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  • 1
    Keywords: Nerves, Peripheral Diseases ; Neuralgia ; Peripheral Nervous System Diseases physiopathology ; Pain etiology ; Neurology ; Fetal Medicine ; Metabolism ; Neuropathology ; Perinatal Medicine ; Aufsatzsammlung ; Peripheres Nervensystem ; Krankheit ; Neuralgie
    Description / Table of Contents: The book takes a novel approach to the subject of pain in peripheral nerve disease by bringing together basic scientists and clinicians with an expertise in the field of neuropathic pain. For the first time, the description of clinically relevant diseases, an up-to-date review of the pathophysiology of neuropathic pain and a comprehensive review of therapeutic options are combined in one book. Furthermore, the anatomy and pathology of peripheral nerve is outlined in the context of neuropathic pain. Peripheral nerve disorders causing pain, the mononeuropathies and polyneuropathies are described in detail including up-to-date summaries of pathogenesis and treatment. Two chapters elucidate the pathophysiology of neuropathic pain, one looking at causes in the periphery and one covering central mechanisms. Treatment options are outlined according to current knowledge from evidence-based medicine and a state-of-the-art treatment algorithm is given to facilitate practical management.Clinicians, neurologists and neurologists in training and basic scientists who are interested in pain will profit most from this book. Painful neuropathies are frequently encountered in clinical practice and are difficult to manage. The book helps to better understand and treat those conditions
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource (X, 202 Seiten)
    Edition: Karger eBooks Collection 1997-2009
    ISBN: 9783318007411
    Series Statement: Pain and headache 13
    DDC: 616.8/7
    RVK:
    Language: English
    Note: Includes bibliographical references and index , ""Contents""; ""Introduction: Linkages between Clinical Observation and Discovery""; ""Chapter 1 Anatomy and Pathology of Peripheral Nerve""; ""Neuropathology of Painful Neuropathies""; ""Chapter 2 Diseases of the Peripheral Nervous System Causing Pain""; ""Clinical Characteristics of Neuropathic Pain""; ""Mononeuropathies""; ""Polyneuropathies""; ""Chapter 3 Pain Mechanisms in Nerve Injury""; ""Peripheral Mechanisms""; ""Central Changes""; ""Why Do Some Patients Develop Neuropathic Pain and Others Not?""; ""Chapter 4 Symptomatic Treatment of Painful Neuropathies"" , ""Pharmacological and Nonpharmacological Treatment of Neuropathic Pain""""Contributors""; ""Subject Index""
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  • 2
    Keywords: Orofacial pain ; Temporomandibular joint Diseases ; Facial Pain ; Pain physiopathology ; Temporomandibular Joint Disorders ; Neurology ; Dental Medicine ; Oral Biology ; Pharmacology ; Physiology ; Aufsatzsammlung ; Orofazialer Schmerz ; Orofazialer Schmerz
    Description / Table of Contents: In recent years, progress in pain research has yielded substantial new insights, and this has profoundly altered our understanding of various orofacial pain conditions. Written by renowned international researchers and clinicians, this state-of-the-art textbook presents recent advances in the understanding of orofacial pain and offers evidence-based management approaches, thus bridging the gap between timely research findings and daily clinical practice. The reader is provided with helpful in-depth information of up-to-date advances in basic research as well as with the present knowledge of the pathophysiology, diagnosis and management of the five most common orofacial pain conditions. In addition, the psychosocial impact of orofacial pain in daily life and future developments are presented. Health care professionals, such as dentists, neurologists, physicians as well as students will find this volume helpful and valuable for an advanced understanding of the diverse orofacial pain conditions and for the improvement of patient care
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource (VI, 254 Seiten)
    Edition: Karger eBooks Collection 1997-2009
    ISBN: 9783318014556
    Series Statement: Pain and headache 15
    DDC: 617.5/22
    RVK:
    RVK:
    Language: English
