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  • 1. Abdelhak, Ahmed
    et al.
    Barba, Lorenzo
    Romoli, Michele
    Benkert, Pascal
    Conversi, Francesco
    D'Anna, Lucio
    Masvekar, Ruturaj R
    Bielekova, Bibiana
    Prudencio, Mercedes
    Petrucelli, Leonard
    Meschia, James F
    Erben, Young
    Furlan, Roberto
    De Lorenzo, Rebecca
    Mandelli, Alessandra
    Sutter, Raoul
    Hert, Lisa
    Epple, Varenka
    Marastoni, Damiano
    Sellner, Johann
    Steinacker, Petra
    Aamodt, Anne Hege
    Heggelund, Lars
    Dyrhol-Riise, Anne Margarita
    Virhammar, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurology.
    Fällmar, David
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Rostami, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury.
    Kumlien, Eva
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurology.
    Blennow, Kaj
    Zetterberg, Henrik
    Tumani, Hayrettin
    Sacco, Simona
    Green, Ari J
    Otto, Markus
    Kuhle, Jens
    Ornello, Raffaele
    Foschi, Matteo
    Abu-Rumeileh, Samir
    Prognostic performance of blood neurofilament light chain protein in hospitalized COVID-19 patients without major central nervous system manifestations: an individual participant data meta-analysis.2023In: Journal of Neurology, ISSN 0340-5354, E-ISSN 1432-1459, Vol. 270, no 7, p. 3315-3328Article in journal (Refereed)
    Abstract [en]

    BACKGROUND AND AIMS: To investigate the prognostic value of blood neurofilament light chain protein (NfL) levels in the acute phase of coronavirus disease 2019 (COVID-19).

    METHODS: We conducted an individual participant data (IPD) meta-analysis after screening on MEDLINE and Scopus to May 23rd 2022. We included studies with hospitalized adult COVID-19 patients without major COVID-19-associated central nervous system (CNS) manifestations and with a measurement of blood NfL in the acute phase as well as data regarding at least one clinical outcome including intensive care unit (ICU) admission, need of mechanical ventilation (MV) and death. We derived the age-adjusted measures NfL Z scores and conducted mixed-effects modelling to test associations between NfL Z scores and other variables, encompassing clinical outcomes. Summary receiver operating characteristic curves (SROCs) were used to calculate the area under the curve (AUC) for blood NfL.

    RESULTS: We identified 382 records, of which 7 studies were included with a total of 669 hospitalized COVID-19 cases (mean age 66.2 ± 15.0 years, 68.1% males). Median NfL Z score at admission was elevated compared to the age-corrected reference population (2.37, IQR: 1.13-3.06, referring to 99th percentile in healthy controls). NfL Z scores were significantly associated with disease duration and severity. Higher NfL Z scores were associated with a higher likelihood of ICU admission, need of MV, and death. SROCs revealed AUCs of 0.74, 0.80 and 0.71 for mortality, need of MV and ICU admission, respectively.

    CONCLUSIONS: Blood NfL levels were elevated in the acute phase of COVID-19 patients without major CNS manifestations and associated with clinical severity and poor outcome. The marker might ameliorate the performance of prognostic multivariable algorithms in COVID-19.

  • 2.
    Alam, Aftab
    et al.
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England..
    Singh, Tanya
    Cardiff Univ, Sch Biosci, Cardiff, Wales.;Cardiff Univ, Neurosci & Mental Hlth Innovat Inst, Cardiff, Wales..
    Kayhanian, Saeed
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England.;Univ Cambridge, Cambridge Biomed Campus, Cambridge CB2 0QQ, England..
    Tjerkaski, Jonathan
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden..
    Garcia, Nuria Marco
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England..
    Carpenter, Keri L. H.
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England..
    Patani, Rickie
    UCL, Inst Neurol, Queen Sq, London, England..
    Lindblad, Caroline
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden..
    Thelin, Eric P. P.
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England.;Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden..
    Syed, Yasir Ahmed
    Cardiff Univ, Sch Biosci, Cardiff, Wales.;Cardiff Univ, Neurosci & Mental Hlth Innovat Inst, Cardiff, Wales..
    Helmy, Adel
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England..
    Modeling the Inflammatory Response of Traumatic Brain Injury Using Human Induced Pluripotent Stem Cell Derived Microglia2023In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 40, no 19-20, p. 2164-2173Article in journal (Refereed)
    Abstract [en]

