10th World Congress on Pain, List of topics

TRAUMATIC NEUROMAS OF THE HUMAN LINGUAL NERVE: AN ULTRASTRUCTURAL STUDY
A.R. Vora, P.P. Boissonade, F.M. Loescher, A.R., Dept of Oral & Maxillofacial Surgery, School of Clinical Dentistry, Sheffield, S10 2TA, United Kingdom

Aim of Investigation To determine the ultrastructural characteristics of axons in traumatic neuromas of the lingual nerve and correlate these with reported symptoms of dysaesthesia.

Methods Using electron microscopy, the morphology of 34 lingual nerve neuromas was determined. The nerves had been damaged during lower third molar removal and the specimens were obtained at the time of nerve repair. Axon diameter, myelin thickness, g-ratio, the number of unmyelinated axons/Schwann cell bundle, and the presence and extent of axonal exposure and apposition were quantified. Comparisons were made with normal lingual nerve (n=8).

Results Mean myelinated axon diameter was lower in neuromas (4.1 +/-0.7µm) than controls (6.3 +/-0.6µm). Mean myelin sheath thickness was also thinner in neuromas (0.6 +/- 0.1µm) than controls (1.1 +/- 0.1µm), but the g-ratio was found to be similar, suggesting a normal process of myelination in neuromas. Unmyelinated axon diameter was smaller in neuromas (0.6 +/-0.1µm) than controls (1.0 +/-0.1µm) and more unmyelinated axons showed signs of axonal exposure (neuromas 26%; controls 5%) and close-apposition with neighbouring axons (neuromas 11%; controls 0.35%). There were no significant differences between the characteristics of neuromas obtained from patients with symptoms, and those without symptoms.

Conclusions These ultrastructural differences may account for some of the altered electrophysiological properties of axons in neuromas. However, as there was no correlation between the reported symptoms of dysaesthesia and the ultrastructural characteristics, these morphological changes are unlikely to be primarily responsible for the initiation of dysaesthesia.

Acknowledgements Supported by Action Research.

PAIN CAUSED BY VASCULAR COMPRESSION OF THE SCIATIC NERVE
M. Koltzenburg, J. Perez, K. Reiners, L. Solymosi, M. Bendszus, Institute of Child Health, University College London, London, United Kingdom , Department of Neurology, University of Wrzburg, Würzburg, Germany , Department of Neurosurgery, University of Wrzburg, Würzburg, Germany , Deptartment of Neuroradiology, University of Wrzburg, Würzburg, Germany

AIM OF INVESTIGATION: Pain radiating into the leg and buttock without focal neurological deficit has a high prevalence in the general population. Here we describe a novel pain syndrome in whom a vascular compression of the sciatic nerve could be identified as the cause.

METHODS: Magnetic-resonance-imaging (MRI) of the pelvis and upper thigh using fat-suppressed T2-weighted images and T1-weighted images prior and after administraion of Gadolinum-DTPA

RESULTS: In 3 patients without focal neurological deficit severe pain radiating into the leg and buttock was provoked by sitting and lying on the affected side and relieved after standing up and walking. MRI showed tubular formations that enhanced intensely after application of Gadolinium DTPA to the same degree as the gluteal and femoral vessels in close vicinity of the sciatic nerve. The diagnosis of varicose veins compressing the sciatic nerve was confirmed during surgical exposure in two patients in whom decompression of the nerve resulted in complete and permanent pain relief whereas in the remaining patient, pain was reduced by carbamazepine treatment.

CONCLUSIONS: Leg or buttock pain in patients with varicosis and pain provoked by sitting or lying may be caused by gluteal varicosis compressing the sciatic nerve. This novel painful focal compression neuropathy of the sciatic nerve can be diagnosed by MRI. As clinical and neurophysiological examination revealed no lesion of the sciatic nerve it is possible that excitation of nervi nervorum caused the pain.

