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151 ALTERED EXPRESSION OF ATF-3 IN PRIMARY AFFERENT NEURONS DURING INFLAMMATORY PAIN
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Oral Presentations / European Journal of Pain 13 (2009) S1–S54
148 SUCCESS AND RETURN TO PLAY STATUS OF PROFESSIONAL FOOTBALL PLAYERS AFTER EPIDURAL STEROID INJECTIONS FOR HERNIATED NUCLEUS PULPOSUS P. Birmingham, M. Drakos, D. Richman *, S. Waldman, S. Williams, L. Weiss. The Hospital for Special Surgery, New York, United States Background and Aims: There is minimal literature on the efficacy of epidural steroid injections in the professional athlete population. Literature regarding long term success of epidural steroid injections is inconclusive, and does not support their use to improve long term functionality or to avoid surgery. Moreover, in the short term, a common criticism of epidural steroid injections is that they do not improve average functional impairment. This study elucidates the dramatic clinical efficacy of epidural steroid injections in the professional athlete. Methods: We performed a retroactive series of case studies of eleven professional football players receiving epidural steroid injections for incapacitating pain secondary to herniated nucleus pulposus. Functional impairment was measured by an initial VAS pain scale, and inability to play. Success was measured simply by return to play status. Results: Eleven players had 25 total injections. Only two did not return to play. Nine did return to play, with 12 total games lost. After 17 of the 25 injections, the player returned to play without missing any games. No complications were reported. Conclusions: In professional athletes with high baseline functionality, results suggest epidural steroid injections are extremely effective in treating symptomatic herniated nucleus pulposus. They appear to be safe and well tolerated, with minimal complications, thus enhancing compliance with physical therapy while reducing the need for surgery.
Free Presentations 12: Best Selected Abstracts 149 5-HT3 RECEPTOR ANTAGONIST ONDANSETRON ATTENUATES MORPHINE WITHDRAWAL INDUCED NEUROTOXICITY, BBB DYSFUNCTION, GLIAL AND HEAT SHOCK PROTEIN ACTIVATION IN RAT BRAIN H.S. Sharma1 *, T. Gordh1 , R. Patnaik2 , S.F. Ali3 . 1 Uppsala University, Anaesthesiology & Intensive Care Medicine, Dept. Surgical Sciences, Uppsala, Sweden; 2 School of Biomedical Engineering, Institute of Technology, Banaras Hindu University, Varanasi-221005, India; 3 Neurochemistry Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research/ US Food and Drug Administration (FDA), 3900 NCTR Road, Jefferson, AR 72079–9502, United States Blockade of 5-HT3 receptors with ondansetron reduces morphine dependence and withdrawal symptoms. However, effects of ondansetron on morphine induced neurotoxicity is still unknown. In this investigation, we examined the effects of ondansetron on morphine neurotoxicity, glial activation and/or HSP response in our rat model. Rats were administered ondansetron (1 mg or 2 mg/kg, s.c) or saline once daily starting from 2 days before morphine administration (10 mg/kg, s.c., single injection for 10 days) and continued up to 2 days after withdrawal. Abrupt cessation of morphine administration in rats on day 11th results in withdrawal symptoms from 24 h and onwards and continued up to 72 h after cessation of morphine administration. Marked increase in blood-brain barrier (BBB) permeability to Evans blue and [131] Iodine was seen in the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus, brain stem and spinal cord on the 2nd day of morphine withdrawal in saline treated animals. These brain areas exhibited profound activation of glial fibrillary acidic protein (GFAP), heat shock protein (HSP 72 kD) immunoreactivity and neuronal damage. Pretreatment with ondansetron exhibited only