    The neuroinflammatory response after traumatic brain injury (TBI) is implicated as a key mediator of secondary injury in both the acute and chronic periods after primary injury. Microglia are the key innate immune cell in the central nervous system, responding to injury with the release of cytokines and chemokines. In this context, we aimed to characterize the downstream cytokine response of human induced pluripotent stem cell (iPSC)-derived microglia when stimulated with five separate cytokines identified after human TBI. The iPSC-derived microglia were exposed to interleukin (IL)-1 & beta;, IL-4, IL-6, IL-10, and tumor necrosis factor (TNF) in the concentration ranges identified in clinical TBI studies. The downstream cytokine response was measured against a panel of 37 separate cytokines over a 72h time-course. The secretome revealed concentration-, time- and combined concentration and time-dependent downstream responses. TNF appeared to be the strongest inducer of downstream cytokine changes (51), followed by IL-1 & beta; (26) and IL-4 (19). IL-10 (11) and IL-6 (10) produced fewer responses. We also compare these responses with our previous studies of iPSC-derived neuronal and astrocyte cultures and the in vivo human TBI cytokine response. Notably, we found microglial culture to induce both a wider range of downstream cytokine responses and a greater fold change in concentration for those downstream responses, compared with astrocyte and neuronal cultures. In summary, we present a dataset for human microglial cytokine responses specific to the secretome found in the clinical context of TBI. This reductionist approach complements our previous datasets for astrocyte and neuronal responses and will provide a platform to enable future studies to unravel the complex neuroinflammatory network activated after TBI.

  • 3.
    Bark, Lovisa
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Larsson, Ing-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Wallin, Ewa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Simren, Joel
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Mölndal, Sweden.;Sahlgrens Univ Hosp, Clin Neurochem Lab, Mölndal, Sweden..
    Zetterberg, Henrik
    Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Mölndal, Sweden.;Sahlgrens Univ Hosp, Clin Neurochem Lab, Mölndal, Sweden.;UCL Inst Neurol, Dept Neurodegenerat Dis, Queen Sq, London, England.;UK Dementia Res Inst UCL, London, England.;Hong Kong Ctr Neurodegenerat Dis, Clear Water Bay, Hong Kong, Peoples R China..
    Lipcsey, Miklós
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care, Hedenstierna laboratory.
    Frithiof, Robert
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Rostami, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Karolinska Inst, Dept Neurosci, Stockholm, Sweden..
    Hultström, Michael
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care. McGill Univ, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ, Canada.;Jewish Gen Hosp, Lady Davis Inst Med Res, Montreal, PQ, Canada..
    Central nervous system biomarkers GFAp and NfL associate with post-acute cognitive impairment and fatigue following critical COVID-192023In: Scientific Reports, E-ISSN 2045-2322, Vol. 13, article id 13144Article in journal (Refereed)
    Abstract [en]

    A high proportion of patients with coronavirus disease 2019 (COVID-19) experience post-acute COVID-19, including neuropsychiatric symptoms. Objective signs of central nervous system (CNS) damage can be investigated using CNS biomarkers such as glial fibrillary acidic protein (GFAp), neurofilament light chain (NfL) and total tau (t-tau). We have examined whether CNS biomarkers can predict fatigue and cognitive impairment 3-6 months after discharge from the intensive care unit (ICU) in critically ill COVID-19 patients. Fifty-seven COVID-19 patients admitted to the ICU were included with analysis of CNS biomarkers in blood at the ICU and at follow up. Cognitive dysfunction and fatigue were assessed with the Montreal Cognitive Assessment (MoCA) and the Multidimensional Fatigue inventory (MFI-20). Elevated GFAp at follow-up 3-6 months after ICU discharge was associated to the development of mild cognitive dysfunction (p = 0.01), especially in women (p = 0.005). Patients who experienced different dimensions of fatigue at follow-up had significantly lower GFAp in both the ICU and at follow-up, specifically in general fatigue (p = 0.009), physical fatigue (p = 0.004), mental fatigue (p = 0.001), and reduced motivation (p = 0.001). Women showed a more pronounced decrease in GFAp compared to men, except for in mental fatigue where men showed a more pronounced GFAp decrease compared to women. NfL concentration at follow-up was lower in patients who experienced reduced motivation (p = 0.004). Our findings suggest that GFAp and NfL are associated with neuropsychiatric outcome after critical COVID-19.

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  • 4.
    Dyhrfort, Philip
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury.
    Lindblad, Caroline
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Univ Uppsala Hosp, Dept Neurosurg, Uppsala, Sweden.;Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Univ Cambridge, Addenbrookes Hosp, Dept Clin Neurosci, Turku, Finland..
    Widgren, Anna
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry.
    Virhammar, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurology. Uppsala Univ Hosp, Dept Neurol, Uppsala, Sweden..
    Piehl, Fredrik
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Acad Specialist Ctr, Ctr Neurol, Stockholm, Sweden..
    Bergquist, Jonas
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry.
    Al Nimer, Faiez
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Acad Specialist Ctr, Ctr Neurol, Stockholm, Sweden..
    Rostami, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Univ Uppsala Hosp, Dept Neurosurg, Uppsala, Sweden.;Karolinska Inst, Dept Neurosci, Stockholm, Sweden..
    Deciphering Proteomic Expression in Inflammatory Disorders: A Mass Spectrometry Exploration Comparing Infectious, Noninfectious, and Traumatic Brain Injuries in Human Cerebrospinal Fluid2024In: NEUROTRAUMA REPORTS, ISSN 2689-288X, Vol. 5, no 1, p. 857-873Article in journal (Refereed)
    Abstract [en]