ASSESSMENT AND FOLLOW-UP OF PAINFUL DIABETIC NEUROPATHY USING QST
G. K Talu1, I. Kara, Department of Algology, Istanbul University, Istanbul, Turkey , Institute of Experimental and Medical Research, Istanbul University, Istanbul, Turkey

Aim of Investigation: To evaluate the sensitivity of QST for the assessment and the treatment follow-up in diabetic neuropathy compared to normal subjects.

Methods: Fifteen patients with diabetic polyneuropathy and twenty healthy volunteers participated. EMG, skin temperature, pin-prick hyperalgesia, allodynia, thermal perceptions for heat and cold, heat and cold pain thresholds (HPT/CPT)and the daily activities evaluated and the intensity of pain was rated (VAS). All measurements were performed at the beginning, one month and two months after the medical treatment using amityriptiline 25 mg and tramadol hydrochloride 50 mg per day. The results from the dominant hands compared with the results of normal volunteers. One-way repeated-measure analysis of variance (ANOVA) was performed for statistical analysis.

Results: The results obtained from the patients at the beginning, one month and two months after the medical treatment regarding skin temperature, cold and heat perceptions, CPT, and HPT were significantly different from the volunteers (p<0.05). There were no significant differences between the results of the patients obtained at the beginning, one month and two months after the medical treatment. Pin-prick hyperalgesia, allodynia, and VAS scores decreased significantly and the skin temperature increased significantly one month and two months after the medical treatment (p<0.05). The daily activities of the patients increased significantly during and at the end of the treatment.

Conclusions: The results of this study suggest that those parameters are appropriate for the assessment of diabetic neuropathy and for therapeutic follow-up. However, the results are individual and the patient's cooperation is needed.

THE TIME FACTOR IN TRICYCLIC TREATMENT OF POSTHERPETIC NEURALGIA (PHN) AND CENTRAL POST-STROKE PAIN (CPSP)
D. Bowsher, PAIN RESEARCH INSTITUTE, LIVERPOOL, United Kingdom

Aim of Investigation: To evaluate the effect of time between acute shingles (HZ) or CPSP onset and initiation of treatment with amitriptyline (TCA) on outcome.

Methods: This time interval (in months) was measured for 262 patients with PHN and 64 patients with CPSP. Successful outcome was taken as >50% reduction in visual analogue pain intensity.

Results: There was a highly significant correlation between HZ onset-treatment initiation interval for PHN: three quarters of those beginning treatment between 3 and 6 months after HZ onset achieved >50% relief, but only one quarter achieved >50% relief of patients beginning treatment between 2 and 3 years after HZ onset.

A less marked, but still significant correlation between the CPSP-treatment interval showed that 89% of those beginning treatment within 6 months of pain onset achieved >50% relief, but only 42% of those not beginning TCA treatment until more than a year.

Conclusions: For TCAs, the interval between HZ or CPSP pain onset and the commencement of treatment is critical to success. The clinical moral is that treatment must be begun at the earliest possible moment. The pathophysiological implication is that both these forms of neuropathic pain are a dynamic process. Unfortunately similar data do not exist for newer treatments with fewer side-effects, notably gabapentin. It is essential that such information be gathered and analysed.

Acknowledgements: This work was supported by The Pain Relief Foundation

DIFFERENTIAL EXPRESSION OF THE SODIUM CHANNEL -3 SUBUNIT IN INJURED HUMAN SENSORY NEURONS
M.A. Casula, A. Powell, I. Kinghorn, C. Plumpton, S. Tate, C. Bountra, R. Birch, P. Anand, Peripheral Neuropathy Unit, Hammersmith Hospital, London, United Kingdom , Neurology, GlaxoSmithKline, Harlow, United Kingdom , Peripheral Nerve Injury Unit, Royal National Orthopaedic Hospital, Stanmore, United Kingdom

Aim: To study the expression of voltage-gated Na+ channel 3 subunit in intact and injured human DRG and peripheral nerves.

