• M J Merkel and A M Brambrink.
• Department of Anesthesiology and Peri-Operative Medicine, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, UHS-2, 97239, Portland, OR 97239, USA.
• Anaesthesist. 2008 Aug 1;57(8):794-802.

AbstractDysregulation of the intracellular calcium concentration is thought to play a key role in the so-called ischemic cascade, as well as for the development of cerebral vasospasm after subarachnoid haemorrhaging (SAH). Therefore, the prophylactic/therapeutic administration of cerebral calcium channel blockers for neurosurgical patients appears to be a compelling idea to prevent ischemic complications. There are abundant data on the efficacy of cerebral calcium antagonists in various animal models of central nervous system pathologies, however, very little clinical evidence exists to justify their use in humans in respective situations. So far there is only evidence for a long-term treatment effect of oral nimodipine in patients suffering from SAH, and this is based essentially on one large controlled clinical trial. Experimental results suggest that blockers of other calcium channel subtypes may be promising for future clinical roles in primary or secondary ischemic brain injury. However, it is also possible that calcium-independent mechanisms play a more important role during the development of the ischemic damage than previously assumed. Currently, there is no clinical evidence to support the prophylactic use of calcium antagonists to prevent ischemic complications in neurosurgical patients without SAH.

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