    The central nervous system (CNS) evokes a complex inflammatory response to injury. Inflammatory cascades are present in traumatic, infectious, and noninfectious disorders affecting the brain. It contains a mixture of pro- and anti-inflammatory reactions involving well-known proteins, but also numerous proteins less explored in these processes. The aim of this study was to explore the distinct inflammatory response in traumatic brain injury (TBI) compared with other CNS injuries by utilization of mass-spectrometry. In total, 56 patients had their cerebrospinal fluid (CSF) analyzed with the use of mass-spectrometry. Among these, CSF was collected via an external ventricular drain (EVD) from n = 21 patients with acute TBI. The resulting protein findings were then compared with CSF obtained by lumbar puncture from n = 14 patients with noninfectious CNS disorders comprising relapsing-remitting multiple sclerosis, anti-N-methyl-d-aspartate-receptor encephalitis, acute disseminated encephalomyelitis, and n = 14 patients with progressive multifocal leukoencephalopathy, herpes simplex encephalitis, and other types of viral meningitis. We also utilized n = 7 healthy controls (HCs). In the comparison between TBI and noninfectious inflammatory CNS disorders, concentrations of 55 proteins significantly differed between the groups. Among them, 23 and 32 proteins were up- and downregulated, respectively, in the TBI group. No proteins were uniquely identified in either group. In the comparison of TBI and HC, 51 proteins were significantly different, with 24 and 27 proteins being up- and downregulated, respectively, in TBI. Two proteins (fibrinogen gamma chain and transketolase) were uniquely identified in all samples of the TBI group. Also in the last comparison, TBI versus infectious inflammatory CNS disorders, 51 proteins differed between the two groups, with 19 and 32 proteins being up- and downregulated, respectively, in TBI, and no unique proteins being identified. Due to large discrepancies between the groups compared, the following proteins were selected for further deeper analysis among those being differentially regulated: APOE, CFB, CHGA, CHI3L1, C3, FCGBP, FGA, GSN, IGFBP7, LRG1, SERPINA3, SOD3, and TTR. We found distinct proteomic profiles in the CSF of TBI patients compared with HC and different disease controls, indicating a specific interplay between inflammatory factors, metabolic response, and cell integrity. In relation to primarily infectious or inflammatory disorders, unique inflammatory pathways seem to be engaged, and could potentially serve as future treatment targets.

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  • 5.
    Froese, Logan
    et al.
    Univ Manitoba, Fac Engn, Biomed Engn, Winnipeg, MB, Canada..
    Hammarlund, Emma
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Perioperat Med & Intens Care, Stockholm, Sweden..
    Åkerlund, Cecilia A. I.
    Karolinska Univ Hosp, Dept Perioperat Med & Intens Care, Stockholm, Sweden.;Karolinska Inst, Dept Physiol & Pharmacol, Sect Perioperat Med & Intens Care, Stockholm, Sweden..
    Tjerkaski, Jonathan
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden..
    Hong, Erik
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden..
    Lindblad, Caroline
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Uppsala Univ Hosp, Dept Neurosurg, Uppsala, Sweden..
    Nelson, David W.
    Karolinska Univ Hosp, Dept Perioperat Med & Intens Care, Stockholm, Sweden.;Karolinska Inst, Dept Physiol & Pharmacol, Sect Perioperat Med & Intens Care, Stockholm, Sweden..
    Thelin, Eric P.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden..
    Zeiler, Frederick A.
    Univ Manitoba, Fac Engn, Biomed Engn, Winnipeg, MB, Canada.;Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Univ Manitoba, Rady Fac Hlth Sci, Dept Surg, Sect Neurosurg, Winnipeg, MB, Canada.;Univ Manitoba, Rady Fac Hlth Sci, Dept Human Anat & Cell Sci, Winnipeg, MB, Canada.;Univ Manitoba, Ctr Aging, Winnipeg, MB, Canada.;Univ Cambridge, Addenbrookes Hosp, Dept Med, Div Anaesthesia, Cambridge, England..
    The impact of sedative and vasopressor agents on cerebrovascular reactivity in severe traumatic brain injury2023In: Intensive Care Medicine Experimental, E-ISSN 2197-425X, Vol. 11, article id 54Article in journal (Refereed)
    Abstract [en]

    Background: The aim of this study is to evaluate the impact of commonly administered sedatives (Propofol, Alfentanil, Fentanyl, and Midazolam) and vasopressor (Dobutamine, Ephedrine, Noradrenaline and Vasopressin) agents on cerebrovascular reactivity in moderate/severe TBI patients. Cerebrovascular reactivity, as a surrogate for cerebral autoregulation was assessed using the long pressure reactivity index (LPRx). We evaluated the data in two phases, first we assessed the minute-by-minute data relationships between different dosing amounts of continuous infusion agents and physiological variables using boxplots, multiple linear regression and ANOVA. Next, we assessed the relationship between continuous/bolus infusion agents and physiological variables, assessing pre-/post- dose of medication change in physiology using a Wilcoxon signed-ranked test. Finally, we evaluated sub-groups of data for each individual dose change per medication, focusing on key physiological thresholds and demographics.