Methods: Using a specific antibody for immunohistochemistry, we have studied postmortem control (n=7) and injured (n=6) human DRG and peripheral nerves (n=14 controls, n=20 injured).

Results: In control DRG, 3 subunit immunostaining was seen in the majority of large (63%) and medium/small diameter neurons (80%). In avulsed DRG, the 3 subunit was observed in fewer large neurons (36%, P<0.035), but was maintained in small/medium cells (70%, P>0.05). Co-localisation studies showed that a sub-set of 3-positive neurons were also stained to trkA, in control (45% small/medium, 33% large) and avulsed DRG (34% small/medium, 15% large). In peripheral nerves, the expression of the 3 subunit as a ratio between the area immunostained by the 3 antibody to the area stained by a neurofilament antibody was significantly increased in nerves with short (< 3 weeks) (P=0.025) and long delay (P=0.027) after injury, in comparison with control nerves.

Conclusion: Our results suggest that unlike 1 and 2 subunits in injured human DRG, which were decreased in parallel to TTX-R sodium channels SNS1/PN3 and NaN/SNS2, the 3 subunit expression was maintained in small sensory neurons in injured DRG, and increased in injured peripheral nerves. The 3 subunit thus appears to be regulated differently, and represents an attractive target for the development of novel selective analgesics for neuropathic pain.

TOPICAL LIDOCAINE TARGETS MYELINATED FIBERS RATHER THAN NOCICEPTORS IN NEUROPATHIC PAIN
G.L. Wasner,^, R. Binder, A. Schattschneider, J. Kleinert, Neurology, University Kiel, Kiel, Germany

Aim of the investigation: Patients with postherpetic neuralgia (PHN) differ concerning their cutaneous nociceptor function and pain generating mechanisms. (1) Pain is caused by pathologically sensitized primary afferent cutaneous nociceptors. Mechanical allodynia is due to central sensitization allowing touch-sensitive A-fibers to activate central nociceptors. (2) Nociceptor function is impaired and the fibers are degenerated. Allodynia is due to anatomical sprouts of A-fibers projecting on central nociceptors. Pain treatment assumed to address the nociceptor should give different results in the two groups.

Methods: Using quantitative sensory testing and the quantitative axon reflex test the cutaneous nociceptor function was identified in 18 PHN patients, prospectively. These data were compared with the results of a randomized, cross over, placebo controlled study with cutaneous lidocaine (5% patch, IBSA). The study was performed according to the Helsinki Declaration.

Results: Six patients (group I) had pathologically sensitized nociceptors with A-mediated allodynia. In 12 patients (group II) nociceptive C-fibers were degenerated and allodynia was mediated by still intact A-fibers. Lidocaine was efficacious in 50% in group I patients (not superior to placebo) but provided significant pain relief in group II patients (75% responder).

Conclusions: Topical lidocaine predominantly acts on myelinated fibers rather than on C-nociceptors. It might be suggested that novel sodium channels are expressed on intact A-fibers in relation to Wallerian degeneration of nociceptors that run in the same nerve.

Acknowledgements: Supported by the Deutsche Forschungsgemeinschaft (DFG Ba 1921/1-1), the Wilhelm Sander-Stiftung and the Institut Biochimique SA (IBSA, Switzerland)

PRIORITIZING CANDIDATE GENES FOR STUDIES OF THE RISK OF CHRONIC NEUROPATHIC PAIN
I. Belfer, M.B. Max, Pain and Neurosensory Mechanisms Branch, National Institute of Dental and Craniofacial Research, Bethesda, MD , Laboratory of Neurogenetics, National Institute on Alcohol Abuse & Alcoholism, Rockville, MD

AIM OF INVESTIGATION: Whole genome studies of human disease risk may evaluate any of the 3 million known variant sites. However, for sample sizes below 500 patients, statistical considerations and current genotyping costs make it more feasible to limit study to 10 - 100 candidate sites.

