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  • 1
    Electronic Resource
    Electronic Resource
    Neue Entwicklungen im Verständnis von Triggerpunkten (1999)
    Springer
    Manuelle Medizin 37 (1999), S. 115-120 
    Details
    ISSN: 1433-0466
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003370050116
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Descending antinociception and fibromyalgia (1998)
    Springer
    Zeitschrift für Rheumatologie 57 (1998), S. S23 
    Details
    ISSN: 0340-1855
    Keywords: Key words Fibromyalgia pain ; descending antinociception ; dorsal horn neurons ; spinal cord block ; Schlüsselwörter ; Fibromyalgie-Schmerzen ; deszendierende Antinozizeption ; Hinterhornneurone ; Kälteblock
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Hypothese wird diskutiert, daß Fibromyalgie-Schmerzen durch eine Dysfunktion des deszendierenden, antinozizeptiven Systems (mit)verursacht sind. Ergebnisse aus Tierexperimenten zeigen, daß eine Unterbrechung des Systems durch Kühlung des Rückenmarks folgende Wirkungen auf nozizeptive Hinterhornneurone hat: 1. Anstieg der Ruheaktivität, 2. Senkung der mechanischen Reizschwelle, und 3. verstärkte Antworten auf Schmerzreize. Die Wirkung der deszendierenden Antinozizeption auf die Reizeffekte von tiefen Nozizeptoren war stärker als die Wirkung auf die Effekte von Nozizeptoren der Haut. Falls ähnliche Effekte auch bei Patienten auftreten, ist zu erwarten, daß eine Störung der deszendierenden Antinozizeption folgende Symptomebewirkt: 1.Spontanschmerzen (Ruheaktivität), 2. Druckschmerzhaftigkeit (Senkung der Schwelle) und 3. Hyperalgesie (verstärkte Antworten auf Schmerzreize). Die Änderungen sollten vorwiegend Schmerzen aus tiefen Geweben betreffen, da die deszendierende Antinozizeption hauptsächlich auf Reizeffekte von tiefen Nozizeptoren wirkt.
    Notes: Summary The hypothesis is discussed that a dysfunction of the descending antinociceptive system may underly the pain of fibromyalgia. Data from animal experimentation show that an interruption of the system by spinal cord cooling leads to (1) increase in ongoing activity, (2) lowering in stimulation threshold, and (3) increase in response magnitude in nociceptive dorsal horn neurons. The influence of the descending system was stronger on the responses to input from deep nociceptors than to input from cutaneous nociceptors. If similar changes occur also in patients, an impairment of the tonicly active descending system should be followed by (1) spontaneous pain (ongoing activity), (2) tenderness (lowering in mechanical threshold), and (3) hyperalgesia (increased responses to noxious stimuli). These changes should affect mainly deep pain, because the antinociceptive system influences predominantly input from deep nociceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003930050229
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  • 3
    Electronic Resource
    Electronic Resource
    Inflammation-induced increase in the density of neuropeptide-immunoreactive nerve endings in rat skeletal muscle (1998)
    Springer
    Experimental brain research 121 (1998), S. 174-180 
    Details
    ISSN: 1432-1106
    Keywords: Key words Substance P ; Nerve growth factor ; Growth-associated protein 43 ; Nerve endings ; Myositis ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The density of substance P (SP)-, calcitonin gene-related peptide (CGRP)- and vasoactive intestinal polypeptide (VIP)-immunoreactive (ir) nerve endings was quantitatively evaluated in intact and inflamed gastrocnemius-soleus muscle of the rat. In persistently inflamed muscle (12 days after a single injection of Freund’s adjuvant into the muscle), the density of SP-ir fibres was significantly increased. CGRP- and VIP-ir fibres displayed an insignificant increase in density. The density of fibres ir for nerve growth factor (NGF) and for growth-associated protein 43 (GAP-43/B-50), a marker for axonal sprouting, regeneration and synaptic reorganisation, increased significantly in persistently inflamed muscle. The data are consistent with the established contribution of NGF on the expression of SP and GAP-43 in afferent neurones under the influence of a persistent inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002210050449
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  • 4
    Electronic Resource
    Electronic Resource
