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  • 1.
    Abu Hamdeh, Sami
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Marklund, Niklas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Lewén, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Howells, Tim
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Raininko, Raili
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Wikström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Enblad, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Intracranial pressure elevations in diffuse axonal injury: association with nonhemorrhagic MR lesions in central mesencephalic structures2019In: Journal of Neurosurgery, ISSN 0022-3085, E-ISSN 1933-0693, Vol. 131, no 2, p. 604-611Article in journal (Refereed)
    Abstract [en]

    Objective: Increased intracranial pressure (ICP) in patients with severe traumatic brain injury (TBI) with diffuse axonal injury (DAI) is not well defined. This study investigated the occurrence of increased ICP and whether clinical factors and lesion localization on MRI were associated with increased ICP in patients with DAI.

    Methods: Fifty-two patients with severe TBI (median age 24 years, range 9–61 years), who had undergone ICP monitoring and had DAI on MRI, as determined using T2*-weighted gradient echo, susceptibility-weighted imaging, and diffusion-weighted imaging (DWI) sequences, were enrolled. The proportion of good monitoring time (GMT) with ICP > 20 mm Hg during the first 120 hours postinjury was calculated and associations with clinical and MRI-related factors were evaluated using linear regression.

    Results: All patients had episodes of ICP > 20 mm Hg. The mean proportion of GMT with ICP > 20 mm Hg was 5%, and 27% of the patients (14/52) spent more than 5% of GMT with ICP > 20 mm Hg. The Glasgow Coma Scale motor score at admission (p = 0.04) and lesions on DWI sequences in the substantia nigra and mesencephalic tegmentum (SN-T, p = 0.001) were associated with the proportion of GMT with ICP > 20 mm Hg. In multivariable linear regression, lesions on DWI sequences in SN-T (8% of GMT with ICP > 20 mm Hg, 95% CI 3%–13%, p = 0.004) and young age (−0.2% of GMT with ICP > 20 mm Hg, 95% CI −0.07% to −0.3%, p = 0.002) were associated with increased ICP.

    Conclusions: Increased ICP occurs in approximately one-third of patients with severe TBI who have DAI. Age and lesions on DWI sequences in the central mesencephalon (i.e., SN-T) are associated with elevated ICP. These findings suggest that MR lesion localization may aid prediction of increased ICP in patients with DAI.

    Abbreviations: ADC = apparent diffusion coefficient; CPP = cerebral perfusion pressure; DAI = diffuse axonal injury; DWI = diffusion-weighted imaging; EVD = external ventricular drain; GCS = Glasgow Coma Scale; GMT = good monitoring time; GOSE = Glasgow Outcome Scale–Extended; ICC = intraclass correlation coefficient; ICP = intracranial pressure; MAP = mean arterial blood pressure; NICU = neurointensive care unit; SN-T = substantia nigra and mesencephalic tegmentum; SWI = susceptibility-weighted imaging; TBI = traumatic brain injury; T2*GRE = T2*-weighted gradient echo.

  • 2. Arakelian, Erebouni
    et al.
    Färdig, Martin
    Nyholm, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Nurses anaesthetists' versus patients' assessment of anxieties in an ambulatory surgery setting.2019In: Journal of perioperative practice, ISSN 2515-7949, article id 1750458919838198Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Failure to assess patients' anxiety perioperatively by means of a validated instrument makes the assessment arbitrary. Studies are lacking about how well nurse anaesthetists estimate patients' preoperative worries.

    PURPOSE: To compare the nurse anaesthetists' estimations of patients' preoperative anxieties with the patients' own assessment of their anxieties.

    DESIGN: Quantitative prospective design.

    METHODS: Eighty-five pairs of patients and nurse anaesthetists in two ambulatory surgery units in a university hospital in Sweden were included. Patients' perioperative anxieties were graded using the Numeric Visual Analogue Anxiety Scale.

