| 1. |
- Andersson, Emma, et al.
(författare)
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A prospective outcome study observing patients with severe traumatic brain injury over 10-15 years
- 2017
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 61:5, s. 502-512
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Tidskriftsartikel (refereegranskat)abstract
- Background: Severe traumatic brain injury (sTBI) can be divided into primary and secondary injuries. Intensive care protocols focus on preventing secondary injuries. This prospective cohort study was initiated to investigate outcome, including mortality, in patients treated according to the Lund Concept after a sTBI covering 10-15 years post-trauma. Methods: Patients were included during 2000-2004 when admitted to the neurointensive care unit, Sahlgrenska University Hospital. Inclusion criteria were: Glasgow coma scale score of 8, need for artificial ventilation and intracranial monitoring. Glasgow Outcome Scale (GOS) was used to evaluate outcome both at 1-year and 10-15 years post-trauma. Results: Ninety-five patients, (27 female and 68 male), were initially included. Both improvement and deterioration were noted between 1- and 10-15 years post-injury. Mortality rate (34/95) was higher in the studied population vs. a matched Swedish population, (Standard mortality rate (SMR) 9.5; P < 0.0001). When dividing the cohort into Good (GOS 4-5) and Poor (GOS 2-3) outcome at 1-year, only patients with Poor outcome had a higher mortality rate than the matched population (SMR 7.3; P < 0.0001). Further, good outcome (high GOS) at 1-year was associated with high GOS 10-15 years post-trauma (P < 0.0001). Finally, a majority of patients demonstrated symptoms of mental fatigue. Conclusion: This indicates that patients with severe traumatic brain injury with Good outcome at 1-year have similar survival probability as a matched Swedish population and that high Glasgow outcome scale at 1-year is related to good long-term outcome. Our results further emphasise the advantage of the Lund concept.
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| 2. |
- Csajbok, Ludvig Z, 1964, et al.
(författare)
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Apolipoprotein E polymorphism in aneurysmal subarachnoid haemorrhage in West Sweden.
- 2016
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Ingår i: Acta neurologica Scandinavica. - : Hindawi Limited. - 1600-0404 .- 0001-6314. ; 133:6, s. 466-474
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Tidskriftsartikel (refereegranskat)abstract
- Aneurysmal subarachnoid haemorrhage (aSAH) is associated with high morbidity and mortality despite novel treatments. Genetic variability may explain outcome differences. Apolipoprotein E (ApoE) is a glycoprotein with a major role in brain lipoprotein metabolism. It has three isoforms encoded by distinct alleles: APOEε2, APOEε3 and APOEε4. The APOEε4 allele is associated with Alzheimer's disease and worse outcome after traumatic brain injury and ischaemic stroke. This prospective blinded study explored the influence of the APOEε4 polymorphism on the risk of aSAH, risk of cerebral vasospasm (CVS) and 1-year neurological outcome.
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| 3. |
- Csajbok, Ludvig Z, 1964
(författare)
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Biochemical and genetic markers after subarachnoid haemorrhage
- 2015
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- ABSTRACT Background: Subarachnoid haemorrhage is a devastating disease with high morbidity and mortality despite novel treatment options are available. There are no established methods to measure the brain damage occurring due to the bleed and its complications and to predict early neurological outcome of the disease. Genetic predisposition is suggested as one of the determinants of outcome. Aim: The aim of this thesis was to investigate nine biochemical neuromarkers’ course and development in the early phase of aneurysmal subarachnoid haemorrhage (aSAH) with special emphasis on C-reactive protein (CRP) and to test if they could be used as markers of disease progression and possibly long-term outcome. As a tool, we aimed to test a novel multiple biochip array for simultaneous monitoring these markers. Finally, we intended to elucidate the effect of two chromosomes with different genetical polymorphisms on the incidence and development of the disease. (Apolipoprotein E and region 9p21) Patients and methods: We have consecutively included patients admitted to the Sahlgrenska University Hospital for SAH, where the causative reason was a ruptured intracranial aneurysm. We have recorded the patients’ admission status with neurological scales and radiological scores for the severity of the haemorrhage. We collected blood sample for determining genetics and continued to collect serum-samples for biochemical marker detection on day0-4, 6, 8, and finally once on days 11-14. We noted the complication cerebral vasospasm (CVS). A long-term follow-up was performed after one year with detailed neurological examinations. For the genetic studies matching controls were recruited among healthy individuals. Results: In 98 endovascularly treated patients, we described the pattern of CRP increase after aSAH. It peaked on day3 with a mean value of 53 mg/l and decreased successively without normalising. This pattern was not dependent of infectious status. We noted a difference in increase between the patients with favourable and unfavourable disease development (i.e. CVS) and long-term outcome, focal neurology and need of assistance with daily activities (ADL) after one year. In a multivariate regression model with initial neurology, radiological severity, CRP was the only parameter showing significant OR. (OR: 1.25/10 units). We could present a predictive curve for poor outcome in relation to CRP values. Furthermore, we tested a 9 potential neuromarker-containing panel in a test series of 41 patients. Six of these markers, TNFR1, IL-6, hs-CRP, DDMR, NGAL and FABP showed significant correlation to CVS development and different outcome results. Four of the markers (TNFR1, hs-CRP, NGAL & FABP) had moderate or good predictive qualities. In a genetic study, ApoE polymorphism on the 19th chromosome, did not present any effect either on the incidence of aneurysm rupture or CVS development and outcome parameters after aSAH in 154 patients and 221 controls. However we have found a single nucleotide polymorphism (SNP) rs10757278 on the 9th chromosome p21 region, which even after controlling for hypertension and smoking showed a significant negative effect on aneurysm rupture in 183 patient and 366 controls Conclusion: CRP proved to be a useful marker for following the course of aSAH and may be applicable for predicting complication or outcome. The tested biochip-neuropanel could be a valuable addition to neuro-monitoring during the initial phase of the aSAH. Finally, not APOE polymorphism, but a genetic variant on 9p21 chromosome region affected negatively the risk of aneurysm rupture in West Sweden.
