Objectives: Quantitative sensory testing (QST) is used to assess sensory dysfunction and nerve damage by examining psychophysical responses to controlled, graded stimuli such as mechanical and thermal detection and pain thresholds. In the breast cancer population, 4 studies have used QST to examine persistent pain after breast cancer treatment, suggesting neuropathic pain being a prominent pain mechanism. However, the agreement and reliability of QST has not been described in the postsurgical breast cancer population, hindering exact interpretation of QST studies in this population. The aim of the present study was to assess test-retest properties of QST after breast cancer surgery.
Methods: A total of 32 patients recruited from a larger ongoing prospective trial were examined with QST 12 months after breast cancer surgery and reexamined a week later. A standardized QST protocol was used, including sensory mapping for mechanical, warmth and cold areas of sensory dysfunction, mechanical thresholds using monofilaments and pin-prick, thermal thresholds including warmth and cold detection thresholds and heat pain threshold, with bilateral examination. Agreement and reliability were assessed by Bland-Altman plots, descriptive statistics, coefficients of variance, and intraclass correlation.
Results: Bland-Altman plots showed high variation on the surgical side. Intraclass coefficients ranged from 0.356 to 0.847 (moderate to substantial reliability). Between-patient variation was generally higher (0.9 to 14.5 SD) than within-patient variation (0.23 to 3.55 SD). There were no significant differences between pain and pain-free patients. The individual test-retest variability was higher on the operated side compared with the nonoperated side.
Discussion: The QST protocol reliability allows for group-to-group comparison of sensory function, but less so for individual follow-up after breast cancer surgery.
*Section for Surgical Pathophysiology
†Department of breast surgery, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Funded by a grant from the Danish Cancer Society (Copenhagen, Denmark), and the study is part of the Europain Collaboration, which has received support from the Innovative Medicines Initiative (www.imi.europa.eu) Joint Undertaking, under grant agreement no 115007, resources of which are composed of financial contribution from the European Union’s Seventh Framework Programme (FP7/2007-2013) and EFPIA companies’ kind contribution. The authors declare no conflict of interest.
Reprints: Kenneth Geving Andersen, MD, Section for Surgical Pathophysiology, 7621, Rigshospitalet, University of Copenhagen, Blegdamsvej 9, DK-2100 Copenhagen, Denmark (e-mail: firstname.lastname@example.org).
Received January 21, 2014
Received in revised form July 29, 2014
Accepted June 30, 2014