- Email: [email protected]
121 THE ROLE OF A-BETA FIBERS IN NEUROPATHIC PAIN
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Oral presentations / European Journal of Pain Supplements 4 (2010) 1–46
118 POSTSURGICAL PAIN – EPIDEMIOLOGY B.H. Smith1,2 . 1 Aberdeen Pain Research Collaboration, University of Aberdeen, Aberdeen, 2 Peterhead Medical Practice, Peterhead, UK The first important contribution that epidemiology made to our understanding of postsurgical pain was to highlight its high prevalence and persistence. Depending on the operation, around 30% of patients go on to experience chronic postsurgical pain (CPSP), and this is severe in around 5% of patients. Secondly, epidemiology is identifying risk factors (surgical and psychosocial) that may be amenable to intervention. This work is important and on-going, but it is also challenging, because identifying and measuring cases, risk factors, and responses to interventions is complex. In particular, quantifying the contribution of neuropathic mechanisms to CPSP is difficult at a population level. This discussion will present some of these challenges, offering some insights into how they might be addressed, and how newer epidemiological studies should take account of current and emerging information on the mechanisms of CPSP.
M6. Role of the A-beta Fibres in Paroxysmal Pain 119 WORKSHOP SUMMARY: ABETA FIBRES IN PAROXYSMAL PAIN A. Truini. Department of Neurological Sciences, University ‘La Sapienza’, Rome, Italy An established notion postulates that whereas neuropathic pain is provoked by nociceptive myelinated A-delta and unmyelinated C-fibre damage, non-nociceptive A-beta-fibre damage manifests only with non-painful sensory disturbances. Patients with neuropathic pain usually describe various types of pain, which include ongoing pain, paroxysmal pain, and provoked pains. Recent clinical-neurophysiological studies in patients with neuropathic pain secondary to peripheral and central nervous system disease (postherpetic neuralgia, carpal tunnel syndrome, and multiple sclerosis) suggest that paroxysmal pain may be related to focally demyelinated A-beta fibres. This workshop deals with the role of non-nociceptive A-beta fibres in neuropathic pain, reports the most recent data on A-beta-fibre function in patients with neuropathic pain and debates whether A-beta fibres can provoke pain per se or rather through central mechanisms. Proposed Program: • Introduction: A historic question that defies an established notion: R. Baron • Evidence from neurophysiological testing: A. Truini • Peripheral or central mechanisms?: R. Baron 120 ROLE OF THE A-BETA FIBRE DAMAGE IN PAROXYSMAL PAIN A. Truini. Department of Neurological Sciences, University Sapienza, Rome, Italy Patients suffering from neuropathic pain often complain of sensory deficits and different types of pain combined in various ways. Neuropathic pain may be ongoing, such as burning pain, or paroxysmal, such as electrical-shock-like sensations, or provoked by various stimuli, e.g. gentle brushing or cold water. Although specific types of pain may predominate in some etiologic categories, none of them are etiologic specific. Hence patients suffering from an identical disease may present with heterogeneous sensory signs and symptoms. Recent studies in patients with neuropathic pain demonstrate that paroxysmal pain is related to abnormalities in neurophysiological tests that assess large-myelinated fibres (Abeta-fibres) function. More specifically, paroxysmal pain correlates with the delay of the Abeta-fibre-mediated blink reflex in patients with postherpetic
