Immunologic Response to Negative Cognition in Persons With Chronic Pain

This study has been completed.
Sponsor:
Collaborator:
American Pain Society
Information provided by:
Oregon Health and Science University
ClinicalTrials.gov Identifier:
NCT00677911
First received: May 13, 2008
Last updated: NA
Last verified: May 2008
History: No changes posted
  Purpose

Principal Investigator/Program Director (Last, First, Middle): Darnall, Beth APS Future Leaders in Pain Small Research Grants Application Page 5 Continuation Format Page

Summary: Chronic pain is stressful, both physically and psychologically. Stressful experiences induce autonomic nervous system arousal, which reliably leads to inflammation and immune suppression. Inflammation then exacerbates existing pain and may be a key factor in both the genesis and maintenance of pain. Stress-induced immune effects are detected two hours (2 hrs) post-stressor, suggesting only a few stressful experiences per day may be sufficient to sustain elevated pain levels1. Cognition has emerged as a potential mediating factor in the relationship between pain and stress. Mentally recreating an emotionally stressful event induces de novo physiological stress1. In other words, thinking about an emotionally charged event down-regulates autonomic stress responses and subsequent immune effects. Therefore, exploring cognition as a mediating factor between stress, pain, and inflammation will inform our understanding of pain pathways, as well as improve treatment for pain.

Study Rationale: The acute stress response induces immunosuppression; however, this relationship has been studied in arbitrary models only (shock avoidance, job interview). This study employs the novel approach of examining stress and immune responses to a personally relevant stressor (pain); prior studies used arbitrary models only (shock avoidance, job interview). Pain offers a highly salient and personal context well-suited for investigation of negative cognitive perseveration. Pain is acutely sensitive to exacerbation via inflammation, and thus the relevance of examining immune effects of rumination on future negative expectations ("expecting the worst") is underscored.

Goal: To test the biological consequences of negative expectations, achieved via an active 10-minute negative cognitive perseveration on a personally relevant stressor: future worsening of one's chronic pain condition. Biological stress response will be measured via heart rate (HR), blood pressure (BP) and serum cortisol. Impact of negative cognition on inflammation will be measured using interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) as biomarkers of immune function, controlling for depression and pain catastrophizing. This study aims to inform the understanding of pain mechanisms.

Aim 1: Determine the magnitude of an autonomic stress response to an induction of negative cognition.

Aim 2: Determine immune effects of the experiment-induced stress response.

Aim 3: Establish whether a pre-existing tendency to catastrophize mediates the relationship between experiment-induced negative perseveration and immune effects.

Aim 4: Establish whether stress-related increases in IL-6 remain elevated post 2 hrs.


Condition Intervention Phase
Chronic Pain
Behavioral: In-vivo pain catastrophizing induction
Phase 0

Study Type: Interventional
Study Design: Allocation: Non-Randomized
Intervention Model: Single Group Assignment
Official Title: Immunologic Response to Negative Cognition in Persons With Chronic Pain

Resource links provided by NLM:


Further study details as provided by Oregon Health and Science University:

Primary Outcome Measures:
  • Interleukin-6 [ Time Frame: cross-sectional ] [ Designated as safety issue: No ]

Enrollment: 47
Study Start Date: February 2007
Study Completion Date: December 2007
Primary Completion Date: December 2007 (Final data collection date for primary outcome measure)
Intervention Details:
    Behavioral: In-vivo pain catastrophizing induction
    All participants underwent a 10-minute in-vivo pain castastrophizing induction.
  Show Detailed Description

  Eligibility

Ages Eligible for Study:   18 Years to 65 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • ages 18-65
  • chronic musculoskeletal pain
  • being treated for chronic pain at OHSU

Exclusion Criteria:

  • suicidality or thought disorder
  • pregnant
  • poor venous access
  • current corticosterioid regimen
  • recent or active virus or infection
  • substance abuse
  • former IV drug user
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00677911

Locations
United States, Oregon
OCTRI; OHSU Mail Code: CHH 13th floor 3303 Bond St.
Portland, Oregon, United States, 97239
Sponsors and Collaborators
Oregon Health and Science University
American Pain Society
  More Information

No publications provided

Responsible Party: Beth Darnall, Assistant Professor, Principal Investigator, Oregon Health & Science University
ClinicalTrials.gov Identifier: NCT00677911     History of Changes
Other Study ID Numbers: OCTRI975
Study First Received: May 13, 2008
Last Updated: May 13, 2008
Health Authority: United States: Institutional Review Board

Keywords provided by Oregon Health and Science University:
Chronic pain
Interleukin-6
pain catastrophizing
cytokines
cortisol

Additional relevant MeSH terms:
Chronic Pain
Pain
Neurologic Manifestations
Nervous System Diseases
Signs and Symptoms

ClinicalTrials.gov processed this record on August 20, 2014