L Arendt-Nielsen

Aalborg University, Ålborg, North Denmark, Denmark

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Publications (395)1136.48 Total impact

  • Michele Curatolo, Lars Arendt-Nielsen
    Physical Medicine and Rehabilitation Clinics of North America 02/2015; · 1.09 Impact Factor
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    ABSTRACT: Biochemical and pain biomarkers can be applied to patients with painful osteoarthritis profiles and may provide more details compared with conventional clinical tools. The aim of this study was to identify an optimal combination of biochemical and pain biomarkers for classification of patients with different degrees of knee pain and joint damage. Such profiling may provide new diagnostic and therapeutic options. A total of 216 patients with different degrees of knee pain (maximal pain during the last 24 hours rated on a visual analog scale [VAS]) (VAS 0-100) and 64 controls (VAS 0-9) were recruited. Patients were separated into 3 groups: VAS 10 to 39 (N = 81), VAS 40 to 69 (N = 70), and VAS 70 to 100 (N = 65). Pressure pain thresholds, temporal summation to pressure stimuli, and conditioning pain modulation were measured from the peripatellar and extrasegmental sites. Biochemical markers indicative for autoinflammation and immunity (VICM, CRP, and CRPM), synovial inflammation (CIIIM), cartilage loss (CIIM), and bone degradation (CIM) were analyzed. WOMAC, Lequesne, and pain catastrophizing scores were collected. Principal component analysis was applied to select the optimal variable subset, and cluster analysis was applied to this subset to create distinctly different knee pain profiles. Four distinct knee pain profiles were identified: profile A (N = 27), profile B (N = 59), profile C (N = 85), and profile D (N = 41). Each knee pain profile had a unique combination of biochemical markers, pain biomarkers, physical impairments, and psychological factors that may provide the basis for mechanism-based diagnosis, individualized treatment, and selection of patients for clinical trials evaluating analgesic compounds. These results introduce a new profiling for knee OA and should be regarded as preliminary.
    Pain 01/2015; 156(1):96-107. · 5.64 Impact Factor
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    ABSTRACT: Background In a cohort of well-characterized patients with different degrees of knee osteoarthritis (OA) and pain, the aims were to utilize mechanism-based quantitative sensory testing (QST) to (1) characterize subgroups of patients; (2) analyse the associations between clinical characteristics and QST; and (3) develop and apply a QST-based knee OA composite pain sensitivity index for patient classification.Methods Two hundred seventeen OA pain patients and 64 controls were included. Kellgren and Lawrence (KL) grading scores were obtained, and pressure pain thresholds (PPTs), temporal summation of pain to repeated painful pressure stimulation and conditioning pain modulation (CPM) were assessed. Associations between pain score/area/duration, radiological findings and QST-related parameters were analysed. A pain sensitivity index was developed and applied based on PPT, temporal summation and CPM. z-Score, as statistical tool, was calculated for statistically comparing the pain index of a single patient with a healthy control group.ResultsHigh knee pain associated with low KL grade showed particular signs of pain sensitization. Patients showed significant associations between clinical knee pain intensity/duration and lowering of knee PPTs (p < 0.01), facilitation of temporal summation (p < 0.01), reduction of CPM function (p < 0.01) and high pain sensitivity index (p < 0.01). The index classified 27–38% of the OA patients and 3% of the controls as highly sensitive with no association to KL. The index increased for high knee pain intensities and long pain duration.Conclusions Radiological scores, contrary to clinical pain intensity/duration, were poorly associated with QST parameters. The pain sensitivity index could classify OA patients with different degrees of OA and pain.
