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This Article Full Text Full Text (PDF) All Versions of this Article: 570/2/421    most recent jphysiol.2005.095562v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lambert, G. Articles by Nitescu, P. Search for Related Content PubMed PubMed Citation Articles by Lambert, G. Articles by Nitescu, P. Related Collections Integrative

Departments of
¹ Clinical Physiology
² Clinical Neurophysiology
³ Anaesthesiology (Pain Section), Sahlgrenska Hospital, 413 45 Göteborg, Sweden
⁴ Department of Analytical Chemistry, Biomedical Centre, Uppsala University, 751 24 Uppsala, Sweden
⁵ Baker Heart Research Institute, Melbourne, Victoria 8008, Australia

Continuous intracisternal infusion of bupivacaine for the management of intractable pain of the head and neck is effective in controlling pain in this patient group. With the catheter tip being located at the height of the C1 vertebral body, autonomic regulatory information may also be influenced by the infusion of bupivacaine. By combining direct sampling of cerebrospinal fluid (CSF), via a percutaneously placed catheter in the cisterna magna, with a noradrenaline and adrenaline isotope dilution method for examining sympathetic and adrenal medullary activity, we were able to quantify the release of brain neurotransmitters and examine efferent sympathetic nervous outflow in patients following intracisternal administration of bupivacaine. Despite severe pain, sympathetic and adrenal medullary activities were well within normal range (4.2 ± 0.6 and 0.7 ± 0.2 nmol min^–1, respectively, mean ±S.E.M.). Intracisternal bupivacaine administration caused an almost instantaneous elevation in mean arterial blood pressure, increasing by 17 ± 7 mmHg after 10 min (P < 0.01). Heart rate increased in parallel (17 ± 5 beats min^–1), and these changes coincided with an increase in sympathetic nervous activity, peaking with an approximately 50% increase over resting level 10 min after injection (P < 0.01). CSF levels of GABA were reduced following bupivacaine (P < 0.05). CSF catecholamines and serotonin, and EEG, remained unaffected. These results show that acutely administered bupivacaine in the cisterna magna of chronic pain sufferers leads to an activation of the sympathetic nervous system. The results suggest that the haemodynamic consequences occur as a result of interference with the neuronal circuitry in the brainstem. Although these effects are transient, they warrant caution at the induction of intracisternal local anaesthesia.

(Received 28 July 2005; accepted after revision 21 October 2005; first published online 27 October 2005)
Corresponding author G. Lambert: Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, VIC 8008, Australia. Email: gavin.lambert{at}baker.edu.au

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