    RESULTS: The nurse anaesthetist overestimated the patients' level of preoperative anxiety in 53% of patients and underestimated patients' anxieties in 31% of the patients. Consensus was seen in 16% of the pairs. In fifty-six pairs (65%), the difference between the estimation of level of patients' anxiety according to Numeric Visual Analogue Anxiety Scale was between -3 (overestimation) and +3 levels (underestimation). Median levels of anxiety were estimated as 3 within the patient group and 4 among the nurse anaesthetists.

    CONCLUSIONS: Systematic assessment of patients' level of anxiety could lead to identifying patients with severe anxiety levels and to offer more individualised treatment. The patients' own estimation must form the basis for the discussion and treatment.

  • 3.
    Arakelian, Erebouni
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Nyholm, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Öster, Caisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Ekselius: Psychiatry.
    How Anesthesiologists and Nurse Anesthetists Assess and Handle Patients' Perioperative Worries Without a Validated Instrument2019In: Journal of Perianesthesia Nursing, ISSN 1089-9472, E-ISSN 1532-8473, Vol. 34, no 4, p. 810-819Article in journal (Refereed)
    Abstract [en]

    PURPOSE: To study how nurse anesthetists and anesthesiologists assess and handle patients' perioperative anxiety without using a validated instrument.

    DESIGN: Qualitative study.

    METHODS: Individual in-depth face-to-face interviews were conducted with nurse anesthetists (n = 9) and anesthesiologists (n = 5) from a university hospital in Sweden. Data were analyzed with thematic analysis according to Braun and Clark.

    FINDINGS: Two themes were identified: (1) I ask about anxiety, look for visual signs, and observe communication and (2) I handle patients' anxieties individually. In addition to subthemes describing assessment and handling of adults, it appeared that parents played an important role in children's perioperative anxiety.

    CONCLUSIONS: When not using a validated instrument, assessing perioperative anxiety is commonly based on the anesthesiologist's and nurse anesthetist's experience, knowledge, views, and attitudes. The evaluator's capability of using different strategies in the assessment and handling of perioperative anxiety is important.

  • 4.
    Berntsson, Shala G.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Gauffin, Helena
    Univ Linköping, Med Fac, Dept Clin & Expt Med, Neurol, Linköping, Sweden.
    Melberg, Atle
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Holtz, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Landtblom, Anne-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology. Univ Linköping, Med Fac, Dept Clin & Expt Med, Neurol, Linköping, Sweden.
    Inherited Ataxia and Intrathecal Baclofen for the Treatment of Spasticity and Painful Spasms2019In: Stereotactic and Functional Neurosurgery, ISSN 1011-6125, E-ISSN 1423-0372, Vol. 97, no 1, p. 18-23Article in journal (Refereed)
    Abstract [en]

    Background: Intrathecal baclofen (ITB) treatment is considered a powerful tool in the management of severe spasticity in neurological conditions such as multiple sclerosis, cerebral palsy, and traumatic spinal cord and brain injury.

    Objectives: The objective of this study was to assess the effectiveness of the ITB in patients with inherited ataxia suffering from severe painful spasms and/or spasticity.

    Method: A total of 5 patients with spinocerebellar ataxia 3 or 7 or Friedreich's ataxia were included in this observational multicenter study. The patients were interviewed and completed outcome measures assessing pain (The Brief Pain Inventory), fatigue (Fatigue Severity Scale), and life satisfaction (LiSAT-9) before and 1 year after the treatment. Spasticity (Modified Ashworth Scale) and spasm frequency (SPFS) were measured objectively for each patient.

    Results: The mean treatment time was 1.9 years. Evaluation of established standard forms revealed symptomatic relief from spasticity, spasms, pain, and fatigue in addition to improved body posture, sleep, and life satisfaction after ITB treatment.

    Conclusions: We report the potential beneficial effects of ITB treatment in patients with inherited ataxia who also suffer from spasticity/spasms. ITB treatment indication in neurological disorders allows for extension to the treatment of spasticity/spasms in patients with hereditary ataxia.