neuralgia, and with reduction of the median nerve sensory conduction velocity in patients with carpal tunnel syndrome. These data suggest that paroxysmal pain reflects demyelination of non-nociceptive, large-myelinated fibres and indicate that, regardless of the disease, paroxysmal pain may be invariably related to Abeta-fibre damage. Consistently with animal studies describing spontaneous ectopic discharges recorded in Abeta-fibre axons after nerve injuries, paroxysmal pain may be related to high-frequency bursts generated in demyelinated Abeta-fibres. Whether these highfrequency bursts in demyelinated Abeta-fibres are sufficient to provoke pain per se or do so only after ephaptic transmission to the neighbouring C fibres, or through the involvement of wide dynamic range neurons is an open matter. Neurophysiological studies showing that paroxysmal pain reflects Abeta-fibre damage suggest that a specific type of pain may arise through the same pathophysiological mechanism, regardless of aetiology. This calls for a change in the way we classify and treat patients with neuropathic pain in clinical practice. Instead of grouping patients by aetiology, they should be probably grouped according to the various qualities of pain. This approach might minimize pathophysiological heterogeneity within the groups under study and increase the power to detect a positive treatment result. 121 THE ROLE OF A-BETA FIBERS IN NEUROPATHIC PAIN R. Baron. Division of Neurological Pain Research and Therapy, Dep. of Neurology, Universitaetsklinikum Schleswig-Holstein, Campus Kiel, Kiel, Germany Normally nociceptive sensations are transmitted to the central nervous system in C- and A-delta primary afferent fibers. After peripheral nerve damage this situation dramatically changes. In these pathological situations A-beta fibers which normally convey only non-noxious information become a major player in abnormal sensory processing. Several lines of evidence underpin this notion: Microneurographic single fiber recordings revealed abnormal ectopic activity of myelinated mechanosensitive fibers in traumatic nerve lesions, entrapment neuropathies, or radiculopathies. Since the ectopic nerve activity correlated in intensity and time course to the perceived paresthesias it is likely that pathological activity in A-fibers is the underlying mechanism. One hallmark of central sensitization of spinal cord neurons in animals is that activity in A-beta fiber mechanoreceptors are allowed to gain access to the nociceptive system and induce pain. This phenomenom is called mechanical allodynia. There is consensus that also in patients dynamic mechanical allodynia is signaled out of the skin by sensitive mechanoreceptors with large myelinated axons that normally encode non-painful tactile stimuli: (1) Reaction time measurements show dynamic mechanical allodynia in patients to be signaled by afferents with conduction velocities appropriate for large myelinated axons, (2) transcutaneous or intraneural stimulation of nerves innervating the allodynic skin can evoke pain at stimulus intensities which only produce tactile sensations in healthy skin, (3) using differential nerve blocks dynamic allodynia is abolished at time points when tactile sensations is lost, but other modalities remain unaffected and (4) mechanical allodynia also occurs in skin which is completely deprived of small afferent fibers. Paroxysmal pain which is characteristic for trigeminal neuralgia also occurs in other neuropathic pain states. To identify the underlying mechanism patients with trigeminal PHN were assessed with blink-reflex recordings and laser evoked potentials and the electrophysiological findings were compared with cutaneous sensory disturbances and the pain quality assessed clinically. The delay in blink reflex latency, a measure of non-nociceptice Abafferent function, correlated with the intensity of paroxysmal pain, whereas the reduction in Ad- and C-fiber evoked potentials correlated with the intensity of constant pain. These neurophysiological-clinical correlations suggest that paroxysmal pain is related to Abeta-fiber demyelination.
Oral presentations / European Journal of Pain Supplements 4 (2010) 1–46
Reference(s) Baron R. Mechanisms of disease: neuropathic pain – a clinical perspective. Nat Clin Pract Neurol 2006; 2: 95–106. Truini A, Galeotti F, Haanpaa M, Zucchi R, Albanesi A, Biasiotta A, Gatti A, Cruccu G. Pathophysiology of pain in postherpetic neuralgia: a clinical and neurophysiological study. Pain. 2008; 140: 405–10.
