• J-M Malinovsky, M Malinge, J-Y Lepage, and M Pinaud.
• Department of Anaesthesia and Intensive Care, Hôtel-Dieu, 44093 Nantes Cedex 1, France. jeanmarc.malinovsky@chu-nantes.fr
• Br J Anaesth. 2003 Jun 1; 90 (6): 742-5.

BackgroundIn patients with spinal cord injury, cephalad spread of intrathecal (i.t.) medication could be delayed.MethodsWe used bispectral index and an observer scale to assess sedation after two different doses of i.t. clonidine in patients with or without spinal cord injury. Twelve patients with neurological deficit caused by trauma (Spinal Cord Injury, SCI) were compared with patients without neurological disease. They received 10 mg of i.t. bupivacaine with clonidine, with either 50 microg (low dose, n=6) or 150 microg (high dose, n=6) at L(2)-L(3). A further 12 patients, six with spinal trauma lesion and six healthy, received i.t. bupivacaine and 150 micro g of i.m. clonidine.ResultsSedation and a decrease in BIS occurred only in patients receiving 150 microg of clonidine. Onset of sedation and the decrease in BIS was delayed in most spinal cord injured patients whatever the route of administration (P<0.001). Duration of sedation was not different between the groups. Delayed sedation and decrease of BIS after i.t. clonidine in patients with spinal cord injury are similar than those observed after i.m. clonidine.ConclusionA systemic effect is likely to be the main reason for sedation.

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