  • 5.
    Borota, Ljubisa
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Mahmoud, Ehab
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Nyberg, Christoffer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Neuroform Atlas stent in treatment of iatrogenic dissections of extracranial internal carotid and vertebral arteries: a single-centre experience2019In: Interventional Neuroradiology, ISSN 1591-0199, E-ISSN 2385-2011, Vol. 25, no 4, p. 390-396Article in journal (Refereed)
    Abstract [en]

    AIM OF THE STUDY: To present our experience in the treatment of iatrogenic dissections of extracranial internal carotid and vertebral arteries with the Neuroform Atlas stent.

    MATERIALS AND METHODS: Between January 2017 and February 2018 we treated iatrogenic dissections of three internal carotid arteries and three vertebral arteries. These iatrogenic dissections occurred during the endovascular treatment of ruptured and unruptured intracranial aneurysms. The indication for stenting was haemodynamically significant, flow-limiting dissection with threatening flow arrest. In all six cases, the dissections were treated by placement of Neuroform Atlas stents in the dissected segments of internal carotid or vertebral arteries. Deployment of the stent was followed by the usual dual antiplatelet regimen.

    RESULTS: Single or multiple Neuroform Atlas stents were deployed without any technical difficulties, and blood flow was restored immediately after placement of the stents in all six cases. Midterm follow-up (6-8 months) showed complete reconstruction of the shape and lumen of all treated arteries, with negligible intimal hyperplasia.

    CONCLUSION: Our results indicate that a favourable outcome can be achieved by treating iatrogenic dissections of extracranial internal carotid and vertebral arteries with the Neuroform Atlas stent.

  • 6.
    Dyhrfort, Philip
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Shen, Qiujin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular tools.
    Clausen, Fredrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience. Uppsala Univ, Dept Neurosci, Sect Neurosurg, Uppsala, Sweden.
    Eriksson, Måns
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Statistics. Uppsala Univ, Dept Stat, Uppsala, Sweden;Univ Edinburgh, Sch Math, Edinburgh, Midlothian, Scotland;Univ Edinburgh, Maxwell Inst Math Sci, Edinburgh, Midlothian, Scotland.
    Enblad, Per
    Kamali-Moghaddam, Masood
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Lewén, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Hillered, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Monitoring of Protein Biomarkers of Inflammation in Human Traumatic Brain Injury Using Microdialysis and Proximity Extension Assay Technology in Neurointensive Care2019In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 36, no 20, p. 2872-2885Article in journal (Refereed)
    Abstract [en]

    Traumatic brain injury (TBI) is followed by secondary injury mechanisms strongly involving neuroinflammation. To monitor the complex inflammatory cascade in human TBI, we used cerebral microdialysis (MD) and multiplex proximity extension assay (PEA) technology and simultaneously measured levels of 92 protein biomarkers of inflammation in MD samples every three hours for five days in 10 patients with severe TBI under neurointensive care. One mu L MD samples were incubated with paired oligonucleotide-conjugated antibodies binding to each protein, allowing quantification by real-time quantitative polymerase chain reaction. Sixty-nine proteins were suitable for statistical analysis. We found five different patterns with either early (<48 h; e.g., CCL20, IL6, LIF, CCL3), mid (48-96 h; e.g., CCL19, CXCL5, CXCL10, MMP1), late (>96 h; e.g., CD40, MCP2, MCP3), biphasic peaks (e.g., CXCL1, CXCL5, IL8) or stable (e.g., CCL4, DNER, VEGFA)/low trends. High protein levels were observed for e.g., CXCL1, CXCL10, MCP1, MCP2, IL8, while e.g., CCL28 and MCP4 were detected at low levels. Several proteins (CCL8, -19, -20, -23, CXCL1, -5, -6, -9, -11, CST5, DNER, Flt3L, and SIRT2) have not been studied previously in human TBI. Cross-correlation analysis revealed that LIF and CXCL5 may play a central role in the inflammatory cascade. This study provides a unique data set with individual temporal trends for potential inflammatory biomarkers in patients with TBI. We conclude that the combination of MD and PEA is a powerful tool to map the complex inflammatory cascade in the injured human brain. The technique offers new possibilities of protein profiling of complex secondary injury pathways.

