Martin Schmelz

Universität Heidelberg, Heidelburg, Baden-Württemberg, Germany

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Publications (296)1175.85 Total impact

  • D Schwab · I Pahl · W Koppert · C Enk · R Sittl · S Mühldorfer · M Schmelz · EG Hahn
    Zeitschrift für Gastroenterologie 08/2015; 41(08). DOI:10.1055/s-0035-1555540 · 1.67 Impact Factor
  • A. Miclescu · M. Schmelz · T. Gordh
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    ABSTRACT: Both peripheral nerve injury and neuroma pain are the result of changes in sodium channel expression. Lidocaine selectively inhibits the spontaneous ectopic activity by binding to sodium channels. Subanesthetics concentrations of lidocaine are able to produce a differential block of the ectopic discharges, but not propagation of impulses, suppressing differentially the associated neuropathic pain symptoms. The aim of this study was to investigate the differences between the analgesic effects of lidocaine 0.5% and a control group of lidocaine 0.1% on several neuroma related pain modalities.
    Scandinavian Journal of Pain 07/2015; 8. DOI:10.1016/j.sjpain.2015.04.026
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    ABSTRACT: Seven patients diagnosed with erythromelalgia (EM) were investigated by microneurography to record from unmyelinated nerve fibers in the peroneal nerve. Two patients had characterized variants of sodium channel Nav1.7 (I848T, I228M) while no mutations of coding regions of Navs were found in 5 EM patients.Irrespective of NaV1.7 mutations, more than 50% of the silent nociceptors in the EM patients showed spontaneous activity. In the patient with mutation I848T all nociceptors, but not sympathetic efferents, displayed enhanced early subnormal conduction in the velocity recovery cycles and the expected late subnormality was reversed to supra-normal conduction. The larger hyperpolarizing shift of activation might explain the difference to the I228M mutation. Sympathetic fibers that lack Nav1.8 did not show supranormal conduction in the patient carrying the I848T mutation, confirming in human subjects that the presence of Nav1.8 crucially modulates conduction in cells expressing EM mutant channels. The characteristic pattern of changes in CV observed in the patient with the I848T gain-of function mutation in Nav1.7 could be explained by axonal depolarization and concomitant inactivation of Nav1.7. If this were true, activity-dependent hyperpolarization would reverse inactivation of Nav1.7 and account for the supranormal CV. This mechanism might explain normal pain thresholds under resting conditions.
    Pain 05/2015; DOI:10.1097/j.pain.0000000000000229 · 5.84 Impact Factor
  • R Jonas · A Klusch · R De Col · M Schmelz · M Petersen · R Carr
    Diabetologie und Stoffwechsel 04/2015; 10(S 01). DOI:10.1055/s-0035-1549567 · 0.31 Impact Factor
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    ABSTRACT: Background Mechano-sensitive and mechano-insensitive C-nociceptors in human skin differ in receptive field sizes and electrical excitation thresholds, but their distinct functional roles are yet unclear.Methods After blocking the lateral femoral cutaneous nerve (NCFL) in eight healthy male subjects (3-mL Naropin® 1%), we mapped the skin innervation territory being anaesthetic to mechanical pin prick but sensitive to painful transcutaneous electrical stimuli. Such ‘differentially anaesthetic zones’ indicated that the functional innervation with mechano-sensitive nociceptors was absent but the innervation with mechano-insensitive nociceptors remained intact. In these areas, we explored heat pain thresholds, low pH-induced pain, cowhage- and histamine-induced itch, and axon reflex flare.ResultsIn differentially anaesthetic skin, heat pain thresholds were above the cut-off of 50°C (non-anaesthetized skin 47 ± 0.4°C). Pain ratings to 30 μL pH 4 injections were reduced compared to non-anaesthetized skin (48 ± 9 vs. 79 ± 6 VAS; p < 0.01). The axon reflex flare area did not differ between these zones (7.8 ± 1.4 cm2 vs. 8.3 ± 0.5 cm2). Histamine iontophoresis still caused pruritus in differentially anaesthetized skin in five of eight subjects (VAS 26 ± 14), whereas itch upon cowhage spicules was absent (VAS 0 vs. 29 ± 11 in non-anaesthetized skin).Conclusions We conclude that activation of mechano-insensitive nociceptors is sufficient to provoke itch by histamine- and acid-induced pain. The mechano-sensitive nociceptors are crucial for cowhage-induced itch and for the assessment of heat pain thresholds.
