Advertisement

Mitochondrial Dysfunction after Traumatic Brain Injury

  • J. Sahuquillo
  • M.-A. Merino
  • C. Airado
Part of the Annual Update in Intensive Care and Emergency Medicine book series (AUICEM, volume 2012)

Abstract

Traumatic brain injury (TBI) is the leading cause of death and disability in the world’s population under 45 years of age. About 10% of cases of TBI are severe (Glasgow Coma Scale [GCS] score ≤ 8 points); in this subgroup, the incidence of poor neurological outcome (severe disability, vegetative state or death) still exceeds 55% inmany centers [2]. The endpoints in the early treatment of TBI are adequate and aggressive resuscitation and patient management in the neurointensive care unit is focused on the avoidance and treatment of high intracranial pressure (ICP). To date, no neuroprotective therapy has proven effective in controlled clinical trials involving severe TBI and the International Mission for Prognosis and Analysis of Clinical Trials inTBI (IMPACT) study showed that despite a significant reduction in mortality, neurological sequelae in TBI survivors have not changed significantly in the last 25 years [3].

Keywords

Traumatic Brain Injury Mitochondrial Dysfunction Traumatic Brain Injury Patient Severe Head Injury Poor Neurological Outcome 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Ekert PG, Vaux DL (2005) The mitochondrial death squad: hardened killers or innocent bystanders? Curr Opin Cell Biol 17: 626–630PubMedCrossRefGoogle Scholar
  2. 2.
    Gomez PA, Lobato RD, Gonzalez P, et al (1999) Severe head injury. Hospital 12 de Octubre data base. Description of the data and analysis of the final outcome. Neurocirugía 10: 297–308Google Scholar
  3. 3.
    Marmarou A, Lu J, Butcher I, et al (2007) IMPACT database of traumatic brain injury: design and description. J Neurotrauma 24: 239–250PubMedCrossRefGoogle Scholar
  4. 4.
    Graham DI, Adams JH, Doyle D (1978) Ischaemic brain damage in fatal non-missile head injuries. J Neurol Sci 39: 213–234PubMedCrossRefGoogle Scholar
  5. 5.
    Graham DI, Ford DI, Adams JH, et al (1989) Ischaemic brain damage is still common in fatal non-missile head injury. J Neurol Neurosurg Psychiatry 52: 346–350PubMedCrossRefGoogle Scholar
  6. 6.
    Marion DW, Darby J, Yonas H (1991) Acute regional cerebral blood flow changes caused by severe head injuries. J Neurosurg 74: 407–414PubMedCrossRefGoogle Scholar
  7. 7.
    Bouma GJ, Muizelaar JP, Stringer WA, et al (1992) Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. J Neurosurgery 77: 360–368CrossRefGoogle Scholar
  8. 8.
    Bellander BM, Cantais E, Enblad P, et al (2004) Consensus meeting on microdialysis in neurointensive care. Intensive Care Med 12: 2166–2169CrossRefGoogle Scholar
  9. 9.
    Hillered L, Vespa PM, Hovda DA (2005) Translational neurochemical research in acute human brain injury: the current status and potential future for cerebral microdialysis. J Neurotrauma 22: 3–41PubMedCrossRefGoogle Scholar
  10. 10.
    Soustiel JF, Larisch S (2010) Mitochondrial damage: a target for new therapeutic horizons. Neurotherapeutics 7: 13–21PubMedCrossRefGoogle Scholar
  11. 11.
    Soustiel JF, Sviri GE (2007) Monitoring of cerebral metabolism: non-ischemic impairment of oxidative metabolism following severe traumatic brain injury. Neurol Res 29: 654–660PubMedCrossRefGoogle Scholar
  12. 12.
    Vespa P, Bergsneider M, Hattori N, et al (2005) Metabolic crisis without brain ischemia is common after traumatic brain injury: a combined microdialysis and positron emission tomography study. J Cereb Blood Flow Metab 25: 763–774PubMedCrossRefGoogle Scholar