mild withdrawal symptoms on the day 2nd and 3rd. Breakdown of the BBB, activation of GFAP and HSP expression and neuronal damage were also considerably reduced in these animals treated with high doses of ondansetron. These observations suggest that blockade of 5-HT3 receptors with ondansetron attenuate morphine withdrawal induced BBB dysfunction leading to reduction in neurotoxicity, stress response and astrocytic activation, not reported earlier. 150 A COMPARISON OF THE US-AMERICAN AND GERMAN GUIDELINE WITH EULAR RECOMMENDATIONS FOR THE MANAGEMENT OF FIBROMYALGIA 1,4 W. Hauser ¨ , K. Thieme2 *, T. Denis3 . 1 Klinikum Saarbr¨ ucken, Saarbr¨ ucken, Germany; 2 Department of Clinical and Cognitive Neuroscience, University of Heidelberg, Central Institute of Mental Health, Mannheim, Germany; 3 Department of Anesthesiology, University of Washington, Seattle, United States; 4 Interdisciplinary center of pain therapy, Saarbr¨ ucken, Germany Objective: To compare evidence-based guidelines for the management of fibromyalgia syndrome (FMS). Methods: Systematic searches up to April 2008 of the US-American National Guideline Clearing House, the Scottish Intercollegiate Guidelines Network, the Association of the Scientific Medical Societies in Germany (AWMF) and Medline were conducted. Three evidence-based guidelines for the management of FMS published by professional organizations were identified: The American Pain Society (APS) (2005), the European League Against Rheumatism (EULAR) (2007), and the AWMF (2008). The composition of panels, search strategies, categorization of evidence and recommendations, methods for developing recommendations and the recommendations of the 3 guidelines were compared and contrasted. Results: The steering committees and panels of APS and AWMF were comprised of multiple disciplines engaged in the management of FMS and included patients, whereas the task force of EULAR only consisted of physicians, predominatly rheumatologists. APS and AWMF ascribed the highest level of evidence to systematic reviews and meta-analyses, whereas EULAR credited the highest level of evidence to randomised controlled studies. Both APS and AWMF assigned the highest level of recommendation to aerobic exercise, cognitive-behavioral therapy, amitriptyline, and multicomponent treatment. In contrast, EULAR assigned the highest level of recommendation to a set of to pharmacological treatment. Conclusion: The APS and AWMF guidelines assigned higher ratings to CBT and multicomponent treatments. The inconsistencies across guidelines are likely attributable to the criteria used for study inclusion, weighting systems, and compositon of the panels. W. Hauser ¨ received honoraria by Elli Lilly, Janssen-Cilag, Mundipharma and Pfizer for educational lectures 151 ALTERED EXPRESSION OF ATF-3 IN PRIMARY AFFERENT NEURONS DURING INFLAMMATORY PAIN D. Nascimento1 *, D. Pozza1 , J.M. Castro-Lopes1,2 , F.L. Neto1 . 1 Instituto de Histologia e Embriologia, Faculdade de Medicina do Porto, Portugal, Oporto, Portugal; 2 Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Oporto, Portugal Background and aims: ATF-3 is a member of the ATF/CREB (activating transcription factor/cAMP responsive element binding protein) transcriptional factors family and its expression has been associated to cellular stress response, anti and pro- apoptosis mechanisms, survival phenomenon and neuropathic pain. ATF-3 has been suggested as an “adaptive response”, as it can decide the cell destiny, according to different stimulus and cellular context. We aimed to study the disease progression and the associated expression of ATF-3 in primary afferent neurons, over time, in a well established model of chronic inflammatory pain.
