Key result
Fibromyalgia patients had weaker blood pressure increments and higher heart rates during the cold pressor test than healthy subjects, correlating with reduced conditioned pain modulation.
Why the study?
Is cardiovascular reactivity to pain associated with conditioned pain modulation dysfunction in patients with fibromyalgia compared to healthy subjects?
Observational (n=47)
Is cardiovascular reactivity to pain associated with conditioned pain modulation dysfunction in patients with fibromyalgia compared to healthy subjects?
Reduced cardiovascular reactivity to pain, specifically blunted blood pressure response, may contribute to diminished endogenous pain inhibition in fibromyalgia.
May link blunted cardiovascular reactivity to impaired pain modulation in fibromyalgia; hypothesis-generating, needs prospective confirmation.
Fibromyalgia (FM) is a chronic widespread pain condition of unknown origin. Reduced endogenous pain inhibition could be related to high pain sensitivity in FM. Associations between conditioned pain modulation (CPM) and cardiovascular responses to pain have been observed in healthy subjects (HS). Because reduced cardiovascular reactivity to various stressors has been reported in FM patients, we investigated relationships between CPM and cardiovascular response to the cold pressor test (CPT) in 22 FM patients and 25 HS. CPM was evaluated by comparing pain intensity produced by a 120-second heat test stimulus (HTS) before and after a CPT (2minutes, 12°C). The CPT, used to activate CPM, produced greater pain intensity in FM patients. Patients with FM had higher heart rates than HS at baseline and during CPT. Higher heart rate was related with higher pain intensity during the CPT. Blood pressure increments during CPT were weaker in the FM group. CPM was less effective in FM patients than in HS. Importantly, systolic blood pressure responses during CPT were positively related to CPM effectiveness, suggesting that reduced blood pressure response during the conditioning stimulus could be involved in CPM dysfunction in the FM group. Higher heart rate could be implicated in the greater sensitivity to cold pain in FM. Patients with FM have reduced blood pressure response to a painful CPT. Reduced cardiovascular reactivity to pain could have important involvement in diminished endogenous pain inhibition efficacy and FM pathophysiology.
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Chalaye et al. (2013) conducted an observational in Fibromyalgia (n=47). Cold pressor test (CPT) vs. Healthy subjects was evaluated on Conditioned pain modulation (CPM) and cardiovascular response to the cold pressor test. Fibromyalgia patients had weaker blood pressure increments and higher heart rates during the cold pressor test than healthy subjects, correlating with reduced conditioned pain modulation.
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