Experts and Doctors on brain injuries in Stockholm, Sweden

Summary

Locale: Stockholm, Sweden
Topic: brain injuries

Top Publications

  1. Günther M, Al Nimer F, Gahm C, Piehl F, Mathiesen T. iNOS-mediated secondary inflammatory response differs between rat strains following experimental brain contusion. Acta Neurochir (Wien). 2012;154:689-97 pubmed publisher
    ..Excessive peroxynitrite formation was probably prevented by limitation of available superoxide. Subsequently, the higher expression of potentially deleterious iNOS in PVGa did not result in increased neuronal death. ..
  2. Skiöld B, Eriksson C, Eliasson A, Adén U, Vollmer B. General movements and magnetic resonance imaging in the prediction of neuromotor outcome in children born extremely preterm. Early Hum Dev. 2013;89:467-72 pubmed publisher
    ..005), whereas sensitivity remained unchanged. The presence of definitely abnormal GMs was predictive of CP: prediction was significantly enhanced when the GMs assessment was combined with findings from MRI obtained at TEA. ..
  3. Lundberg J, Le Blanc K, Söderman M, Andersson T, Holmin S. Endovascular transplantation of stem cells to the injured rat CNS. Neuroradiology. 2009;51:661-7 pubmed publisher
    ..The method is significantly more efficient than the intravenous route and causes no side effects in the current model. The technique can potentially be used for repeated transplantation to the CNS after TBI and in other diseases. ..
  4. Lindblom R, Ström M, Heinig M, Al Nimer F, Aeinehband S, Berg A, et al. Unbiased expression mapping identifies a link between the complement and cholinergic systems in the rat central nervous system. J Immunol. 2014;192:1138-53 pubmed publisher
  5. Holmberg P, Liljequist S, Wagner A. Secondary brain injuries in thalamus and hippocampus after focal ischemia caused by mild, transient extradural compression of the somatosensori cortex in the rat. Curr Neurovasc Res. 2009;6:1-11 pubmed
  6. Boman I, Lindberg Stenvall C, Hemmingsson H, Bartfai A. A training apartment with a set of electronic memory aids for patients with cognitive problems. Scand J Occup Ther. 2010;17:140-8 pubmed publisher
  7. Huang M, Risling M, Baker D. The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury. Psychoneuroendocrinology. 2016;63:398-409 pubmed publisher
    ..MEG signal may serve as a sensitive imaging marker for mTBI, distinguishable from abnormalities generated in association with PTSD. More work is needed to fully describe physiological mechanisms of post-concussive symptoms. ..
  8. Bellander B, Lidman O, Ohlsson M, Meijer B, Piehl F, Svensson M. Genetic regulation of microglia activation, complement expression, and neurodegeneration in a rat model of traumatic brain injury. Exp Brain Res. 2010;205:103-14 pubmed publisher
    ..Genetic factors that regulate inflammation elicited by brain trauma may be important for the development of secondary brain damage. ..
  9. Nekludov M, Antovic J, Bredbacka S, Blomback M. Coagulation abnormalities associated with severe isolated traumatic brain injury: cerebral arterio-venous differences in coagulation and inflammatory markers. J Neurotrauma. 2007;24:174-80 pubmed
    ..IL-6 and activation of the complement system (C5b-9) co-vary with hemostatic parameters in TBI patients. ..