Oral Presentations / European Journal of Pain 13 (2009) S1–S54
Methods: The monoarthritis (MA) model induced by injection of CFA (Complete Freud’s Adjuvant) in the tibiotarsal joint was used. Immunohistochemistry against ATF-3 at timepoints 2, 4, 7 and 14 days post-CFA injection was performed in ipsi- and contralateral L3 , L4 and L5 Dorsal Root Ganglions (DRGs). Control rats were injected with saline or vehicle and sacrificed after 2 days. Results: Expression of ATF-3 was significantly increased at 2 and 4 days of MA, but it started diminishing after that period although in 7 and 14 days MA was still higher than controls. Rises were more considerable in L5 . Control DRGs showed no significant ATF-3 expression. Conclusion: Data suggest ATF-3 expression, at early timepoints, is involved in the inflammatory pain process, at the periphery. Further studies are necessary to clarify the ATF-3 signaling pathways associated to this condition and the underlying mechanisms that contribute to this particular expression pattern. 152 AN EVIDENCE-BASED MODEL OF CHRONIC WIDESPREAD PAIN IN CHRONIC FATIGUE SYNDROME J. Nijs1,2 *, J. Van Oosterwijck1 , M. Meeus1,2 . 1 Vrije Universiteit Brussel Department of Human Physiology, Brussels, Belgium; 2 Artesis University College Antwerp, Division of Musculoskeletal Physiotherapy, Antwerp (Merksem), Belgium Background and Aims: Although fatigue is the primary characteristic of chronic fatigue syndrome (CFS), the majority of CFS patients experience chronic widespread pain. Pain appears to be equally debilitating as fatigue to patients with CFS. Until recently, there was a dearth of knowledge on chronic widespread pain in CFS. Contrary to the multiple studies on pain in fibromyalgia, a disease considerably overlapping with CFS, studies in CFS were scarce. At present, a series of studies have provided more insight into the nature of chronic widespread pain in CFS. The present study aimed at critically assessing the existing knowledge on chronic widespread pain in CFS. Methods: Systematic literature review. Results: First, various studies have provided evidence indicating that a number of psychological factors like pain catastrophizing, depressive symptoms and coping strategies influence chronic widespread pain in those with CFS. These factors may contribute to pain facilitation. Second, impairments in pain inhibitory mechanisms at rest and during physical activity have been observed. Impaired pain inhibition accounts in part for postexertional malaise as typically seen in CFS. Third, exercise-mediated increases in oxidative stress contribute to pain in patients with CFS. Finally, cognitive therapies like cognitive behaviour therapy and pain neurophysiology education re able to improve chronic widespread pain in those with CFS.
Figure 1. Model for chronic widespread pain in chronic fatigue syndrome. Conclusions: Based on the available evidence, a model of chronic widespread pain in CFS was constructed (figure 1). This pain model for CFS n be used to steer treatment.
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153 CAN PATIENTS WITH CENTRAL POST-STROKE PAIN BE IDENTIFIED USING A QUESTIONNAIRE? H. Klit1 *, N.B. Finnerup2 , K. Overvad3 , G. Andersen4 , T.S. Jensen5 . 1 Danish Pain Research Center, Aarhus, Denmark; 2 Danish Pain Research Center, Aarhus, Denmark; 3 Department of Clinical Epidemiology, Aarhus University Hospital, Aalborg, Denmark; 4 Department of Neurology, Aarhus University Hospital, Aarhus, Denmark; 5 Danish Pain Research Center & Dept of Neurology, Aarhus C, Denmark Central post-stroke pain (CPSP) is seen in 8% following stroke. Aim: To identify patients with CPSP using 4 predefined criteria, based on the newly proposed diagnostic criteria for neuropathic pain (Treede et al. 2008), and the S-LANSS scale (Bennett et al 2005) and to validate the findings by clinical examination. All surviving stroke patients (N = 964, F=457, M=507), registered in the National Indicator Project stroke database in Aarhus County, Denmark, between March 2004 and February 2005, were mailed a questionnaire about development of chronic pain after stroke. A sex- and age-matched reference group (N = 957, F=456, M=501) served as control. Results: Response rates were 66.5% and 59.5% (p < 0.05), respectively. High S-LANSS scores were more common in stroke patients than controls (51/128=39.8% vs. 16/67=23.9% (p = 0.03)). The 4 CPSP criteria were fulfilled by 10.4% of stroke patients and 0.4% of control subjects. Both S-LANSS and CPSP criteria were fulfilled by 30 patients, whereas 21 patients fulfilled only S-LANSS and 33 only CPSP criteria. 