270 OBJECTIVE MEASUREMENT OF SUBJECTIVE PAIN PERCEPTION BY CONTACT HEAT EVOKED POTENTIALS

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European Journal of Pain 2006, Vol 10 (suppl S1)

OPT (mA mean±SD) SuPT (mA) SePT (mA) APT (mA) Pain tolerance (s)

Abstracts, 5th EFIC Congress, Free Presentations

S

AT

PM

NM

30(±9) 30(±9) 20(±5) 29(±8) 23(±16)

30(±9) 35(±12)* 24(±8)* 32(±9)* 28(±17)*

31(±9) 37(±16)* 24(±7)* 35(±12)* 27(±15)*

29(±9) 32(±13) 22(±7) 31(±12) 22(15)

*p < 0.05

Music eliciting positive emotions as well as distraction induced analgesic effects probably mediated supraspinaly as the nociceptive spinal reflex was not influenced. Whether music could be used to modulate pain perception in chronic pain patients is still to be determined.

267 MODIFICATION OF CORTICAL EVOKED POTENTIALS DURING SURAL NERVE STIMULATION IN FAILED BACK SURGERY SYNDROME PATIENTS TREATED WITH SPINAL CORD STIMULATION H. Polacek1 ° , J. Kozak2 , I. Vrba3 , J. Vrana1 , A. Stancak1 . 1 Dept. Normal, Path., Clin. Physiol., Third Fac. Med., Charles University Prague, 2 Pain Manag. Res. Centre, Fac. Hosp. Motol, Prague, 3 Dept. Anaesthesiol. Resusc., Hosp. Na Homolce, Prague, Czech Republic We analyzed whether cortical processing of cutaneous sural nerve stimuli would be altered by spinal cord stimulation (SCS) in patients with failed back surgery syndrome. In nine patients (4 women, 5 men, age 39–56 years) suffering from intractable pain in their left leg and back, the left sural nerve was stimulated with 0.2 ms square pulses (13–34 mA) and 5–8 s inter-stimulus intervals. The evoked potentials (111 EEG electrodes), that were recorded during ongoing SCS or in absence of SCS, were modeled using BESA™ (MEGIS, Germany). The source model encompassed four source dipoles located in the following regions: the right primary somatosensory cortex (S1, 87 ms), the left and right secondary somatosensory cortex (S2, 161 and 167 ms, respectively), and the mid-cingulate cortex (314 ms). The source amplitudes of the S1 and of both S2 source dipoles were reduced during periods of SCS compared to periods without SCS (P < 0.05). In contrast to the S1 and S2 sources, the amplitude of the mid-cingulate source was increased during SCS (P < 0.05). Subjective intensity of sural nerve stimuli, evaluated using visual analogue scale, was not affected by SCS (P > 0.05). While reduced amplitudes of S1 and S2 sources during SCS suggest inhibition of afferent input possibly occurring at segmental level, the increased source activity in the cingulate cortex points to a positive interaction between SCS and the sural nerve stimulation. These cortical activation changes are not associated with subjective intensity measures of the sural nerve stimuli. Supported by GAUK 66/2005, IGA 8232, RG 0021620816, LC 550 and CNS 1M0517.

268 INTENSITY MODULATION OF CUTANEOUS ELECTRICAL STIMULATION: EPS AND SUBJECTIVE RATINGS E.M. van der Heide ° , J.R. Buitenweg, E. Marani, W.L.C. Rutten. Institute for Biomedical Technology (BMTI), Department EEMCS, Biomedical Signals and Systems Group, University of Twente, Enschede, The Netherlands Background and Aims: Chronic pain research is increasingly focused on neuroplastic mechanisms underlying subjective pain experience. Both sensation and cortical representation depend on central modulation of applied stimuli. In multiple mechanisms, both tactile and nociceptive activations interact, indicating that the distribution of activated afferents is relevant for correct interpretation of results. From this perspective, the traditional use of amplitude modulated single electrical pulses (SP) might not be optimal for studying central processing of pain as the amplitude changes this distribution (depending on local fiber densities). Pulse trains