A6. Clinical Assessment of Neuropathic Pain: The NeuPSIG Recommendations 122 WORKSHOP SUMMARY: CLINICAL ASSESSMENT OF NEUROPATHIC PAIN: THE NEUPSIG RECOMMENDATIONS N. Attal1 , T. Nurmikko2 , R.D. Treede3 . 1 Centre d’Evaluation et de Traitement de la Douleur, INSERM U 987 and APHP, Boulogne Billancourt, France; 2 University of Liverpool, Liverpool, UK; 3 Institute of physiology and pathophysiology, Mainz, Germany Clinical assessment of neuropathic pain (NP) is crucial for a better understanding of its mechanisms and for implementing appropriate treatment. Over the past years a number of questionnaires have been developed specifically for the assessment of NP or its impact on quality of life. Quantitative sensory testing is also increasingly used for clinical research and practice and normative data based on large population groups have appeared a few years ago. The objectives of this workshop will be to present evidence based recommendations from the NeuPsig on neuropathic pain assessment for both clinical practice and research. Nadine Attal (France) will present outcome measures used in NP trials with special emphasis on specific questionnaires and their relevance to assess efficacy of treatments. Turo Nurmikko (UK) will present quality of life instruments with focus on recently validated tools specifically for NP. Finally Rolf Detlef Treede (Germany) will present evidence based recommendations on quantitative sensory testing for assessing pain mechanisms and treatments effects. 123 CLINICAL OUTCOME MEASURES IN NEUROPATHIC PAIN THERAPEUTIC TRIALS N. Attal. Centre d’Evaluation et de Traitement de la Douleur, INSERM U 987 and APHP, Boulogne Billancourt, France A number of pain scales and questionnaire have been used in clinical trials to assess the efficacy of therapeutic interventions in NP from simple VAS or numerical scales to assess pain intensity to more complex multidimensional scales to assess neuropathic pain symptoms, quality or life or disability [1, 2]. Numerical scales or VAS remain the most suitable to assess effects of treatment on pain intensity and clinical global impression and responder rates are recommended to asssess overall change of neuropathic pain under treatment. However these scales cannot capture the various dimensions of neuropathic pain experience (ie, burning pain, paroxysmal pain . . . ). Several neuropathic pain quality measures have been devoloped and found useful to discriminate between various pain mechanisms associated with distinct dimensions of neuropathic pain experience (1). These scales are recommended by NeuPsig as secondary outcomes in neuropathic pain clinical trials. Furthermore one major utility of these scales should be to attempt to help better define responder profiles to particular treatments. Reference(s) [1] Gilron I, Attal N, Bouhassira D, Dworkin RH Assessment of Neuropathic Pain (NP). In: Handbook of Pain Assessment, Turk D and Melzack R (editors), Guilford Press, 3rnd edition, in press. [2] Haanpa¨ a¨ ML, Backonja MM, Bennett MI, Bouhassira D, Cruccu G, Hansson PT, Jensen TS, Kauppila T, Rice AS, Smith BH, Treede RD, Baron R. Assessment of neuropathic pain in primary care. Am J Med. 2009 Oct; 122(10 Suppl): S13–21.
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124 NEUROPATHIC PAIN AND QUALITY OF LIFE – DO SCALES MEASURE IT RIGHT? T. Nurmikko. School of Clinical Sciences, University of Liverpool, Liverpool, UK Health-related quality-of-life (HRQOL) is increasingly considered as an important measure of the impact of disease on the patient’s physical, psychological and social functioning. My presentation will be an overview of the scales commonly used in the assessment of HRQOL in patients with neuropathic pain. From a systematic review of the topic, which included 61 papers in which generic HRQOL scales were used (Nurmikko et al., unpublished) I will provide answers to the following questions: (1) what is the effect on HRQOL of neuropathic pain per se, (2) does HRQOL correlate with the severity of neuropathic pain and related functional disability, and (3) is improvement in neuropathic pain reflected in HRQOL. While the answers to these questions are affirmative, there are discrepancies and inconsistencies that I will discuss, against the background of lack of consensus on what constitutes a clinically meaningful change, and how HRQOL as an outcome measure is frequently misconstrued. Two patient-oriented, condition-specific tools are available for the measurement of HRQOL in neuropathic pain, NePIQol suited for both of peripheral and central neuropathic pain (Poole et al., 2009) and Neuroqol (Vileikyte et al., 2005), developed for diabetic neuropathy and vasculopathy. I will discuss the usefulness and limitations of these two scales, as well as some condition-specific proxy tools available for diabetic neuropathy and herpes zoster (BPI-DPN, ZIQ, ZBPI) (Zelman et al., 2005, Coplan et al., 2005). I will finish my presentation with a set of recommendations regarding the choice of an appropriate HRQOL tool for specific purposes (e.g., epidemiological studies, clinical trials or routine data collection in the clinic), recently used as discussion paper for the deliberations of the Assessment Subcommittee of NeuPSIG. Reference(s) Coplan PM, Schmader K, Nikas A et al. Development of a measure due to the burden of pain of herpes zoster and postherpetic neuralgia for prevention trials: adaptation of the Brief Pain Inventory. J Pain 2004; 5: 344–356. Poole HM, Murphy P, Nurmikko TJ. Development and preliminary validation of the NePIQol: a quality of life measure for neuropathic pain. J Pain Symptom Manage 2009; 37: 233–245. Vileikyte L, Peyrot M, Bundy C, et al. The development and validation of a neuropathy- and foot ulcer-specific quality of life instrument. Diab Care 2003; 26: 2549–2555. Zelman DC, Gore M, Dukes E, et al. Validation of a modified version of the Brief Pain Inventory for painful diabetic peripheral neuropathy. J Pain Symptom Manage 2005; 29: 401–410.