    European journal of pain (London, England) 04/2015; DOI:10.1002/ejp.710 · 3.22 Impact Factor
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    ABSTRACT: Following each action potential, C-fiber nociceptors undergo cyclical changes in excitability, including a period of superexcitability, before recovering their basal excitability state. The increase in superexcitability during this recovery cycle depends upon their immediate firing history of the axon, but also determines the instantaneous firing frequency that encodes pain intensity. To explore the mechanistic underpinnings of the recovery cycle phenomenon a biophysical model of a C-fiber has been developed. The model represents the spatial extent of the axon including its passive properties as well as ion channels and the Na/K-ATPase ion pump. Ionic concentrations were represented inside and outside the membrane. The model was able to replicate the typical transitions in excitability from subnormal to supernormal observed empirically following a conducted action potential. In the model, supernormality depended on the degree of conduction slowing which in turn depends upon the frequency of stimulation, in accordance with experimental findings. In particular, we show that activity-dependent conduction slowing is produced by the accumulation of intraaxonal sodium. We further show that the supernormal phase results from a reduced potassium current Kdr as a result of accumulation of periaxonal potassium in concert with a reduced influx of sodium through Nav1.7 relative to Nav1.8 current. This theoretical prediction was supported by data from an in vitro preparation of small rat dorsal root ganglion somata showing a reduction in the magnitude of tetrodotoxin-sensitive relative to tetrodotoxin -resistant whole cell current. Furthermore, our studies provide support for the role of depolarization in supernormality, as previously suggested, but we suggest that the basic mechanism depends on changes in ionic concentrations inside and outside the axon. The understanding of the mechanisms underlying repetitive discharges in recovery cycles may provide insight into mechanisms of spontaneous activity, which recently has been shown to correlate to a perceived level of pain. Copyright © 2015 Biophysical Society. Published by Elsevier Inc. All rights reserved.
    Biophysical Journal 03/2015; 108(5):1057-71. DOI:10.1016/j.bpj.2014.12.034 · 3.97 Impact Factor
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    ABSTRACT: Excessive Ultraviolet (UV) exposure of the skin causes sunburn which is characterized by an acute cutaneous inflammatory response including skin tissue injury, dermal vasodilation, leukocyte infiltration and pain. Several studies have indicated that cytokines and chemokines are important mediators in UVB-induced skin damage (1,2). Besides their role in inducing and regulating the immune response, cytokines and chemokines have been implicated in modulating inflammatory pain perception (3). Recently, Dawes et al. reported the chemokine CXCL5, also known as epithelial-derived neutrophil-activating peptide 78 (ENA-78) in humans and liposaccharide-induced CXC chemokine (LIX) in rodents, as a novel mediator of UVB-induced mechanical hypersensitivity. Substantially increased CXCL5 mRNA expression was found in human and rodent skin punch biopsies after UV treatment (4). However, the regulation of CXCL5 in human non-immune skin cells after UV exposure has not been investigated in detail. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Experimental Dermatology 02/2015; 24(4). DOI:10.1111/exd.12652 · 4.12 Impact Factor
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    ABSTRACT: Background Inflammatory mediators activate and sensitize nociceptors. Tissue acidosis with low pH of 5.5 often accompanies inflammation and could enhance inflammatory pain and sensitization.Methods Action potentials from single mechano-responsive (CM) and mechano-insensitive (CMi) C-nociceptors of cutaneous fascicles of the peroneal nerve in healthy volunteers were recorded by microneurography. Low pH solutions with and without prostaglandin E2 (PGE2) were injected twice (with an interval of approximately 5 min) into two spots of the receptive fields of C-fibres. Heat thresholds of the C-fibres were obtained before and after each injection.ResultsInjections of the low pH solutions immediately induced phasic responses in CM nociceptors, whereas CMi fibres responded after a delay of several seconds with a sustained response. More CMi fibres than CM fibres showed ongoing discharge after low pH injection, but the duration and intensity of the responses to the first low pH injection did not differ between them. Upon repetition, duration and intensity of the pH responses increased more than twofold in CMi fibres only. Furthermore, combined application of pH and PGE2 sensitized the response in CMi fibres only. In contrast, heat activation thresholds were sensitized by the combination of low pH and PGE2 in both fibre classes.Conclusions Our results confirm nociceptor class independent heat sensitization by PGE2 which is probably mediated by transient receptor potential vanilloid 1 phosphorylation. However, prolonged and increased pain responses in humans upon low pH/PGE2 stimulation appear to be primarily dependent on CMi fibres, whereas CM nociceptors appear crucial for phasic responses.
