Acta Neurochirurgica

, Volume 129, Issue 3, pp 152–157

Effect of intraventricular haemorrhage and rebleeding following subarachnoid haemorrhage on CSF eicosanoids


  • J. D. Pickard
    • Academic Neurosurgical UnitUniversity of Cambridge
    • Clinical Neurological Sciences GroupUniversity of Southampton
  • V. Walker
    • Department of Clinical BiochemistryUniversity of Southampton
  • L. Brandt
    • University Department of Neurosurgery
  • S. Zygmunt
    • University Department of Neurosurgery
    • Department of NeurosurgeryUniversity Hospital of Northern Sweden
  • J. Smythe
    • Department of Clinical BiochemistryUniversity of Southampton
Clinical Articles

DOI: 10.1007/BF01406495

Cite this article as:
Pickard, J.D., Walker, V., Brandt, L. et al. Acta neurochir (1994) 129: 152. doi:10.1007/BF01406495


CSF eicosanoid levels are raised following subarachnoid haemorrhage but not sufficiently to be vasoactive per se within the cerebral circulation. Rebleeding and intraventricular haemorrhage are two factors associated with a worse outcome after aneurysmal SAH. We have examined the effects of these two factors on the CSF levels of TXB2 (TXA2 metabolite), PG 6-keto F (prostacyclin metabolite), PGF and PGE2 in 44 patients following subarachnoid haemorrhage. In 15 patients who had received no non-steroidal antiinflammatory agent or dexamethasone, intraventricular haemorrhage increased the median levels of all four eicosanoids in ventricular CSF by 2.1–5.1-fold. In 4 patients who rebled, the CSF median levels of all four eicosanoids were raised up to 250-fold over the normal range. These concentrations are just sufficient to have cerebrovascular and neuromodulatory effects.


Cerebrospinal fluideicosanoidsprostaglandinssubarachnoid haemorrhagethromboxane

Copyright information

© Springer-Verlag 1994