(PT) with a variable number of fixed amplitude pulses might be more suitable as they resemble the coding of stimulus intensity by skin receptors. In this study, we compared Numeric Rating Scale (NRS) and evoked potentials (EP) components obtained with SP and PT modulated intensity (I). Method: A total of 30 healthy subjects were electrically stimulated at the left forearm or middle fingertip. NRS scores and EPs were averaged from 105 randomized stimuli at 5 levels. Results: Both the I-EP (components) and the I-NRS relationships differed depending on the modulation method and stimulus location. Although the repeatedly reported NRS-EP (N150-P200) correlation was reproduced for SP at the fingertip, no significant correlation was found with stimulation at the forearm. For PT the NRS-EP (N150-P200) correlation was found for both stimulus locations. Conclusion: These findings support the view that SP and PT offer a different excitation of neural mechanisms, which might be fruitful for future observation of the central mechanisms underlying chronification of pain. 269 HABITUATION EFFECTS ON SOMATOSENSORY EVENT-RELATED POTENTIALS (SEPS) ELICITED BY PAINFUL ELECTRICAL STIMULI C.M. van Rijn1 ° , M.L.A. Jongsma1,3 , E. van den Broeke1 , S. Postma1 , R. van der Lubbe3 , J.R. Buitenweg4 , M. Arns5 , R. Quian Quiroga6 , H. van Goor2 , M. Luckers2 , O.H.G. Wilder-Smith2 . 1 NICI, Radboud University, Nijmegen, 2 Pain and Nociception Research Group, Pain Knowledge Centre, St Radboud University Medical Centre, Nijmegen, 3 Department of Psychonomics and Human Performance Technology, University Twente, Enschede, 4 Insitute for Biomedical Technology (BMTI), University Twente, Enschede, 5 The Brain Resource Company, Nijmegen, The Netherlands, 6 Department of Engineering, University of Leicester, Leicester, UK Background and Aims: Pain perception is typically measured by questionnaires and behavioural responses. Somatosensory Evoked Potentials (SEPs), however, provide a direct measure of stimulus processing in the brain. We studied how stimulus repetition influences the SEPs. Methods: A multi-channel EEG was recorded (band pass 0.1−100Hz, sample frequency 1000Hz) from 11 volunteers. Electrical stimuli were applied to the middle phalange of the left ring finger. Each trial consisted of 30 stimuli (1 s duration); inter-stimulus interval of 4 seconds. Three trials were recorded, corresponding with subjective intensity levels 5 (pain detection), 7 (moderate pain) and 9 (pain tolerance). Electric stimuli thus ranged from 1 to 25 mA. Mean amplitudes were extracted from single EEG epochs at Cz: N1: 115–125 ms, P2: 185–195 ms, N2: 195–205 ms and P3: 250–270 ms. Results and Discussion: The N1 component of the SEP decreased between the first and second stimulus. The P3 wave decreased slower; over 4 to 5 stimuli. For the amplitude of the N1 no differences were observed between the three VAS scores. For those of the P3, the amplitudes of the VAS 5 were lower than those of the two higher VAS scores. The amplitude of the N1 reaching an asymptotic level after the second stimulus in the trains, is consistent with those of many earlier studies [ref: J. Kekoni]. The slow habituation of the P3 component contrasts the sensitization in subjective VAS scores found in a parallel experiment. It will be interesting to study whether this SEP habituation differs between chronic pain patients and healthy volunteers. 270 OBJECTIVE MEASUREMENT OF SUBJECTIVE PAIN PERCEPTION BY CONTACT HEAT EVOKED POTENTIALS Y. Granovsky, M. Granot, R. Nir, D. Yarnitsky ° . Neurology Department, Rambam Medical Center, Haifa, Israel Background and Aims: The method of pain evoked potentials gained considerable accreditation along the last 3 decades regarding its objectivity,