    European journal of pain (London, England) 12/2014; · 3.37 Impact Factor
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    ABSTRACT: Objectives: This study focused on the biomechanical implications of knee osteoarthritis (OA) and the association with pain. The plantar loading force distribution of the foot was determined and correlated to degenerative knee changes, function, pain intensity, and pain sensitization. Method: Knee OA patients (n = 34) with moderate and mild knee pain were characterized and compared to matched controls (n = 16). The Plantar Foot Posture Index (FPI) and mean maximum plantar forces were determined by pressure-sensitive insoles. Pain intensity and function were assessed by the Western Ontario and McMaster Universities Arthritis Index (WOMAC) and the Brief Pain Inventory (BPI). Local knee pain sensitization was assessed by pressure pain thresholds (PPTs) from eight knee locations. Spreading sensitization was assessed by PPTs from two extra-segmental test sites. Temporal summation to repeated pressure stimulation (knee and extra-segmental stimulation) and conditioning pain modulation (CPM) were assessed, representing central pain mechanisms. Results: The maximum force (MF) applied by the medial forefoot correlated to knee PPTs (r = 0.524, p < 0.001), CPM potency (r = 0.532, p < 0.001), and BPI (r = -0.325, p < 0.05) and WOMAC scores (pain r = -0.425, p < 0.01; stiffness r = -0.386, p < 0.01; function r = -0.378, p < 0.05). The MF applied by the medial hindfoot correlated negatively to scores on the FPI (r = -0.394, p < 0.01) and the Kellgren-Lawrence (K-L) grading scale (r = -0.330, p < 0.05). The MF applied by the medial forefoot correlated to extra-segmental PPTs (r = 0.554, p < 0.001) and the potency of CPM (r = 0.561, p < 0.0001). The MF applied by the lateral hindfoot correlated negatively to the PPT assessed extra-segmentally (r = -0.367, p < 0.05) and positively to CPM potency (r = 0.322, p < 0.05). Conclusions: This study shows that mean maximum plantar foot force distribution in patients with painful knee OA is associated with specific pain mechanisms, function, radiological findings, and pain intensity.
    Scandinavian journal of rheumatology. 10/2014;
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    ABSTRACT: Osteoarthritis (OA) is the most common degenerative joint disease, of which the pathogenesis is inadequately understood. Hypertrophy-like changes have been observed as part of the progression of OA. The aim of the study was to develop and characterize a novel biomarker of chondrocytes hypertrophy and investigate how this marker was associated with cartilage degradation and inflammation in patients with various degrees of OA.
    BMC Musculoskeletal Disorders 09/2014; 15(1):309. · 1.90 Impact Factor
  • Jesper Elberling, Lars Arendt-Nielsen
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    ABSTRACT: Chronic itch is an annoying and disabling symptom that severely affects patients' quality of life in several dermatological as well as non-dermatological disorders. Chronic itch may be maintained and even aggravated by sensitization of peripheral and central neuronal structures. The possibilities to effectively relieve chronic itch are often limited and the need of more specific, effective and quick-acting treatment options is huge. This review summarizes the fundamental aspects of itch, the neuronal transmission and modulation of itch, and discusses new treatment opportunities.
    Ugeskrift for laeger 08/2014; 176(32).
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    ABSTRACT: Generalized hyperalgesia, a widespread increased sensitivity to painful stimuli, has been demonstrated in a range of chronic pain conditions including low-back pain. The evidence suggests, that generalized hyperalgesia may be an important factor in the development of chronicity, but it is not commonly assessed in clinical practice. Whereas a range of tools and procedures for the quantitative sensory testing of pain sensitivity is available for laboratory pain research, most experimental pain stimuli are not well suited for clinical practice. In the current study, a simple and inexpensive mechanical spring-clamp was tested as a potential experimental pain stimulus.
    Chiropractic & Manual Therapies. 08/2014; 22(1):30.
