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Sensory signs in complex regional pain syndrome and peripheral nerve injury

Gierthmühlen, Jannea,*,1; Maier, Christophb,1,2; Baron, Ralfa,2; Tölle, Thomasc,2; Treede, Rolf-Detlefd,2; Birbaumer, Nielse; Huge, Volkerf; Koroschetz, Janaa; Krumova, Elena K.b; Lauchart, Meikef; Maihöfner, Christiang; Richter, Helmutb; Westermann, Andreabthe German Research Network on Neuropathic Pain (DFNS) study group

doi: 10.1016/j.pain.2011.11.009
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Summary QST revealed more similarities than differences between CRPS-I, CRPS-II, and PNI: sensory loss occurred in 63% of CRPS-I and sensory gain in 81% of PNI patients.

This study determined patterns of sensory signs in complex regional pain syndrome (CRPS) type I and II and peripheral nerve injury (PNI). Patients with upper-limb CRPS-I (n = 298), CRPS-II (n = 46), and PNI (n = 72) were examined with quantitative sensory testing according to the protocol of the German Research Network on Neuropathic Pain. The majority of patients (66%–69%) exhibited a combination of sensory loss and gain. Patients with CRPS-I had more sensory gain (heat and pressure pain) and less sensory loss than patients with PNI (thermal and mechanical detection, hypoalgesia to heat or pinprick). CRPS-II patients shared features of CRPS-I and PNI. CRPS-I and CRPS-II had almost identical somatosensory profiles, with the exception of a stronger loss of mechanical detection in CRPS-II. In CRPS-I and -II, cold hyperalgesia/allodynia (28%–31%) and dynamic mechanical allodynia (24%–28%) were less frequent than heat or pressure hyperalgesia (36%–44%, 67%–73%), and mechanical hypoesthesia (31%–55%) was more frequent than thermal hypoesthesia (30%–44%). About 82% of PNI patients had at least one type of sensory gain. QST demonstrates more sensory loss in CRPS-I than hitherto considered, suggesting either minimal nerve injury or central inhibition. Sensory profiles suggest that CRPS-I and CRPS-II may represent one disease continuum. However, in contrast to recent suggestions, small fiber deficits were less frequent than large fiber deficits. Sensory gain is highly prevalent in PNI, indicating a better similarity of animal models to human patients than previously thought. These sensory profiles should help prioritize approaches for translation between animal and human research.

aDivision of Neurological Pain Research and Therapy, Department of Neurology, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel, Germany

bDepartment of Pain Management, BG Universitätsklinikum Bergmansheil, Ruhr-University Bochum, Bochum, Germany

cDepartment of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany

dChair of Neurophysiology, Center of Biomedicine and Medical Technology Mannheim (CBTM), Medical Faculty Mannheim, Heidelberg University, Germany

eInstitute of Medical Psychology and Behavioral Neurobiology, University of Tübingen, Tübingen, Germany

fDepartment of Anaesthesiology, Ludwig–Maximilians-Universität München, Munich, Germany

gDepartment of Neurology, University of Erlangen-Nuremberg, Germany

*Corresponding author. Address: Division of Neurological Pain Research and Therapy, Department of Neurology, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Arnold-Heller-Strasse 3, Haus 41, Kiel 24105, Germany. Tel.: +49 431 597 8510; fax: +49 431 597 8530.

E-mail: j.gierthmuehlen@neurologie.uni-kiel.de

1These authors contributed equally to this work.

E-mail: j.gierthmuehlen@neurologie.uni-kiel.de

2These authors are on the German Research Network on Neuropathic Pain (DFNS) Steering Committee.

3German Research Network on Neuropathic Pain (DFNS) study group: Prof. Dr. med. Ralf Baron, Dr. med. Janne Gierthmühlen, Dr. med. Andreas Binder, Jana Koroschetz, Division of Neurological Pain Research and Therapy, Department of Neurology, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Germany; Prof. Dr. med. Christoph Maier, Helmut Richter, Dr. med. Elena K. Krumova, Dr. med. Andrea Westermann, Department of Pain Management, BG Universitätsklinikum Bergmansheil, Ruhr-University Bochum, Germany; Prof. D. med. Thomas Tölle, PD Dr. med. Achim Berthele, PD Dr. med. Till Sprenger, Dr. med. Michael Valet, Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany; Prof. Dr. med. Rolf-Detlef Treede, PD Dr. rer. biol. hum. Walter Magerl, Dr. med. Thomas Klein, Chair of Neurophysiology, Center of Biomedicine and Medical Technology Mannheim (CBTM), Medical Faculty Mannheim, Heidelberg University, Germany; Prof. Dr. med. Frank Birklein, Dr. med. Christian Geber, Dr. med. Roman Rolke, Department of Neurology, Johannes Gutenberg-University, Mainz, Germany; PD Dr. med. Christian Maihöfner, Department of Neurology, University of Erlangen - Nuremberg, Germany; PD Dr. med. Shahnaz Christina Azad, Dr. med. Antje Beyer, Dr. med. Volker Huge, Dr. med. Meike Lauchart, Department of Anaesthesiology, Ludwig–Maximilians-Universität München, Munich, Germany; Prof. Dr. med. Niels Birbaumer, Dipl.-Psych Anja Schwarz, Institute of Medical Psychology and Behavioral Neurobiology, University of Tübingen, Tübingen, Germany; Prof. Dr. G.B. Landwehrmeyer, Department of Neurology, University of Ulm, Ulm, Germany.

Submitted March 7, 2011; revised October 1, 2011; accepted November 7, 2011.

© 2012 Lippincott Williams & Wilkins, Inc.
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