125 ROLE OF QUANTITATIVE SENSORY TESTING FOR ASSESSING MECHANISMS AND TREATMENT OF NEUROPATHIC PAIN R.-D. Treede. Lehrstuhl f¨ ur Neurophysiologie, Medizinische Fakult¨ at Mannheim, Universit¨ at Heidelberg, Mannheim, Germany Neuropathic pain is frequently associated with negative or positive sensory signs or both in the painful body region (Geber et al. 2009). These signs can be documented by various combinations of Quantitative Sensory Testing (QST) and electrophysiology (standard neurography, microneurography, laser-evoked potentials; Cruccu et al. 2004). Animal models of neuropathic pain rely heavily on measurement of increased responsiveness to external stimuli. Thus, positive sensory signs in QST lend themselves for a direct comparison of mechanisms between patients and animal models. QST profiles from the patient database of the DFNS (German Research Network on Neuropathic Pain) for polyneuropathy and peripheral nerve injury have been compared with animal models. Whereas no single sensory test was pathological in all patients, QST profiling identified a substantial number of patients with positive
Oral presentations / European Journal of Pain Supplements 4 (2010) 1–46
118 POSTSURGICAL PAIN – EPIDEMIOLOGY B.H. Smith1,2 . 1 Aberdeen Pain Research Collaboration, University of Aberdeen, Aberdeen, 2 Peterhead Medical Practice, Peterhead, UK The first important contribution that epidemiology made to our understanding of postsurgical pain was to highlight its high prevalence and persistence. Depending on the operation, around 30% of patients go on to experience chronic postsurgical pain (CPSP), and this is severe in around 5% of patients. Secondly, epidemiology is identifying risk factors (surgical and psychosocial) that may be amenable to intervention. This work is important and on-going, but it is also challenging, because identifying and measuring cases, risk factors, and responses to interventions is complex. In particular, quantifying the contribution of neuropathic mechanisms to CPSP is difficult at a population level. This discussion will present some of these challenges, offering some insights into how they might be addressed, and how newer epidemiological studies should take account of current and emerging information on the mechanisms of CPSP.