    European journal of pain (London, England) 02/2015; 19(2). DOI:10.1002/ejp.532 · 3.22 Impact Factor
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    ABSTRACT: Introduction: Nerve growth factor (NGF) induces profound hyperalgesia. We explored patterns of NGF sensitization in muscle and fascia of distal and paraspinal sites.Methods: We injected 1 µg NGF into human (n=8) tibialis anterior and erector spinae muscles and their fasciae. The spatial extent of pressure sensitization, pressure pain threshold, and mechanical hyperalgesia (150 kPa, 10 sec) was assessed at days 0.25, 1, 3, 7, 14, and 21. Chemical sensitization was explored by acidic buffer injections (pH4, 100 µl) at days 7 and 14.Results: The mechanical hyperalgesia area was larger in tibial fascia than in muscle. Pressure pain thresholds were lower, tonic pressure pain ratings, and citrate buffer evoked pain higher in fascia than in muscle.Conclusions: Spatial mechanical sensitization differs between muscle and fascia. Thoracolumbar fasciae appear more sensitive than tibial fasciae and might be important structures contributing to low back pain, but the temporal sensitization profile is similar between paraspinal and distal sites. This article is protected by copyright. All rights reserved.
    Muscle & Nerve 12/2014; DOI:10.1002/mus.24537 · 2.31 Impact Factor
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    ABSTRACT: Background and aims “Gain-of-function” mutations in voltage-gated sodium channel NaV1.7 have been linked to erythromelalgia (EM), characterized by painful hot and red hands and feet. We investigated the proportion of patients with EM that carry a mutation in NaV1.7 or in other pain-related genes and studied possible clinical differences. Methods In this study, 48 patients with EM were screened for mutations in a total of 29 candidate genes, including all sodium channel subunits, transient receptor potential channels (TRPA1, TRPV1, TRPM8), neurotrophic factors (NGF, NGFR, BDNF, GDNF, NTRK1 and WNK1) and other known pain-related genes (CACNG2, KCNS1, COMT, P2RX3, TAC1, TACR1), using a combination of next generation sequencing and classical Sanger sequencing. Results In 7/48 patients protein-modifying mutations of NaV1.7 (P187L, I228M, I848T (n = 4) and N1245S) were identified. Patients with the I848T mutation could be identified clinically based on early onset and severity of the disease. In contrast, there were no clinical characteristics that differentiated the other patients with NaV1.7 mutation from those patients without. We also found more than twenty rare protein-modifying genetic variants in the genes coding for sodium channels (NaV1.8, NaV1.9, NaV1.6, NaV1.5, NaV2.1, SCN1B, SCN3B), transient receptor potential channel (TRPA1, TRPV1), and other pain-related targets (WNK1 and NGFR). Conclusions We conclude that functionally characterized mutations of NaV1.7 (I848T) are present only in a minority of patient with EM. Albeit the majority of patients (27/48) carried rare protein-modifying mutations the vast majority of those will most probably not be causally linked to their disease. Implications The key question remaining to be solved is the possible role of rare variants of NaV1.8, NaV1.9, or beta-subunits in provoking chronic pain conditions or even EM.