METHODS: To plan a study of the genetic risk factors for chronic sciatica after disc herniation, we listed the 200+ pain-related molecules mentioned in the Wall/Melzack textbook and recent Soc Neurosci abstracts and review articles and assigned 0-3 points for strength of association with neuropathic pain. We then searched PubMed for "[name of molecule] and human and polymorphism," and assigned two additional 0-3 scores based on the population frequency and evidence that the variant affects either cellular function or risk of any disease. RESULTS: In order of priority scores, variants include: IL-6 (G -174 C promoter); neuronal nitric oxide synthase (AAT VNTR); TNF-alpha (G -308 A promoter); serotonin transporter (44 bp insertion/deletion in promoter); IL-1 beta (C -31 T promoter); bradykinin receptor 2 (C -58 T promoter); IL-10 (A - 1082 G promoter); inducible nitric oxide synthase (CCTTTn repeat); prodynorphin (68 base pair repeat).

CONCLUSIONS: Cytokine genes carry many of the common, functionally significant human variants of genes whose products may process neuropathic pain. Association studies of these and other common variants may help to prioritize targets for drug development.

ACKNOWLEDGEMENTS: We thank J Neubert, H-S Kim, A Kingman, S Diehl, M Iadarola, and R Dionne for suggestions. Supported by NIDCR ZO1 DE00366

HYPEREXCITABLE C NOCICEPTORS CAUSING CAPSAICIN-LIKE ERYTHRALGIA (ABC SYNDROME), POST FLU. SERUM ANTI VR1 RECEPTOR ACTIVITY. RESPONSE TO IV IMMUNOGLOBULIN
J.L. Ochoa^, J. Campero, M. Serra, Bostock, H., Oregon Nerve Center, Good Samaritan Hospital, Oregon Health Sciences University, Portland, OR

AIM OF INVESTIGATION: To characterize the clinical and neurophysiological profile of a patient with acute, post-infectious, ABC syndrome. Test C nociceptors through microneurography. Evaluate anti VR1 immune activity. Therapeutic trial with human immunoglobulin.

METHODS: Rigorous clinical neurological examination, supplemented by quantitative sensory thermotest, thermography, microneurography and automated latency tracking of identified C nociceptors supplying symptomatic skin. Immunological challenge with the patient's serum of Western blots containing extracts from VR1-expressing fibroblasts (supplied by the Julius Lab, UCSF). Treatment: intravenous immunoglobulin.

RESULTS: The girl had spontaneous burning pain in the feet, heat and mechanical hyperalgesia relieved by passive cooling, and thermographic signs of cutaneous inflammation. Large caliber sensory and motor nerve functions were intact. Microneurography revealed spontaneous firing and abnormal afterdischarges of C nociceptors, which did not respond to activation of neighboring C sympathetic efferent fibers (superficial peroneal nerves). Immunological testing showed cross reactivity between serum and Western blots containing VR1 membrane receptors. After treatment, pain gradually diminished and narcotics were withdrawn. On follow-up, four months later, the patient was asymptomatic except for minor hyperalgesia in the hands.

Conclusions: We attribute this case of painful neuropathy to hyperexcitability of human C nociceptors caused by autoimmune disruption of the VR1 membrane receptor. Further immunological studies are in progress.

ACKNOWLEDGEMENTS: Supported by Grant NIH RO1 NS39761.

NA_V1.7/PN1 SODIUM CHANNEL EXPRESSION IN HUMAN LINGUAL NERVE NEUROMAS
E.V. Bird^, P.P. Boissonade, F.M. Oral and Maxillofacial Surgery, School of Clinical Dentistry, University of Sheffield, Sheffield, United Kingdom

Aim of Investigation: To examine the expression of the sodium channel subtype Na_v1.7/PN1 in damaged human lingual nerve, and to identify any association between Na_v1.7/PN1 expression and reported symptoms of dysaesthesia.

