stroke is the second leading cause of death worldwide. The prognostic influence of body temperature on acute stroke in patients has been recently reported; however, hypothermia has confounded experimental results in animal stroke models. This work aimed to investigate how body temperature could prognose stroke severity as well as reveal a possible mitochondrial mechanism in the association of body temperature and stroke severity. Lipopolysaccharide (LPS) compromises mitochondrial oxidative phosphorylation in cerebrovascular endothelial cells (CVECs) and worsens murine experimental stroke. In this study, we report that LPS (0.1 mg/kg) exacerbates stroke infarction and neurological deficits, in the mean time LPS causes temporary hypothermia in the hyperacute stage during 6 hours post-stroke. Lower body temperature is associated with worse infarction and higher neurological deficit score in the LPS-stroke study. However, warming of the LPS-stroke mice compromises animal survival. Furthermore, a high dose of LPS (2 mg/kg) worsens neurological deficits, but causes persistent severe hypothermia that conceals the LPS exacerbation of stroke infarction. Mitochondrial respiratory chain complex I inhibitor, rotenone, replicates the data profile of the LPS-stroke study. Moreover, we have confirmed that rotenone compromises mitochondrial oxidative phosphorylation in CVECs. Lastly, the pooled data analyses of a large sample size (n=353) demonstrate that stroke mice have lower body temperature compared to sham mice within 6 hours post-surgery; the body temperature is significantly correlated with stroke outcomes; linear regression shows that lower body temperature is significantly associated with higher neurological scores and larger infarct volume. We conclude that post-stroke body temperature predicts stroke severity and mitochondrial impairment in CVECs plays a pivotal role in this hypothermic response. These novel findings suggest that body temperature is prognostic for stroke severity in experimental stroke animal models and may have translational significance for clinical stroke patients -targeting endothelial mitochondria may be a clinically useful approach for stroke therapy.

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An early rise in body temperature is related to unfavorable outcome after stroke: data from the PAIS study

Cited by 40 publications

References 23 publications

Reduction of the systemic inflammatory induced by acute cerebral infarction through ultra-early thrombolytic therapy

Reduction of the systemic inflammatory induced by acute cerebral infarction through ultra-early thrombolytic therapy

Cerebral Vascular Control and Metabolism in Heat Stress

Mitochondrial Impairment in Cerebrovascular Endothelial Cells is Involved in the Correlation between Body Temperature and Stroke Severity

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