  • K. WANG, T. HE, Q. XIE, Y. KANG, G. YANG, Y. HE, M. CAO, Y. LUO, L. ARENDT-NIELSEN
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    ABSTRACT: The assessment of the dentinal hypersensitivity usually depends on subjective responses to clinically applied stimuli and lack of standardized and quantified testing methods. Objective: This study is to apply standardized mechanical, thermal, and electrical stimuli on the teeth with dentinal hypersensitivity providing an objective evaluation method of diagnosis and treatment evaluation of dentinal hypersensitivity. Method: Twenty-three subjects (aged 20-40) with unilateral hypersensitivity in incisor/cuspid/pre-molar (S-Tooth) participated in a three-session experiment. The contralateral tooth was selected as control (C-Tooth). Mechanical Stimuli Sensitivity (MSS), Cold Detection Threshold (CDT), Warm Detection Threshold (WDT), Electrical Detection Threshold (EDT), and Electrical Pain Threshold (EPT) were tested on both S-Tooth and C-Tooth at the first day (Day-1) before and immediately after manual toothbrushing using the commercial Crest Pro-health Clinical Sensitivity Dentifrice. The subjects were instructed to perform standard toothbrushing twice daily for seven days. The testing was repeated on the second day (Day-2) and the seventh day (Day-7) after toothbrushing. Data were analyzed with ANOVAs. The study was approved by the local ethical committee and performed at Peking University School of Stomatology. Result: The S-Tooth was significantly more sensitive in MSS (P=0.033) compared with the C-Tooth. That e S-Tooth was significantly less sensitive in MSS (P=0.004), CDT (P=0.041), WDT (P=0.010), EPT (P=0.047) on Day-7 compared with Day-1, and significantly less sensitive in EPT on both Day-2 (P=0.041) and Day-7 (P=0.001) compared with Day-1. The sensitivity of the C-Tooth was also significantly changed in MSS (P=0.020) and EPT (P=0.004) on Day-7. Conclusion: The established quantitative sensory testing methods are suitable for use in clinical trials and provide important information on diagnosis and treatment evaluation of dentinal hypersensitivity. The test dentifrice provided a rapid desensitizing effect. Further study with placebo control is required.
    IADR General Session and Exhibition 2014; 06/2014
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    ABSTRACT: Activation of TRPM8 and TRPA1 receptors generates cold and cold pain sensations, respectively, and is presumably important in clinical pain manifestations, such as cold hyperalgesia. This study investigated the interaction between TRPM8 and TRPA1 receptors through stimulation of glabrous human skin (volar forearm) by topical administration of 40% L-menthol and 10% trans-cinnamaldehyde (CA), individually and in combination. Sensory manifestations were assessed in 10 healthy volunteers via a platform of 11 quantitative sensory (thermal and mechanical stimuli) and vasomotor tests (skin temperature, perfusion and axon-reflex-flare) in a double-blinded randomized crossover design. Cold pain threshold was increased (p < 0.01, cold allodynia) by L-menthol alone and L-menthol + CA in combination but unaffected by CA. Mechanical pain threshold was significantly decreased (mechanical hyperalgesia) by all three substances (p < 0.01), with a significant intergroup difference found between CA alone and the less decreased L-menthol + CA (p < 0.05). Application of CA alone and L-menthol + CA in combination showed an increase in skin temperature and perfusion significantly larger than that induced by L-menthol alone (p < 0.05). An axon-reflex-flare was present after CA administration, but was significantly reduced upon addition of L-menthol (p < 0.01). This study elucidates the potential of L-menthol as a counter-irritant to secondary neurogenic inflammation and provides evidence of an intricate interplay between cold receptors TRPA1 and TRPM8, warranting further investigation of the neural coding of cold pain perception.
    European journal of pain (London, England) 03/2014; · 3.37 Impact Factor
  • Lars Arendt-Nielsen, Thomas Arendt Nielsen, Parisa Gazerani
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    ABSTRACT: Translation of the analgesic efficacy of investigational neurotherapeutics from pre-clinical pain models into clinical trial phases is associated with a high risk of failure. Application of human pain biomarkers in early stages of clinical trials can potentially enhance the rate of successful translation, which would eventually reduce both length and costs of drug development after the pre-clinical stage. Human pain biomarkers are based on the standardized activation of pain pathways followed by the assessment of ongoing and paroxysmal pain, plus evoked responses which can be applied to healthy individuals and patients prior to and after pharmacological interventions. This review discusses the rationality and feasibility of advanced human pain biomarkers in early phases of drug development for pain management which is still an unmet medical need.
    Expert Review of Neurotherapeutics 02/2014; · 2.96 Impact Factor
  • Ann G Hayes, Lars Arendt-Nielsen, Simon Tate
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    ABSTRACT: Recent advances in understanding the pathophysiology of pain have led to a wealth of molecular targets for novel analgesic drugs and many clinical drug trials. There have been successes, like the gabapentinoids for neuropathic pain and calcium channel blockers for otherwise intractable pain states; and drugs which show promise in clinical trials, like nerve growth factor inhibitors and p38 kinase inhibitors. Unfortunately there have also been a number of failures. We suggest factors which might predispose to success, for example some clinical precedence for the mechanism in pain or a genetic link for the mechanism, for example a mutation linked to a pain syndrome. We also stress the importance of demonstrating molecular target engagement with a novel compound and suggest pain biomarkers which can be used for mechanistic drug profiling.
