Aktuelle Erkenntnisse zur Pathophysiologie des CRPS I

Zusammenfassung

In den letzten Jahren konnten zur Pathophysiologie des komplexen regionalen Schmerzsyndroms (CRPS) einige neue Erkenntnisse gewonnen werden. Während in der Vergangenheit das Konzept des sympathisch unterhaltenen Schmerzes („sympathetically maintained pain”, SMP) im Vordergrund stand, stellt sich nun die Erkrankung als komplexes Zusammenspiel von somatosensorischen, motorischen, inflammatorischen und autonomen Veränderungen dar. Wie bei anderen neuropathischen Schmerzsyndromen kommt es beim CRPS zu einer peripheren und zentralen Sensibilisierung. Hierbei sind unter anderem postsynaptische NMDA-Rezeptoren im Hinterhorn beteiligt. Auch das endogene Schmerzhemmsystem ist bei CRPS-Patienten defizient. Zentrale neuroplastische Veränderungen im Bereich des somatosensorischen Kortex bedingen sensible Phänomene. Häufige motorische Störungen können durch zentrale Reorganisationsvorgänge im motorischen Kortex erklärt werden. Im Bereich der neurogenen Inflammation beim CRPS konnten neben dem Calcitonin-gene related peptide (CGRP) und Substanz P inzwischen weitere beteiligte proinflammatorische Zytokine identifiziert werden. Hinsichtlich des sympathischen Nervensystems weisen aktuelle Erkenntnisse weniger auf eine erhöhte efferente Aktivität, als auf eine Sensibilisierung peripherer adrenerger Rezeptoren hin. Insbesondere die Expression von α₁-Adrenozeptoren auf C-Fasern spielt hier eine Rolle. Diese im Artikel weiter ausgeführten Konzepte schließen sich keineswegs aus, vielmehr ergänzen sie sich. Die verschiedenen Pathomechanismen greifen ineinander. Das intra- und interindividuell variable klinische Erscheinungsbild des CRPS wird durch die unterschiedliche Beteiligung der Systeme erklärbar.

Abstract

Knowledge about the pathophysiology underlying the complex regional pain syndrome (CRPS) has increased over the last years. Classically, CRPS has been considered to be mainly driven by sympathetic dysfunction with sympathetically maintained pain being its major pathogenetic mechanism. Currently, the disease is understood as result of a complex interplay between altered somatosensory, motor, autonomic and inflammatory systems. Peripheral and central sensitization is a common feature in CRPS as in other neuropathic pain syndromes. One important mechanism is the sensitization of spinal dorsal horn cells via activation of postsynaptic NMDA-receptors by chronic C-fiber input. Differential activity of endogenous pain modulating systems may play a pivotal role in the development of CRPS, too. Neuronal plasticity of the somatosensory cortex accounts for central sensory signs. Also the motor system is subject to central adaptive changes in patients with CRPS. Calcitonin-gene related peptide (CGRP) and substance P mediate neurogenic inflammation. Additionally other proinflammatory cytokines involved in the inflammatory response in CRPS have been identified. In terms of the sympathetic nervous system, recent evidence rather points to a sensitization of adrenergic receptors than to increased efferent sympathetic activity. Particularly the expression of α₁-adrenoceptors on nociceptive C-fibers may play a major role. These pathophysiological ideas do not exclude each other. In fact they complement one another. The variety of the involved systems may explain the versatile clinical picture of CRPS.

Schlüsselwörter

Pathophysiologie - CRPS - neuropathischer Schmerz - Neuroplastizität

Key words

pathophysiology - CRPS - neuropathic pain - neuroplasticity

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1 Beide Autoren sind gleichberechtigte Autoren.

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