  • 7.
    Elf, Kristin
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Rostedt Punga: Clinical Neurophysiology.
    Ronne-Engström, Elisabeth
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Semnic, Robert
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Radiology.
    Rostami-Berglund, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Sundblom, Jimmy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Zetterling, Maria
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Continuous EEG monitoring after brain tumor surgery2019In: Acta Neurochirurgica, ISSN 0001-6268, E-ISSN 0942-0940, Vol. 161, no 9, p. 1835-1843Article in journal (Refereed)
    Abstract [en]

    Background

    Prolonged seizures generate cerebral hypoxia and increased intracranial pressure, resulting in an increased risk of neurological deterioration, increased long-term morbidity, and shorter survival. Seizures should be recognized early and treated promptly.

    The aim of the study was to investigate the occurrence of postoperative seizures in patients undergoing craniotomy for primary brain tumors and to determine if non-convulsive seizures could explain some of the postoperative neurological deterioration that may occur after surgery.

    Methods

    A single-center prospective study of 100 patients with suspected glioma. Participants were studied with EEG and video recording for at least 24 h after surgery.

    Results

    Seven patients (7%) displayed seizure activity on EEG recording within 24 h after surgery and another two patients (2%) developed late seizures. One of the patients with early seizures also developed late seizures. In five patients (5%), there were non-convulsive seizures. Four of these patients had a combination of clinically overt and non-convulsive seizures and in one patient, all seizures were non-convulsive. The non-convulsive seizures accounted for the majority of total seizure time in those patients. Non-convulsive seizures could not explain six cases of unexpected postoperative neurological deterioration. Postoperative ischemic lesions were more common in patients with early postoperative seizures.

    Conclusions

    Early seizures, including non-convulsive, occurred in 7% of our patients. Within this group, non-convulsive seizure activity had longer durations than clinically overt seizures, but only 1% of patients had exclusively non-convulsive seizures. Seizures were not associated with unexpected neurological deterioration.

  • 8.
    Grönholdt-Klein, Max
    et al.
    Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden.
    Altun, Mikael
    Karolinska Inst, Dept Lab Med, Huddinge, Sweden.
    Becklen, Meneca
    Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden.
    Kahm, Emelie Dickman
    Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden.
    Fahlström, Andreas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery. Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden.
    Rullman, Eric
    Karolinska Inst, Dept Lab Med, Huddinge, Sweden.
    Ulfhake, Brun
    Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden.
    Muscle atrophy and regeneration associated with behavioural loss and recovery of function after sciatic nerve crush2019In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 227, no 3, article id e13335Article in journal (Refereed)
    Abstract [en]

    Aim To resolve timing and coordination of denervation atrophy and the re-innervation recovery process to discern correlations indicative of common programs governing these processes. Methods Female Sprague-Dawley (SD) rats had a unilateral sciatic nerve crush. Based on longitudinal behavioural observations, the triceps surae muscle was analysed at different time points post-lesion. Results Crush results in a loss of muscle function and mass (-30%) followed by a recovery to almost pre-lesion status at 30 days post-crush (dpc). There was no loss of fibres nor any significant change in the number of nuclei per fibre but a shift in fibres expressing myosins I and II that reverted back to control levels at 30 dpc. A residual was the persistence of hybrid fibres. Early on a CHNR -epsilon to -gamma switch and a re-expression of embryonic MyHC showed as signs of denervation. Foxo1, Smad3, Fbxo32 and Trim63 transcripts were upregulated but not Myostatin, InhibinA and ActivinR2B. Combined this suggests that the mechanism instigating atrophy provides a selectivity of pathway(s) activated. The myogenic differentiation factors (MDFs: Myog, Myod1 and Myf6) were upregulated early on suggesting a role also in the initial atrophy. The regulation of these transcripts returned towards baseline at 30 dpc. The examined genes showed a strong baseline covariance in transcript levels which dissolved in the response to crush driven mainly by the MDFs. At 30 dpc the naive expression pattern was re-established. Conclusion Peripheral nerve crush offers an excellent model to assess and interfere with muscle adaptions to denervation and re-innervation.