    Current Opinion in Pharmacology 02/2014; 14:11–17. · 4.23 Impact Factor
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    ABSTRACT: Hip disorder patients typically present with extensive pain referral and hyperalgesia. To better understand underlying mechanisms an experimental hip pain model was established where pain referrals and hyperalgesia could be studied under standardized conditions. In sixteen healthy subjects, pain was induced by hypertonic saline injection into the gluteus medius tendon (GMT), addutor longus tendon (ALT), or gluteus medius muscle (GMM). Isotonic saline was injected contralaterally as control. Pain intensity was assessed on a visual analogue scale (VAS) and subjects mapped the pain distribution. Before, during and after injections, passive hip joint pain provocation tests were completed together with quantitative sensory testing: Pressure pain thresholds (PPTs), cuff algometry pain thresholds (cuff-PPTs), cutaneous pin-prick sensitivity, and thermal pain thresholds. Hypertonic saline injected into the GMT caused higher VAS scores than hypertonic injections into the ALT and GMM (P<0.05). Referred pain areas spread to larger parts of the leg after GMT and GMM injections compared with more regionalized pain pattern after ALT injections (P<0.05). PPTs at the injection site were decreased after hypertonic saline injections into GMT and GMM compared with baseline, ALT injections, and isotonic saline. Cuff-PPTs from the thigh were decreased after hypertonic saline injections into the ALT compared with baseline, GMT injections, and isotonic saline (P<0.05). More subjects had positive joint pain provocation tests after hypertonic compared with isotonic saline injections (P<0.05) indicating that this provocation test also assess hyperalgesia in extra-articular soft tissues. The experimental models may open for better understanding of pain mechanisms associated with painful hip disorders.
    Pain 01/2014; · 5.64 Impact Factor
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    Lars Arendt-Nielsen, Brian Edwin Cairns
    The Lancet Neurology 01/2014; 13(1):22-23. · 21.82 Impact Factor
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    ABSTRACT: In the trigeminal ganglion (TG), satellite glial cells (SGCs) form a functional unit with neurons. It has been proposed that SGCs participate in regulating extracellular glutamate levels and that dysfunction of this SGC capacity can impact nociceptive transmission in craniofacial pain conditions. This study investigated whether SGCs release glutamate and whether elevation of TG glutamate concentration alters response properties of trigeminal afferent fibers. Immunohistochemistry was used to assess glutamate content and the expression of excitatory amino acid transporter (EAAT)1 and EAAT2 in TG sections. SGCs contained glutamate and expressed EAAT1 and EAAT2. Potassium chloride (10 mM) was used to evoke glutamate release from cultured rat SGCs treated with the EAAT1/2 inhibitor (3S)-3-[[3-[[4-(trifluoromethyl)ben zoyl]amino]phenyl]methoxy]-l-aspartic acid (TFB-TBOA) or control. Treatment with TFB-TBOA (1 and 10 μM) significantly reduced the glutamate concentration from 10.6 ± 1.1 to 5.8 ± 1.4 μM and 3.0 ± 0.8 μM, respectively (p < 0.05). Electrophysiology experiments were conducted in anaesthetized rats to determine the effect of intraganglionic injections of glutamate on the response properties of ganglion neurons that innervated either the temporalis or masseter muscle. Intraganglionic injection of glutamate (500 mM, 3 μl) evoked afferent discharge and significantly reduced muscle afferent mechanical threshold. Glutamate-evoked discharge was attenuated by the N-methyl-d-aspartate receptor antagonist 2-amino-5-phosphonovalerate (APV) and increased by TFB-TBOA, whereas mechanical sensitization was only sensitive to APV. Antidromic invasion of muscle afferent fibers by electrical stimulation of the caudal brainstem (10 Hz) or local anesthesia of the brainstem with lidocaine did not alter glutamate-induced mechanical sensitization. These findings provide a novel mechanism whereby dysfunctional trigeminal SGCs could contribute to cranial muscle tenderness in craniofacial pain conditions such as migraine headache.
