Now Available: Final Rule for FDAAA 801 and NIH Policy on Clinical Trial Reporting

Neural Mechanisms in Asthma

This study has been completed.
Information provided by (Responsible Party):
University of Wisconsin, Madison Identifier:
First received: June 30, 2010
Last updated: September 30, 2015
Last verified: December 2014

June 30, 2010
September 30, 2015
October 2011
November 2014   (final data collection date for primary outcome measure)
  • Neural activity in response to stress [ Time Frame: duration of stress (30 minutes) ] [ Designated as safety issue: No ]
    positron emission tomography
  • inflammation [ Time Frame: 24 hours ] [ Designated as safety issue: No ]
    infiltration of eosinophils into lung sputum, percentage of blood eosinophils, exhaled nitric oxide, glucocorticoid sensitivity of peripheral blood leukocytes
  • lung function [ Time Frame: 24 hours ] [ Designated as safety issue: No ]
    peak expiratory volume in 1 sec effort
  • peripheral acute stress reactivity [ Time Frame: 60 minutes ] [ Designated as safety issue: No ]
    salivary cortisol and alpha amylase in response to acute stressor
Same as current
Complete list of historical versions of study NCT01155843 on Archive Site
Not Provided
Not Provided
Not Provided
Not Provided
Neural Mechanisms in Asthma
Neural Mechanisms by Which Chronic Stress Regulates Inflammation in Asthma
Asthma is a chronic disease that affects nearly 13% of adults in the U.S., causing substantial impairment that is reflected in the tens of millions of missed days of work, and doctors' and emergency room visits it leads to annually. Those who have asthma are twice as likely to develop depression and anxiety, which are associated with more frequent and severe asthma symptoms, especially in those under chronic stress. The project proposed here seeks to understand the role of the brain in these associations and to evaluate the neural mechanisms through which a safe, low-cost intervention, that influences the function of body via the mind, may diminish the expression of asthma symptoms.
Not Provided
Observational Model: Case Control
Time Perspective: Cross-Sectional
Not Provided
Not Provided
Non-Probability Sample
Community sample
Not Provided
  • Asthmatic, chronic stress
  • Asthmatic, non-stress
Not Provided

*   Includes publications given by the data provider as well as publications identified by Identifier (NCT Number) in Medline.
November 2014
November 2014   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Asthmatics:

    • Physician diagnosed asthma with previous use of asthma medication
  • Controls:

    • negative skin-prick test to cat dander or house dust mite and have no history of asthma
  • Chronic Stress:

    • score 3 or above on any subscale of the UCLA (University of California Los Angeles) chronic stress interview

No chronic stress:

score 1.5 or below on all subscales of the UCLA chronic stress interview

Exclusion Criteria:

  • Individuals with severe asthma, or those whom currently require the use of corticosteroids
  • Individuals with significant medical problems
  • Individuals who smoke cigarettes
  • Individuals a previous adverse reaction to corticosteroids, a recent (< 1 month) viral illness, a history of severe asthma or anaphylaxis.
  • Breastfeeding women or women who are, suspect they might be or are trying to become pregnant
18 Years to 45 Years   (Adult)
Contact information is only displayed when the study is recruiting subjects
United States
Not Provided
Not Provided
University of Wisconsin, Madison
University of Wisconsin, Madison
Not Provided
Not Provided
University of Wisconsin, Madison
December 2014

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP