期刊
RHEUMATOLOGY INTERNATIONAL
卷 33, 期 9, 页码 2365-2372出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00296-013-2725-0
关键词
Central sensitization; Electromyography; Pain; Muscle; Depression; Autonomic nervous system
类别
资金
- International Association for the Study of Pain
- Colorado Clinical & Translational Institute [NIH KL2RR025779]
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [KL2TR001080, UL1TR001082] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [KL2RR025779] Funding Source: NIH RePORTER
Fibromyalgia syndrome (FMS) is a widespread musculoskeletal pain condition with unclear physiologic mechanisms. The purpose of this investigation was to compare the responsiveness of nociceptive flexion reflex (NFR) pathways between women with and without FMS. A secondary purpose was to examine the influence of depression, fibromyalgia symptom severity, and cardiovascular health on NFR responses among women with FMS. Fifteen women with FMS and 14 healthy controls participated in an experimental session to assess NFR responses to sural nerve stimulation, resting mean arterial pressure (MAP) and heart rate (HR), and scores on the Beck Depression Inventory (BDI) and Fibromyalgia Impact Questionnaire (FIQ). NFR responses were successfully elicited from all healthy individuals, but only eight (53 %) of the women with FMS. These women did not differ in the minimum stimulus intensity required to elicit an NFR response compared to healthy controls (p a parts per thousand yen 0.35). Further, these women had lower BDI (p = 0.04) and FIQ (p = 0.02) scores compared to women with FMS from whom NFR responses could not be elicited. Resting HR was higher in both groups of women with FMS compared to healthy individuals (p < 0.05), and MAP was strongly associated with NFR thresholds only among women with FMS (r = 0.88, p < 0.01). Findings from this preliminary investigation suggest that NFR pathways are impaired in women who are more severely impacted by symptoms of depression and fibromyalgia, potentially due to desensitization of NFR pathways with chronic autonomic arousal.
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