Current Diabetes Reports

, Volume 12, Issue 4, pp 393–402 | Cite as

Neuropathic Pain: Is Quantitative Sensory Testing Helpful?

  • Elena K. KrumovaEmail author
  • Christian Geber
  • Andrea Westermann
  • Christoph Maier
Microvascular Complications—Neuropathy (D Ziegler, Section Editor)


Neuropathic pain arises as a consequence of a lesion or disease affecting the somatosensory system and is characterised by a combination of positive and negative sensory symptoms. Quantitative sensory testing (QST) examines the sensory perception after application of different mechanical and thermal stimuli of controlled intensity and the function of both large (A-beta) and small (A-delta and C) nerve fibres, including the corresponding central pathways. QST can be used to determine detection, pain thresholds and stimulus–response curves and can thus detect both negative and positive sensory signs, the second ones not being assessed by other methods. Similarly to all other psychophysical tests QST requires standardised examination, instructions and data evaluation to receive valid and reliable results. Since normative data are available, QST can contribute also to the individual diagnosis of neuropathy, especially in the case of isolated small-fibre neuropathy, in contrast to the conventional electrophysiology which assesses only large myelinated fibres. For example, detection of early stages of subclinical neuropathy in symptomatic or asymptomatic patients with diabetes mellitus can be helpful to optimise treatment and identify diabetic foot at risk of ulceration. QST assessed the individual’s sensory profile and thus can be valuable to evaluate the underlying pain mechanisms which occur in different frequencies even in the same neuropathic pain syndromes. Furthermore, assessing the exact sensory phenotype by QST might be useful in the future to identify responders to certain treatments in accordance to the underlying pain mechanisms.


Quantitative sensory testing Somatosensory profile Neuropathic pain Diabetic polyneuropathy Pain mechanisms Mechanism-based treatment 



Conflicts of interest: C.M., E.K., and A.W. are members of the German Research Network on Neuropathic Pain (German Ministry for Education and Research, grants 01EM0107, 01EM0502, 01EM0506) and the Europain Collaboration, which has received support from the Innovative Medicines Initiative Joint Undertaking, under grant agreement no 115007, resources of which are composed of financial contribution from the European Union’s Seventh Framework Programme (FP7/20072013) and EFPIA companies (AstraZeneca, Pfizer, Esteve, UCB-Pharma, Sanofi Aventis, Grünenthal, Eli Lilly, Neuroscience Technologies und Boehringer Ingelheim) in kind contribution. C.M. has received research grants from Pfizer, MSD, Mundipharma, Grünenthal, Astellas, and Lilly; he has also received consultant and/or speaker fees from Astellas, Sanofi Aventis, Wyeth, Pfizer, Mundipharma and Eli Lilly. E.K. is supported by intramural funding of the Ruhr-University Bochum (FoRUM grant K046-10). C.G. is supported by the “Foundation Rhineland—Palatinate, project 936” and the “Kalkhof-Rose-Stiftung.”


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Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Elena K. Krumova
    • 1
    • 3
    Email author
  • Christian Geber
    • 2
  • Andrea Westermann
    • 1
  • Christoph Maier
    • 1
  1. 1.Department of Pain Medicine, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil GmbHRuhr-University BochumBochumGermany
  2. 2.Klinik und Poliklinik für NeurologieUniversitätsmedizin der Johannes-Gutenberg UniversitätMainzGermany
  3. 3.Department of Neurology, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil GmbHRuhr University BochumBochumGermany

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