Methods: Eleven nerve-end neuromas (NENs) and 11 neuromas-in-continuity (NICs) were studied; all were obtained at the time of surgical repair of damaged lingual nerves. The specimens were categorised as being obtained from patients with symptoms or without symptoms, according to the degree of pain, tingling or discomfort that had been experienced. Following removal, the specimens were placed in 2% Zamboni's fixative, cryoprotected in 30% sucrose and processed for indirect immunofluorescence. Frozen, 14m sections were dual labelled for the general neuronal marker, protein gene-product 9.5 (PGP 9.5) and Na_v1.7/PN1 (antibody provided by GlaxoSmithKline). Image analysis was used to quantify the percentage area of PGP 9.5 labelled tissue that contained Na_v1.7/PN1.

Results: The extent of labelling varied greatly between the specimens, ranging from 0% to 81.2%. However, there was no significant difference between the level of the Na_v1.7/PN1 labelling in patients with symptoms and those without symptoms (NICs: no symptoms 36% (mean), symptoms 33.7%, NENs: no symptoms 24.5%, symptoms 30.1%; Unpaired t-test p>0.05).

Conclusions: The data reveal that the sodium channel Na_v1.7/PN1 is expressed in human lingual nerve neuromas but does not appear to play a primary role in initiating the painful symptoms of dysaesthesia.

USE OF GABAPENTIN IN THE CONTROL OF NEURITIS IN HANSEN`S PATIENTS
L.C. Pelloso, D.D. Almeida1, M.A. Allet1, Anestesiologia, Instituto de Especialidades de Mato Grosso, Cuiabá, Brazil , Anestesiologia, Medicine School, Sao Paulo, Brazil

AIM OF INVESTIGATION: To evaluate the use of Gabapentin in patients with Hansens disease with neuritis undergoing treatment with prednisolone.

METHODS: Ethical approval and informed consent were obtained. We studied 22 patients with Hansen's disease, 16 males and 6 females between 18 and 66 years of age. The disease was classified as: 11 virchovian, 10 dimorphous, and 1 tuberculoid. Patients were using daily Prednisolone in doses ranging from 0 to 60 mg. For painful neuritis, the treatment was Gabapentin (400 to 800 mg) and Amitriptyline (0 to 25 mg). To evaluate the pain we used a visual analgesic scale on the first day (VAS0) and after 30 days (VAS30). Predinosolone dosage was reduced with decrease of pain, and side effects were controlled and related comorbidities were shown.

RESULTS: There was a decreased in pain (VAS0 8 2,8 and VAS30 1,9 1,9; p < 0,001) and in use of Prednisolone ( Pred0 15,4 15, 6 and Pred30 7,2 8,1; p < 0,005). The initial consumption of Gabapentin was 400 123,4 and after 30 days, 427,2 187,0, and the initial consumption of Amitriptyline was 17,0 9,8 and after 30 days, 16,6 10,0.

CONCLUSIONS: The association between Gabapentin and Amitriptyline was effective in pain control, decreasing the consumption of Predinisolone and its side effects without significant side effects. We found drowsiness in 10 patients, epigastralgia in 3, and conjunctival hyperemia in 1 patient. The comorbidities related to the use of Prednisolone were diabetes in 4 patients, hypertension in 6, osteoporosis in 1, and herpes zoster in 1.

COMMON NEUROPATHIC PAIN
D. Roy,^,Anesthesiology, Private Practice, Calcutta, India

AIM OF INVESTIGATION: Neuropathic pain of various etiologies and anatomical structures makes up 15% of the total patient attendance at my Pain Clinic. The main objective of this study was to ascertain: (a) etiology and altered pathology; (b) to formulate treatment programs; (c) research aspect of treatment; and (d) logical conclusion about the prognosis in individual cases of: (1) non-diabetic and diabetic neuropathic pain of plantar nerve, peroneal nerve, saphenous nerve distribution, and (2) blunt injury of sciatic nerve causing neuropathic pain: (A) partial injury (fall, direct blunt injury, e.g., hit) and (b) chronic compressive ischemic injury (chronic constrictive injury).