73 surviving patients with possible central post-stroke pain are invited to participate in an examination including bedside sensory testing in order to validate the diagnosis of CPSP. At present, 50 of these have been reviewed. Further data will be presented at the congress. Conclusion: Patients with high likelihood of CPSP can be identified using a questionnaire. 154 DNIC AND THE ‘NO-PAIN INHIBITS PAIN’ PHENOMENON R.R. Nir1 *, M. Granot2 , E. Sprecher1 , D. Yarnitsky1 . 1 Neurology Department, Rambam Health Care Campus, and Laboratory of Clinical Neurophysiology, Faculty of Medicine, Technion – Israel Institute of Technology, Haifa, Israel; 2 Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel Background and Aims: DNIC is usually induced by painful conditioning stimulation intensities (CSIs), though some demonstrated its induction also by non-painful CSIs. We aimed at investigating whether ’no-pain inhibits pain’ is equivalent to ’pain inhibits pain’ by exploring the transition zone characteristics of the conditioning stimulation and its effects on DNIC. Methods: CSIs consisting of innocuous 44.5ºC and noxious 45.5 and 46.5ºC hand water immersion were used to induce DNIC in the parallel paradigm (N = 28). Contact-heat test-pain at ‘pain-60’ intensity was delivered before and during conditioning. Results: While the two painful CSIs induced significant DNICs (Ps < 0.01), of similar extents, 44.5ºC did not. However, the direction of change in endogenous pain modulation under the latter was indicative of DNIC occurrence observed under the painful CSIs: 100% of subjects demonstrating a test-pain decrease under CSI of 44.5ºC consistently expressed DNIC under both painful CSIs. Despite conditioning stimuli covered both innocuous and noxious intensities, magnitudes of test-pain reduction under all CSIs were positively inter-correlated (Ps < 0.01). Conclusions: These findings suggest that (i) endogenous pain inhibition follows a ’step function’ pattern, suggesting a critical painful CSI is required to induce DNIC, which will not further increase under more painful CSIs; (ii) occurrence of ’no-pain inhibits pain’ testifies to an individual’s predisposition to express DNIC; and
Oral Presentations / European Journal of Pain 13 (2009) S1–S54
148 SUCCESS AND RETURN TO PLAY STATUS OF PROFESSIONAL FOOTBALL PLAYERS AFTER EPIDURAL STEROID INJECTIONS FOR HERNIATED NUCLEUS PULPOSUS P. Birmingham, M. Drakos, D. Richman *, S. Waldman, S. Williams, L. Weiss. The Hospital for Special Surgery, New York, United States Background and Aims: There is minimal literature on the efficacy of epidural steroid injections in the professional athlete population. Literature regarding long term success of epidural steroid injections is inconclusive, and does not support their use to improve long term functionality or to avoid surgery. Moreover, in the short term, a common criticism of epidural steroid injections is that they do not improve average functional impairment. This study elucidates the dramatic clinical efficacy of epidural steroid injections in the professional athlete. Methods: We performed a retroactive series of case studies of eleven professional football players receiving epidural steroid injections for incapacitating pain secondary to herniated nucleus pulposus. Functional impairment was measured by an initial VAS pain scale, and inability to play. Success was measured simply by return to play status. Results: Eleven players had 25 total injections. Only two did not return to play. Nine did return to play, with 12 total games lost. After 17 of the 25 injections, the player returned to play without missing any games. No complications were reported. Conclusions: In professional athletes with high baseline functionality, results suggest epidural steroid injections are extremely effective in treating symptomatic herniated nucleus pulposus. They appear to be safe and well tolerated, with minimal complications, thus enhancing compliance with physical therapy while reducing the need for surgery.