    Increased spinal expression of c-Fos following stimulation of the lower urinary tract in chronic spinal cord-injured rats (1999)
    Springer
    Histochemistry and cell biology 112 (1999), S. 63-72 
    Details
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  c-Fos expression was studied in the lumbar and sacral spinal cord regions involved in processing afferent input from the lower urinary tract and a comparison was made between spinal cord-injured (SCI) animals and control animals with intact neuraxes. Afferent pathways from the lower urinary tract were activated either by insertion of a catheter through the urethra into the urinary bladder or by catheterisation plus induction of reflex micturition contractions by intravesical saline infusion. Placement of a catheter alone elicited Fos expression in a similar number of neurones in SCI and control rats mainly in the medial dorsal horn (MDH) and dorsal commissure (DCM) in the segments L1–2 and L5–S1 with a maximum in L5. Additional saline infusion induced low-frequency, high-amplitude, rhythmic bladder contractions of long duration in the rats with intact spinal cords, whereas in SCI rats, bladder distension elicited reflex contractions at a higher frequency, smaller amplitude and shorter duration. However, the basal and mean bladder pressure, as well as the total contraction time relative to the whole recording time, was not significantly different. Distension-induced bladder contractions markedly increased Fos expression primarily in the spinal segments L5–S1 in the control rats, where the majority of bladder and urethral afferent fibres terminates. Fos-positive cells were located in the MDH, lateral dorsal horn (LDH), DCM and the lateral aspect of laminae V–VII. Compared to controls, Fos expression after spinal cord injury (SCI) occurred in a significantly greater number of neurones throughout the segments L3–S1 following induction of bladder reflexes. The greatest proportional increase in the number of Fos-positive cells occurred in L3–5 which normally receive only little afferent input from the urinary bladder. Cell numbers predominantly increased in the LDH and lateral lamina V–VII. The data are consistent with the concept of a neuroplastic reorganisation of spinal pathways after SCI. Unmasking of silent synapses or formation of new connections by afferent axonal sprouting caudal to the lesion, as evident from the increased numbers of cells expressing Fos after bladder distension, could be factors underlying the emergence of reflexogenic micturition in chronic SCI rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004180050392
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  • 5
    Electronic Resource
    Electronic Resource
    Neurobiologische Grundlagen von Muskelschmerz (1999)
    Springer
    Der Schmerz 13 (1999), S. 3-17 
    Details
    ISSN: 1432-2129
    Keywords: Schlüsselwörter Muskelschmerz ; Nozizeptor ; Rückenmark ; Neuroplastizität ; Key words Muscle pain ; Nociceptor ; Spinal cord ; Neuroplasticity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Mechanisms in the lesioned muscle: The peripheral mechanism underlying the tenderness and pain during movement of a damaged muscle is the sensitization of muscle nociceptors. Ongoing activity of nociceptors causes spontaneous pain in addition to tenderness. Muscle pain (particularly that originating in myofascial trigger points) is often mislocalized because it is referred to other deep somatic tissues. The development of trigger points is a purely peripheral event, whereas the referral of muscle pain is based on central nervous mechanisms. Mechanisms at the spinal level: The input from muscle nociceptors induces neuroplastic changes in the spinal cord and higher centres of the central nervous system. These changes are associated with an overexcitability of neurones (central sensitization) and contribute to hyperalgesia of patients. Resting activity of spinal neurones (and hence spontaneous pain) is strongly dependent on nitric oxide (NO). A muscle lesion is likely to lead to an inhibition of the homonymous muscle, it can, however, elicit spasm in another muscle. Supraspinal mechanisms: Spinal neurones that mediate muscle pain are subjected to a strong descending inhibitory influence. The inhibitory tracts originate in the mesencephalon and medulla oblongata. A dysfunction of this inhibitory system might be involved in the pathogenesis of fibromyalgia.