Topic B: SYSTEMS (PHYSIOLOGY, ANATOMY, ANIMAL MODELS)

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repeatability and quantitability. Yet, this method’s penetration into clinical practice has lagged behind its scientific development. In the present study, a contact heat rather than the conventionally used laser stimulator was applied to explore whether the relationship between pain evoked potentials and pain psychophysics obtained by the laser prevail for contact heat stimuli as well. Methods: Evoked potentials (EP) were recorded in response to contact heat stimuli at different body sites in 27 healthy volunteers. Four temperatures (43, 46, 49 and 52ºC) were applied at the forearm and two temperatures (46 and 49ºC) at the leg. Results: EP amplitudes were strongly associated with intensity of applied stimuli and with subjective pain perception, though analysis revealed pain perception and not stimulus intensity as the major contributing factor. This is in accordance with past results of LEP studies. Further, within each painfully stimulating temperature, a correlation was found between amplitude and pain perception. Significant correlation was found between responses from forearm and leg. Conclusions: This study demonstrates the association between the subjective pain experience and the objective measure of pain perception as assessed by contact heat EPs amplitude, which was consistent between body sites for individual subjects. Significance: This work strengthens the role of contact heat EPs for objective pain assessment.

272 DIFFERENT MICE STRAINS SHOW DIVERSE INTERLEUKIN-1 RECEPTOR TYPE I DISTRIBUTION IN DORSAL ROOT GANGLIA FOLLOWING SPINAL NERVE INJURY

B07 ENDOGENOUS PAIN MODULATION 271 ROLE OF NUCLEUS RAPHE MAGNUS AND NUCLEUS RETICULARIS GIGANTOCELLULARIS/PARAGIGANTOCELLULARIS COMPLEX-SEROTONERGIC RECEPTORS IN THE ANTINOCICEPTION EVOKED BY EITHER FEAR-INDUCED DEFENSIVE BEHAVIOR OR CONVULSIVE REACTIONS Oliveira1 ,

Oliveira1 ,

Ferreira1 ,

Elias-Filho1 ,

R. de R.C. de C.M.R. D.H. I. Tracey2 , N.C. Coimbra1 ° . 1 Laboratory of Neuroanatomy & Neuropsychobiology, Department of Pharmacology, School of Medicine or Ribeir˜ao Preto of the University of S˜ao Paulo (FMRP-USP), Ribeir˜ao Preto (SP), Brazil, 2 Pain Imaging Neuroscience Group, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford UK This work studied the effect of microinjections of ritanserin either in the nucleus raphe magnus (NRM) or in the nucleus reticularis gigantocellularis/paragigantocellularis complex (Gi/PGi) on the antinociception evoked either by electrical stimulation of the mesencephalic tectum or by chemically induced tonic-clonic seizures. Wistar rats (n-8, per group), weighing 200–250 g, were submitted to a stereotaxic surgery for the introduction of a guide-cannula aiming the NRM or Gi/PGi. In some groups, the continuum comprised by the deep layers of the superior colliculus (dlSC) and dorsolateral periaqueductal gray matter (dlPAG) was concomitantly targeted using a bipolar electrode. After 5 days of post-operative recovery, the tail-flick baseline was recorded, and the tail-withdrawal latency was measured again at 0, 10, 20, 30, 40, 60, 120, 150 and 180 min after escape behavior (elicited by electrical stimulation of dlSC/dlPAG) or after seizures evoked by intraperitoneal injection pentylenetetrazole (PTZ) (at 64 mg/kg). After 24 h, 5.0 mg/0.5 mL (10.46 nmol) of ritanserin + tween 80 (RBI), or physiological saline + tween 80 were microinjected into the NMR or Gi/PGi, and, after 5 min, the escape behavior or tonic-clonic seizures were evoked again, following the TFL recording. The electrical stimulation of dlSC/dlPAG caused fear-induced antinociception for 60 min, and tonic-clonic seizures elicited a long lasting postictal antinociception for 120 min. Microinjections of ritanserin in either the NRM or in the Gi/PGi nuclei antagonized both the antinociceptive phenomena, suggesting the involvement of serotonin and 5-HT2A/2C receptors of the NRM and of Gi/PGi nuclei in these different kind of hypalgesia.