M6. Role of the A-beta Fibres in Paroxysmal Pain 119 WORKSHOP SUMMARY: ABETA FIBRES IN PAROXYSMAL PAIN A. Truini. Department of Neurological Sciences, University ‘La Sapienza’, Rome, Italy An established notion postulates that whereas neuropathic pain is provoked by nociceptive myelinated A-delta and unmyelinated C-fibre damage, non-nociceptive A-beta-fibre damage manifests only with non-painful sensory disturbances. Patients with neuropathic pain usually describe various types of pain, which include ongoing pain, paroxysmal pain, and provoked pains. Recent clinical-neurophysiological studies in patients with neuropathic pain secondary to peripheral and central nervous system disease (postherpetic neuralgia, carpal tunnel syndrome, and multiple sclerosis) suggest that paroxysmal pain may be related to focally demyelinated A-beta fibres. This workshop deals with the role of non-nociceptive A-beta fibres in neuropathic pain, reports the most recent data on A-beta-fibre function in patients with neuropathic pain and debates whether A-beta fibres can provoke pain per se or rather through central mechanisms. Proposed Program: • Introduction: A historic question that defies an established notion: R. Baron • Evidence from neurophysiological testing: A. Truini • Peripheral or central mechanisms?: R. Baron 120 ROLE OF THE A-BETA FIBRE DAMAGE IN PAROXYSMAL PAIN A. Truini. Department of Neurological Sciences, University Sapienza, Rome, Italy Patients suffering from neuropathic pain often complain of sensory deficits and different types of pain combined in various ways. Neuropathic pain may be ongoing, such as burning pain, or paroxysmal, such as electrical-shock-like sensations, or provoked by various stimuli, e.g. gentle brushing or cold water. Although specific types of pain may predominate in some etiologic categories, none of them are etiologic specific. Hence patients suffering from an identical disease may present with heterogeneous sensory signs and symptoms. Recent studies in patients with neuropathic pain demonstrate that paroxysmal pain is related to abnormalities in neurophysiological tests that assess large-myelinated fibres (Abeta-fibres) function. More specifically, paroxysmal pain correlates with the delay of the Abeta-fibre-mediated blink reflex in patients with postherpetic
neuralgia, and with reduction of the median nerve sensory conduction velocity in patients with carpal tunnel syndrome. These data suggest that paroxysmal pain reflects demyelination of non-nociceptive, large-myelinated fibres and indicate that, regardless of the disease, paroxysmal pain may be invariably related to Abeta-fibre damage. Consistently with animal studies describing spontaneous ectopic discharges recorded in Abeta-fibre axons after nerve injuries, paroxysmal pain may be related to high-frequency bursts generated in demyelinated Abeta-fibres. Whether these highfrequency bursts in demyelinated Abeta-fibres are sufficient to provoke pain per se or do so only after ephaptic transmission to the neighbouring C fibres, or through the involvement of wide dynamic range neurons is an open matter. Neurophysiological studies showing that paroxysmal pain reflects Abeta-fibre damage suggest that a specific type of pain may arise through the same pathophysiological mechanism, regardless of aetiology. This calls for a change in the way we classify and treat patients with neuropathic pain in clinical practice. Instead of grouping patients by aetiology, they should be probably grouped according to the various qualities of pain. This approach might minimize pathophysiological heterogeneity within the groups under study and increase the power to detect a positive treatment result. 121 THE ROLE OF A-BETA FIBERS IN NEUROPATHIC PAIN R. Baron. Division of Neurological Pain Research and Therapy, Dep. of Neurology, Universitaetsklinikum Schleswig-Holstein, Campus Kiel, Kiel, Germany Normally nociceptive sensations are transmitted to the central nervous system in C- and A-delta primary afferent fibers. After peripheral nerve damage this situation dramatically changes. In these pathological situations A-beta fibers which normally convey only non-noxious information become a major player in abnormal sensory processing. Several lines of evidence underpin this notion: Microneurographic single fiber recordings revealed abnormal ectopic activity of myelinated mechanosensitive fibers in traumatic nerve lesions, entrapment neuropathies, or radiculopathies. Since the ectopic nerve activity correlated in intensity and time course to the perceived paresthesias it is likely that pathological activity in A-fibers is the underlying mechanism. One hallmark of central sensitization of spinal cord neurons in animals is that activity in A-beta fiber mechanoreceptors are allowed to gain access to the nociceptive system and induce pain. This phenomenom is called mechanical allodynia. There is consensus that also in patients dynamic mechanical allodynia is signaled out of the skin by sensitive mechanoreceptors with large myelinated axons that normally encode non-painful tactile stimuli: (1) Reaction time measurements show dynamic mechanical allodynia in patients to be signaled by afferents with conduction velocities appropriate for large myelinated axons, (2) transcutaneous or intraneural stimulation of nerves innervating the allodynic skin can evoke pain at stimulus intensities which only produce tactile sensations in healthy skin, (3) using differential nerve blocks dynamic allodynia is abolished at time points when tactile sensations is lost, but other modalities remain unaffected and (4) mechanical allodynia also occurs in skin which is completely deprived of small afferent fibers. Paroxysmal pain which is characteristic for trigeminal neuralgia also occurs in other neuropathic pain states. To identify the underlying mechanism patients with trigeminal PHN were assessed with blink-reflex recordings and laser evoked potentials and the electrophysiological findings were compared with cutaneous sensory disturbances and the pain quality assessed clinically. The delay in blink reflex latency, a measure of non-nociceptice Abafferent function, correlated with the intensity of paroxysmal pain, whereas the reduction in Ad- and C-fiber evoked potentials correlated with the intensity of constant pain. These neurophysiological-clinical correlations suggest that paroxysmal pain is related to Abeta-fiber demyelination.