  • 9.
    Juratli, Tareq A.
    et al.
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Med, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Med, Boston, MA 02115 USA;Tech Univ Dresden, Dept Neurosurg, Fac Med, Dresden, Germany;Tech Univ Dresden, Carl Gustav Carus Univ Hosp, Dresden, Germany.
    Jones, Pamela S.
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02115 USA.
    Wang, Nancy
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Med, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Med, Boston, MA 02115 USA.
    Subramanian, Megha
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Med, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Med, Boston, MA 02115 USA.
    Aylwin, Simon J. B.
    Kings Coll Hosp London, Dept Endocrinol, London, England.
    Odia, Yazmin
    Baptist Hlth South Florida, Miami Canc Inst, Miami, FL USA.
    Rostami, Elham
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Gudjonsson, Olafur
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Shaw, Brian L.
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Med, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Med, Boston, MA 02115 USA.
    Cahill, Daniel P.
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02115 USA.
    Galanis, Evanthia
    Mayo Clin, Div Med Oncol, Dept Oncol, Dept Mol Med, Rochester, MN USA.
    Barker, Fred G., II
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02115 USA.
    Santagata, Sandro
    Harvard Med Sch, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
    Brastianos, Priscilla K.
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Neurol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Neurooncol,Dept Med, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurosurg, Div Hematol Oncol,Dept Med, Boston, MA 02115 USA.
    Targeted treatment of papillary craniopharyngiomas harboring BRAF V600E mutations2019In: Cancer, ISSN 0008-543X, E-ISSN 1097-0142, Vol. 125, no 17, p. 2910-2914Article in journal (Other academic)
    Abstract [en]

    Papillary craniopharyngiomas (PCPs) are characterized by the presence of BRAF V600E mutations, which are emerging as a useful guide for diagnosis and treatment decision making. The ongoing multicenter phase 2 Alliance A071601 trial is evaluating the efficacy of BRAF and mitogen-activated protein kinase kinase (MEK) inhibitors for patients with PCPs. With continued successful responses, it is proposed that BRAF (and MEK) inhibitors be evaluated for the neoadjuvant treatment of patients with PCPs.

  • 10.
    Lenell, Samuel
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Nyholm, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Lewén, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Enblad, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Clinical outcome and prognostic factors in elderly traumatic brain injury patients receiving neurointensive care2019In: Acta Neurochirurgica, ISSN 0001-6268, E-ISSN 0942-0940, Vol. 161, no 6, p. 1243-1254Article in journal (Refereed)
    Abstract [en]

    Background: The probability of favorable outcome after traumatic brain injury (TBI) decreases with age. Elderly,≥60 years, are an increasing part of our population. Recent studies have shown an increase of favorable outcome in elderly over time. However,the optimal patient selection and neurointensive care (NIC) treatments may differ in the elderly and the young. The aims of this study were to examine outcome in a larger group of elderly TBI patients receiving NIC and to identify demographic and treatmentrelated prognostic factors.

    Methods: Patients with TBI≥60 years receiving NIC at our department between 2008 and 2014 were included. Demographics, co-morbidity, admission characteristics, and type of treatments were collected. Clinical outcome at around 6 months was assessed. Potential prognostic factors were included in univariate and multivariate regression analysis with favorable outcomeas dependent variable.

    Results: Two hundred twenty patients with mean age 70 years (median 69; range 60–87) were studied. Overall, favorable outcome was 46% (Extended Glasgow Outcome Scale (GOSE) 5–8), unfavorable outcome 27% (GOSE 2–4), and mortality 27% (GOSE 1). Significant independent negative prognostic variables were high age (p< 0.05), multiple injuries (p<0.05),GCSM≤3 on admission (p< 0.05), and mechanical ventilation (p<0.001).