    Neuroscience 01/2014; 256:23–35. · 3.33 Impact Factor
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    ABSTRACT: Around 20% of patients with osteoarthritis (OA) have chronic post-operative pain after total knee arthroplasty (TKA) and often undergo revision surgery with unfavourable pain outcome. This study compared sensitization in pain patients with knee OA and after revision TKA (re-TKA). Median pressure pain thresholds (PPTs) assessed from the most affected knee (localized sensitization) were used to subgroup 53 patients with OA pain and 20 patients with pain after re-TKA: group 1: OA and high-knee PPT; group 2: OA and low-knee PPT; group 3: re-TKA and high-knee PPT; group 4: re-TKA and low-knee PPT. Clinical pain intensity was assessed using a visual analogue scale (VAS). Bilateral PPTs were measured from the lower leg and forearm (spreading sensitization). Furthermore, the pain intensities evoked by 10 repeated pressure pain stimuli (temporal summation) at the knee and lower leg were assessed on an electronic VAS. The mean clinical pain intensity was not significantly different between groups. The PPTs from both lower leg and forearm were significantly lower in group 4 compared to groups 1, 2, and 3 and in groups 2 and 3 compared to group 1 (p < 0.05). Temporal summations from the knee and lower leg were significantly facilitated in groups 3 and 4 compared to groups 1 and 2 (p < 0.05). Despite similar pain intensities, facilitated temporal summation is worse in re-TKA than in OA and patients with high local knee hyperalgesia show more prominent spreading sensitization. The study suggests that sensitization should be considered in knee OA especially before re-TKA.
    European journal of pain (London, England) 12/2013; 18(7). · 3.37 Impact Factor
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    ABSTRACT: Osteoarthritis (OA) is a degenerative disease with a subset of patients experiencing joint inflammation, but C-reactive protein (CRP) has shown limited use in OA as a diagnostic marker. The aim was to identify subpopulations of patients with high or low levels of acute (hsCRP) and/or matrix metalloproteinase (MMP) derived inflammation (CRPM) and investigate the subpopulations' association with biomarkers of collagen degradation and Kellgren-Lawrence score (KL). hsCRP, CRPM and MMP-degraded type I, II and III collagen (C1M, C2M and C3M) were quantified by ELISA in serum of 342 patients with symptomatic knee OA of which 60 underwent total knee replacement (TKR). KL was obtained. Patients were divided into quartiles by hsCRP and CRPM levels, where Q1 and Q4 were low or high in both. The biomarker levels of healthy adults provided in the ELISA kits were used as reference level. hsCRP was elevated in TKR (5.9(3.6-8.2 95% CI)μg/mL) compared to reference level (3μg/mL), while CRPM was highly elevated with OA independent of KL (10-14ng/mL) compared to reference level (5ng/mL). Q4 had higher KL than Q1 (P<0.001), Q2 (P=0.017) and Q3 (P<0.001). C1M, C2M and C3M were lowest in Q1. C1M was elevated in Q3 compared to Q2 (P<0.001), whereas C3M was lower (P=0.019). A bigger proportion of patients were elevated in CRPM compared to hsCRP, indicating MMP-derived inflammation as a component of OA. Moreover, the levels of MMP-degraded collagens differed between the subgroups segregated by inflammation, indicating distinctively different subpopulation selected by inflammation.