    Results: Of the 475 patients with an average stay of 10 days resulting in over 3000 days of recorded information 367 (77.3%) were male with a median Glasgow coma score of 7 (4-9). The results of this retrospective observational study confirmed that the infusion of most administered agents do not impact cerebrovascular reactivity, which is confirmed by the multiple linear regression components having p value > 0.05. Incremental dose changes or bolus doses in these medications in general do not lead to significant changes in cerebrovascular reactivity (confirm by Wilcoxon signed-ranked p value > 0.05 for nearly all assessed relationships). Within the sub-group analysis that separated the data based on LPRx pre-dose, a significance between pre-/post-drug change in LPRx was seen, however this may be more of a result from patient state than drug impact.

    Conclusions: Overall, this study indicates that commonly administered agents with incremental dosing changes have no clinically significant influence on cerebrovascular reactivity in TBI (nor do they impair cerebrovascular reactivity). Though further investigation in a larger and more diverse TBI patient population is required.

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  • 6.
    Hong, Erik
    et al.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurosurg, Stockholm, Sweden..
    Froese, Logan
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Univ Manitoba, Fac Engn, Biomed Engn, Winnipeg, MB, Canada..
    Ponten, Emeli
    Karolinska Inst, Dept Mol Med & Surg MMK, Stockholm, Sweden.;Skane Univ Hosp, Dept Neurosurg, Lund, Sweden..
    Fletcher-Sandersjoo, Alexander
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurosurg, Stockholm, Sweden..
    Tatter, Charles
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Soder Sjukhuset, Dept Radiol, Stockholm, Sweden..
    Hammarlund, Emma
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Perioperat Med & Intens Care, Stockholm, Sweden..
    Akerlund, Cecilia A. I.
    Karolinska Univ Hosp, Dept Perioperat Med & Intens Care, Stockholm, Sweden.;Karolinska Inst, Dept Physiol & Pharmacol, Sect Perioperat Med & Intens Care, Stockholm, Sweden..
    Tjerkaski, Jonathan
    Danderyd Hosp, Dept Cardiol, Stockholm, Sweden..
    Alpkvist, Peter
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurosurg, Stockholm, Sweden..
    Bartek Jr, Jiri
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurosurg, Stockholm, Sweden..
    Raj, Rahul
    Univ Helsinki, Dept Neurosurg, Helsinki, Finland..
    Lindblad, Caroline
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Univ Uppsala Hosp, Dept Neurosurg, Uppsala, Sweden..
    Nelson, David W.
    Karolinska Univ Hosp, Dept Perioperat Med & Intens Care, Stockholm, Sweden.;Karolinska Inst, Dept Physiol & Pharmacol, Sect Perioperat Med & Intens Care, Stockholm, Sweden..
    Zeiler, Frederick A.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Univ Manitoba, Fac Engn, Biomed Engn, Winnipeg, MB, Canada.;Univ Manitoba, Rady Fac Hlth Sci, Dept Surg, Sect Neurosurg, Winnipeg, MB, Canada.;Pan Am Clin Fdn, Winnipeg, MB, Canada.;Univ Manitoba, Ctr Aging, Winnipeg, MB, Canada..
    Thelin, Eric P.
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden..
    Critical thresholds of long-pressure reactivity index and impact of intracranial pressure monitoring methods in traumatic brain injury2024In: Critical Care, ISSN 1364-8535, E-ISSN 1466-609X, Vol. 28, no 1, article id 256Article in journal (Refereed)
    Abstract [en]

    Background: Moderate-to-severe traumatic brain injury (TBI) has a global mortality rate of about 30%, resulting in acquired life-long disabilities in many survivors. To potentially improve outcomes in this TBI population, the management of secondary injuries, particularly the failure of cerebrovascular reactivity (assessed via the pressure reactivity index; PRx, a correlation between intracranial pressure (ICP) and mean arterial blood pressure (MAP)), has gained interest in the field. However, derivation of PRx requires high-resolution data and expensive technological solutions, as calculations use a short time-window, which has resulted in it being used in only a handful of centers worldwide. As a solution to this, low resolution (longer time-windows) PRx has been suggested, known as Long-PRx or LPRx. Though LPRx has been proposed little is known about the best methodology to derive this measure, with different thresholds and time-windows proposed. Furthermore, the impact of ICP monitoring on cerebrovascular reactivity measures is poorly understood. Hence, this observational study establishes critical thresholds of LPRx associated with long-term functional outcome, comparing different time-windows for calculating LPRx as well as evaluating LPRx determined through external ventricular drains (EVD) vs intraparenchymal pressure device (IPD) ICP monitoring.