    Notes: Zusammenfassung Mechanismen im Muskel: Der periphere Mechanismus für die Druck- und Bewegungsempfindlichkeit des verletzten Muskels besteht in der Sensibilisierung von Nozizeptoren. Wenn Nozizeptoren eine Ruheaktivität entwickeln, tritt zusätzlich zur Überempfindlichkeit Spontanschmerz auf. Muskelschmerzen (besonders die von myofaszialen Triggerpunkten) werden oft in andere tiefe Gewebe übertragen und damit subjektiv fehllokalisiert. Die Entstehung von Triggerpunkten ist ein rein peripherer Vorgang; die Übertragung der Schmerzen basiert dagegen auf Mechanismen im Zentralnervensystem. Mechanismen auf Rückenmarkebene: Der Impulseinstrom von Muskelnozizeptoren bewirkt neuroplastische Veränderungen im Rückenmark und höheren Zentren des Zentralnervensystems. Diese Veränderungen sind mit einer Erregbarkeitssteigerung der Neuronen (einer zentralen Sensibilisierung) verbunden, die bei Patienten eine Hyperalgesie mitverursacht. Die Ruheaktivität der spinalen nozizeptiven Zellen (und damit der spontane Muskelschmerz) sind stark von Stickstoffmonoxid (Stickoxid, NO) abhängig. Eine Muskelläsion führt meist zu einer Hemmung des homonymen Muskels, kann jedoch in anderen Muskeln einen Spasmus auslösen. Supraspinale Mechanismen: Spinale Neuronen, die Muskelschmerz vermitteln, sind einer tonischen deszendierenden Hemmung unterworfen. Die hemmenden Bahnen haben ihren Ursprung im Mesenzephalon und in der Medulla oblongata. Eine Fehlfunktion dieses Hemmsystems könnte bei der Pathogenese der Fibromyalgie beteiligt sein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004820050179
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  • 6
    Electronic Resource
    Electronic Resource
    The controversy about spinal neuronal nitric oxide synthase: under which conditions is it up- or downregulated? (1999)
    Springer
    Cell & tissue research 295 (1999), S. 183-194 
    Details
    ISSN: 1432-0878
    Keywords: Key words Nitric oxide synthase ; NADPH-dependent diaphorase ; Spinal cord ; Pathological circumstances ; Nociception
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In recent years, the regulation of the synthesis of nitric oxide (NO) in the central nervous system has attracted much interest because it has been shown that NO is involved in a wide variety of functions such as neuroprotection, neurotoxicity, neurotransmission, and neuroplas- ticity under physiological and pathophysiological conditions. However, the use of different detection techniques for neuronal nitric oxide synthase (nNOS), different animal species, and different experimental lesions has led to contradictory results concerning the direction of changes in spinal nNOS expression. This paper summarizes the available data on the expression on nNOS in the spinal cord under physiological and pathological conditions and tries to extract some of the basic mechanisms that underlie neuronal up- or downregulation of this enzyme. Wherever possible, results obtained with the NADPH-dependent diaphorase reaction are also included for reasons of comparison. The main conclusion is that changes in spinal nNOS expression critically depend on the type of afferent fibres activated by a specific lesion as well as the intensity and duration of input to the spinal cord. This input may be further modified by supraspinal influences. Thus the exact composition of these factors, which is undoubtfully highly variable between different experimental models, appears to determine whether the spinal NO system responds with an up- or downregulation of nNOS expression or in a bidirectional way. With regard to the diaphorase reaction it is becoming increasingly clear that under pathological conditions data obtained with this reaction differ markedly from those obtained with immunohistochemical visualization of nNOS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410051224
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