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Neurobiologie viszeraler Schmerzen

Neurobiology of visceral pain

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Zusammenfassung

Viszerale Schmerzen werden diffus lokalisiert und in andere Gewebe übertragen, sind häufig nicht mit aktuellen viszeralen Entzündungen korreliert, werden bevorzugt von vegetativen und motorischen Reflexen begleitet und zeichnen sich durch starke negative Affekte aus. Sie gehören zusammen mit anderen Schmerzen und Körperempfindungen in den Bereich der Interozeption. 1) Viszerale Schmerzen sind mit der Erregung spinaler (thorakolumbaler, sakraler) viszeraler Afferenzen korreliert und (mit einigen Ausnahmen) nicht mit der Erregung vagaler Afferenzen. Spinale viszerale Afferenzen sind polymodal und werden adäquat durch mechanische sowie chemische Reize aktiviert. Alle Gruppen spinaler viszeraler Afferenzen können sensibilisiert werden (z. B. durch Entzündungen). Stumme (mechanisch nichterregbare) spinale viszerale Afferenzen werden bei Entzündungen rekrutiert. 2) Spinale viszerale afferente Neurone projizieren in die Laminae I, II (äußere Schicht IIo) und V des Hinterhorns über mehrere Segmente, mediolateral über die gesamte Breite des Hinterhorns und nach kontralateral. Ihre Aktivität wird in die Laminae I, IIo und tieferen Laminae auf viszerosomatische Konvergenzneurone übertragen, die ebenso afferente synaptische (meist nozizeptive) Eingänge von der Haut und von tiefen somatischen Geweben der entsprechenden Dermatome, Myotome und Sklerotome erhalten. 3) Die Sekundärneurone bestehen aus erregenden und hemmenden Interneuronen (etwa 90 % aller Hinterhornneurone) und Traktneuronen, die in Lamina I monosynaptisch von viszeralen afferenten Neuronen und in tieferen Laminae di- oder polysynaptisch aktiviert werden. 4) An der Sensibilisierung viszerosomatischer Konvergenzneurone (zentrale Sensibilisierung) sind die Sensibilisierung spinaler viszeraler afferenter Neurone, lokale spinale erregende und hemmende Interneurone und supraspinale endogene Kontrollsysteme beteiligt. Die Mechanismen dieser zentralen Sensibilisierung sind wenig erforscht. 5) Viszerosomatische Traktneurone projizieren über den kontralateralen ventrolateralen spinalen Trakt und vermutlich andere aszendierende Trakte zum unteren und oberen Hirnstamm, zum Hypothalamus und über den Thalamus zu verschiedenen Kortexarealen. 6) Viszeraler Schmerz ist vermutlich (zusammen mit anderen viszeralen Empfindungen und nozizeptiven sowie nichtnozizeptiven somatischen Körperempfindungen) primär im posterioren dorsalen Inselkortex („primärer interozeptiver Kortex“) repräsentiert. Dieses Kortexareal erhält bei Primaten seine spinalen synaptischen Eingänge hauptsächlich von den Lamina-I-Traktneuronen über den Nucleus ventromedialis posterior des Thalamus. 7) Die Impulsübertragung viszeraler Afferenzen im Rückenmark wird hemmend und erregend durch endogene anti- und pronozizeptiv wirkende Kontrollsysteme im oberen und unteren Hirnstamm moduliert. Diese Kontrollsysteme stehen unter kortikaler Kontrolle. 8) Viszerale Schmerzen werden in tiefe somatische Gewebe, in die Haut und in andere viszerale Organe übertragen. Diese Übertragung besteht aus Spontanschmerz und mechanischer Hyperalgesie. Die Mechanismen der Übertragung und der sie begleitenden Gewebeveränderungen sind wenig erforscht worden.