    Methods: The study included a total of n = 435 TBI patients from the Karolinska University Hospital. Patients were dichotomized into alive vs. dead and favorable vs. unfavorable outcomes based on 1-year Glasgow Outcome Scale (GOS). Pearson's chi-square values were computed for incrementally increasing LPRx or ICP thresholds against outcome. The thresholds that generated the greatest chi-squared value for each LPRx or ICP parameter had the highest outcome discriminatory capacity. This methodology was also completed for the segmentation of the population based on EVD, IPD, and time of data recorded in hospital stay.

    Results: LPRx calculated with 10-120-min windows behaved similarly, with maximal chi-square values ranging at around a LPRx of 0.25-0.35, for both survival and favorable outcome. When investigating the temporal relations of LPRx derived thresholds, the first 4 days appeared to be the most associated with outcomes. The segmentation of the data based on intracranial monitoring found limited differences between EVD and IPD, with similar LPRx values around 0.3.

    Conclusion: Our work suggests that the underlying prognostic factors causing impairment in cerebrovascular reactivity can, to some degree, be detected using lower resolution PRx metrics (similar found thresholding values) with LPRx found clinically using as low as 10 min-by-minute samples of MAP and ICP. Furthermore, EVD derived LPRx with intermittent cerebrospinal fluid draining, seems to present similar outcome capacity as IPD. This low-resolution low sample LPRx method appears to be an adequate substitute for the clinical prognostic value of PRx and may be implemented independent of ICP monitoring method when PRx is not feasible, though further research is warranted.

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  • 7.
    Jirlow, Unni
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Hossain, Iftakher
    Turku Univ Hosp, Dept Neurosurg, Neuroctr, Turku, Finland.;Univ Cambridge, Addenbrookes Hosp, Dept Clin Neurosci, Neurosurg Unit, Cambridge, England..
    Korhonen, Otto
    Turku Univ Hosp, Dept Neurosurg, Neuroctr, Turku, Finland..
    Depreitere, Bart
    Univ Hosp Leuven, Dept Neurosurg, Leuven, Belgium..
    Rostami, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Karolinska Inst, Dept Neurosci, Solna, Sweden..
    Cerebral contusions - Pathomechanism, predictive factors for progression and historical and current management2024In: BRAIN AND SPINE, ISSN 2772-5294, Vol. 4, article id 103329Article in journal (Refereed)
    Abstract [en]

    Introduction: Cerebral contusions (CCs) are common traumatic brain injuries known for their propensity to progress. Understanding their mechanical pathogenesis and predictive factors for progression is crucial for optimal management.

    Research question: To provide an overview of current knowledge on CCs, including pathomechanisms, predictive factors of contusion progression, and management strategies.

    Material and methods: A literature search was conducted using PubMed, Scopus and ISI web of knowledge focused on articles in English with the words "cerebral contusion" together with the words "traumatic brain injury", "pathomechanism", "progression of contusion", "predictive factors" and "management" alone or in combination.

    Results: The management of CCs has evolved alongside the advances in neurointensive care, yet there is no consensus. Evidence on the effectiveness of early surgery, importantly, for the group which has the potential to expand, is limited. Some predictive factors for contusion progression have been identified, including age, injury mechanism, coagulopathy and initial contusion volume which could help to guide decision-making.

    Discussion and conclusion: While various theories exist on pathomechanisms and several predictive factors for progression have been proposed, consensus on optimal management remains elusive. Individualized care guided by the predictive factors is essential. Challenges posed by antithrombotic medications highlight the need for early intervention strategies. Decompressive craniectomy could serve as a potential tool in severe traumatic brain injury management including contusions. Conducting large cohort studies to refine predictive models and harmonizing management approaches would help to improve outcomes of patients with CCs.

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  • 8.
    Lindblad, Caroline
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Uppsala Univ Hosp, Dept Neurosurg, Akad Sjukhuset, Entrance 85 Floor 2, S-75185 Uppsala, Sweden; Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
    Rostami, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Uppsala Univ Hosp, Dept Neurosurg, Akad Sjukhuset, Entrance 85 Floor 2, S-75185 Uppsala, Sweden; Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Helmy, Adel
    Univ Cambridge, Dept Clin Neurosci, Div Neurosurg, Cambridge, England.
    Interleukin-1 Receptor Antagonist as Therapy for Traumatic Brain Injury2023In: Neurotherapeutics, ISSN 1933-7213, Vol. 20, no 6, p. 1508-1528Article, review/survey (Refereed)
    Abstract [en]

