4.4 Article

Asymmetries in reciprocal baroreflex mechanisms and chronic pain severity: Focusing on irritable bowel syndrome

Journal

NEUROGASTROENTEROLOGY AND MOTILITY
Volume 30, Issue 2, Pages -

Publisher

WILEY
DOI: 10.1111/nmo.13186

Keywords

asymmetrical baroreflex reciprocity; chronic pain severity; heart rate variability; irritable bowel syndrome; pain resilience and adaptation; systolic blood pressure

Funding

  1. National Institutes of Health [R21 AT003221, R24 AT002681]
  2. Gail and Gerald Oppenheimer Family Foundation
  3. Russian Humanitarian Scientific Foundation [14-06-00304a]

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Background: Objective measures of pain severity remain ill defined, although its accurate measurement is critical. Reciprocal baroreflex mechanisms of blood pressure (BP) control were found to impact differently on pain regulation, and thus their asymmetry was hypothesized to also connect to chronic pain duration and severity. Methods: Seventy-eight female patients with irritable bowel syndrome (IBS) and 27 healthy women were assessed for IBS severity and chronicity, negative affect, and various measures of resting autonomic function including BP, heart rate and its variability (HRV), baroreceptor-sensitivity to activations and inhibitions, gains of brady-and tachy-cardiac baro-responses, gains of BP falls/rises, and BP start points for these spontaneous baroreflexes. Key Results: IBS directly and indirectly (through increased negative affect) was associated with asymmetry between baroreceptor activations/inhibitions compared to symmetrical baroreflex reciprocity in the healthy women. In the IBS group, independently of specific IBS symptoms, pain chronicity was associated with (i) decreased BP falls coupled with either (a) decreased tachycardia associated with lower disease severity (earlier pain resilience mechanism), or (b) decreased bradycardia associated with higher disease severity (later pain decompensation mechanism), or (ii) increased BP start point for baroreceptor activations coupled with either (a) BP increase (delayed pain adaptation mechanism) or (b) affect-related HRV decrease (delayed pain aggravation mechanism). Conclusion and Inferences: We anticipate the findings to be a starting point for validating these autonomic metrics of pain suffering and pain coping mechanisms in other chronic pain syndromes to suggest them as biomarkers of its severity and duration for profiling and correct management of chronic pain patients.

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