Background and Goal of Study: Cerebral processing of painful stimuli is investigated by EEG and imaging techniques. For contact heat evoked potentials (CHEP) specific brain areas have been identified . Based on Low Resolution Brain Electro-magnetic Tomography (LORETA) source localization, the present study analyses effects of subanaesthetic concentrations of propofol and remifentanil on these areas.
Materials and Methods: Approved by the university's ethics committee, 30 healthy male volunteers participated in the study. Standard monitoring parameters and 32 channel electroencephalogram (EEG) were recorded. For CHEP, heat pain was applied at the individual pain threshold by a CHEP stimulator (CHEPS Medoc, Israel). At baseline, CHEP were recorded without drug. Then, for each 15 subjects, CHEP were recorded under either propofol (0.5 μg/ml) or remifentanil (0.05 μg/kg/min). Cerebral activity of CHEP was analysed by LORETA power estimation (0.5-30 Hz EEG bandwidth, 350-500ms post-stimulus) in the frontal and somatosensory cortices and the limbic system. Drug induced changes were analysed with the Wilcoxon two-sample test (p< 0.05).
Results and Discussion: Estimated LORETA power of specific cerebral regions is affected differently by propofol and remifentanil. For propofol, LORETA power decreases in the limbic system, somatosensory and mainly frontal cortex. For remifentanil, no effects are detected in the frontal cortex. Power decreases in the somatosensory cortex and significantly in the limbic system.
Conclusion(s): Previous analysis of CHEP showed similar antinociceptive effects of propofol and remifentanil [2, 3]. The current results indicate differentiated drug specific mechanisms of analgesic effects. For propofol, the distinctive decrease of cerebral power in the frontal cortex suggests analgesic effects caused by reduced conscious pain processing. In contrast, remifentanil does not seem to influence the conscious processing of pain, but the pain perception itself. Strong effects in the limbic system are in accordance with the role of μ-agonists in mediating opioid analgesia .
 BMC Anesthesiology 2008, 8:8
 Anesthesiology 2008, 109 A1298
 Eur J Anaesthesiol 2008, 25 (suppl. 44) 14AP12-4
 J Neurophysiol 2000, 84: 525-533