Skip to main content
Log in

Does a routine operation for intracranial aneurysm incur brain damage?

  • Clinical Articles
  • Published:
Acta Neurochirurgica Aims and scope Submit manuscript

Summary

A biochemical marker of brain cell damage, the BB-isozyme of the intracellular enzyme Creatine Kinase (CK), was used to evaluate any possible injury to the brain, caused by an operation for a ruptured intracranial aneurysm (SAH).

CSF-CK BB was assessed before and at intervals after operation in a series of 60 patients, aged 29–71 (mean 51 years) operated on for intracranial aneurysms, all but one after SAH. The m/f ratio was 18/42. 35 of the 60 patients were operated on acutely, i.e. within 72 hours after the SAH. CK BB was determined as CKB-activity after immunological inactivation of CKM. Normally there should be almost no detectable enzyme activity in the CSF.

The pre-operative CK BB-activity was 0.01 + −0.01 mikrokatal in the patients in Hunt & Hess grade I who were operated on > 7 days after their SAH, and 0.05 + −0.04 in those operated on acutely, probably still reflecting the effects of the SAH on the brain. The mean per-operative CKBB increase was 0.11 + −0.17 for patients who had an uneventful postoperative course, compared to 0.39 + −0.49 for those showing some degree of immediate postoperative deterioration. This difference is significant at the 1% level. 52 of the 60 patients showed a rise of CK BB after operation. The mean increase for those patients operated upon in a good state and without any complication or postoperative deterioration was 0.02 + −0.03 mikrokatal, which could therefore be considered as a “normal” or acceptable elevation. The per-operative increase for the whole group was 0.14 + −0.19 and 0.28 + −0.38 after late and early operation respectively. A temporary arterial clip was applied for 1 to 27 (totally) minutes in 18 patients. The mean increase for that group did not differ significantly from the rest.

The study shows that an operation for intracranial aneurysm causes at least some brain cell damage even in the absence of any clinical signs of deterioration, and more so with early than with late operation. The use of a temporary clip, at least for less than 7 minutes, does not per se cause any further brain cell damage, as mirrored by the CK BB.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  1. Auer LM, Kassel N (eds) (1985) Timing of aneurysm surgery. Berlin, 685 pp

  2. Charbel FD, Ausman JI, Diaz FG, Malik GM, Dujovny M, Sanders J (1991) Temporary clipping in aneurysm surgery: technique and results. Surg Neurol 36: 83–90

    PubMed  Google Scholar 

  3. Hans P, Born JD, Albert A (1987) Extrapolated creatine kinase-BB isoenzyme activity in assessment of initial brain damage after severe head injury. J Neurosurg 66: 714–717

    PubMed  Google Scholar 

  4. Hunt WE, Kassell N, Pertuiset B, Sano K, Teasdale G, De Villier JC, Drake CG (1988) Report of the World Federation of Neurological Surgeons Committee on a Universal Subarachnoid Hemorrhage Grading Scale. J Neurosurg 68: 985–986

    PubMed  Google Scholar 

  5. Kassell NF, Torner JC, Haley EC Jr, Jane JA, Adams HP, Kongable GL, and Participants (1990) The International Co-operative Study on the timing of aneurysm surgery. Part I: overall management results. J Neurosurg 73: 18–36

    PubMed  Google Scholar 

  6. Ljunggren B, Säveland H, Brandt L, Kågström E, Rehncrona S, Nilsson PE (1983) Temporary clipping during early operation for ruptured aneurysm: preliminary report. Neurosurgery 12: 525–530

    PubMed  Google Scholar 

  7. Moma F, Wang AD, Symon L (1987) Effects of temporary arterial occlusion on somatosensory evoked responses in aneurysm surgery. Surg Neurol 27: 343–352

    PubMed  Google Scholar 

  8. Persson L, Hårdemark H-G, Gustafsson J, Rundström G, Mendel-Hartvig I, Esscher T, and Påhlman S (1987) S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system. Stroke 18: 911–918

    PubMed  Google Scholar 

  9. Pool JL (1961) Aneurysms of the anterior communicating artery. J Neurosurg 18: 98–111

    PubMed  Google Scholar 

  10. Rabow L, Hedman G (1979) CKBB-isoenzymes as a sign of cerebral injury. Acta Neurochir (Wien) [Suppl] 28: 108–112

    Google Scholar 

  11. Rabow L, DeSalles AA, Becker DPet al (1986) CSF brain creatine kinase level and lactic acidosis in severe head injury. J Neurosurg 65: 625–629

    PubMed  Google Scholar 

  12. Rabow L, Cook D, Lipper MHet al (1989) Relationship CT attenuation changes and post-traumatic CSF-CKBB-activity after severe head injury in man. Acta Neurochir (Wien) 100: 155–157

    Google Scholar 

  13. Säveland H, Hillman J, Brandt L, Edner G, Jakobsson K-E, Algers G (1992) Overall outcome in aneurysmal subarachnoid hemorrhage. J Neurosurg 76: 729–734

    PubMed  Google Scholar 

  14. Skogseid IM, Nordby HK, Urdal P, Paus E, Lilleaas F (1992) Increased serum creatine kinase BB and neuron specific enolase following head injury indicates brain damage. Acta Neurochir (Wien) 115: 106–111

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Rabow, L., Algers, G., Elfversson, J. et al. Does a routine operation for intracranial aneurysm incur brain damage?. Acta neurochir 133, 13–16 (1995). https://doi.org/10.1007/BF01404941

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01404941

Keywords

Navigation