Posters / Clinical Neurophysiology 117 (2006) S121–S336
Supported by the Swedish Research Council and CIHR Grant MOP-9772. doi:10.1016/j.clinph.2006.06.418
P22.2 Effect of perineurally administered tramadol on nerve conduction M. Beyazova 1, E. Ozturk 2, M. Zinnuroðlu 1, I. Gokyar 2, A. Babacan 2, K. Kaya 2 1
Gazi University, Medical Faculty, Physical Medicine and Rehabilitation, Turkey 2 Gazi University, Medical Faculty, Anesthesiology, Turkey Background: It has been shown that the admixture of tramadol with mepivacaine for axillary plexus block provides a prolongation of blockade. Moreover, it was postulated that tramadol has local anesthetic-like effect in an invitro study. Objective: By using an electroneurographical method, we investigated if tramadol had a nerve conduction blocking effect when administered perineurally in vivo. Methods: After approval by the Ethics Committee of our institution and obtaining informed consent from healthy volunteers, 24 cases were randomized into four equal groups [saline (placebo), 0.5% tramadol, 1% tramadol and 1.5% tramadol]. The study was designed to be double-blinded. Two milliliters of working solution was administered to sural nerve perineurally at the level of ankle using a nerve stimulator. Sensory response amplitudes were recorded electroneurographically. A minimum of 20% decrement with respect to control amplitude was sought to accept that the block had occurred. Results: According to electroneurographical recordings, none of the volunteers in saline group had block. However, the block rates with 0.5%, 1% and 1.5% tramadol were 1/6, 4/6 and 6/6, respectively (p < 0.05). The maximum decrement in the sensory response amplitudes with respect to control amplitudes given as median values were as follows: 7.8% with saline; 12.5% with 0.5% tramadol; 38.5% with 1% tramadol; 77.5% with 1.5% tramadol (p < 0.05). While the median duration of sensory block with 1% tramadol was 15 min, it was 35 min with 1.5% tramadol. Conclusion: Perineural tramadol blocks sensory conduction in peripheral nerves. doi:10.1016/j.clinph.2006.06.419
3
S219
Radcliffe Infirmary, Neurosurgery, Oxford, UK
Background: In the treatment of deep brain stimulation (DBS), brain activity can be electrically detected and modulated via the surgically implanted multi-contact macroelectrodes. Both the injected current and the recorded signal travel across the electrode–brain interface (EBI) consisting of the electrode, the surrounding brain tissue and the space between the two. Objectives: To quantitatively identify the modulated electrical potential in situ specifically related to the EBI in patients with DBS under physiological condition. Methods: We quantitatively identified the physiologically modulated electrode potentials by decomposing the local field potentials (LFPs) recorded from 11 patients (18 electrodes in four different brain regions of the globus pallidus, the periventricular gray, the subthalamic nucleus and the thalamus) who underwent DBS, and correlated them with simultaneously recorded physiological signals of blood pressure (BP) and respiration. Results: Results showed that the electrode potential related to the EBI in the human brains under physiological conditions was not constant but modulated by brain pulsations. The rhythmically modulated electrode potentials could be detected as a specific component of the compound LFP signals at the frequency range of the heart beat with a mean (±SD) amplitude of 6.9 lV±1.7 lV. The positive detection rate and amplitude of the modulated electrode potentials were independent from brain regions and neurological disorders. Conclusions: The electrode potential of the EBI temporally correlates with changes in systemic blood pressure and respiration under physiological condition, and is independent from brain location and neurological disorder. This study will lead us to investigate the effects of the EBI in situ on the ’crossing’ currents in the recording and stimulation procedures, and to contribute to the understanding of the DBS mechanism. doi:10.1016/j.clinph.2006.06.420
P22.4 Investigating the mechanism of deep brain stimulation using a dynamic complex model of the head incorporated with a complete model of electrode R. Bayford 1, A. Tizzard 1, N. Yousif 2, X. Liu 2 1
Middlesex University, Biomedical Science, UK Charing Cross Hospital and Imperial College, Department of Clinical Neuroscience, UK
2
P22.3 The physiologically modulated electrode potentials at the depth electrode–brain interface in humans X. Liu 1, K. Xie 2, S. Wang 2, J. Stein 2, T. Aziz 3 1
Charing Cross Hospital, Neurosciences, UK University of Oxford, University Laboratory of Physiology, UK
2
Background: The use of deep brain stimulation (DBS) for clinical treatment for various neurological disorders, particularly movement disorders such as Parkinson’s disease is on the increase. However, the mechanism by which this electrical stimulation acts on neuronal activity is unclear. Experimental in situ investigation of the mecha-