    Scandinavian Journal of Pain 10/2014; 5(4). DOI:10.1016/j.sjpain.2014.09.002
  • B. Weinkauf · O. Obreja · M. Schmelz · R. Rukwied
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    ABSTRACT: Background Nerve growth factor (NGF) causes early heat and delayed mechanical hyperalgesia. Axonal transport might contribute to lasting responses. Temporal hyperalgesia development was investigated by administering NGF in paraspinal skin. Transient receptor potential ankyrin 1 (TRPA1) is up-regulated by NGF and chemical responsiveness to cinnamon aldehyde (TRPA1 agonist) was quantified.Methods Eight healthy volunteers received 1 μg human recombinant NGF (i.d. 50 μL) to L4/L5 processi spinosi skin. Mechanical, thermal and electrical sensitization was assessed at 3–6 h and at days 1, 2, 3, 5, 7, 10, 14 and 21, and pain upon cinnamon aldehyde (20%, 60 μL) recorded at days 3 and 21.ResultsHeat hyperalgesia developed with an initial maximum at 3 h [heat pain threshold −3.9°; peak pain ratings +22 visual analogue scale (VAS)] that decreased by day 1, subsequently increased to a maximum around day 5 (−5 ± 0.2 °C, +41 ± 4 VAS), and thereafter declined to ∼20% at day 21. Mechanical and electrical hyperexcitability developed within 3 days and gradually increased to peak between days 14 and 21. Pain intensity upon cinnamon aldehyde stimulation was doubled at the NGF site at day 3 and was still increased by about 50% at day 21.ConclusionsNGF causes immediate heat hyperalgesia probably linked to an up-regulation and sensitization of transient receptor potential vanilloid 1 and possibly other proteins involved in heat transduction. The delayed mechanical hyperalgesia is apparently independent of the time required for axonal transport of NGF receptor complexes. Local mRNA translation at axonal terminals and protein accumulation is hypothesized being involved in sustained NGF-evoked hyperalgesia.
    European journal of pain (London, England) 10/2014; 19(6). DOI:10.1002/ejp.603 · 3.22 Impact Factor
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    ABSTRACT: Cutaneous pain sensations are mediated largely by C-nociceptors consisting of both mechano-sensitive (CM) and mechano-insensitive (CMi) fibres that can be distinguished from one another according to their characteristic axonal properties. In healthy skin and relative to CMi fibres, CM fibres show a higher initial conduction velocity, less activity-dependent conduction velocity slowing, and less prominent post-spike supernormality. However, after sensitization with nerve growth factor, the electrical signature of CMi fibres changes towards a profile similar to that of CM fibres. Here we take a combined experimental and modelling approach to examine the molecular basis of such alterations to the excitation thresholds. Changes in electrical activation thresholds and activity-dependent slowing were examined in vivo using single-fibre recordings of CM and CMi fibres in domestic pigs following NGF application. Using computational modelling, we investigated which axonal mechanisms contribute most to the electrophysiological differences between the fibre classes. Simulations of axonal conduction suggest that the differences between CMi and CM fibres are strongly influenced by the densities of the delayed rectifier potassium channel (Kdr), the voltage-gated sodium channels NaV1.7 and NaV1.8, and the Na+/K+-ATPase. Specifically, the CM fibre profile required less Kdr and NaV1.8 in combination with more NaV1.7 and Na+/K+-ATPase. The difference between CM and CMi fibres is thus likely to reflect a relative rather than an absolute difference in protein expression. In support of this, it was possible to replicate the experimental reduction of the ADS pattern of CMi nociceptors towards a CM-like pattern following intradermal injection of nerve growth factor by decreasing the contribution of Kdr (by 50%), increasing the Na+/K+-ATPase (by 10%), and reducing the branch length from 2 cm to 1 cm. The findings highlight key molecules that potentially contribute to the NGF-induced switch in nociceptors phenotype, in particular NaV1.7 which has already been identified clinically as a principal contributor to chronic pain states such as inherited erythromelalgia.
    PLoS ONE 08/2014; 9(8):e103556. DOI:10.1371/journal.pone.0103556 · 3.23 Impact Factor
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  • R Rukwied · B Weinkauf · M Main · O Obreja · M Schmelz
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    ABSTRACT: Both nerve growth factor (NGF) and ultraviolet-B (UV-B) irradiation sensitize nociceptive nerve endings and increase axonal excitability of nociceptors. Combining NGF and UV-B treatment is supra-additive for sensory sensitization and even caused spontaneous pain in about 70% of the subjects. UV-B irradiation was performed at day 21 after intradermal NGF injection in 13 volunteers. Pain thresholds, electrically induced axon reflex erythema and pain (1.5-fold pain threshold, 5-100 Hz) was analysed at days 22, 24, 28, 35, 49 and 70 and correlated to hyperalgesia and spontaneous pain. Electrical pain threshold after combined NGF/UVB was reduced below single treatment at 24 h but not at 72 h post-UV-B irradiation. At the NGF/UV-B site, electrical pain was enhanced at all frequencies compared with single NGF and UV-B sites at 24 and 72 h with pain ratings exceeding control values about twofold to threefold [65 ± 7 vs. 25 ± 8 visual analogue scale (VAS) (24 h) and 55 ± 9 vs. 22 ± 5 VAS (72 h)]. Hyperalgesia to electrical stimulation correlated with hyperalgesia to pinprick (Spearman r = 0.44; p < 0.001, Bonferroni corr.) and supra-threshold heat (Spearman r = 0.55; p < 0.001) stimulation at 24 h only. Electrical pain thresholds at the NGF/UV-B site weakly correlated to spontaneous pain levels (Spearman r = 0.3; p = 0.025, without Bonferroni correction). In contrast, electrically induced pain or axon reflex erythema did not correlate to spontaneous pain levels. The combination of NGF and UV-B increases axonal excitability that contributes to hyperalgesia and might also facilitate ongoing spontaneous pain.