  13. 13.
    Vilalta A, Sahuquillo J, Merino MA, et al (2011) Normobaric hyperoxia in traumatic brain injury. Does brain metabolic state influence the response to hyperoxic challenge? J Neurotrauma 28: 1139–1148PubMedCrossRefGoogle Scholar
  14. 14.
    Soustiel JF, Vlodavsky E, Milman F, Gavish M, Zaaroor M (2011) Improvement of cerebral metabolism mediated by Ro5-4864 is associated with relief of intracranial pressure and mitochondrial protective effect in experimental brain injury. Pharm Res 28: 2945–2953PubMedCrossRefGoogle Scholar
  15. 15.
    Timofeev I, Carpenter KL, Nortje J, et al (2011) Cerebral extracellular chemistry and outcome following traumatic brain injury: a microdialysis study of 223 patients. Brain 134: 484–494PubMedCrossRefGoogle Scholar
  16. 16.
    Fink M (1997) Cytopathic hypoxia in sepsis. Acta Anesthesiol Scand (Suppl) 110: 87–95CrossRefGoogle Scholar
  17. 17.
    Siggäard-Andersen O, Ulrich A, Gothgen IH (1995) Classes of tissue hypoxia. Acta Anaesthesiol Scand 39: 137–142CrossRefGoogle Scholar
  18. 18.
    Nelson DW, Thornquist B, Maccallum RM, et al (2011) Analyses of cerebral microdialysis in patients with traumatic brain injury: relations to intracranial pressure, cerebral perfusion pressure and catheter placement. BMC Med 9: 21PubMedCrossRefGoogle Scholar
  19. 19.
    Connett RJ, Honig CR, Gayeski TE, Brooks GA (1990) Defining hypoxia: a systems view of VO2, glycolysis, energetics, and intracellular PO2. J Appl Physiol 68: 833–842PubMedGoogle Scholar
  20. 20.
    Siggäard-Andersen O, Fogh-Andersen N, Gothgen IH, Larsen VH (1995) Oxygen status of arterial and mixed venous blood. Crit Care Med 23: 1284–1293PubMedCrossRefGoogle Scholar
  21. 21.
    Harzing AW (2007) Publish or Perish. Available at http://www.harzing.com/pop.htm. Accessed Nov 2011Google Scholar
  22. 22.
    Siggäard-Andersen O, Gothgen IH (1995) Oxygen and acid-base parameters of arterial and mixed venous blood, relevant versus redundant. Acta Anaesthesiol Scand 39: 21–27CrossRefGoogle Scholar
  23. 23.
    Siggaard-Andersen M, Siggaard-Andersen O (1995) Oxygen status algorithm, version 3, with some applications. Acta Anaesthesiol Scand 39: 13–20CrossRefGoogle Scholar
  24. 24.
    Sahuquillo J, Poca MA, Amoros S (2001) Current aspects of pathophysiology and cell dysfunction after severe head injury. Curr Pharm Des 7: 1475–503PubMedCrossRefGoogle Scholar
  25. 25.
    Marin-Caballos AJ, Murillo-Cabezas F, Dominguez-Roldan JM, et al (2008) [Monitoring of tissue oxygen pressure (PtiO2) in cerebral hypoxia: diagnostic and therapeutic approach.] Med Intensiva 32: 81–90PubMedCrossRefGoogle Scholar
  26. 26.
    Poca MA, Sahuquillo J, Mena MP, Vilalta A, Riveiro M (2005) [Recent advances in regional cerebral monitoring in the neurocritical patient: brain tissue oxygen pressure monitoring, cerebral microdialysis and near-infrared spectroscopy.] Neurocirugía (Astur) 16: 385–410Google Scholar
  27. 27.
    Gilmer LK, Roberts KN, Joy K, Sullivan PG, Scheff SW (2009) Early mitochondrial dysfunction after cortical contusion injury. J Neurotrauma 26: 1271–1280PubMedCrossRefGoogle Scholar
  28. 28.
    Clausen TF, Zauner AF, Levasseur Je FAU, Rice Ac FAU, Bullock R (2001) Induced mitochondrial failure in the feline brain: implications for understanding acute post-traumatic metabolic events. Brain Res 908: 35–48PubMedCrossRefGoogle Scholar
  29. 29.
    Obrist WD, Langfitt TW, Jaggi JL, Cruz J, Gennarelli TA (1984) Cerebral blood flow and metabolism in comatose patients with acute head injury.Relationship to intracranial hypertension. J Neurosurg 61: 241–253PubMedCrossRefGoogle Scholar