METHODS: Etiology, pathophysiology, and neuropathology were determined by clinical, hematological, neurophysiological, biochemical, radiological, immunological, and Doppler study. Symptomatic pharmacological treatment: diabetic management, steroid therapy, central skeletal muscle relaxant, antidepressant, NSAID drugs, anticonvulsants, NMDA receptor blockers, antioxidants, vitamins, and vasodilators were used.

RESULTS: Multimodal physical therapy, weight reduction, diet and exercise, assisted devices, e.g., special shoes and special chairs, rehabilitation program, psychotherapy, and regular follow-up strategy, etc., cured or improved the majority with 10% short recurrence and 5% dropouts.

CONCLUSIONS: Neuropathic pain of certain etiologies have more knowledge to medical and pain specialists than others, hence a continued research will even bring answers to preventive aspects.

TREATMENT OF POSTSURGICAL NEUROPATIC PAIN
A. Koulousakis, M. Lenartz, D. Weber, Stereotaxy, University of Cologne, Cologne, Germany

Postsurgical pain occurs when the surgical procedure was accompanied by iatrogenic damage of the nerve fibers. Such pain in the area of the face occurs after maxillofacial surgery, called symptomatic trigeminal neuralgia. Similar pain of the body and extremities arises as pain after surgical procedures, known as postthoracotomy syndrome with intercostal neuralgia, neuralgia of the inguinal nerve or genitofemoral nerve after hernia surgery, phantom pain after amputation, sympathetic pain after surgical or orthopedic surgery (CRPS) and most often the neuropathic pain of herniated disc surgery (FBSS Syndrom).

Nowadays there is no indication for destructive surgery with neuropathic pain. More often used are two methods of modula-tion. These are the electrostimulation of peripheral nerves or spinal cord (ganglion gasseri stimulation, S.C.S., PNS) or the intrathecal application of opioids. In the last 15 years we have treated 360 patients with SCS-Therapy and 180 patients with intrathecal morphine for postsurgical, neuropathic pain of diffe-rent origin; in most cases after FBSS (320 SCS-152 pumps). Short term results of stimulation methods are good with 70%. Only gradually a decrease of the positive effect of stimulation os developed. Follow-ups to 10 years show a relief of pain for 40% of patients. Similar or even better results can be achieved with intrathecal application of opioids, either as monoapplication (Morphine, Buprenorphine) or in combination with other drugs such as Baclofen or Clonidine. The good or very good results are around 70% and the stay constant with only minimal dose adjustment during a period of time of up to 8 years.

Comparing the two methods, the intrathecal application of opioids is superior to the epidural stimulation. The two methods and their results are presented in detail.

ADRENERGIC SENSITIZATION OF C-FIBERS IN PAINFUL AND NON-PAINFUL HUMAN POLYNEUROPATHY
J. Schattschneider, A. Binder, S. Kloehn, H. Kjos-Poetsch, R. Baron, Dept of Neurology, Univ of Kiel, Kiel, Germany , Dept of Medicine, Univ of Kiel, Kiel, Germany

AIM OF INVESTIGATION: After nerve lesions nociceptor activity can be influenced by the sympathetic nervous system. Sensitization of C-fibers by norepinephrine (NE) has been demonstrated in normal and capsaicin-treated human skin.In the present study contribution of sympathetic afferent coupling to pain in polyneuropathy was investigated.

METHODS: 9 patients (PAT) with painful (PN), 7 PAT with non-painful neuropathy (NN) and 7 controls (CON) were examined. Warm and heat pain thresholds were measured on the dorsum of the foot before and after iontophoresis of NE and NaCl 0,9%. Cutaneous blood flow (CBF) at the site of iontophoresis was monitored. Function of sympathetic efferents was measured by quantitative evaluation of the decrease in CBF after deep inspiration.

