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Numbness in clinical and experimental pain – A cross-sectional study exploring the mechanisms of reduced tactile function

Geber, Christiana,b,*; Magerl, Walterb,d; Fondel, Ricardac; Fechir, Marcela; Rolke, Romana; Vogt, Thomasa; Treede, Rolf-Detlefd; Birklein, Franka

doi: 10.1016/j.pain.2008.03.006

Pain patients often report distinct numbness of the painful skin although no structural peripheral or central nerve lesion is obvious. In this cross-sectional study we assessed the reduction of tactile function and studied underlying mechanisms in patients with chronic pain and in healthy participants exposed to phasic and tonic experimental nociceptive stimulation. Mechanical detection (MDT) and pain thresholds (MPT) were assessed in the painful area and the non-painful contralateral side in 10 patients with unilateral musculoskeletal pain. Additionally, 10 healthy participants were exposed to nociceptive stimulation applied to the volar forearms (capsaicin; electrical stimulation, twice each). Areas of tactile hypaesthesia and mechanical hyperalgesia were assessed. MDT and MPT were quantified adjacent to the stimulation site. Tactile hypaesthesia in pain patients and in experimental pain (MDT-z-scores: −0.66 ± 0.30 and −0.42 ± 0.15, respectively, both p < 0.01) was paralleled by mechanical hyperalgesia (MPT-z-scores: +0.51 ± 0.27, p < 0.05; and +0.48 ± 0.10, p < 0.001). However, hypaesthesia and hyperalgesia were not correlated. Although 9 patients reported numbness, only 3 of them were able to delineate circumscript areas of tactile hypaesthesia. In experimental pain, the area of tactile hypaesthesia could be mapped in 31/40 experiments (78%). Irrespective of the mode of nociceptive stimulation (phasic vs. tonic) tactile hypaesthesia and hyperalgesia developed with a similar time course and disappeared within approximately 1 day. Hypaesthesia (numbness) often encountered in clinical pain can be reproduced by experimental nociceptive stimulation. The time course of effects suggests a mechanism involving central plasticity.

aNeurologische Universitätsklinik Mainz, Germany

bInstitut für Physiologie und Pathophysiologie, Mainz, Germany

cKlinik für Anästhesiologie der Universität Mainz, Germany

dLehrstuhl für Neurophysiologie, CBTM, Medizinische Fakultät Mannheim der Universität Heidelberg, Germany

*Corresponding author. Address: Klinik und Poliklinik für Neurologie, Johannes-Gutenberg Universität, Langenbeckstrasse 1, 55131 Mainz, Germany. Tel.: +49 6131 17 4588; fax: +49 6131 17 3271.


Submitted January 11, 2008; revised March 2, 2008; accepted March 5, 2008.

© 2008 Lippincott Williams & Wilkins, Inc.
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