    Traumatic brain injury is a common type of acquired brain injury of varying severity carrying potentially deleterious consequences for the afflicted individuals, families, and society. Following the initial, traumatically induced insult, cellular injury processes ensue. These are believed to be amenable to treatment. Among such injuries, neuroinflammation has gained interest and has become a specific focus for both experimental and clinical researchers. Neuroinflammation is elicited almost immediately following trauma, and extend for a long time, possibly for years, after the primary injury. In the acute phase, the inflammatory response is characterized by innate mechanisms such as the activation of microglia which among else mediates cytokine production. Among the earliest cytokines to emerge are the interleukin- (IL-) 1 family members, comprising, for example, the agonist IL-1β and its competitive antagonist, IL-1 receptor antagonist (IL-1ra). Because of its early emergence following trauma and its increased concentrations also after human TBI, IL-1 has been hypothesized to be a tractable treatment target following TBI. Ample experimental data supports this, and demonstrates restored neurological behavior, diminished lesion zones, and an attenuated inflammatory response following IL-1 modulation either through IL-1 knock-out experiments, IL-1β inhibition, or IL-1ra treatment. Of these, IL-1ra treatment is likely the most physiological. In addition, recombinant human IL-1ra (anakinra) is already approved for utilization across a few rheumatologic disorders. As of today, one randomized clinical controlled trial has utilized IL-1ra inhibition as an intervention and demonstrated its safety. Further clinical trials powered for patient outcome are needed in order to demonstrate efficacy. In this review, we summarize IL-1 biology in relation to acute neuroinflammatory processes following TBI with a particular focus on current evidence for IL-1ra treatment both in the experimental and clinical context.

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  • 9. Molero, Yasmina
    et al.
    Sharp, David J.
    D’Onofrio, Brian M.
    Lichtenstein, Paul
    Larsson, Henrik
    Fazel, Seena
    Rostami, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury.
    Medication utilization in traumatic brain injury patients: insights from a population-based matched cohort study2024In: Frontiers in Neurology, E-ISSN 1664-2295, Vol. 15, article id 1339290Article in journal (Refereed)
    Abstract [en]

    Introduction: Traumatic brain injury (TBI) is associated with health problems across multiple domains and TBI patients are reported to have high rates of medication use. However, prior evidence is thin due to methodological limitations. Our aim was thus to examine the use of a wide spectrum of medications prescribed to address pain and somatic conditions in a population-based cohort of TBI patients, and to compare this to a sex- and age-matched cohort. We also examined how patient factors such as sex, age, and TBI severity were associated with medication use.

    Methods: We assessed Swedish nationwide registers to include all individuals treated for TBI in hospitals or specialist outpatient care between 2006 and 2012. We examined dispensed prescriptions for eight different non-psychotropic medication classes for the 12 months before, and 12 months after, the TBI. We applied a fixed-effects model to compare TBI patients with the matched population cohort. We also stratified TBI patients by sex, age, TBI severity and carried out comparisons using a generalized linear model.

    Results: We identified 239,425 individuals with an incident TBI and 239,425 matched individuals. TBI patients were more likely to use any medication [Odds ratio (OR) = 2.03, 95% Confidence Interval (CI) = 2.00–2.05], to present with polypharmacy (OR = 1.96, 95% CI = 1.90–2.02), and to use each of the eight medication classes before their TBI, as compared to the matched population cohort. Following the TBI, TBI patients were more likely to use any medication (OR = 1.83, 95% CI = 1.80–1.86), to present with polypharmacy (OR = 1.74, 95% CI = 1.67–1.80), and to use all medication classes, although differences were attenuated. However, differences increased for antibiotics/antivirals (OR = 2.02, 95% CI = 1.99–2.05) and NSAIDs/antirheumatics (OR = 1.62, 95% CI = 1.59–1.65) post-TBI. We also found that females and older patients were more likely to use medications after their TBI than males and younger patients, respectively. Patients with more severe TBIs demonstrated increased use of antibiotics/ antivirals and NSAIDs/antirheumatics than those with less severe TBIs.

    Discussion: Taken together, our results point to poor overall health in TBI patients, suggesting that medical follow-up should be routine, particularly in females with TBI, and include a review of medication use to address potential polypharmacy.