RESULTS: Pathological warm thresholds were detected in PAT with PN (44,5C0,7) and NN (43,5C1,6). After deep inspiration the mean decrease in CBF was 33%5,5 in PN and 45,510 in NN. After application of NE a significant decrease in heat pain thresholds and CBF occurred which was not observed after NaCl iontophoresis. There was no significant differences in the decrease in heat pain thresholds between PN PAT (1,1C0,2), NN PAT(1,6C0,4) or CON (1,3C0,3). There were no correlations between the degree of afferent C-fiber damage or function of sympathetic efferents and sensitization of heat responsive C-fibers due to NE.

CONCLUSIONS: The present study could not confirm the assumption that adrenergic mechanisms are involved in generation of pain in human polyneuropathy.

Acknowledgments: This work was supported by the Deutsche Forschungs Gesellschaft (DFG) Ba 1921/1-1

BEHAVIORAL AND HISTOLOGICAL STUDY OF SCIATIC NERVE IN NEUROPATHIC RATS FOLLOWING SPINAL TRANSPLANTATION OF CHROMAFFIN CELLS
F. Nezhad,^, G. Manaheji, H., Dept of Physiology, Shahid Beheshti Medical Univ, Tehran, Iran

AIM OF INVESTIGATION: The aim of this study was to determine the effects of spinal transplantation of chromaffin cells on peripheral nerve regeneration in neuropathic rats.

METHODS: For this reason the left sciatic nerve of adult rats were ligated by 4 loose ligatures around it. One week after nerve injury some animals were implanted with either isolated chromaffin cells or control striated muscle at the level of L1-L2. Behavioral evaluation were repeated after nerve injury and transplantation. After 2 months the animals were anesthetized and the proximal and distal parts of sciatic nerve were isolated and prepared for histological studies.

RESULTS: The results showed that in animals with chromaffin cells implants allodynia and hyperalgesia which are the signs of neuropathic pain were markedly reduced or eliminated. Also in the chromaffin transplanted animals marked increase in the number of myelinated fiber in the distal segment compare to untransplanted and muscle transplanted animals was observed. These animals showed increase in the thickness of myelin sheath comparing to other groups.

CONCLUSIONS: Our observation showed that molecules such as neurotrophic factors secreted by the chromaffin cells could accelerate the regeneration of neurons after injury of sciatic nerve.

ACKNOWLEDGEMENTS: Supported by the grants from neuroscience research center.

TREATMENT OF NEUROPATHIC PAIN WITH IMPULSE ELECTROMAGNETIC FIELDS
A.V. Musayev, S.S. Huseynova, S.G., Researh Inst of Medical Rehabilitation, Baki, Azerbaijan

AIM OF INVESTIGATION: To evaluate the efficacy of impulse electromagnetic fields (IEMF) for neuropathic pain treatment.

METHODS: Pain syndromes caused by diabetic polyneuropathy (DP - 120 patients) and traumatic neuropathy (TN - 36 patients) served as a model of neuropathic pain before and after treatment. All of the patients underwent cliniconeurological and pathopsychological (visual-analogous scale - VAS and McGill Questionnaire. The analgesic effect ratio (AER) had also been determined.

RESULTS: The driving clinical sign of DP was pain syndrome (89.2%) with the intensity according to VAS 5.30.3. TN patients developed pain syndrome in 58.3% of cases, median intensity value according to VAS comprised 4.10.2. A total number of descriptors according to sensor and affective scales was 9.10.9, a range total number - 17.00.1. Significant reduction of pain syndrome intensity (p<0.001) after treatment showed two groups. AER (DP - 0.5, TN - 0.4) counted after treatment allowed us to justify the analgesic effect of IEMF as of mean significance. The descriptor index had been reduced to 3.50.7, the range index - to 6.10.9 by the end of treatment.

CONCLUSIONS: Thus, IEMF showed a positive effect on neuropathic pain the reason of which was the reduction of structurally functional alterations in peripheral and central parts of the nervous system due to the improved neuropathic processes resulting in the attenuation of pathologic algic system.