  30. 30.
    Burwell LS, Nadtochiy SM, Brookes PS (2009) Cardioprotection by metabolic shut-down and gradual wake-up. J Mol Cell Cardiol 46: 804–810PubMedCrossRefGoogle Scholar
  31. 31.
    Vespa PM, McArthur D, O’Phelan K, et al (2003) Persistently low extracellular glucose correlates with poor outcome 6 months after human traumatic brain injury despite a lack of increased lactate: a microdialysis study. J Cereb Blood Flow Metab 23: 865–877PubMedCrossRefGoogle Scholar
  32. 32.
    Bullock R, Maxwell WL, Graham DI, Teasdale GM, Adams JH (1991) Glial swelling following human cerebral contusion: an ultrastructural study. J Neurol Neurosurg Psychiatry 54: 427–434PubMedCrossRefGoogle Scholar
  33. 33.
    Verweij BH, Muizelaar JP, Vinas FC, et al (1997) Mitochondrial dysfunction after experimental and human brain injury and its possible reversal with a selective N-type calcium channel antagonist (SNX-111). Neurol Res 19: 334–339PubMedGoogle Scholar
  34. 34.
    Xiong Y, Peterson PL, Verweij BH, et al (1998) Mitochondrial dysfunction after experimental traumatic brain injury: combined efficacy of SNX-111 and U-101033E. J Neurotrauma 15: 531–544PubMedCrossRefGoogle Scholar
  35. 35.
    Geller RJ, Barthold C, Saiers JA, Hall AH (2006) Pediatric cyanide poisoning: causes, manifestations, management, and unmet needs. Pediatrics 118: 2146–2158PubMedCrossRefGoogle Scholar
  36. 36.
    Fink MP (2002) Bench-to-bedside review: Cytopathic hypoxia. Crit Care 6: 491–499PubMedCrossRefGoogle Scholar
  37. 37.
    Zhang J, Dawson VL, Dawson TM, Snyder SH (1994) Nitric oxide activation of poly(ADPribose) synthetase in neurotoxicity. Science 263: 687–689PubMedCrossRefGoogle Scholar
  38. 38.
    Szabó C, Zingarelli B, O’Connor M, Salzman AL (1996) DNA strand breakage, activation of poly (ADP-ribose) synthetase, and cellular energy depletion are involved in the cytotoxicity of macrophages and smooth muscle cells exposed to peroxynitrite. Proc Natl Acad Sci USA 93: 1753–1758PubMedCrossRefGoogle Scholar
  39. 39.
    Baines CP (2009) The molecular composition of the mitochondrial permeability transition pore. J Mol Cell Cardiol 46: 850–857PubMedCrossRefGoogle Scholar
  40. 40.
    Kroemer G, Reed JC (2000) Mitochondrial control of cell death. Nat Med 6: 513–519PubMedCrossRefGoogle Scholar
  41. 41.
    Halestrap AP (2009) What is the mitochondrial permeability transition pore? J Mol Cell Cardiology 46: 821–831CrossRefGoogle Scholar
  42. 42.
    Magnoni S, Ghisoni L, Locatelli M, et al (2003) Lack of improvement in cerebral metabolism after hyperoxia in severe head injury: a microdialysis study. J Neurosurgery 98: 952–958CrossRefGoogle Scholar
  43. 43.
    Menzel M, Doppenberg EM, Zauner A, et al (1999) Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury. J Neurosurgery 91: 1–10CrossRefGoogle Scholar
  44. 44.
    Manabe H, Okonkwo DO, Gainer JL, Clarke RH, Lee KS (2010) Protection against focal ischemic injury to the brain by trans-sodium crocetinate. Laboratory investigation. J Neurosurg 113: 802–809PubMedCrossRefGoogle Scholar
  45. 45.
    Stennett AK, Dempsey GL, Gainer JL (2006) Trans-Sodium crocetinate and diffusion enhancement. J Phys Chem B 110: 18078–18080PubMedCrossRefGoogle Scholar
  46. 46.
    Lo EH, Dalkara T, Moskowitz MA (2003) Mechanisms, challenges and opportunities in stroke. Nat Rev Neurosci 4: 399–415PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2012

Authors and Affiliations

  • J. Sahuquillo
  • M.-A. Merino
  • C. Airado

There are no affiliations available

Personalised recommendations