More Information

Publications30

  1. Nekludov M, Bellander B, Blomback M, Wallen H. Platelet dysfunction in patients with severe traumatic brain injury. J Neurotrauma. 2007;24:1699-706 pubmed
    ..The observed platelet dysfunction appears to involve the cyclooxygenase pathway. TEG-PM analysis can be used to identify patients with a high risk of bleeding complications. ..
  2. Froelich M, Ni Q, Wess C, Ougorets I, Hartl R. Continuous hypertonic saline therapy and the occurrence of complications in neurocritically ill patients. Crit Care Med. 2009;37:1433-41 pubmed publisher
    ..However, there was a significant risk of developing hypernatremia. We conclude that CHS administration in patients with severe injuries is safe as long as sodium levels are carefully monitored. ..
  3. Ho J, Kleiven S. Can sulci protect the brain from traumatic injury?. J Biomech. 2009;42:2074-80 pubmed publisher
    ..The results suggested that the inclusion of sulci should be considered for future FE head models as it alters the strain and strain distribution in an FE model. ..
  4. Xie C, Ginet V, Sun Y, Koike M, Zhou K, Li T, et al. Neuroprotection by selective neuronal deletion of Atg7 in neonatal brain injury. Autophagy. 2016;12:410-23 pubmed publisher
  5. Lundberg J, Sodersten E, Sundström E, Le Blanc K, Andersson T, Hermanson O, et al. Targeted intra-arterial transplantation of stem cells to the injured CNS is more effective than intravenous administration: engraftment is dependent on cell type and adhesion molecule expression. Cell Transplant. 2012;21:333-43 pubmed publisher
    ..In addition, we conclude that careful analysis of cells intended for local, intra-arterial transplantation with respect to integrin expression is important. ..
  6. Nelson D, Nyström H, MacCallum R, Thornquist B, Lilja A, Bellander B, et al. Extended analysis of early computed tomography scans of traumatic brain injured patients and relations to outcome. J Neurotrauma. 2010;27:51-64 pubmed publisher
    ..Finally we present a practical clinical "rule of thumb" to help predict the probability of unfavorable outcome using clinical and CT variables. ..
  7. Nygren De Boussard C, Holm L, Cancelliere C, Godbolt A, Boyle E, Stålnacke B, et al. Nonsurgical interventions after mild traumatic brain injury: a systematic review. Results of the International Collaboration on Mild Traumatic Brain Injury Prognosis. Arch Phys Med Rehabil. 2014;95:S257-64 pubmed publisher
    ..Well-designed intervention studies are required to develop effective treatments and improve outcomes for adults and children at risk for persistent symptoms after MTBI. ..
  8. von Holst H, Li X, Kleiven S. Increased strain levels and water content in brain tissue after decompressive craniotomy. Acta Neurochir (Wien). 2012;154:1583-93 pubmed publisher
    ..Hence, this new numerical method provides more insight of the consequences following DC and may be used to better define the most optimal size and area of the craniotomy in reducing the strain level development. ..
  9. Rostami E, Davidsson J, Gyorgy A, Agoston D, Risling M, Bellander B. The terminal pathway of the complement system is activated in focal penetrating but not in mild diffuse traumatic brain injury. J Neurotrauma. 2013;30:1954-65 pubmed publisher
    ..The role of complement activation in TAI is unclear, but might indicate an alternative function following rot-TBI, such as opsonizing the synapses for elimination. ..
  10. Rostami E, Krueger F, Zoubak S, Dal Monte O, Raymont V, Pardini M, et al. BDNF polymorphism predicts general intelligence after penetrating traumatic brain injury. PLoS ONE. 2011;6:e27389 pubmed publisher
    ..Identifying the underlying mechanism of this brain-derived neurotrophic factor effect could provide insight into an important aspect of post-traumatic cognitive recovery. ..
  11. Witman N, Behm M, Ohman M, Morrison J. ADAR-related activation of adenosine-to-inosine RNA editing during regeneration. Stem Cells Dev. 2013;22:2254-67 pubmed publisher
    ..The link between RNA editing and regeneration provides further insights into how lower organisms, such as the newt, can activate essential molecular pathways via the discrete alteration of RNA sequences...
  12. von Holst H, Li X. Numerical impact simulation of gradually increased kinetic energy transfer has the potential to break up folded protein structures resulting in cytotoxic brain tissue edema. J Neurotrauma. 2013;30:1192-9 pubmed publisher
    ..The definition of mild, moderate, and severe TBI should thus be looked upon as the same condition and separated only by a gradual severity of impact. ..
  13. Thelin E, Johannesson L, Nelson D, Bellander B. S100B is an important outcome predictor in traumatic brain injury. J Neurotrauma. 2013;30:519-28 pubmed publisher
    ..Early samples of S100B, within 12?h after trauma, appear to have little prognostic value, and S100B should likely be sampled 12-36?h following trauma to best enhance TBI outcome prediction. ..
  14. Plantman S. Osteopontin is upregulated after mechanical brain injury and stimulates neurite growth from hippocampal neurons through ?1 integrin and CD44. Neuroreport. 2012;23:647-52 pubmed publisher
    ..Finally, growth on OPN was mediated through ?1 intregrins and CD44. These findings indicate that injury-induced OPN may support neurite sprouting, suggesting a role for this molecule in recovery from central nervous system trauma. ..
  15. Kenne E, Erlandsson A, Lindbom L, Hillered L, Clausen F. Neutrophil depletion reduces edema formation and tissue loss following traumatic brain injury in mice. J Neuroinflammation. 2012;9:17 pubmed publisher
    ..Our results suggest that neutrophils are involved in the edema formation, but not the extravasation of large proteins, as well as contributing to cell death and tissue loss following TBI in mice. ..
  16. Nakahara M, Ericson K, Bellander B. Diffusion-weighted MR and apparent diffusion coefficient in the evaluation of severe brain injury. Acta Radiol. 2001;42:365-9 pubmed
    ..To study apparent diffusion coefficient (ADC) maps in severely brain-injured patients...
  17. Nelson D, Thornquist B, MacCallum R, Nyström H, Holst A, Rudehill A, et al. Analyses of cerebral microdialysis in patients with traumatic brain injury: relations to intracranial pressure, cerebral perfusion pressure and catheter placement. BMC Med. 2011;9:21 pubmed publisher
    ..This suggests that disturbances other than pressure and/or flow have a dominant influence on MD levels in patients with TBI. ..
  18. Sköld M, von Gertten C, Sandberg Nordqvist A, Mathiesen T, Holmin S. VEGF and VEGF receptor expression after experimental brain contusion in rat. J Neurotrauma. 2005;22:353-67 pubmed
    ..The data provide a foundation for future pharmacological intervention studies focusing on posttraumatic angiogenesis and possible injury repair effects of the VEGF system in TBI. ..
  19. Al Nimer F, Ström M, Lindblom R, Aeinehband S, Bellander B, Nyengaard J, et al. Naturally occurring variation in the Glutathione-S-Transferase 4 gene determines neurodegeneration after traumatic brain injury. Antioxid Redox Signal. 2013;18:784-94 pubmed publisher
    ..A naturally occurring variation in Gsta4 expression in rats affects neurodegeneration after TBI. Further studies are needed to explore if genetic variability in Gsta4 can be associated to outcome also in human TBI. ..
  20. Lu M, Zhang X, Mix E, Quezada H, Jin T, Zhu J, et al. TNF-alpha receptor 1 deficiency enhances kainic acid-induced hippocampal injury in mice. J Neurosci Res. 2008;86:1608-14 pubmed publisher
    ..These data suggest that TNF-alpha may play a protective role through TNFR1 signaling. ..
  21. Gahm C, Holmin S, Rudehill S, Mathiesen T. Neuronal degeneration and iNOS expression in experimental brain contusion following treatment with colchicine, dexamethasone, tirilazad mesylate and nimodipine. Acta Neurochir (Wien). 2005;147:1071-84; discussion 1084 pubmed
    ..Early neuroprotection may to some extent target iNOS via different pathways since all tested drugs affected both iNOS expression and neuronal degeneration. ..