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J Neurol Neurosurg Psychiatry 2003;74:765-770 doi:10.1136/jnnp.74.6.765
  • Paper

Cerebrovascular pressure reactivity is related to global cerebral oxygen metabolism after head injury

  1. L A Steiner1,
  2. J P Coles1,
  3. M Czosnyka2,
  4. P S Minhas2,
  5. T D Fryer1,
  6. F I Aigbirhio1,
  7. J C Clark1,
  8. P Smielewski1,
  9. D A Chatfield3,
  10. T Donovan1,
  11. J D Pickard2,
  12. D K Menon3
  1. 1Wolfson Brain Imaging Centre, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK
  2. 2Academic Neurosurgery, Addenbrooke’s Hospital
  3. 3University Department of Anaesthesia, Addenbrooke’s Hospital
  1. Correspondence to:
 Dr Luzius A Steiner, Academic Neurosurgery, Box 167, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK; 
 las30{at}cam.ac.uk
  • Received 7 August 2002
  • Accepted 4 February 2003
  • Revised 29 January 2003

Abstract

Background: After head injury, impaired cerebrovascular autoregulation has been associated with abnormally high or low cerebral blood flow. The physiological relevance of cerebral blood flow levels is difficult to assess in these patients, whose cerebral metabolic rate for oxygen (CMRo2) is known to be abnormal. Investigation of these relations requires quantitative measures of cerebral blood flow and CMRO2, to allow assessment of oxygen supply and demand relations.

Objectives: To investigate the relation between dysautoregulation and global cerebral oxygen metabolism following head injury.

Methods: Using positron emission tomography, global cerebral blood flow, CMRo2, and oxygen extraction fraction were determined in 22 patients who were investigated in 26 examinations on days 1 to 11 (mean (SD), 3.5 (2.3)) after head injury. Cerebrovascular pressure reactivity was assessed using a pressure reactivity index, calculated as the moving linear correlation coefficient between mean arterial blood pressure and intracranial pressure. Outcome was assessed six months after injury using the Glasgow outcome scale.

Results: Low CMRo2 was associated with disturbed pressure reactivity (inverse function, R2 = 0.21, p = 0.018) and there was a correlation between disturbed pressure reactivity and oxygen extraction fraction (quadratic function, R2 = 0.55, p = 0.0001). There was no significant relation between pressure reactivity and cerebral blood flow. An unfavourable outcome was associated with disturbed pressure reactivity. There was no significant relation between outcome and CMRo2 or oxygen extraction fraction.

Conclusions: There is a close relation between dysautoregulation and abnormal cerebral metabolism but not blood flow. Further studies are needed to determine whether metabolic dysfunction is a result of or a cause of disturbed pressure reactivity, and to establish if there is a relation between cerebral oxygen metabolism and outcome.

Footnotes

  • Competing interests: none declared

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