    European journal of pain (London, England) 07/2014; 18(6). DOI:10.1002/j.1532-2149.2013.00423.x · 3.22 Impact Factor
  • B. Weinkauf · R. Rukwied · M. Schmelz
    Acta Physiologica 03/2014; 210:38-38. · 4.25 Impact Factor
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    ABSTRACT: Action potential initiation and conduction along peripheral axons is a dynamic process that displays pronounced activity dependence. In patients with neuropathic pain, differences in the modulation of axonal conduction velocity by activity suggest that this property may provide insight into some of the pathomechanisms. To date, direct recordings of axonal membrane potential have been hampered by the small diameter of the fibres. We have therefore adopted an alternative approach to examine the basis of activity-dependent changes in axonal conduction by constructing a comprehensive mathematical model of human cutaneous C-fibres. Our model reproduced axonal spike propagation at a velocity of 0.69 m/s commensurate with recordings from human C-nociceptors. Activity-dependent slowing (ADS) of axonal propagation velocity was adequately simulated by the model. Interestingly, the property most readily associated with ADS was an increase in the concentration of intraaxonal sodium. This affected the driving potential of sodium currents, thereby producing latency changes comparable to those observed for experimental ADS. The model also adequately reproduced post action potential excitability changes (i.e., recovery cycles) observed in-vivo. We performed a series of control experiments replicating blockade of particular ion channels as well as changing temperature and extracellular ion concentrations. In the absence of direct experimental approaches, the model allows specific hypotheses to be formulated regarding the mechanisms underlying activity-dependent changes in C-fibre conduction. As ADS might functionally act as a negative feedback to limit trains of nociceptor activity, we envisage that identifying its mechanisms may also direct efforts aimed at alleviating neuronal hyperexcitability in pain patients.
    Journal of Neurophysiology 12/2013; 111(9). DOI:10.1152/jn.00777.2012 · 3.04 Impact Factor
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    ABSTRACT: Even though itch is a common syndrome of many diseases there is only little knowledge about sex and gender differences in pruritus, especially in central itch perception and modulation. To our knowledge, this is the first fMRI study examining sex differences in perception and its modulation by distraction. Experimental itch was induced by application of histamine (0.1 mM) via microdialysis fibers twice at the left forearm and twice at the left lower leg in 33 healthy volunteers (17 females, 16 males). The brain activation patterns were assessed by fMRI during itch without and with distraction (Stroop task). Between the various conditions, subjects were asked to rate itch intensity, desire to scratch and pain intensity. In a second experiment in 10 of the 33 volunteers histamine was replaced by saline solution to serve as control for the 'Stroop' condition. Women generally presented higher itch intensities compared to men during itch over the course of the experiment. A more specific analysis revealed higher itch intensities and desire to scratch in women during experimental induced itch that can be reduced by distraction at the lower legs when itch is followed by 'Stroop'. In contrast, men depicted significant reduction of 'itch' by 'Stroop' at the forearms. Women depicted higher brain activation of structures responsible for integration of sensory, affective information and motor integration/planning during 'itch' and 'Stroop' condition when compared to men. No sex differences were seen in the saline control condition. Women and men exhibited localisation dependent differences in their itch perception with women presenting higher itch intensities and desire to scratch. Our findings parallel clinical observations of women reporting higher itch intensities depending on itch localisation and suffering more from itch as compared to men.