    Note: Includes bibliographical references and indexes , Orofacial pain : a challenge and chance (not only) for dentistry , Characteristics of muscle nociception , Nociceptors of the joint with particular reference to silent nociceptors , Inflammatory mediators in temporomandibular joint pain , The role of reproductive hormones in orofacial pain , Pathophysiology of orofacial pain , Dental pain : pathophysiology and management , Myofascial temporomandibular disorder pain : pathophysiology and management , Painful arthrogenous temporomandibular disorders : pathophysiology, diagnosis, management and prognosis , Neuralgic and idiopathic facial pain : pathophysiology and management , Burning mouth syndrome : pathophysiology and management , Psychosocial impact of orofacial pain , A rationale for the classification of orofacial pain , Orofacial pain: past and future , The end of an era: orofacial pain enters the genomic age : implications and opportunities for research and the care of patients
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  • 3
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Although it has been postulated that adult neurogenesis, i.e. the generation of functional neurons from progenitor cells in the mammalian brain, is involved in both the pathogenesis of depressive disorders and the therapeutic effect of antidepressant drugs, its regulation is still poorly understood. Nitric oxide, a gaseous messenger molecule, represents a possible modulating agent as it is involved in learning and memory formation as well as synapto- and morphogenesis. Here we investigated whether adult neurogenesis is altered in mice lacking endothelial nitric oxide synthase (NOS-III). Compared to wild-type littermates, NOS-III-deficient mice showed a significant reduction in neuronal progenitor cell proliferation in the dentate gyrus, suggesting a role for NOS-III in the stimulation of neuroneogenesis. NeuN, β-III-tubulin and GFAP double-immunolabelling demonstrated that proliferating progenitor cells differentiate preferentially into neurons but not into astrocytes. However, when the survival rate of newly formed cells was examined no difference between wild-type and NOS-III knockout mice was found, suggesting that NOS-III selectively exerts its effects on the proliferation of progenitor cells. This might be mediated by a decrease in vascular endothelial growth factor (VEGF) transcripts in the hippocampus of knockout animals. At the behavioural level, while NOS-III knockout mice displayed better and faster learning in a learned helplessness paradigm, no depression-like behaviours were observed. In conclusion, our results indicated that NOS-III is involved in the proliferation of neuronal progenitor cells, although behavioural analysis does not provide evidence for a pro-depressive effect of reduced neuroneogenesis.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Chronic constriction of the sciatic nerve, leading to a hyperalgesic state, results in a partial lesion wherein some axons are injured and others remain intact. Here we sought to characterize reactive changes which occur in DRG cell bodies of injured and uninjured axons projecting to skin and muscle. Using immunohistochemistry combined with flurorogold and fluororuby retrograde labelling to define DRG cell bodies associated with injured and uninjured axons, we analysed the DRG immunoreactivity (IR) for tumour necrosis factor-alpha (TNF), interleukin-10 (IL-10), the sensory neuron-specific channel vanilloid receptor 1 (VR1), isolectin B4 (IB4) and calcitonin-gene-related peptide (CGRP) 4 days after a unilateral chronic constriction injury (CCI) of the rat sciatic nerve. TNF IR was predominantly localized in neuronal DRG cells. In DRG with an intact nerve, TNF IR was present in 45%, IL-10 IR in 46%, VR1 IR in 44%, IB4 IR in 51% and CGRP IR in 40% of all neuronal profiles. Four days after CCI, TNF IR was increased in medium-sized neurons, whereas IR for IL-10, VR1 and IB4, predominantly present in small neurons, was reduced. Importantly, not only injured but also adjacent spared neurons contributed markedly to increased TNF IR. Neurons projecting to both muscle and skin displayed upregulated TNF IR after CCI. TNF in medium-sized neurons colocalized with neurofilament and trkB, but not with IB4, trkA or RET, suggesting a selective phenotypic switch in presumably low-threshold myelinated primary afferents. Spared myelinated fibres with intact sensory functions but upregulated TNF expression may contribute to behavioural changes observed after nerve injury.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 90 (1995), S. 478-485 