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| 6. |
- Ladenvall, Claes, 1974, et al.
(författare)
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Association between factor XIII single nucleotide polymorphisms and aneurysmal subarachnoid hemorrhage Clinical article
- 2009
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Ingår i: JOURNAL OF NEUROSURGERY. - 0022-3085. ; 110:3, s. 475-481
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Tidskriftsartikel (refereegranskat)abstract
- Object Family studies have suggested a role of genetic factors in susceptibility to aneurysmal subarachnoid hemorrhage (aSAH), but the underlying genetic risk factors remain poorly defined. There is an activation of the fibrinolytic system in aSAH, and fibrinolytic markers may be useful in predicting outcome. The authors investigate associations between putative functional variants in genes of importance for fibrinolysis and aSAH and/or outcome following aSAH. Methods One hundred eighty-three patients presenting with aSAH at a neurointensive care unit were consecutively recruited. Two healthy controls per case, matched for age, sex, and geographic region, were randomly recruited. Outcome was assessed after 1 year according to the extended Glasgow Outcome Scale. Single nucleotide polymorphisms (SNPs) in the tissue-type plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), and factor XIII (FXIII) genes were investigated. Results Participants carrying the FXIII 34Leu allele showed an increased risk of aSAH. When adjusting for smoking and hypertension, 2 haplotypes, differing on either the FXIII Val34Leu or the Pro564Leu position, showed an association to aSAH. No significant association was observed for the tPA -7351 C > T, PAI-1 -675 4G > 5G, or TAFI Ala147Thr SNPs. No specific SNP or haplotype was associated with outcome after aSAH, whereas a weak association was observed for a tPA/PAI-1 genotype combination. Conclusions Polymorphisms in the FXIII gene showed association to aSAH. The finding of an increased risk of bleeding in FXIII 34Leu carriers is biologically plausible.
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| 7. |
- Nylén, Karin, 1961, et al.
(författare)
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CSF -neurofilament correlates with outcome after aneurysmal subarachnoid hemorrhage.
- 2006
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Ingår i: Neurosci Lett. - : Elsevier BV. - 0304-3940. ; 404:1-2, s. 132-6
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Tidskriftsartikel (refereegranskat)abstract
- Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating event. Following the bleeding, a number of pathophysiological changes and clinical factors determine outcome. Not surprisingly, attempts to predict outcome based on a single factor have failed. The neurological status graded at admission to hospital and distributions of the blood on CT are the strongest predictors. There is evidence that cerebrospinal fluid (CSF) proteins may serve as markers of the extent of brain damage. The present study is focused on the light unit of neurofilament protein (NFL), previously not evaluated in aSAH. Lumbar puncture (LP), neurological grading according to World Federation of Neurological Surgeons (WFNS) and neurological examination according to the National Institute of Health Stroke Scale (NIHSS) were performed in 48 consecutive patients with aSAH 10-14 days after the hemorrhage. CSF-NFL concentrations were analyzed using an ELISA. Outcome was assessed after 1 year and categorised according to the extended Glasgow Outcome Scale (GOSE). A significant correlation between CSF-NFL and GOSE was detected at follow up after 1 year. CSF-NFL also correlated with WFNS and NIHSS on the day of the lumbar puncture. CSF-NFL is a biochemical marker of brain damage correlating to neurological status and long-term outcome after aneurysmal subarachnoid hemorrhage.
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| 8. |
- Nylen, K, et al.