Oral presentations / European Journal of Pain Supplements 4 (2010) 1–46
Reference(s) Baron R. Mechanisms of disease: neuropathic pain – a clinical perspective. Nat Clin Pract Neurol 2006; 2: 95–106. Truini A, Galeotti F, Haanpaa M, Zucchi R, Albanesi A, Biasiotta A, Gatti A, Cruccu G. Pathophysiology of pain in postherpetic neuralgia: a clinical and neurophysiological study. Pain. 2008; 140: 405–10.
A6. Clinical Assessment of Neuropathic Pain: The NeuPSIG Recommendations 122 WORKSHOP SUMMARY: CLINICAL ASSESSMENT OF NEUROPATHIC PAIN: THE NEUPSIG RECOMMENDATIONS N. Attal1 , T. Nurmikko2 , R.D. Treede3 . 1 Centre d’Evaluation et de Traitement de la Douleur, INSERM U 987 and APHP, Boulogne Billancourt, France; 2 University of Liverpool, Liverpool, UK; 3 Institute of physiology and pathophysiology, Mainz, Germany Clinical assessment of neuropathic pain (NP) is crucial for a better understanding of its mechanisms and for implementing appropriate treatment. Over the past years a number of questionnaires have been developed specifically for the assessment of NP or its impact on quality of life. Quantitative sensory testing is also increasingly used for clinical research and practice and normative data based on large population groups have appeared a few years ago. The objectives of this workshop will be to present evidence based recommendations from the NeuPsig on neuropathic pain assessment for both clinical practice and research. Nadine Attal (France) will present outcome measures used in NP trials with special emphasis on specific questionnaires and their relevance to assess efficacy of treatments. Turo Nurmikko (UK) will present quality of life instruments with focus on recently validated tools specifically for NP. Finally Rolf Detlef Treede (Germany) will present evidence based recommendations on quantitative sensory testing for assessing pain mechanisms and treatments effects. 123 CLINICAL OUTCOME MEASURES IN NEUROPATHIC PAIN THERAPEUTIC TRIALS N. Attal. Centre d’Evaluation et de Traitement de la Douleur, INSERM U 987 and APHP, Boulogne Billancourt, France A number of pain scales and questionnaire have been used in clinical trials to assess the efficacy of therapeutic interventions in NP from simple VAS or numerical scales to assess pain intensity to more complex multidimensional scales to assess neuropathic pain symptoms, quality or life or disability [1, 2]. Numerical scales or VAS remain the most suitable to assess effects of treatment on pain intensity and clinical global impression and responder rates are recommended to asssess overall change of neuropathic pain under treatment. However these scales cannot capture the various dimensions of neuropathic pain experience (ie, burning pain, paroxysmal pain . . . ). Several neuropathic pain quality measures have been devoloped and found useful to discriminate between various pain mechanisms associated with distinct dimensions of neuropathic pain experience (1). These scales are recommended by NeuPsig as secondary outcomes in neuropathic pain clinical trials. Furthermore one major utility of these scales should be to attempt to help better define responder profiles to particular treatments. Reference(s) [1] Gilron I, Attal N, Bouhassira D, Dworkin RH Assessment of Neuropathic Pain (NP). In: Handbook of Pain Assessment, Turk D and Melzack R (editors), Guilford Press, 3rnd edition, in press. [2] Haanpa¨ a¨ ML, Backonja MM, Bennett MI, Bouhassira D, Cruccu G, Hansson PT, Jensen TS, Kauppila T, Rice AS, Smith BH, Treede RD, Baron R. Assessment of neuropathic pain in primary care. Am J Med. 2009 Oct; 122(10 Suppl): S13–21.