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  • 10.
    Pietilä, Riikka
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Del Gaudio, Francesca
    Karolinska Inst, Dept Med Huddinge, S-14157 Huddinge, Sweden.;Karolinska Inst, Dept Cell & Mol Biol, S-17177 Stockholm, Sweden..
    He, Liqun
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Vázquez-Liébanas, Elisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Vanlandewijck, Michael
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology. Karolinska Inst, Dept Med Huddinge, S-14157 Huddinge, Sweden.
    Muhl, Lars
    Karolinska Inst, Dept Med Huddinge, S-14157 Huddinge, Sweden..
    Mocci, Giuseppe
    Karolinska Inst, Dept Med Huddinge, S-14157 Huddinge, Sweden..
    Bjørnholm, Katrine D.
    Karolinska Inst, Ctr Alzheimer Res, Dept Neurobiol Care Sci & Soc, Div Neurogeriatr, S-17177 Stockholm, Sweden..
    Lindblad, Caroline
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Karolinska Inst, Dept Clin Neurosci, S-17177 Stockholm, Sweden; Department of Neurosurgery, Uppsala University Hospital.
    Fletcher-Sandersjöö, Alexander
    Karolinska Inst, Dept Clin Neurosci, S-17177 Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurosurg, S-17176 Stockholm, Sweden..
    Svensson, Mikael
    Karolinska Inst, Dept Clin Neurosci, S-17177 Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurol, S-17176 Stockholm, Sweden..
    Thelin, Eric P.
    Karolinska Inst, Dept Clin Neurosci, S-17177 Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurol, S-17176 Stockholm, Sweden..
    Liu, Jianping
    Karolinska Inst, Dept Med Huddinge, S-14157 Huddinge, Sweden..
    van Voorden, A. Jantine
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Torres, Monica
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Antila, Salli
    Univ Helsinki, Wihuri Res Inst, Helsinki 00014, Finland.;Univ Helsinki, Translat Canc Med Program, Helsinki 00014, Finland..
    Xin, Li
    Univ Bern, Theodor Kocher Inst, CH-3012 Bern, Switzerland..
    Karlström, Helena
    Karolinska Inst, Ctr Alzheimer Res, Dept Neurobiol Care Sci & Soc, Div Neurogeriatr, S-17177 Stockholm, Sweden..
    Storm-Mathisen, Jon
    Univ Oslo, Inst Basic Med Sci, Dept Mol Med, Div Anat, N-0317 Oslo, Norway..
    Bergersen, Linda Hildegard
    Univ Oslo, Inst Oral Biol, Brain & Muscle Energy Grp, N-0316 Oslo, Norway.;Univ Copenhagen, Ctr Hlth Aging, DK-2200 Copenhagen, Denmark..
    Moggio, Aldo
    Karolinska Inst, Dept Cell & Mol Biol, S-17177 Stockholm, Sweden.;Tech Univ Munich, German Heart Ctr Munich, Dept Cardiol, D-80333 Munich, Germany..
    Hansson, Emil M.
    Karolinska Inst, Dept Cell & Mol Biol, S-17177 Stockholm, Sweden..
    Ulvmar, Maria H.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Nilsson, Per
    Karolinska Inst, Ctr Alzheimer Res, Dept Neurobiol Care Sci & Soc, Div Neurogeriatr, S-17177 Stockholm, Sweden..
    Mäkinen, Taija
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Andaloussi Mäe, Maarja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Alitalo, Kari
    Univ Helsinki, Wihuri Res Inst, Helsinki 00014, Finland.;Univ Helsinki, Translat Canc Med Program, Helsinki 00014, Finland..
    Proulx, Steven T.
    Univ Bern, Theodor Kocher Inst, CH-3012 Bern, Switzerland..
    Engelhardt, Britta
    Univ Bern, Theodor Kocher Inst, CH-3012 Bern, Switzerland..
    McDonald, Donald M.
    Univ Calif San Francisco, Cardiovasc Res Inst, UCSF Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.;Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA..
    Lendahl, Urban
    Karolinska Inst, Dept Cell & Mol Biol, S-17177 Stockholm, Sweden..
    Andrae, Johanna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Betsholtz, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology. Karolinska Inst, Dept Med Huddinge, S-14157 Huddinge, Sweden.
    Molecular anatomy of adult mouse leptomeninges2023In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 111, no 23Article in journal (Refereed)
    Abstract [en]

    Leptomeninges, consisting of the pia mater and arachnoid, form a connective tissue investment and barrier enclosure of the brain. The exact nature of leptomeningeal cells has long been debated. In this study, we iden-tify five molecularly distinct fibroblast-like transcriptomes in cerebral leptomeninges; link them to anatomically distinct cell types of the pia, inner arachnoid, outer arachnoid barrier, and dural border layer; and contrast them to a sixth fibroblast-like transcriptome present in the choroid plexus and median eminence. Newly identified transcriptional markers enabled molecular characterization of cell types responsible for adherence of arach-noid layers to one another and for the arachnoid barrier. These markers also proved useful in identifying the molecular features of leptomeningeal development, injury, and repair that were preserved or changed after traumatic brain injury. Together, the findings highlight the value of identifying fibroblast transcriptional subsets and their cellular locations toward advancing the understanding of leptomeningeal physiology and pathology.

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  • 11.
    Svedung-Wettervik, Teodor
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery.
    Engquist, Henrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
    Hånell, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery.
    Howells, Timothy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery.
    Rostami, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury.
    Ronne-Engström, Elisabeth
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery.
    Lewén, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery.
    Enblad, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Neurosurgery.
    Cerebral Microdialysis Monitoring of Energy Metabolism: Relation to Cerebral Blood Flow and Oxygen Delivery in Aneurysmal Subarachnoid Hemorrhage2023In: Journal of Neurosurgical Anesthesiology, ISSN 0898-4921, E-ISSN 1537-1921, Vol. 35, no 4, p. 384-393Article in journal (Refereed)
    Abstract [en]

    Introduction: In this study, we investigated the roles of cerebral blood flow (CBF) and cerebral oxygen delivery (CDO2) in relation to cerebral energy metabolism after aneurysmal subarachnoid hemorrhage (aSAH).

