Individuals with vs without Raynaud phenomenon (RP) may experience bilateral pressure pain hypersensitivity, according to a study published in Pain Medicine.

Although RP pathogenesis is not clearly understood, the pain component is thought to result from hyperactivation of nociceptors and ischemia in deep and peripheral tissues, respectively. This hyperactivation of nociceptors may contribute to the maintenance of peripheral sensitization and lead to central sensitization.

A total of 57 participants age >18 years were enrolled for this preliminary case-control study. Study participants were classified as having primary RP (n=18; mean age, 28.4 years; 72.2% women; mean time since onset, 11.4 years), secondary RP (n=19; mean age, 55.8 years; 78.9% women; mean time since onset, 17.3 years), or healthy controls (n=20; mean age, 47.3 years; 80.0% women). Sociodemographic information, clinical/vascular data, and information on several pain features were collected. Among the pain components evaluated were pain intensity assessed with a visual analog scale; bilateral pressure pain sensitivity and thresholds; catastrophizing evaluated with the Pain Catastrophizing Scale; central sensitization (CS) assessed using the CS Inventory; and pain intensity and thresholds, which were evaluated using the Pain Matcher device. Participants answered questionnaires regarding pain variables, then underwent thermography, followed by pain evaluation using the Pain Matcher with algometry.

The 3 groups differed in age, with participants in the primary RP group being younger than those in the control group (P =.004) or in the secondary RP group (P <.001). There were also significant differences in thermography between participants with primary or secondary RP vs control individuals (P ≤.012), with patients in the primary and secondary RP groups registering lower temperatures than those in the control arm (P ≤.007 and P ≤.046, respectively). Pain intensity in patients with secondary RP was higher compared with that of healthy controls (P =.001) and with patients with primary RP (P <.001). Electrical pain magnitude was greater in both RP groups vs the control group (P <.001), and pressure pain thresholds and electrical pain thresholds were lower in participants with primary or secondary RP compared with healthy controls (P ≤.05 and P <.001).

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Only patients with secondary RP had evidence of central sensitization, as indicated by higher CS Inventory scores compared with those in the primary RP and control groups (P =.001 for both). Catastrophizing was higher in both RP vs control groups, as indicated by higher Pain Catastrophizing Scale scores (P ≤.001). There were no correlations between any of the pain variables and vasoconstriction severity.

Study limitations include a small sample size, significant between-group age differences, lack of control for age as a possible confounder, and a cross-sectional design that precludes causal inference.

“These findings can thus stimulate future research efforts to obtain information of value in efforts to improve the diagnosis and treatment of this disorder,” noted the authors.

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Reference

Tapia-Haro RM, Guisado-Barrilao R, García-Ríos MDC, Raya-Álvarez E, Pérez-Mármol JM, Aguilar-Ferrándiz ME. Pain intensity, pressure pain hypersensitivity, central sensitization, and pain catastrophizing related to vascular alterations in Raynaud’s phenomenon: a preliminary case–control study [published online April 15, 2019]. Pain Med. doi:10.1093/pm/pnz089