E. Gabay1 ° , Y. Shavit2 , R. Yirmiya2 , M. Tal1 . 1 Department of Anatomy and Cell Biology, Faculty of Medicine, 2 Department of Psychology, Hebrew University, Jerusalem, Israel Previous studies in animal models of neuropathic pain showed elevated levels of proinflammatory cytokines, particularly IL-1. To examine the effect of IL-1ˆa on DRG neurons we studied IL-1 receptor type I (IL-1 RI) distribution on the different sensory neuron types in the DRG. Our aim was to determine whether there is a correlation between IL-1 RI distribution and neuropathic pain behavior. Various mice strains whose neuropathic pain behavior and electrophysiological characteristics had been phenotyped were used. Neuropathy was induced by cutting the L4 and L5 spinal nerves on one side in 28 mice; a sham operation was performed in another 28 mice. By the day 7 post operative, frozen sections of DRG L4, L5 were immunostained for IL-1 RI and Nissl stain. The neurons were classified as large >1100mm2, medium > 600 mm2 and small < 600 mm2. The results showed that following nerve injury the high autotomy CBA/J mice showed a marked increase of IL-1 RI labeling expressed only in the large neurons (from 4.1±0.6% to 7.6±2.7%, p = 0.02), that was 2.33±0.45 times greater than in all the other mouse strains. In conclusion, the correlation between the neuropathic pain behavior and the electrophysiological characteristics and the IL-1 RI labeling pattern in the DRG neurons in the CBA/J mice strain suggest that IL-1 signaling plays an important role in the neuropathic pain mechanism. The increased labeling of IL-1 RI in large neurons in the nerve-injured CBA/J mice implies that IL-1 signaling might underlie neuronal Aˆa pain mechanisms.

273 ENHANCED DIFFUSE NOXIOUS INHIBITORY CONTROL (DNIC) IN MALES DOES NOT DEPEND ON THE MODALITY OF CONDITIONING STIMULUS M. Granot1 ° , D. Pud1 , Y. Granovsky2 , E. Sprecher2 , J. Krispel2 , D. Yarnitsky2 . 1 Faculty of Social Welfare and Health Studies, University of Haifa, 2 Laboratory of Clinical Neurophysiology, Technion Faculty of Medicine, Haifa, Israel Background and Aims: Mechanisms of descending inhibition is expressed by the phenomenon of (DNIC). This study aimed to evaluate association between modality of the conditioning stimulus, gender and personality variables and DNIC response. Methods: Contact heat pain was applied by thermal sensory analyzer as conditioned stimulus (one minute) to the non-dominant forearm in 31 healthy volunteers (21 men, 10 women). Stimulation temperature was administered at an intensity that evoked pain scores of 60 in 0−100 numerical pain scale. The conditioning stimulus was immersion of the dominant hand in cold or hot water of 12ºC, 15ºC, 18ºC, 33ºC, 44ºC and 46.5ºC, while the same conditioned stimulus was given simultaneously to the other hand. DNIC response was defined as the difference between pain score from the first to the second conditioned stimuli. State and trait anxiety, and pain catastrophizing scores were assessed before the subjects were exposed to the painful tests. Results: Significant reduction in pain scores were found for both heat (46.5ºC) and cold (12ºC) painful conditioning stimuli (p < 0.0001) but not for the non-painful conditions. ANOVA revealed significant gender effect with greater DNIC response in male (p = 0.012), but no effect of the conditioning pain modality (cold or hot pain) or personality. Conclusions: The association between mechanisms of endogenous inhibition and gender was not influenced neither by pain modality nor by personality. Enhanced DNIC response in male emphasizes the role of gender in the investigation of pain processing via advanced psychophysical tests.