    ISSN: 1432-0533
    Keywords: Key words Chronic constriction injury ; Crush ; Dorsal horn ; Hyperalgesia ; Neurotransmitters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We tested the hypothesis that neurochemical changes in the spinal cord dorsal horn associated with neuropathic pain states differ from those seen in association with non-painful neuropathies. Immunohistochemistry was performed on spinal cord sections from rats with a chronic constriction injury (CCI), which develop hyperalgesia, and from animals with a nerve crush injury, which do not develop hyperalgesia or other signs of a painful syndrome. Immunohistochemistry was quantified by computer-assisted densitometry. Calcitonin gene-related peptide (CGRP) immunoreactivity and substance P (SP) immunoreactivity were decreased from 1 to 4 weeks after injury in CCI and from 2 to 6 weeks in crush. Gamma-aminobutyric acid immunoreactivity was unchanged in both conditions at all time points. Met-enkephalin (Met-enk) immunoreactivity was increased in CCI and unchanged in crush. Although SP and CGRP are involved in pain transmission, we conclude that their decrease in immunoreactivity is not specific for the CCI model, but rather a more general event in nerve de- and regeneration. The increase in immunoreactivity for the opioid peptide Met-enk, however, was only seen in the late phase of CCI, and may be specific for conditions associated with neuropathic pain and its resolution.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0533
    Keywords: Key words Glucocorticosteroids ; Apoptosis ; Guillain-Barré syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lipocortin-1 exerts a potent immunosuppressive effect on pathogenic T cells. In multiple sclerosis and experimental autoimmune encephalomyelitis levels of lipocortins are raised, suggesting their involvement in the recovery from an immunological insult or in neural regeneration. To further understand the role of lipocortins in the peripheral nervous system we have characterized lipocortin-1 levels and cellular distribution of lipocortin-1 immunoreactivity in sciatic nerves of rats with experimental autoimmune neuritis (EAN), a model of human Guillain-Barré syndrome. EAN was induced actively by immunization with bovine peripheral myelin (active EAN) or by adoptive-transfer (AT-EAN) of P2-specific T cells. Cellular infiltrates in serial and semithin cryosections were characterized by immunohistochemistry. In parallel, lipocortin-1 levels in tissue extracts were quantified by a sandwich-ELISA. Only weak lipocortin-1 immunoreactivity was found in nerves of control animals injected with non-pathogenic T cells. The majority of macrophages and lymphocytes in EAN lesions exhibited lipocortin-1 immunoreactivity. Some very heavily stained cells showed a distribution and morphology similar to ED-2-positive macrophages which were abundant during early stages of EAN. Lipocortin-1 expression in T cells and macrophages was proven by immunocytochemical studies in semithin serial sections. In tissue extracts, lipocortin-1 levels increased from 0.24 ± 0.14 μg/mg protein in controls receiving non-pathogenic T cells to a maximum of 0.55 ± 0.1 μg/mg protein in AT-EAN at the peak of disease, and then slowly decreased during clinical recovery but still remained elevated. In dose-response studies in AT-EAN, highest values of lipocortin-1 (0.71 ± 0.23 μg/mg protein) were recorded after transfer of 2 × 107 T cells. Increased levels of lipocortin-1 were also measured in active EAN but occurred during the recovery phase (0.65 ± 0.27 μg/mg protein). By analogy with other immune-mediated disorders, increased lipocortin-1 expression in the inflamed sciatic nerve in EAN may exert immunoregulatory functions in-situ and contribute to the termination of the autoimmune response.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0533
