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Pathophysiologie der Schmerzen bei diabetischer Polyneuropathie

Pathophysiology of pain in diabetic polyneuropathy

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Zusammenfassung

Die diabetische Polyneuropathie (dPNP) stellt die häufigste Ursache von Polyneuropathien dar. In ca. 20 % der Fälle ist sie mit Schmerzen assoziiert. Diese müssen jedoch nicht zwangsläufig neuropathischer Genese sein. Die differenzialdiagnostische Abgrenzung gegenüber Schmerzen z. B. im Rahmen einer zusätzlich vorliegenden pAVK (periphere arterielle Verschlusskrankheit) oder durch muskuläre Imbalancen bei Afferenzstörung ist für den Behandlungserfolg essenziell. Der Nachweis einer Schädigung des somatosensorischen Systems ist Voraussetzung für die Kategorisierung der Schmerzen als neuropathisch. Pathophysiologisch ist die Ursache der dPNP sowie auch der neuropathischen Schmerzen komplex. Neben die Ätiologie übergreifenden allgemeinen Pathomechanismen neuropathischer Schmerzen wurden auch diabetesspezifische Faktoren wie der Stoffwechselmetabolit Methylglyoxal oder unabhängige Faktoren wie „gain of function mutations“ am NaV1.7 (spannungsabhängiger Natriumionenkanal) als Ursache neuropathischer Schmerzen identifiziert. Auch eine zu rasche Senkung des Blutzuckerspiegels nach langjähriger diabetischer Stoffwechsellage kann zur schmerzhaften „treatment-induced neuropathy of diabetes“ (TIND) führen. Diese pathophysiologische Vielfalt der Schmerzen bei dPNP verdeutlicht eindrücklich, dass „Schmerz nicht gleich Schmerz ist“.

Abstract

Diabetic polyneuropathy (dPNP) is the most common cause of polyneuropathy. In about 20% it is associated with pain. However, pain does not have to be neuropathic. The differentiation of the pain, e. g. in the context of a present arterial occlusive disorder or by muscular imbalances in case of impaired afferent nerve function, is essential for the success of the treatment. Proof of damage to the somatosensory nervous system is a prerequisite for categorizing pain as neuropathic. Pathophysiologically, the cause of dPNP as well as neuropathic pain is complex. In addition to generally valid pathomechanisms of neuropathic pain, diabetes-specific factors such as the metabolite methylglyoxal or independent “gain of function” mutations on the NaV1.7 channel on nociceptive afferents as a cause of neuropathic pain have been identified. Also, a rapid normalization of blood glucose after years of diabetes can lead to the painful “treatment-induced neuropathy of diabetes” (TIND). This pathophysiological diversity of pain makes it clear that the term “pain is not pain” might be particularly true in dPNP.

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Abbreviations

ADP:

Adenosindiphosphat

AGE:

„Advanced glycation end products“

ATPase:

Adenosintriphosphatase

dPNP:

Diabetische Polyneuropathie

GABA:

Gammaaminobuttersäure

NaV :

Spannungsabhängiger Natriumionenkanal

NGF:

„Nerve growth factor“

pAVK:

Periphere arterielle Verschlusskrankheit

PNP:

Polyneuropathie

QST:

Quantitative sensorische Testung

TIND:

„Treatment-induced neuropathy of diabetes“

TRPA1:

„Transient receptor potential cation channel, subfamily A, member 1“

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Authors and Affiliations

  1. Klinik und Poliklinik für Neurologie, Universitätsmedizin Mainz, Langenbeckstraße 1, 55131, Mainz, Deutschland

    Christian Geber &  Frank Birklein

  2. DRK Schmerz-Zentrum Mainz, Auf der Steig 14–16, 55131, Mainz, Deutschland

    Christian Geber

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  1. Christian Geber
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  2. Frank Birklein
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Correspondence to Frank Birklein.

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Interessenkonflikt

C. Geber und F. Birklein geben an, dass kein Interessenkonflikt besteht.

Für diesen Beitrag wurden von den Autoren keine Studien an Menschen oder Tieren durchgeführt. Für die aufgeführten Studien gelten die jeweils dort angegebenen ethischen Richtlinien.

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Geber, C., Birklein, F. Pathophysiologie der Schmerzen bei diabetischer Polyneuropathie. Diabetologe 15, 641–646 (2019). https://doi.org/10.1007/s11428-019-0479-3

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  • DOI: https://doi.org/10.1007/s11428-019-0479-3

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