    Osteoarthritis and Cartilage 11/2013; · 4.26 Impact Factor
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    Dataset: Fulltext p9
  • Lars Arendt-Nielsen, Michele Curatolo
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    ABSTRACT: Background Mechanistic, translational, human experimental pain assessment technologies (pain biomarkers) can be used for: (1) profiling the responsiveness of various pain mechanisms and pathways in healthy volunteers and pain patients, and (2) profiling the effect of new or existing analgesic drugs or pain management procedures. Translational models, which may link mechanisms in animals to humans, are important to understand pain mechanisms involved in pain patients and as tools for drug development. This is urgently needed as many drugs which are effective in animal models fail to be efficient in patients as neither the mechanisms involved in patients nor the drugs’ mechanistic actions are known. Aim The aim of the present topical review is to provide the basis for how to use mechanistic human experimental pain assessment tools (pain biomarkers) in the development of new analgesics and to characterise and diagnose pain patients. The future aim will be to develop such approaches into individualised pain management regimes. Method Experimental pain biomarkers can tease out mechanistically which pain pathways and mechanisms are modulated in a given patient, and how a given compound modulates them. In addition, pain biomarkers may be used to assess pain from different structures (skin, muscle and viscera) and provoke semi-pathophysiological conditions (e.g. hyperalgesia, allodynia and after-sensation) in healthy volunteers using surrogate pain models. Results With this multi-modal, multi-tissue, multi-mechanism pain assessment regime approach, new opportunities have emerged for profiling pain patients and optimising drug development. In this context these technologies may help to validate targets (proof-of-concept), provide dose–response relationships, predicting which patient population/characteristics will respond to a given treatment (individualised pain management), and hence provide better understanding of the underlying cause for responders versus non-responders to a given treatment. Conclusion In recent years, pain biomarkers have been substantially developed to have now a role to play in early drug development, providing valuable mechanistic understanding of the drug action and used to characterise/profile pain patients. In drug development phase I safety volunteer studies, pain biomarkers can provide indication of efficacy and later if feasible be included in clinical phase II, III, and IV studies to substantiate mode-of-action. Implications Refining and optimising the drug development process ensures a higher success rate, i.e. not discarding drugs that may be efficient and not push non-efficient drugs too far in the costly development process. Mechanism-based pain bio-markers can help to qualify the development programmes and at the same time help qualifying them by pain profiling (phenotyping) and recognising the right patients for specific trials. The success rate from preclinical data to clinical outcome may be further facilitated by using specific translational pain bio-markers. As human pain biomarkers are getting more and more advanced it could be expected that FDA and EMA in the future will pay more attention to such mechanism-related measures in the approval phase as proof-of-action.
    Scandinavian Journal of Pain 10/2013; 4(4):226–230.
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    ABSTRACT: Ethnic differences in pain experiences have been widely assessed in various pathological and experimental conditions. However, limited sensory modalities have been described in previous research, and the affective-motivational factors have so far been estimated to be the main mediator for the ethnic differences. This study aimed to detect the ethnic differences of oro-facial somatosensory profiles related to the sensory-discriminative dimension in healthy volunteers. The standardised quantitative sensory testing battery developed by the German Research Network on Neuropathic Pain was performed bilaterally in the infraorbital and mental regions on age- and gender-matched healthy Chinese and Danes, 29 participants each group. The influences of ethnicity, gender and test site on the somatosensory profile were evaluated by three-way anova. The ethnic disparities were also presented by Z-scores. Compared to Danes, Chinese were more sensitive to thermal detection, thermal pain, mechanical deep pain and mechanical pain rating parameters (P < 0·002) related to small fibre functions. However, the inverse results were observed for mechanical tactile modality related to large fibre function (P < 0·001) and wind-up ratio (P = 0·006). Women presented higher sensitivity compared to men. The mean Z-scores of all the parameters from Chinese group were in the normal zone created by Danish Caucasians' means and SDs. The ethnic disparities in somatosensory profile illustrated the necessity of establishing the reference data for different ethnic groups and possibly individual pain management strategies for the different ethnic groups.
    Journal of Oral Rehabilitation 08/2013; · 1.93 Impact Factor
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    ABSTRACT: Cold allodynia and cold hyperalgesia are both elusive features of neuropathic pain, particularly in patients with various polyneuropathies. Numerous studies have suggested that topical application of L-menthol causes temporary cold hypersensitivity and thus acts as a proxy for associated symptoms. This review summarizes studies on L-menthol-induced nociception, cold allodynia and cold hyperalgesia in vitro, in animals and in humans. A comprehensive literature search was performed using the PubMed and Google Scholar databases until February 2013. Obtained manuscripts were reviewed for relevancy and reference lists of the retrieved articles were cross-checked for additional important studies. Solely the literature regarding topical application of L-menthol in humans was attained systematically. Of the total identified studies (96), 10 met the inclusion criteria being controlled studies applying L-menthol at a concentration of ≥30%. The extracted data are meticulously compared and presented with emphasis on clarity and transparency. In seven animal studies, cold allodynia or hyperalgesia was successfully established utilizing various methods. Eight studies in healthy volunteers unanimously reported a significant increase in cold pain threshold, representing cold allodynia and increased supra-threshold cold pain sensitivity, thus demonstrating cold hyperalgesia. Topical high-concentration L-menthol consistently induces cold hypersensitivity in animals and humans, thus constituting a predictable surrogate model of cold allodynia and hyperalgesia. Understanding translational features of this model and its underlying mechanisms could be valuable in preclinical and human phases of drug development and in improving current treatment of patients with polyneuropathy.