    Keywords: HLA-DR ; Neuropathies ; Macrophages Fibroblasts ; Schwann cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The expression of HLA-DR and the macrophage marker CD 68 was studied in 44 sural nerve biopsies from patients with inflammatory and non-inflammatory neuropathies and controls using immunohistochemistry on non-osmicated semithin sections, a technique that has not been used before in such a biopsy study. Most HLA-DR-immunoreactive (ir) cells were fibroblasts, macrophages on perineurial cells, some were perivascular and endothelial cells, and only few were Schwann cells. Counts of immunoreactive cells revealed (a) increased HLA-DR expression in severe as compared to less severe neuropathies and to controls, (b) no correlation between the numbers of HLA-DR-ir cells and CD 68-ir macrophages, and (c) no close correlation between diagnostic groups and the number of HLA-DR-ir cells, but higher numbers in inflammatory neuropathies. We conclude that endoneurial fibroblasts and macrophages as antigen-presenting cells may be mediators in various peripheral nerve diseases, not only in inflammatory disorders.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 90 (1995), S. 478-485 
    ISSN: 1432-0533
    Keywords: Chronic constriction injury ; Crush ; Dorsal horn ; Hyperalgesia ; Neurotransmitters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We tested the hypothesis that neurochemical changes in the spinal cord dorsal horn associated with neuropathic pain states differ from those seen in association with non-painful neuropathies. Immunohistochemistry was performed on spinal cord sections from rats with a chronic constriction injury (CCI), which develop hyperalgesia, and from animals with a nerve crush injury, which do not develop hyperalgesia or other signs of a painful syndrome. Immunohistochemistry was quantified by computer-assisted densitometry. Calcitonin gene-related peptide (CGRP) immunoreactivity and substance P (SP) immunoreactivity were decreased from 1 to 4 weeks after injury in CCI and from 2 to 6 weeks in crush. Gammaaminobutyric acid immunoreactivity was unchanged in both conditions at all time points. Met-enkephalin (Metenk) immunoreactivity was increased in CCI and unchanged in crush. Although SP and CGRP are involved in pain transmission, we conclude that their decrease in immunoreactivity is not specific for the CCI model, but rather a more general event in nerve de- and regeneration. The increase in immunoreactivity for the opioid peptide Met-enk, however, was only seen in the late phase of CCI, and may be specific for conditions associated with neuropathic pain and its resolution.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Der Schmerz 13 (1999), S. 315-323 
    ISSN: 1432-2129
    Keywords: Schlüsselwörter Schmerz ; Chronifizierung ; Tierexperiment ; Zytokine ; Key words Chronic pain ; Neuropathic pain ; Cytokines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract When pain becomes chronic this is a process that takes place at several levels of the peripheral and central nervous systems. In recent years, proinflammatory substances like bradykinin, prostaglandins and signal molecules like cytokines have been identified as algogenic factors. In the present paper we examined whether cytokines play a role also in non-inflammatory peripheral nerve lesions, i.e. whether they are of importance in the causation of pain in general and whether their antagonists can be used therapeutically. The development of pain after peripheral nerve lesion in animal models follows the process of Wallerian degeneration. During Wallerian degeneration the expression of proinflammatory cytokines in the nerve is upregulated. Here we studied the temporal course of cytokine expression with several different analytical methods, analyzing tumor necrosis factor-α (TNF) and interleukin-β (IL-β) in the mouse model of chronic constrictive injury (CCI) of the sciatic nerve. This model is associated with reproducible pain related behavior in the animals. We found an early increase of TNF 12 hours after injury. Neutralizing antibodies to TNF were able to reduce the hyperalgesia that evolved due to the nerve injury. As TNF exerts its effects via two receptors, TNF receptor 1 (TNF-R1) and TNF receptor 2 (TNF R2), we also investigated, which of the receptors is relevant to the causation of pain in this model. It turned out that antibodies to TNF-R1, but not to TNF-R2 reduced hyperalgesia, indicating that TNF-R1 is the receptor concerned. Neu-tralizing antibodies to IL-1 receptor and to IL-6 receptor also reduced pain related behavior. These results lead to the conclusion that proinflammatory cytokines are involved not only in inflammatory pain but also in neuropathic pain. Therapeutic strategies involving cytokine inhibition have been tested experimentally and are already being used in preliminary clinical studies in immune-mediated diseases. In the future, they might be a useful addition to the range of treatments for patients with neuropathic pain.