Free Presentations 12: Best Selected Abstracts 149 5-HT3 RECEPTOR ANTAGONIST ONDANSETRON ATTENUATES MORPHINE WITHDRAWAL INDUCED NEUROTOXICITY, BBB DYSFUNCTION, GLIAL AND HEAT SHOCK PROTEIN ACTIVATION IN RAT BRAIN H.S. Sharma1 *, T. Gordh1 , R. Patnaik2 , S.F. Ali3 . 1 Uppsala University, Anaesthesiology & Intensive Care Medicine, Dept. Surgical Sciences, Uppsala, Sweden; 2 School of Biomedical Engineering, Institute of Technology, Banaras Hindu University, Varanasi-221005, India; 3 Neurochemistry Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research/ US Food and Drug Administration (FDA), 3900 NCTR Road, Jefferson, AR 72079–9502, United States Blockade of 5-HT3 receptors with ondansetron reduces morphine dependence and withdrawal symptoms. However, effects of ondansetron on morphine induced neurotoxicity is still unknown. In this investigation, we examined the effects of ondansetron on morphine neurotoxicity, glial activation and/or HSP response in our rat model. Rats were administered ondansetron (1 mg or 2 mg/kg, s.c) or saline once daily starting from 2 days before morphine administration (10 mg/kg, s.c., single injection for 10 days) and continued up to 2 days after withdrawal. Abrupt cessation of morphine administration in rats on day 11th results in withdrawal symptoms from 24 h and onwards and continued up to 72 h after cessation of morphine administration. Marked increase in blood-brain barrier (BBB) permeability to Evans blue and [131] Iodine was seen in the cerebral cortex, hippocampus, cerebellum, thalamus, hypothalamus, brain stem and spinal cord on the 2nd day of morphine withdrawal in saline treated animals. These brain areas exhibited profound activation of glial fibrillary acidic protein (GFAP), heat shock protein (HSP 72 kD) immunoreactivity and neuronal damage. Pretreatment with ondansetron exhibited only
mild withdrawal symptoms on the day 2nd and 3rd. Breakdown of the BBB, activation of GFAP and HSP expression and neuronal damage were also considerably reduced in these animals treated with high doses of ondansetron. These observations suggest that blockade of 5-HT3 receptors with ondansetron attenuate morphine withdrawal induced BBB dysfunction leading to reduction in neurotoxicity, stress response and astrocytic activation, not reported earlier. 150 A COMPARISON OF THE US-AMERICAN AND GERMAN GUIDELINE WITH EULAR RECOMMENDATIONS FOR THE MANAGEMENT OF FIBROMYALGIA 1,4 W. Hauser ¨ , K. Thieme2 *, T. Denis3 . 1 Klinikum Saarbr¨ ucken, Saarbr¨ ucken, Germany; 2 Department of Clinical and Cognitive Neuroscience, University of Heidelberg, Central Institute of Mental Health, Mannheim, Germany; 3 Department of Anesthesiology, University of Washington, Seattle, United States; 4 Interdisciplinary center of pain therapy, Saarbr¨ ucken, Germany Objective: To compare evidence-based guidelines for the management of fibromyalgia syndrome (FMS). Methods: Systematic searches up to April 2008 of the US-American National Guideline Clearing House, the Scottish Intercollegiate Guidelines Network, the Association of the Scientific Medical Societies in Germany (AWMF) and Medline were conducted. Three evidence-based guidelines for the management of FMS published by professional organizations were identified: The American Pain Society (APS) (2005), the European League Against Rheumatism (EULAR) (2007), and the AWMF (2008). The composition of panels, search strategies, categorization of evidence and recommendations, methods for developing recommendations and the recommendations of the 3 guidelines were compared and contrasted. Results: The steering committees and panels of APS and AWMF were comprised of multiple disciplines engaged in the management of FMS and included patients, whereas the task force of EULAR only consisted of physicians, predominatly rheumatologists. APS and AWMF ascribed the highest level of evidence to systematic reviews and meta-analyses, whereas EULAR credited the highest level of evidence to randomised controlled studies. Both APS and AWMF assigned the highest level of recommendation to aerobic exercise, cognitive-behavioral therapy, amitriptyline, and multicomponent treatment. In contrast, EULAR assigned the highest level of recommendation to a set of to pharmacological treatment. Conclusion: The APS and AWMF guidelines assigned higher ratings to CBT and multicomponent treatments. The inconsistencies across guidelines are likely attributable to the criteria used for study inclusion, weighting systems, and compositon of the panels. W. Hauser ¨ received honoraria by Elli Lilly, Janssen-Cilag, Mundipharma and Pfizer for educational lectures 151 ALTERED EXPRESSION OF ATF-3 IN PRIMARY AFFERENT NEURONS DURING INFLAMMATORY PAIN D. Nascimento1 *, D. Pozza1 , J.M. Castro-Lopes1,2 , F.L. Neto1 . 