    Conclusions: Overall, the elderly TBI patients> 60 years receiving modern NIC in this study had a fair chance of favorable outcome without large risks for severe deficits and vegetative state, also in patients over 75 years of age. High age, multiple injuries, GCS M≤3 on admission, and mechanical ventilation proved to be independent negative prognostic factors. The results underline that a selected group of elderly with TBI should have access to NIC

  • 11. Niemelä, Valter
    et al.
    Landtblom, Anne-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Landtblom: Neurology.
    Nyholm, Dag
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Kneider, Maria
    Sahlrenska akademin, Göteborgs universitet.
    Constantinescu, Radu
    Sahlrenska akademin, Göteborgs universitet.
    Paucar, Martin
    Karolinska institutet.
    Svenningsson, Per
    Karolinska institutet.
    Abujrais, Sandy
    Uppsala University.
    Shevchenko, Ganna
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Bergquist, Jonas
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Sundblom, Jimmy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    CSF Proenkephalin decreases with the progression of Huntington's diseaseManuscript (preprint) (Other academic)
    Abstract [en]

    Identifying molecular changes that contribute to the onset and progression of Huntington's disease (HD) is of importance for the development and evaluation of potential therapies. We conducted an unbiased mass-spectrometry proteomic analysis on the cerebrospinal fluid of 12 manifest HD patients (ManHD), 13 presymptomatic gene expansion carriers (pGEC) and 38 controls. In ManHD compared to pGEC 10 proteins were downregulated, and 43 upregulated. Decreased levels of proenkephalin (PENK) and transthyretin along with upregulated proteins (VASN, STC2, SGCE and C7) were all closely linked to HD symptom severity. The decreased PENK levels were replicated in a separate cohort of 23 ManHD and 23 controls where absolute quantitation was performed. We hypothesize that declining PENK levels reflect the degeneration of medium spiny neurons (MSNs) that produce PENK, and that assays for PENK may serve as a surrogate marker for the state of MSNs in HD.   

  • 12.
    Sundblom, Jimmy
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Gallinetti, Sara
    Uppsala University, Disciplinary Domain of Science and Technology, Technology, Department of Engineering Sciences, Applied Materials Sciences.
    Birgersson, Ulrik
    Karolinska Inst, Div Imaging & Technol, Dept Clin Sci Intervent & Technol, Huddinge, Sweden.
    Engqvist, Håkan
    Uppsala University, Disciplinary Domain of Science and Technology, Technology, Department of Engineering Sciences, Applied Materials Sciences.
    Kihlström, Lars
    Karolinska Univ Hosp, Clin Neurosci, Dept Neurosurg, Stockholm, Sweden;Karolinska Inst, Stockholm, Sweden.
    Gentamicin loading of calcium phosphate implants: implications for cranioplasty2019In: Acta Neurochirurgica, ISSN 0001-6268, E-ISSN 0942-0940, Vol. 161, no 6, p. 1255-1259Article in journal (Refereed)
    Abstract [en]

    BackgroundSurgical site infections (SSI) are a significant risk in cranioplasty, with reported rates of around 8-9%. The most common bacteria associated with these nosocomial infections are of the Staphylococcus species, which have the ability to form biofilm. The possibility to deliver antibiotics, such as gentamicin, locally rather than systemically could potentially lower the early postoperative SSI. Various antibiotic dosages are being applied clinically, without any true consensus on the effectiveness.MethodsDrug release from calcium phosphate (CaP), polyetheretherketone (PEEK), and titanium (Ti) samples was evaluated. Microbiological studies with Staphylococcus aureus (SA) and Staphylococcus epidermidis (SE) including strains from clinical infection were used to establish clinically relevant concentrations.ResultsThe CaP samples were able to retain and release gentamicin overtime, whereas the Ti and PEEK samples did not show any drug uptake or release. A gentamicin loading concentration of 400g/ml was shown to be effective in in vitro microbiological studies with both SA and SE.ConclusionsOut of the three materials studied, only CaP could be loaded with gentamicin. An initial loading concentration of 400g/ml appears to establish an effective gentamicin concentration, possibly translating into a clinical benefit in cranioplasty.

