Cerebral Blood Flow and Metabolism in Severe Head Injury

  • F. Della Corte
  • A. Caricato
  • F. Pappalardo
Conference paper


Primary neurologic injury due to any kind of insult (traumatic, ischemic, hypoxic, metabolic) can be followed by a chain of pathological events, that can worsen or perpetuate the primary lesion within minutes, hours or days. This group of derangements is traditionally defined as secondary damage, and its principal determinant, regardless of the producing cause, is ischemia-anoxia.


Cerebral Blood Flow Head Injury Cerebral Perfusion Pressure Severe Head Injury Head Injured Patient 
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  1. 1.
    Bouma GJ, Muizelaar JP, Choi SC et al (1991) Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg 75: 685–693PubMedCrossRefGoogle Scholar
  2. 2.
    Gopinath SP, Robertson CS, Contant CF et al (1994) Jugular venous desaturation and outcome after head injury. J Neurol Neurosurg Psychiatry 57: 717–723PubMedCrossRefGoogle Scholar
  3. 3.
    Robertson CS, Contant CF, Gokaslan ZL et al (1992) Cerebral blood flow, arteriovenous oxygen difference, and outcome in head injured patients. J Neurol Neurosurg Psychiatry 55: 594–603PubMedCrossRefGoogle Scholar
  4. 4.
    Kelly DF, Martin NA, Kordestani R et al (1997) Cerebral blood flow as a predictor of outcome following traumatic brain injury. J Neurosurg 86: 633–641PubMedCrossRefGoogle Scholar
  5. 5.
    Delia Corte F, Giordano A, Pennisi MA et al (1997) Quantitative cerebral blood flow and metabolism determination in the first 48 hours after severe head injury with a new dynamic spect device. Acta Neurochirurgica, July (in press)Google Scholar
  6. 6.
    Jaggi JL, Obrist WD, Gennarelli TA et al (1990) Relationship of early cerebral blood flow and metabolism to outcome in acute head injury. J Neurosurg 72: 176–182PubMedCrossRefGoogle Scholar
  7. 7.
    Sakas DE, Bullock MR, Patterson JP et al (1995) Focal cerebral hyperemia after focal head injury in humans: a benign phenomenon? J Neurosurg 83: 277–284PubMedCrossRefGoogle Scholar
  8. 8.
    Goodman JC, Gopinath SP, Valadka AB et al (1996) Lactic acid and aminoacid fluctuations measured using microdialysis reflect physiological derangements in head injury. Acta Neuroch [Suppl]67: 37–39Google Scholar
  9. 9.
    Santbrink H, Maas AIR, Avezaas CJJ (1996) Continuous monitoring of partial pressure of brain tissue oxygen in patients with severe head injury. Neurosurg 38: 21–31CrossRefGoogle Scholar
  10. 10.
    Menzel M, Doppenberg E, Zauner A (1997) Can we improve brain tissue oxygenation with increased inspired oxygen concentration? Acta Neuroch [Suppl] (in press)Google Scholar
  11. 11.
    Bellinzona G, Bruzzone P, Imberti R et al (1997) Effects of cerebral perfusion pressure on brain tissue PO2 in patients with severe head injury. Acta Neuroch [Suppl] (in press)Google Scholar
  12. 12.
    Doppenberg E, Zauner A, Bullock MR et al (1997) Determination of the ischemic threshold for brain tissue oxygenation in the severely head injured patient. Acta Neuroch [Suppl] (in press)Google Scholar
  13. 13.
    Zauner A, Doppenberg E, Menzel M et al (1997) Relationship of brain oxygen to GCS, ICP, CPP, and outcome in severely head injured patients. Acta Neuroch [Suppl] (in press)Google Scholar

Copyright information

© Springer-Verlag Italia, Milano 1998

Authors and Affiliations

  • F. Della Corte
  • A. Caricato
  • F. Pappalardo

There are no affiliations available

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