PHARMACOLOGICAL TREATMENT OF SUSPECTED NEUROPATHIC PAIN. RESPONSE IS NOT RELATED TO EVIDENCE OF NERVOUS SYSTEM LESION
P.V. Rasmussen, S.H. Sindrup, F.W. Bach, Danish Pain Research Center, Aarhus University Hospital, Aarhus, Denmark , ² Neurological Dep., Odense University Hospital, Odense, Denmark

AIM OF INVESTIGATION: Unpredictability of outcome is a major problem in pharmacological treatment of patients suspected of neuropathic pain (NP). We examined if patients with firm nervous system lesion respond better to neuropathic pharmacological therapy than patients with less evidence of nerve lesion.

METHOD: We included 188 patients with suspected NP. Clinical pain diagnosis ranged from e.g. neuropathy, peripheral nerve lesion, central pain and PHN to myofascial pain.

Based on pain descriptors, a standardized bed side sensory examination and quantitative sensory testing on all patients, and relevant electrophysiological and imaging examinations patients were divided into 4 groups with increasing evidence of nerve lesion. Depression was tested by a questionnaire: Major Depression Inventory (MDI). Patients were treated in a standardized manner with imipramine guided by serum concentrations. In case of contraindications or treatment failure, gabapentine was given. Primary end point was pain relief (0-100)

RESULTS: Pain relief of 0-25%, 26-50%, 51-75%, and 76-100% were reported by 44% resp. 17%, 22% and 17% of the patients. There was no difference in degree of pain relief between the 4 groups (p<0.793). The groups were similar with respect to the ratio of patients treated with imipramine respectively gabapentine, imipramine dose and serum concentration, gabapentine dose, MDI score and gender.

CONCLUSION: Evidence of nerve lesion is not a predictor for outcome of pharmacological therapy with imipramine and gabapentine in patients suspected of NP.

ACKNOWLEDGEMENTS: Supported by grants from Pfizer and Danish Medical Research Council (22-00-0547).

EFFECTS OF IV LIDOCAINE ON SPONTANEOUS AND EVOKED PAINS DUE TO PERIPHERAL NERVE INJURY AND PREDICTORS OF THE RESPONSE
J. Rouaud^,-Joindreau, M. Chauvin, D. Bouhassira, Centre d'Evaluation et de Traitement de la Douleur, Hpital Ambroise Par, Boulogne, France

AIM OF INVESTIGATION: This study used a double blind cross-over placebo-controlled design to evaluate the effects of iv lidocaine on spontaneous and evoked pains due to peripheral nerve injury and to provide informations about the mechanisms involved.

METHODS: 22 patients (14 men, 8 women) with postherpetic neuralgia (n=8) or nerve trauma (n=14) were included and gave informed consent. Lidocaine or saline were administered (5 mg/kg iv over 30 minutes) at 2 weeks interval. Spontaneous pain and brush-evoked allodynia were rated on a VAS scale. Von Frey hairs and a thermotest device were used to determine detection, pain thresholds and pains evoked by suprathreshold stimuli.

RESULTS: Lidocaine was superior to placebo in reducing ongoing pain, an effect that persisted for 6 hours, but recovered at day 1. Lidocaine reduced mechanical dynamic allodynia and static punctate hyperalgesia, but failed to modify thermal allodynia/hyperalgesia. There was an inverse correlation between the magnitude of thermal deficits, the decrease in mechanical pain thresholds on the painful side, and the effects of lidocaine on spontaneous pain.

CONCLUSIONS: IV lidocaine reduces spontaneous pain due to peripheral nerve injury, an effect that outlasts the half life of the drug. Patients with mechanical hyperalgesia and/or minor thermal deficit are better responders to lidocaine. Lidocaine induces modality specific effects on mechanical allodynia/hyperalgesia, as previously reported by our group in central pain patients. A study using nerve blocks with lidocaine is in progress to differentiate between the peripheral and central mechanisms of action of the drug

10th World Congress on Pain, List of topics

10th World Congress on Pain. International Association for the Study of Pain, San Diego, California, USA August 17-22, 2002