  • 13.
    Svedung-Wettervik, Teodor
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Howells, Timothy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Enblad, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Lewén, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Temporal Neurophysiological Dynamics in Traumatic Brain Injury: Role of Pressure Reactivity and Optimal Cerebral Perfusion Pressure for Predicting Outcome2019In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 36, no 11, p. 1818-1827Article in journal (Refereed)
    Abstract [en]

    Intracranial pressure (ICP), cerebral perfusion pressure (CPP), and the pressure reactivity index (PRx) have been shown to correlate with outcome after traumatic brain injury (TBI), but their temporal evolution is less studied. Optimal CPP (CPPopt; i.e., the CPP with the lowest [optimal] PRx value) has been proposed as a dynamic, individualized CPP target. Our aim was to map the temporal course of these parameters and their relation to outcome, in particular the extent and impact of CPP insults based both on fixed CPP thresholds and on divergence from CPPopt. Data from 362 TBI patients with ICP-monitoring treated at the neurointensive care unit of Uppsala University Hospital, Uppsala, Sweden, between 2008-2016 were retrospectively analyzed for the temporal course of ICP, mean arterial blood pressure, CPP, PRx, PRx55-15 (a variant of PRx), and CPPopt the first 10 days post-injury. PRx and PRx55-15 showed significantly lower/better values for those with favorable outcome, most pronounced on Days 2 to 5. PRx55-15 gave better separation between the two groups. In the univariate analysis, CPP insults (both fixed and CPPopt-thresholds) were significantly correlated with outcome on these days. Multi-variate logistic regression showed that age, Glasgow Coma Score Motor, pupillary abnormality at admission, CPP > CPPopt, and PRx55-15 were significant independent outcome predictors. PRx was significant when PRx55-15 was excluded. High PRx55-15 and high grade of monitoring time with CPP > CPPopt, but not the traditional fixed CPP thresholds, were strong predictors for worse clinical outcome. The study supports the concept that CPPopt is an important parameter in TBI management.

  • 14.
    Wettervik, Teodor Svedung
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
    Howells, Timothy
    Hillered, Lars
    Nilsson, Pelle
    Engquist, Henrik
    Lewén, Anders
    Enblad, Per
    Rostami, Elham
    Mild hyperventilation in traumatic brain injury - relation to cerebral energy metabolism, pressure autoregulation and clinical outcome.2019In: World Neurosurgery, ISSN 1878-8750, E-ISSN 1878-8769, article id S1878-8750(19)32530-6Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Hyperventilation is a controversial treatment in traumatic brain injury (TBI). Prophylactic severe hyperventilation below 3.3 kPa/25 mm Hg) is generally avoided, due to the risk of cerebral ischemia. Mild hyperventilation (arterial pCO2 within 4.0-4.5 kPa/30-34 mm Hg) in cases of intracranial hypertension is commonly used, but its safety and benefits are not fully elucidated. The aim of this study was to evaluate the use of mild hyperventilation and its relation to, cerebral energy metabolism, pressure autoregulation and clinical outcome in TBI.

    METHOD: This retrospective study was based on 120 patients with severe TBI treated at the neurointensive care unit, Uppsala university hospital, Sweden, 2008-2018. Data from cerebral microdialysis (glucose, pyruvate and lactate), arterial pCO2 and pressure reactivity index (PRx55-15) were analyzed for the first three days post-injury.

    RESULTS: Mild hyperventilation 4.0-4.5 kPa (30-34 mm Hg) was more frequently used early and the patients were gradually normoventilated. Low pCO2 was associated with slightly higher intracranial pressure and slightly lower cerebral perfusion pressure (p-value < 0.01). There was no univariate correlation between low pCO2 and worse cerebral energy metabolism. Multiple linear regression analysis showed that mild hyperventilation was associated with lower PRx55-15 day 2 (p-value = 0.03), suggesting better pressure autoregulation. Younger age and lower ICP were also associated with lower PRx55-15.

    CONCLUSIONS: These findings support the notion that mild hyperventilation is safe and may improve cerebrovascular reactivity.

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