    Methods: Fifty-seven adult aSAH patients treated on the neurointensive care unit at Uppsala, Sweden between 2012 and 2020, with at least 1 xenon-enhanced computed tomography (Xe-CT) scan in the first 14 days after ictus and concurrent microdialysis (MD) monitoring, were included in this retrospective study. CBF was measured globally and focally (around the MD catheter) with Xe-CT, and CDO2 calculated. Cerebral energy metabolites were measured using MD.

    Results: Focal ischemia (CBF <20 mL/100 g/min around the MD catheter was associated with lower median [interquartile range]) MD-glucose (1.2 [0.7 to 2.2] mM vs. 2.3 [1.3 to 3.5] mM; P=0.05) and higher MD-lactate-pyruvate (LPR) ratio (34 [29 to 66] vs. 25 [21 to 32]; P=0.02). A compensated/normal MD pattern (MD-LPR <25) was observed in the majority of patients (22/23, 96%) without focal ischemia, whereas 4 of 11 (36%) patients with a MD pattern of poor substrate supply (MD-LPR >25, MD-pyruvate <120 µM) had focal ischemia as did 5 of 20 (25%) patients with a pattern of mitochondrial dysfunction (MD-LPR >25, MD-pyruvate >120 µM) (P=0.04). Global CBF and CDO2, and focal CDO2, were not associated with the MD variables.

    Conclusions: While MD is a feasible tool to study cerebral energy metabolism, its validity is limited to a focal area around the MD catheter. Cerebral energy disturbances were more related to low CBF than to low CDO2. Considering the high rate of mitochondrial dysfunction, treatments that increase CBF but not CDO2, such as hemodilution, may still benefit glucose delivery to drive anaerobic metabolism.

  • 12.
    Wood, Sara
    et al.
    Karolinska Univ Hosp, ECMO Ctr Karolinska, Intens Care & Transport, Pediat Perioperat Med & Intens Care, Akad Straket 14, S-17176 Stockholm, Sweden..
    Iacobelli, Riccardo
    Karolinska Univ Hosp, ECMO Ctr Karolinska, Intens Care & Transport, Pediat Perioperat Med & Intens Care, Akad Straket 14, S-17176 Stockholm, Sweden..
    Kopfer, Sarah
    Karolinska Univ Hosp, ECMO Ctr Karolinska, Intens Care & Transport, Pediat Perioperat Med & Intens Care, Akad Straket 14, S-17176 Stockholm, Sweden..
    Lindblad, Caroline
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Acquired brain injury. Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Uppsala Univ Hosp, Dept Neurosurg, Uppsala, Sweden..
    Thelin, Eric Peter
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurol, Stockholm, Sweden..
    Fletcher-Sandersjoo, Alexander
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.;Karolinska Univ Hosp, Dept Neurosurg, Stockholm, Sweden..
    Broman, Lars Mikael
    Karolinska Univ Hosp, ECMO Ctr Karolinska, Intens Care & Transport, Pediat Perioperat Med & Intens Care, Akad Straket 14, S-17176 Stockholm, Sweden.;Karolinska Inst, Dept Physiol & Pharmacol, Stockholm, Sweden..
    Predictors of intracranial hemorrhage in neonatal patients on extracorporeal membrane oxygenation2023In: Scientific Reports, E-ISSN 2045-2322, Vol. 13, no 1, article id 19249Article in journal (Refereed)
    Abstract [en]

    Extracorporeal membrane oxygenation (ECMO) is a life-supportive treatment in neonatal patients with refractory lung and/or heart failure. Intracranial hemorrhage (ICH) is a severe complication and reliable predictors are warranted. The aims of this study were to explore the incidence and possible predictors of ICH in ECMO-treated neonatal patients. We performed a single-center retrospective observational cohort study. Patients aged <= 28 days treated with ECMO between 2010 and 2018 were included. Exclusion criteria were ICH, ischemic stroke, cerebrovascular malformation before ECMO initiation or detected within 12 h of admission, ECMO treatment < 12 h, or prior treatment with ECMO at another facility > 12 h. The primary outcome was a CT-verified ICH. Logistic regression models were employed to identify possible predictors of the primary outcome. Of the 223 patients included, 29 (13%) developed an ICH during ECMO treatment. Thirty-day mortality was 59% in the ICH group and 16% in the non-ICH group (p < 0.0001). Lower gestational age (p < 0.01, odds ratio (OR) 0.96; 95%CI 0.94-0.98), and higher pre-ECMO lactate levels (p = 0.017, OR 1.1; 95%CI 1.01-1.18) were independently associated with increased risk of ICH-development. In the clinical setting, identification of risk factors and multimodal neuromonitoring could help initiate steps that lower the risk of ICH in these patients.

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