    European journal of pain (London, England) 08/2013; · 3.37 Impact Factor

Publication Stats

11k Citations
1,136.48 Total Impact Points

Institutions

  • 1987–2014
    • Aalborg University
      • • Department of Health Science and Technology
      • • Faculty of Medicine
      • • Department of Electronic Systems
      Ålborg, North Denmark, Denmark
  • 2013
    • University of Mazandaran
      Meshed-i-Sar, Māzandarān, Iran
  • 2010
    • Regionspsykiatrien Viborg-Skive
      Viborg, Central Jutland, Denmark
  • 1989–2010
    • Aarhus University
      • • Department of Dentistry
      • • Department of Neurology
      • • Royal Dental College
      • • Department of Anaesthesiology
      Aars, Region North Jutland, Denmark
  • 2009
    • Academisch Centrum Tandheelkunde Amsterdam
      Amsterdamo, North Holland, Netherlands
    • Hospital Clínico San Carlos
      Madrid, Madrid, Spain
    • Fourth Military Medical University
      • School of Stomatology
      Xi’an, Liaoning, China
  • 2007–2009
    • King Juan Carlos University
      • Departamento de Fisioterapia, Terapia Ocupacional, Rehabilitación y Medicina Física
      Móstoles, Madrid, Spain
  • 1997–2009
    • Aalborg University Hospital
      • • Department of Gastroenterology and Hepatology
      • • Department of Internal Medicine
      Ålborg, North Denmark, Denmark
    • Odense University Hospital
      • Department of Neurology - N
      Odense, South Denmark, Denmark
  • 2008
    • The Royal Marsden NHS Foundation Trust
      Londinium, England, United Kingdom
  • 2006–2007
    • University of British Columbia - Vancouver
      • Faculty of Pharmaceutical Sciences
      Vancouver, British Columbia, Canada
    • Sapienza University of Rome
      • Department of Anatomical, Histological, Forensic Medicine and Orthopedic Science
      Roma, Latium, Italy
  • 2005–2006
    • University of Haifa
      • Faculty of Social Welfare and Health Sciences
      H̱efa, Haifa District, Israel
    • Otto-Friedrich-Universität Bamberg
      Bamberg, Bavaria, Germany
  • 2001–2006
    • University of Southern Denmark
      • • Speciality in Clinical Pharmacology
      • • Institute of Public Health
      Copenhagen, Capital Region, Denmark
    • Politecnico di Torino
      • DET - Department of Electronics and Telecommunications
      Torino, Piedmont, Italy
    • University of Toronto
      • Faculty of Dentistry
      Toronto, Ontario, Canada
    • Universität Bern
      Berna, Bern, Switzerland
  • 1998–2003
    • Inselspital, Universitätsspital Bern
      • Department of Anesthesiology and Pain Therapy
      Bern, BE, Switzerland
    • Johannes Gutenberg-Universität Mainz
      • Institut für Physiologie und Pathophysiologie
      Mainz, Rhineland-Palatinate, Germany
    • University Hospital Linköping
      • Department of Anaesthesiology
      Linköping, Östergötland, Sweden
  • 2002
    • Curtin University Australia
      • School of Physiotherapy
      Bentley, Western Australia, Australia
  • 1992–2002
    • Aarhus University Hospital
      • • Department of Neurology
      • • Department of Anaesthesiology
      Århus, Central Jutland, Denmark
    • Royal Australasian College of Dental Surgeons
      Денмарк, Western Australia, Australia
  • 2000
    • Catholic University of the Sacred Heart
      • Institute of Neurology
      Roma, Latium, Italy
  • 1999
    • Friedrich-Alexander Universität Erlangen-Nürnberg
      Erlangen, Bavaria, Germany
  • 1988
    • University of Groningen
      • Department of Neurology
      Groningen, Province of Groningen, Netherlands