Fortschr Neurol Psychiatr 2002; 70(2): 88-94
DOI: 10.1055/s-2002-19922
Originalarbeit
Georg Thieme Verlag Stuttgart · New York

Neuropathische Schmerzen - Mechanismen und Therapie

Mechanism-Based Treatment Principles of Neuropathic PainF.  Birklein1
  • 1Neurologische Universitätsklinik Mainz (Direktor: Prof. Dr. M. Dieterich)
Diese Arbeit wurde von der DFG, SFB 353, C3 und vom Forschungsnetzwerk „Neuropathischer Schmerz” des BMBF unterstützt.
Further Information

Publication History

Publication Date:
01 February 2002 (online)

Zusammenfassung

Neuropathische Schmerzen treten dann auf, wenn das Nervensystem selbst geschädigt ist. In der gängigen Klassifikation werden neuropathische Schmerzen noch nach deren Ätiologie eingeteilt. Durch die Forschung der letzten Jahre gelang es jedoch, die wichtigsten molekularen Mechanismen neuropathischer Schmerzen aufzuklären. Es hat sich dabei gezeigt, dass diese Mechanismen prinzipiell unabhängig von der Ätiologie der Nervenschädigung sind. Die wichtigsten Mechanismen sind die Akkumulation von spannungsabhängigen Na+-Kanälen im verletzten Nerv, die pathologische Kopplung zwischen sympathischen und nozizeptiven Axonen, die Disinhibition der Schmerzempfindung auf Rückenmarksebene, die zentrale (spinale) und die periphere nozizeptive Sensibilisierung. Gegen jeden einzelnen Mechanismus gibt es bereits heute therapeutische Optionen. Das Ziel einer erfolgreichen Schmerztherapie muss also sein, individuelle Schmerzmechanismen und nicht ätiologische Krankheitsentitäten zu bekämpfen. Die Aufgaben der klinischen Forschung in den nächsten Jahren liegen darin, dazu die nötigen Instrumentarien zu liefern. Nur so wird jeder Patient mit neuropathischen Schmerzen die für ihn effiziente Therapie bekommen können.

Abstract

Traditionally, neuropathic pain has been classified due to aetiology of nerve damage-traumatic, inflammatory or metabolic, for instance. Based on this classification, pain therapy often is insufficient. Recent research revealed different mechanisms, which are responsible for the generation of pain after nerve lesion. These mechanisms seem to be independent of aetiology of the nerve damage. The most important mechanisms are accumulation of sodium channels on injured nerves, pathological sympatho-afferent coupling, disinhibition of nociception and central or peripheral nociceptive sensitisation. Each individual mechanism could be treated specifically by current available drugs, or by non-drug therapy. However, future research has to focus on exploring tools to recognise individual pain mechanisms in single patients. Thereby treatment will become more effective.

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PD Dr. F. Birklein

Neurologische Universitätsklinik

Langenbeckstraße 1

55101 Mainz

Email: birklein@neurologie.klinik.uni-mainz.de