    Notes: Zusammenfassung Hintergrund: Die Chronifizierung von Schmerz erfolgt auf mehreren Ebenen des peripheren und zentralen Nervensystems. In den letzten Jahren sind aus der Entzündungsforschung proinflammatorische Substanzen, wie Bradykinin, Prostaglandine und Signalmoleküle, wie Zytokine, als algogene Mechanismen identifiziert worden. Untersuchungen: In der vorliegenden Arbeit wurde tierexperimentell untersucht, ob Zytokine auch bei nichtentzündlichen peripheren Nervenläsionen bedeutsam sind, also eine allgemeingültige Bedeutung für die Schmerzentstehung besitzen und ob sich die Antagonisierung dieser Prozesse therapeutisch nutzen läßt. Schmerzentstehung nach Nervenläsion im Tiermodell ist an den Ablauf der Waller-Degeneration gekoppelt. Bei der Waller-Degeneration wird im Nerv die Expression proinflammatorischer Zytokine hochreguliert. Am Mausmodell der chronischen Konstriktionsläsion des N. ischiadicus (chronic constrictive nerve injury, CCI), das mit reproduzierbarem Schmerz-assoziiertem Verhalten einhergeht, wurde mit verschiedenen analytischen Methoden der Zeitverlauf der Zytokinexpression für Tumornekrosefaktor α (TNF) und Interleukin-1β (IL-1β) untersucht. Ergebnisse: Dabei zeigte sich, daß TNF sehr früh, schon 12 h nach der Läsion, erhöht ist. Durch die Gabe von neutralisierenden Antikörpern gegen TNF konnte die in Folge der Läsion entstehende Hyperalgesie reduziert werden. Da TNF seine Wirkung über 2 Rezeptoren vermittelt, TNF-Rezeptor 1 (TNF-R1) und 2 (TNF-R2), wurde auch untersucht, welcher der beiden Rezeptoren für die Schmerzauslösung in diesem Modell relevant ist. Es stellte sich heraus, daß Antikörper gegen TNF-R1, nicht aber Antikörper gegen TNF-R2 die Hyperalgesie reduzierten, so daß TNF-R1 der hier relevante Rezeptor ist. Auch neutralisierende Antikörper gegen den IL-1- sowie den IL-6-Rezeptor reduzierten das Schmerz-assoziierte Verhalten. Diskussion: Aus diesen Ergebnissen läßt sich schließen, daß proinflammatorische Zytokine nicht nur beim Entzündungsschmerz, sondern auch beim neuropathischen Schmerz eine Rolle spielen. Therapeutische Strategien zur Zytokinhemmung sind experimentell und in ersten klinischen Studien bei Immunkrankheiten bereits im Einsatz. Sie könnten das therapeutische Spektrum für Patienten mit neuropathischen Schmerzen in Zukunft bereichern.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Archives of microbiology 167 (1997), S. 384-391 
    ISSN: 1432-072X
    Keywords: Key words Xanthobacter flavus ; Dichlorobenzene ; Biodegradation ; Modified ortho pathway ; Toxicity ; Chloromuconate cycloisomerase ; Dienelactone ; hydrolase ; Maleylacetate reductase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Xanthobacter flavus 14p1 used 1,4-dichlorobenzene as the sole source of carbon and energy but did not grow on other (chloro)aromatic compounds. 1,4-Dichlorobenzene was attacked by a chlorobenzene dioxygenase, and the intermediate chlorocatechol was metabolized by the modified ortho pathway. All enzymes necessary to convert 1,4-dichlorobenzene to 3-oxoadipate showed a low substrate specificity and also accepted the respective intermediates of chlorobenzene or 1,3-dichlorobenzene degradation. Of the three compounds chlorobenzene, 1,4-dichlorobenzene, and 1,3-dichlorobenzene, the latter was the most toxic for X. flavus 14p1. Furthermore, 1,3-dichlorobenzene did not induce chlorocatechol 1,2-dioxygenase activity of the organism. Chlorobenzene, however, induced chlorocatechol 1,2-dioxygenase, dienelactone hydrolase, and maleylacetate reductase activities. As demonstrated by chloride release, also chlorobenzene dioxygenase, chlorobenzene cis-dihydrodiol dehydrogenase, and chloromuconate cycloisomerase activities were present in chlorobenzene-induced cells, but chlorobenzene failed to support growth. Presumably a toxic compound was formed from one of the intermediates.
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