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- Cronberg, Tobias, et al.
(författare)
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Long-term neurological outcome after cardiac arrest and therapeutic hypothermia.
- 2009
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Ingår i: Resuscitation. - : Elsevier BV. - 1873-1570 .- 0300-9572. ; 80, s. 1119-1123
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Tidskriftsartikel (refereegranskat)abstract
- AIM OF THE STUDY: To analyse the neurological status of survivors after cardiac arrest (CA) treated with hypothermia. METHODS: We prospectively included all patients with CA treated with hypothermia at intensive care units (ICU) in two university hospitals and one regional hospital. All adult survivors at 6 months after CA, n=48, were invited for neurological follow-up and 43 accepted. History, clinical status, ability testing and questionnaires were administered to screen for difficulties, including Assessment of Motor and Process Skills, Neurobehavioral Cognitive Status Examination, Frontal Lobe Assessment Battery, EQ-VAS quality of life scale, Skåne Sleep Index, Hospital Anxiety and Depression Rating Scale, Self-reported Montgomery and Astrand Depression Rating Scale, Global Deterioration Scale, Rivermead Behavioural Memory Test, and the Cerebral Performance Categories (CPC). RESULTS: No patient was found to be in a chronic vegetative state and all patients were living at home, one with extensive help. Thirty-six patients were in CPC1 at follow-up, and some degree of neurological sequelae was found in 40 patients, but was mild in all but 3. Three patients had no subjective complaints, nor could any deficits be detected. Initial defects improved over-time. Short-term memory loss, executive frontal lobe dysfunction along with mild depression and sleep rhythm disturbances were the most common findings. CONCLUSIONS: Mild cognitive impairment is common following hypothermia-treated cardiac arrest but has little effect on activities of daily living or quality of life.
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| 5. |
- Markus, Tina, et al.
(författare)
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Tumor necrosis factor receptor-1 is essential for LPS-induced sensitization and tolerance to oxygen-glucose deprivation in murine neonatal organotypic hippocampal slices.
- 2009
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Ingår i: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 1559-7016. ; 29, s. 73-86
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Tidskriftsartikel (refereegranskat)abstract
- Inflammation and ischemia have a synergistic damaging effect in the immature brain. The role of tumor necrosis factor (TNF) receptors 1 and 2 in lipopolysaccharide (LPS)-induced sensitization and tolerance to oxygen-glucose deprivation (OGD) was evaluated in neonatal murine hippocampal organotypic slices. Hippocampal slices from balb/c, C57BL/6 TNFR1(-/-), TNFR2(-/-), and wild-type (WT) mice obtained at P6 were grown in vitro for 9 days. Preexposure to LPS immediately before OGD increased propidium iodide-determined cell death in regions CA1, CA3, and dentate gyrus from 4 up to 48 h after OGD (P<0.001). Extending the time interval between LPS exposure and OGD to 72 h resulted in tolerance, that is reduced neuronal cell death after OGD (P<0.05). Slices from TNFR1(-/-) mice showed neither LPS-induced sensitization nor LPS-induced tolerance to OGD, whereas both effects were present in slices from TNFR2(-/-) and WT mice. Cytokine secretion (TNFalpha and interleukin-6) during LPS exposure was decreased in TNFR1(-/-) slices and increased in TNFR2(-/-) as compared with WT slices. We conclude that LPS induces sensitization or tolerance to OGD depending on the time interval between exposure to LPS and OGD in murine hippocampal slice cultures. Both paradigms are dependent on signaling through TNFR1.Journal of Cerebral Blood Flow & Metabolism advance online publication, 27 August 2008; doi:10.1038/jcbfm.2008.90.
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- Rundgren, Malin, et al.
(författare)
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Neuron specific enolase and S-100B as predictors of outcome after cardiac arrest and induced hypothermia.
- 2009
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Ingår i: Resuscitation. - : Elsevier BV. - 1873-1570 .- 0300-9572. ; 80, s. 784-789
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To assess the prognostic value of repetitive serum samples of neuron specific enolase (NSE) and S-100B in cardiac arrest patients treated with hypothermia. METHODS: In a three-centre study, comatose patients after cardiac arrest were treated with hypothermia at 33 degrees C for 24h, regardless of cause or the initial rhythm. Serum samples were collected at 2, 24, 48 and 72h after the arrest and analysed for NSE and S-100B in a non-blinded way. The cerebral performance categories scale (CPC) was used as the outcome measure; a best CPC of 1-2 during 6 months was regarded as a good outcome, a best CPC of 3-5 a poor outcome. RESULTS: One centre was omitted in the NSE analysis due to missing 24 and 48h samples. Two partially overlapping groups were studied, the NSE group (n=102) and the S-100B group (n=107). NSE at 48h >28mug/l (specificity 100%, sensitivity 67%) and S-100B >0.51mug/l at 24h (specificity 96%, sensitivity 62%) correlated with a poor outcome, and so did a rise in NSE of >2mug/l between 24 and 48h (odds ratio 9.8, CI 3.5-27.7). A majority of missing samples (n=123) were from the 2h sampling time (n=56) due to referral from other hospitals or inter-hospital transfer. CONCLUSION: NSE was a better marker than S-100B for predicting outcome after cardiac arrest and induced hypothermia. NSE above 28mug/l at 48h and a rise in NSE of more than 2mug/l between 24 and 48h were markers for a poor outcome.
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| 7. |
- Rytter, Anna, et al.
(författare)
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The temperature dependence and involvement of mitochondria permeability transition and caspase activation in damage to organotypic hippocampal slices following in vitro ischemia.
- 2005
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Ingår i: Journal of Neurochemistry. - : Wiley. - 1471-4159 .- 0022-3042. ; 95:4, s. 1108-1117
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Tidskriftsartikel (refereegranskat)abstract
- The aggravating effect of hyperglycemia on ischemic brain injury can be mimicked in a model of in vitro ischemia (IVI) using murine hippocampal slice cultures. Using this model, we found that the damage in the CA1 region following IVI in the absence or presence of 40 mM glucose (hyperglycemia) is highly temperature dependent. Decreasing the temperature from 35 to 31 degrees C during IVI prevented cell death, whereas increasing the temperature by 2 degrees C markedly aggravated damage. As blockade of the mitochondrial permeability transition (MPT) is equally effective as hypothermia in preventing ischemic cell death in vivo, we investigated whether inhibition of MPT or of caspases was protective following IVI. In the absence of glucose, the MPT blockers cyclosporin A and MeIle(4)-CsA but not the immunosuppressive compound FK506 diminished cell death. In contrast, following hyperglycemic IVI, MPT blockade was ineffective. Also, the pan-caspase inhibitor Boc-Asp(OMe)fluoromethyl ketone did not decrease cell death in the CA1 region following IVI or hyperglycemic IVI. We conclude that cell death in the CA1 region of organotypic murine hippocampal slices following IVI is highly temperature dependent and involves MPT. In contrast, cell death following hyperglycemic IVI, although completely prevented by hypothermia, is not mediated by mechanisms that involve MPT or caspase activation
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