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Papers of the Week


Papers: 4 May 2019 - 10 May 2019


Human Studies


2019 Jun


Pain


160


6

Quantitative Assessment of Non-Pelvic Pressure Pain Sensitivity in Urological Chronic Pelvic Pain Syndrome: A MAPP Research Network Study.

Authors

Harte SE, Schrepf A, Gallop R, Kruger GH, Lai HH, Sutcliffe S, Halvorson M, Ichesco E, Naliboff BD, Afari N, Harris RE, Farrar JT, Tu F, Landis RJ, Clauw DJ
Pain. 2019 Jun; 160(6):1270-1280.
PMID: 31050659.

Abstract

Experimental pain sensitivity was assessed in individuals with urologic chronic pelvic pain syndrome (UCPPS) as part of the Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network. A series of computer-controlled pressure stimuli were delivered to the thumbnail bed, an asymptomatic site distant from the area of UCPPS pain that is considered to be indicative of overall body pain threshold. Stimuli were rated according to a standardized magnitude estimation protocol. Pain sensitivity in UCPPS participants was compared to healthy controls and a mixed pain group composed of individuals with other chronic overlapping pain conditions, including fibromyalgia, chronic fatigue, and irritable bowel syndromes. Data from six participating MAPP testing sites were pooled for analysis. UCPPS participants (n = 153) exhibited an intermediate pain sensitivity phenotype: they were less sensitive relative to the mixed pain group (n = 35) but significantly more sensitive than healthy controls (n = 100). Increased pain sensitivity in UCPPS patients was associated with both higher levels of clinical pain severity and more painful body areas outside the pelvic region. Exploratory analyses in UCPPS participants revealed that pain sensitivity increased during periods of urological symptom flare and that less pressure pain sensitivity at baseline was associated with a greater likelihood of subsequent genitourinary pain improvement one year later. The finding that individuals with UCPPS demonstrate non-pelvic pain hypersensitivity that is related to clinical symptoms suggests that central nervous system mechanisms of pain amplification contribute to UCPPS.