    PLoS ONE 11/2013; 8(11):e79123. DOI:10.1371/journal.pone.0079123 · 3.23 Impact Factor
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    ABSTRACT: Background and aims: The use of pigs in translational pain research is increasing. However, only few methods are available to behaviourally quantify porcine nociceptive thresholds. Our aim was to determine baseline mechanical and thermal nociceptive thresholds using behavioural assays in pig with the tail root as stimulation site. Methods: Eight female pigs were used (50±5 kg, 15 weeks of age) and habituated to procedures before testing. Two mechanical (von Frey filaments (vF), pressure application measurement device (PAM)) and one thermal assay (CO2 laser) were used. Behavioural responses to stimulation at a 2 x 2 cm test area on the dorsal tail base were measured during one test session while the pigs were kept in a test cage and accompanied by a pen mate for social support. Within the test session each assay involved three stimulations per pig. Results: All assays provided robust values for nociceptive thresholds, with a mean of 5±1 sec (CO2); 422±35 gf (PAM) and 73±11 gf (vF). The responses to the 24 single stimulations ranged from 1-17 sec, 212-890 gf and 26-300 gf for CO2, PAM and vF. The observed behavioural responses were tail flicks (88, 8 and 29 %), tail clamps (0, 0 and 63 %), rump flinches (4, 83 and 0 %) and body movements (8, 8 and 8 %) respectively. Conclusions: Using these experimental approaches and behavioural assays already described for rodents, it was possible to quantify mechanical and thermal nociceptive thresholds on the tail roots of standing pigs.
    8th Congress of the European Federation of IASP Chapters (EFIC), Florence, Italy.; 10/2013
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    ABSTRACT: Background and aims: We investigated effects of intradermal NGF injection on cutaneous mechanical and thermal sensitivity in pigs. Methods: Eight female pigs (50±5kg; 15 weeks of age) were habituated to the procedures before testing. Treatment pigs (n=4) received either 10μg NGF (in PBS; 0.1% BSA) or PBS vehicle (control) in 25 x 20μl intradermal injections into a 5x5cm area tail root. Two mechanical (von Frey filaments (vF), pressure application measurement device (PAM)) and one thermal assay (CO2 laser) were used. Behavioural responses (skin twitch, tail flick and clamp) to stimulation at a 2x2cm test area on the dorsal tail base were measured during test sessions at 1 day before and 3, 7, 14 and 21 days after NGF or vehicle administration, while the pigs were kept in a test cage and accompanied by a pen mate for social support. Within the test session each assay involved three stimulations per pig. Data were analysed by GLM repeated measures ANOVA. Results: NGF injection induced increased (p<0.05) punctate mechanical sensitivity 3-7 days post injection, compared with controls. At 14 and 21 days no significant effects on noxious sensitivity were detected. Conclusions: In this pilot study we showed signs of NGF-induced mechanical hyperalgesia on day 3 and 7, but the measurements of cutaneous sensitivity appeared to differ depending on the mode of stimulation used. Further research is needed to clarify whether these findings, apparently differing from the temporal profiles found in humans, are species differences or can be explained by methodological differences.
    8th Congress of the European Federation of IASP Chapters (EFIC), Florence, Italy, October 9-12, 2013.; 10/2013
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    Scandinavian Journal of Pain 10/2013; 4(4):258. DOI:10.1016/j.sjpain.2013.07.012

Publication Stats

10k Citations
1,175.85 Total Impact Points


  • 2003–2015
    • Universität Heidelberg
      • • Faculty of Medicine Mannheim and Clinic Mannheim
      • • Department of Intensive Care Medicine
      Heidelburg, Baden-Württemberg, Germany
    • University of Münster
      Muenster, North Rhine-Westphalia, Germany
    • Wake Forest University
      • Department of Dermatology
      Winston-Salem, North Carolina, United States
  • 2006–2012
    • Universität Mannheim
      Mannheim, Baden-Württemberg, Germany
  • 2007
    • GlaxoSmithKline plc.
      • Clinical Pharmacology and Discovery Medicine
      London, ENG, Belgium
  • 1994–2005
    • Universitätsklinikum Erlangen
      • • Department of Anaesthesiology
      • • Department of Dermatology
      Erlangen, Bavaria, Germany
  • 2004
    • CUNY Graduate Center
      New York, New York, United States
    • Johannes Gutenberg-Universität Mainz
      • Neurobiology
      Mainz, Rhineland-Palatinate, Germany
  • 1994–2004
    • Friedrich-Alexander Universität Erlangen-Nürnberg
      • • Department of Neurology
      • • Department of Anaesthesiology
      • • Institute of Physics
      • • Department of Physiology and Pathophysiology
      Erlangen, Bavaria, Germany