1 Instituto de Histologia e Embriologia, Faculdade de Medicina do Porto, Portugal, Oporto, Portugal; 2 Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Oporto, Portugal Background and aims: ATF-3 is a member of the ATF/CREB (activating transcription factor/cAMP responsive element binding protein) transcriptional factors family and its expression has been associated to cellular stress response, anti and pro- apoptosis mechanisms, survival phenomenon and neuropathic pain. ATF-3 has been suggested as an “adaptive response”, as it can decide the cell destiny, according to different stimulus and cellular context. We aimed to study the disease progression and the associated expression of ATF-3 in primary afferent neurons, over time, in a well established model of chronic inflammatory pain.
Oral Presentations / European Journal of Pain 13 (2009) S1–S54
Methods: The monoarthritis (MA) model induced by injection of CFA (Complete Freud’s Adjuvant) in the tibiotarsal joint was used. Immunohistochemistry against ATF-3 at timepoints 2, 4, 7 and 14 days post-CFA injection was performed in ipsi- and contralateral L3 , L4 and L5 Dorsal Root Ganglions (DRGs). Control rats were injected with saline or vehicle and sacrificed after 2 days. Results: Expression of ATF-3 was significantly increased at 2 and 4 days of MA, but it started diminishing after that period although in 7 and 14 days MA was still higher than controls. Rises were more considerable in L5 . Control DRGs showed no significant ATF-3 expression. Conclusion: Data suggest ATF-3 expression, at early timepoints, is involved in the inflammatory pain process, at the periphery. Further studies are necessary to clarify the ATF-3 signaling pathways associated to this condition and the underlying mechanisms that contribute to this particular expression pattern. 152 AN EVIDENCE-BASED MODEL OF CHRONIC WIDESPREAD PAIN IN CHRONIC FATIGUE SYNDROME J. Nijs1,2 *, J. Van Oosterwijck1 , M. Meeus1,2 . 1 Vrije Universiteit Brussel Department of Human Physiology, Brussels, Belgium; 2 Artesis University College Antwerp, Division of Musculoskeletal Physiotherapy, Antwerp (Merksem), Belgium Background and Aims: Although fatigue is the primary characteristic of chronic fatigue syndrome (CFS), the majority of CFS patients experience chronic widespread pain. Pain appears to be equally debilitating as fatigue to patients with CFS. Until recently, there was a dearth of knowledge on chronic widespread pain in CFS. Contrary to the multiple studies on pain in fibromyalgia, a disease considerably overlapping with CFS, studies in CFS were scarce. At present, a series of studies have provided more insight into the nature of chronic widespread pain in CFS. The present study aimed at critically assessing the existing knowledge on chronic widespread pain in CFS. Methods: Systematic literature review. Results: First, various studies have provided evidence indicating that a number of psychological factors like pain catastrophizing, depressive symptoms and coping strategies influence chronic widespread pain in those with CFS. These factors may contribute to pain facilitation. Second, impairments in pain inhibitory mechanisms at rest and during physical activity have been observed. Impaired pain inhibition accounts in part for postexertional malaise as typically seen in CFS. Third, exercise-mediated increases in oxidative stress contribute to pain in patients with CFS. Finally, cognitive therapies like cognitive behaviour therapy and pain neurophysiology education re able to improve chronic widespread pain in those with CFS.
