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. 2013 Feb;154(2):257-262.
doi: 10.1016/j.pain.2012.10.020. Epub 2012 Nov 2.

Hypertension prevalence and diminished blood pressure-related hypoalgesia in individuals reporting chronic pain in a general population: the Tromsø study

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Hypertension prevalence and diminished blood pressure-related hypoalgesia in individuals reporting chronic pain in a general population: the Tromsø study

Roy Bjørkholt Olsen et al. Pain. 2013 Feb.

Abstract

Resting blood pressure (BP) is inversely related to pain sensitivity in individuals free of chronic pain, reflecting homeostatic interactions between cardiovascular and pain modulatory systems. Several laboratory studies indicate that BP-related hypoalgesia is diminished in chronic pain patients, suggesting dysfunction in these interacting systems. Separate epidemiological findings reveal elevated hypertension prevalence in the chronic pain population. This study for the first time simultaneously evaluated both hypertension prevalence and BP-related hypoalgesia as they relate to chronic pain in the same sample. Resting BP and pain sensitivity were evaluated in a large general population sample (n=10,135, aged 30-87years). Subjects participated in a standardized 106s cold pressor test, providing pain ratings at 9s intervals. Self-reported presence of chronic pain and history of hypertension and use of antihypertensive medication were assessed. Significant interactions between chronic pain status and resting systolic (P<.001) and diastolic BP (P<.001) on mean pain ratings were observed. These interactions were due to significant (P<.001) BP-related hypoalgesia in individuals free of chronic pain that was twice the magnitude of the hypoalgesia observed in the group reporting chronic pain. Presence of chronic pain was associated with significantly increased odds of comorbid hypertension (P<.001). Within the chronic pain group, higher chronic pain intensity was a significant predictor of positive hypertension status beyond the effects of traditional demographic risk factors (P<.05). Results are consistent with the hypothesis that increased hypertension risk in the chronic pain population might be linked in part to chronic pain-related dysfunction in interacting cardiovascular-pain modulatory systems.

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