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124 NEUROPATHIC PAIN AND QUALITY OF LIFE – DO SCALES MEASURE IT RIGHT? T. Nurmikko. School of Clinical Sciences, University of Liverpool, Liverpool, UK Health-related quality-of-life (HRQOL) is increasingly considered as an important measure of the impact of disease on the patient’s physical, psychological and social functioning. My presentation will be an overview of the scales commonly used in the assessment of HRQOL in patients with neuropathic pain. From a systematic review of the topic, which included 61 papers in which generic HRQOL scales were used (Nurmikko et al., unpublished) I will provide answers to the following questions: (1) what is the effect on HRQOL of neuropathic pain per se, (2) does HRQOL correlate with the severity of neuropathic pain and related functional disability, and (3) is improvement in neuropathic pain reflected in HRQOL. While the answers to these questions are affirmative, there are discrepancies and inconsistencies that I will discuss, against the background of lack of consensus on what constitutes a clinically meaningful change, and how HRQOL as an outcome measure is frequently misconstrued. Two patient-oriented, condition-specific tools are available for the measurement of HRQOL in neuropathic pain, NePIQol suited for both of peripheral and central neuropathic pain (Poole et al., 2009) and Neuroqol (Vileikyte et al., 2005), developed for diabetic neuropathy and vasculopathy. I will discuss the usefulness and limitations of these two scales, as well as some condition-specific proxy tools available for diabetic neuropathy and herpes zoster (BPI-DPN, ZIQ, ZBPI) (Zelman et al., 2005, Coplan et al., 2005). I will finish my presentation with a set of recommendations regarding the choice of an appropriate HRQOL tool for specific purposes (e.g., epidemiological studies, clinical trials or routine data collection in the clinic), recently used as discussion paper for the deliberations of the Assessment Subcommittee of NeuPSIG. Reference(s) Coplan PM, Schmader K, Nikas A et al. Development of a measure due to the burden of pain of herpes zoster and postherpetic neuralgia for prevention trials: adaptation of the Brief Pain Inventory. J Pain 2004; 5: 344–356. Poole HM, Murphy P, Nurmikko TJ. Development and preliminary validation of the NePIQol: a quality of life measure for neuropathic pain. J Pain Symptom Manage 2009; 37: 233–245. Vileikyte L, Peyrot M, Bundy C, et al. The development and validation of a neuropathy- and foot ulcer-specific quality of life instrument. Diab Care 2003; 26: 2549–2555. Zelman DC, Gore M, Dukes E, et al. Validation of a modified version of the Brief Pain Inventory for painful diabetic peripheral neuropathy. J Pain Symptom Manage 2005; 29: 401–410.
125 ROLE OF QUANTITATIVE SENSORY TESTING FOR ASSESSING MECHANISMS AND TREATMENT OF NEUROPATHIC PAIN R.-D. Treede. Lehrstuhl f¨ ur Neurophysiologie, Medizinische Fakult¨ at Mannheim, Universit¨ at Heidelberg, Mannheim, Germany Neuropathic pain is frequently associated with negative or positive sensory signs or both in the painful body region (Geber et al. 2009). These signs can be documented by various combinations of Quantitative Sensory Testing (QST) and electrophysiology (standard neurography, microneurography, laser-evoked potentials; Cruccu et al. 2004). Animal models of neuropathic pain rely heavily on measurement of increased responsiveness to external stimuli. Thus, positive sensory signs in QST lend themselves for a direct comparison of mechanisms between patients and animal models. QST profiles from the patient database of the DFNS (German Research Network on Neuropathic Pain) for polyneuropathy and peripheral nerve injury have been compared with animal models. Whereas no single sensory test was pathological in all patients, QST profiling identified a substantial number of patients with positive