Figure 1. Model for chronic widespread pain in chronic fatigue syndrome. Conclusions: Based on the available evidence, a model of chronic widespread pain in CFS was constructed (figure 1). This pain model for CFS n be used to steer treatment.
S53
153 CAN PATIENTS WITH CENTRAL POST-STROKE PAIN BE IDENTIFIED USING A QUESTIONNAIRE? H. Klit1 *, N.B. Finnerup2 , K. Overvad3 , G. Andersen4 , T.S. Jensen5 . 1 Danish Pain Research Center, Aarhus, Denmark; 2 Danish Pain Research Center, Aarhus, Denmark; 3 Department of Clinical Epidemiology, Aarhus University Hospital, Aalborg, Denmark; 4 Department of Neurology, Aarhus University Hospital, Aarhus, Denmark; 5 Danish Pain Research Center & Dept of Neurology, Aarhus C, Denmark Central post-stroke pain (CPSP) is seen in 8% following stroke. Aim: To identify patients with CPSP using 4 predefined criteria, based on the newly proposed diagnostic criteria for neuropathic pain (Treede et al. 2008), and the S-LANSS scale (Bennett et al 2005) and to validate the findings by clinical examination. All surviving stroke patients (N = 964, F=457, M=507), registered in the National Indicator Project stroke database in Aarhus County, Denmark, between March 2004 and February 2005, were mailed a questionnaire about development of chronic pain after stroke. A sex- and age-matched reference group (N = 957, F=456, M=501) served as control. Results: Response rates were 66.5% and 59.5% (p < 0.05), respectively. High S-LANSS scores were more common in stroke patients than controls (51/128=39.8% vs. 16/67=23.9% (p = 0.03)). The 4 CPSP criteria were fulfilled by 10.4% of stroke patients and 0.4% of control subjects. Both S-LANSS and CPSP criteria were fulfilled by 30 patients, whereas 21 patients fulfilled only S-LANSS and 33 only CPSP criteria. 73 surviving patients with possible central post-stroke pain are invited to participate in an examination including bedside sensory testing in order to validate the diagnosis of CPSP. At present, 50 of these have been reviewed. Further data will be presented at the congress. Conclusion: Patients with high likelihood of CPSP can be identified using a questionnaire. 154 DNIC AND THE ‘NO-PAIN INHIBITS PAIN’ PHENOMENON R.R. Nir1 *, M. Granot2 , E. Sprecher1 , D. Yarnitsky1 . 1 Neurology Department, Rambam Health Care Campus, and Laboratory of Clinical Neurophysiology, Faculty of Medicine, Technion – Israel Institute of Technology, Haifa, Israel; 2 Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel Background and Aims: DNIC is usually induced by painful conditioning stimulation intensities (CSIs), though some demonstrated its induction also by non-painful CSIs. We aimed at investigating whether ’no-pain inhibits pain’ is equivalent to ’pain inhibits pain’ by exploring the transition zone characteristics of the conditioning stimulation and its effects on DNIC. Methods: CSIs consisting of innocuous 44.5ºC and noxious 45.5 and 46.5ºC hand water immersion were used to induce DNIC in the parallel paradigm (N = 28). Contact-heat test-pain at ‘pain-60’ intensity was delivered before and during conditioning. Results: While the two painful CSIs induced significant DNICs (Ps < 0.01), of similar extents, 44.5ºC did not. However, the direction of change in endogenous pain modulation under the latter was indicative of DNIC occurrence observed under the painful CSIs: 100% of subjects demonstrating a test-pain decrease under CSI of 44.5ºC consistently expressed DNIC under both painful CSIs. Despite conditioning stimuli covered both innocuous and noxious intensities, magnitudes of test-pain reduction under all CSIs were positively inter-correlated (Ps < 0.01). Conclusions: These findings suggest that (i) endogenous pain inhibition follows a ’step function’ pattern, suggesting a critical painful CSI is required to induce DNIC, which will not further increase under more painful CSIs; (ii) occurrence of ’no-pain inhibits pain’ testifies to an individual’s predisposition to express DNIC; and