Abstract

Visceral pain is diffusely localized, referred into other tissues, frequently not correlated with visceral traumata, preferentially accompanied by autonomic and somatomotor reflexes, and associated with strong negative affective feelings. It belongs together with the somatic pain sensations and non-painful body sensations to the interoception of the body. (1) Visceral pain is correlated with the excitation of spinal (thoracolumbar, sacral) visceral afferents and (with a few exceptions) not with the excitation of vagal afferents. Spinal visceral afferents are polymodal and activated by adequate mechanical and chemical stimuli. All groups of spinal visceral afferents can be sensitized (e.g., by inflammation). Silent mechanoinsensitive spinal visceral afferents are recruited by inflammation. (2) Spinal visceral afferent neurons project into the laminae I, II (outer part IIo) and V of the spinal dorsal horn over several segments, medio-lateral over the whole width of the dorsal horn and contralateral. Their activity is synaptically transmitted in laminae I, IIo and deeper laminae to viscero-somatic convergent neurons that receive additionally afferent synaptic (mostly nociceptive) input from the skin and from deep somatic tissues of the corresponding dermatomes, myotomes and sclerotomes. (3) The second-order neurons consist of excitatory and inhibitory interneurons (about 90 % of all dorsal horn neurons) and tract neurons activated monosynaptically in lamina I by visceral afferent neurons and di- or polysynaptically in deeper laminae. (4) The sensitization of viscero-somatic convergent neurons (central sensitization) is dependent on the sensitization of spinal visceral afferent neurons, local spinal excitatory and inhibitory interneurons and supraspinal endogenous control systems. The mechanisms of this central sensitization have been little explored. (5) Viscero-somatic tract neurons project through the contralateral ventrolateral tract and presumably other tracts to the lower and upper brain stem, the hypothalamus and via the thalamus to various cortical areas. (6) Visceral pain is presumably (together with other visceral sensations and nociceptive as well as non-nociceptive somatic body sensations) primarily represented in the posterior dorsal insular cortex (primary interoceptive cortex). This cortex receives in primates its spinal synaptic inputs mainly from lamina I tract neurons via the ventromedial posterior nucleus of the thalamus. (7) The transmission of activity from visceral afferents to second-order neurons in spinal cord is modulated in an excitatory and inhibitory way by endogenous anti- and pronociceptive control systems in the lower and upper brain stem. These control systems are under cortical control. (8) Visceral pain is referred to deep somatic tissues, to the skin and to other visceral organs. This referred pain consists of spontaneous pain and mechanical hyperalgesia. The mechanisms underlying referred pain and the accompanying tissue changes have been little explored.

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Notes

  1. Die Existenz des VMpo im Thalamus von Primaten, seine hauptsächlichen aszendierenden synaptischen Eingänge von spinalen und trigeminalen Lamina I Neuronen und die Projektion der VMpo-Neurone zum dorsalen posterioren Inselkortex wurde zuerst von Craig und Mitarbeitern beschrieben [37, 39, 42]. Die Existenz und funktionelle Bedeutung des VMpo wird in der Literatur kontrovers diskutiert und von einigen Experimentatoren bezweifelt [38, 98, 135].

  2. Die Idee der sensorischen Innervation der Knochen geht auf Déjerine [41] zurück. Inman u. Saunders [75] haben die räumliche Ausdehnung der sensorischen Innervation der Knochen der oberen Extremitäten, des Schultergürtels, der unteren Extremitäten und des Beckengürtels durch die Spinalnerven zum ersten Mal systematisch untersucht sowie beschrieben und die Knochenbereiche, die durch einen Spinalnerven innerviert werden, als Sklerotom bezeichnet. Die Sklerotome wurden mit modernen Methoden allerdings nie nachuntersucht. Insgesamt ist die direkte experimentelle Evidenz für die segmentale Innervation des Knochenapparats und damit für die Existenz der Sklerotome bisher nicht gut belegt worden [76].

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Interessenkonflikt. Mit Unterstützung der Deutschen Forschungsgemeinschaft. W. Jänig gibt an, dass kein Interessenkonflikt besteht. Alle nationalen Richtlinien zur Haltung und zum Umgang mit Labortieren wurden eingehalten und die notwendigen Zustimmungen der zuständigen Behörden liegen vor.

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  1. Physiologisches Institut, Christian-Albrechts-Universität, Olshausenstr. 40, 24098, Kiel, Deutschland

    W. Jänig

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Diese Publikation ist eine aktualisierte Version von Jänig W, Häbler HJ (2002) Physiologie und Pathophysiologie viszeraler Schmerzen. Schmerz 16:429–446.

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Jänig, W. Neurobiologie viszeraler Schmerzen. Schmerz 28, 233–251 (2014). https://doi.org/10.1007/s00482-014-1402-x

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