(författare)
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Increased serum-GFAP in patients with severe traumatic brain injury is related to outcome
- 2006
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Ingår i: J Neurol Sci. - : Elsevier BV. - 0022-510X. ; 240:1-2, s. 85-91
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Several studies have established the relevance of S-100 in blood as a marker of brain damage after traumatic brain injury. However, a more specific marker is required and glial fibrillary acidic protein (GFAP) is considered to be a good candidate. METHODS: In order to assess the increase of GFAP in serum (s-GFAP) after a severe traumatic brain injury (TBI) we collected daily serum samples from 59 patients with severe TBI starting on the day of the trauma. S-GFAP was measured using a sandwich ELISA. The Glasgow outcome scale (GOS) assessed outcome after 1 year. RESULTS: All but one patient had maximal s-GFAP values above the laboratory reference value (median increased 10-fold). The highest detected levels were seen during the first days after TBI and then decreased gradually. Patients with unfavourable outcome had significantly (p<0.001) higher maximal s-GFAP values in the acute phase compared with patients with favourable outcome. All patients (n=5) with s-GFAP>15.04 microg /L died (reference level<0.15 microg/L). We found no significant difference in the maximal s-GFAP levels of patients with isolated brain injury in comparison with patients with multiple traumas. CONCLUSION: Serum-GFAP is increased during the first days after a severe traumatic brain injury and related to clinical outcome.
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| 9. |
- Nylén, Karin, 1961, et al.
(författare)
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Serum glial fibrillary acidic protein is related to focal brain injury and outcome after aneurysmal subarachnoid hemorrhage.
- 2007
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Ingår i: Stroke. - 1524-4628. ; 38:5, s. 1489-94
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: Aneurysmal subarachnoid hemorrhage (aSAH) stands out from other subtypes of stroke because of the high early mortality and the risk of complications. Serum glial fibrillary acidic protein (s-GFAP) concentrations are increased after stroke. The aim of this study was to investigate whether s-GFAP could be used as a marker of brain damage and outcome after aSAH. METHODS: Serum samples were obtained on a regular basis from 116 adults during a 2-week period after aSAH and analyzed using an enzyme-linked immunosorbent assay. The World Federation of Neurological Surgeons scale was used for neurological evaluation. Outcome was assessed after 1 year and categorized according to the Extended Glasgow Outcome Scale. RESULTS: Increased s-GFAP levels were seen in 81 of the 116 patients. Maximum s-GFAP correlated with World Federation of Neurological Surgeons scale on arrival and on days 10 to 15 (r=0.37, P<0.001 and r=0.47, P<0.001, respectively). Furthermore, maximum s-GFAP levels were increased in the patient group with radiological signs of focal lesions acute or at 1 year, compared with the group without focal lesions (P<0.001 in both comparisons). Patients with secondary events (re-bleeding or ischemia) reached maximum levels later in the series and both maximum and final s-GFAP levels increased compared with the levels in patients without secondary events (P<0.001 in all 3 comparisons). Finally, maximum s-GFAP correlated with outcome (r=-0.48, P<0.001) and s-GFAP was an independent predictor of dichotomized outcome. CONCLUSIONS: s-GFAP provides information about brain injury severity and outcome after aSAH, which can be useful as a complement to clinical data.
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| 10. |
- Nylén, Karin, 1961, et al.
(författare)
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Serum levels of S100B, S100A1B and S100BB are all related to outcome after severe traumatic brain injury.
- 2008
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Ingår i: Acta neurochirurgica. - : Springer Science and Business Media LLC. - 0942-0940 .- 0001-6268. ; 150:3
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: S100B is an established marker of brain damage. Used in the context as a biochemical marker, S100B denotes a measurement of all S100 proteins, including at least one S100B monomer, i.e. the sum of the two dimers S100A1B and S100BB. Almost all published studies are based on this "sum concentration". However, the brain specificity of S100B has been questioned and increased serum levels have also been reported after trauma without head injury. Since the S100B monomer dominates in the brain, we hypothesised that the S100BB dimer should be better related to outcome after severe traumatic brain injury than S100A1B or the "sum concentration". METHODS: Daily serum samples were collected from 59 patients with severe traumatic brain injury. Three different ELISA methods were used for measurements of S100B, S100A1B and S100BB respectively. Outcome was assessed after one year and categorised according to the Glasgow Outcome Scale. RESULTS: Serum levels of S100B, S100A1B and S100BB followed the same temporal course, with early maximum and rapidly decreasing values over the first days after the trauma. Maximum serum concentrations of each of the parameters were increased in the patient group with an unfavourable outcome compared with those with a favourable outcome (p = 0.01, 0.006 and 0.004, respectively). CONCLUSION: Both S100A1B and S100BB were related to outcome after severe traumatic brain injury. Even though this study is small, it seems unlikely that separate analyses of the dimers are of any advantage compared with measuring S100B alone.
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