Prognostic Value of Measures of the Central Hypersensitivity in Patients With Acute Low Back Pain

This study is currently recruiting participants.
Verified December 2012 by University Hospital Inselspital, Berne
Sponsor:
Information provided by (Responsible Party):
University Hospital Inselspital, Berne
ClinicalTrials.gov Identifier:
NCT00892411
First received: May 1, 2009
Last updated: December 17, 2012
Last verified: December 2012

May 1, 2009
December 17, 2012
February 2009
December 2013   (final data collection date for primary outcome measure)
Presence or absence of chronic low back pain [ Time Frame: 6 months after the acute episode ] [ Designated as safety issue: No ]
Same as current
Complete list of historical versions of study NCT00892411 on ClinicalTrials.gov Archive Site
Mechanisms of central hypersensitivity [ Time Frame: During the acute episode of low back pain ] [ Designated as safety issue: No ]
Same as current
Not Provided
Not Provided
 
Prognostic Value of Measures of the Central Hypersensitivity in Patients With Acute Low Back Pain
Prognostic Value of Measures of Central Hypersensitivity in Patients With Low Back Pain

Background. Patients with chronic low back pain display hyperexcitability of the central nervous system (central hypersensitivity). Such hypersensitivity may occur in the acute phase and represent a risk factor for the development of chronic pain.

Objective. To determine the prognostic value of central hypersensitivity for the development of chronic low back pain.

Design. Prospective cohort study.

Setting. Primary care.

Patients. 140 individuals with acute low back pain and no history of chronic pain.

Outcomes. Primary prognostic variable will be the pain tolerance threshold at the second toe (the pressure intensity at which a further increase in pressure is deemed intolerable). Exploratory secondary prognostic variables are measures of mechanisms related to central hypersensitivity: stimulus-specific hypersensitivity (pressure, electrical, heat and cold stimulation); tissue-specific hypersensitivity (skin vs. muscle stimulation); localized vs. widespread hypersensitivity; spinal cord modulation (electrophysiological measures of hypersensitivity and changes in receptive fields); modulation at brain level (descending modulation of nociceptive input and cortical plasticity). Clinical primary outcome will be the occurrence of chronic low back pain at follow-up.

Main analysis. The investigators will use least square logistic regression models to determine the association of central hypersensitivity with prognosis.

Relevance. An understanding of the prognostic value of central hypersensitivity may allow an early stratification for treatment of individuals at risk of developing chronic low back pain. Subgroups of patients may be selected for clinical trials on novel pharmacological approaches for the prevention and treatment of central hypersensitivity.

Background

Prolonged afferent nociceptive input induces an increase in the excitability of central sensory neurons and plasticity changes that cause hyperexcitability of the central nervous system (central hypersensitivity. The hyperexcitable central nervous system amplifies the nociceptive signal, thereby producing an exaggerated pain response even in the presence of limited tissue damage.

Using quantitative sensory tests, central hypersensitivity has been detected in different chronic musculoskeletal pain syndromes. Patients with chronic low back pain display increased pain sensitivity and enlargement of the areas of referred pain after stimulation of tissues around and distant from the site of pain (i.e. the leg or the thumb), suggesting that widespread central hypersensitivity is associated with this condition. Functional reorganization of the cortex has been detected in different pain conditions, including low back pain. Using equal levels of sensory stimulation in patients and pain-free controls, patients with chronic low back pain showed more extensive patterns of neuronal activation in pain-related cortical areas.

An investigation on patients after a whiplash injury found that those patients with persistent moderate or severe symptoms at 6 months had displayed, soon after injury, widespread hypersensitivity. Therefore, central hypersensitivity may be an indicator of poor prognosis. An acute peripheral lesion may induce plasticity changes leading to central hypersensitivity in a subset of individuals. Such a hypersensitivity would facilitate the transition from acute to chronic pain and disability. This hypothesis has been investigated using a limited number of tests only in a limited number of individuals with whiplash injury, but not in any other condition.

Objective

To determine the prognostic value of different measures of mechanisms of central hypersensitivity in patients with acute low back pain.

Methods

140 consecutive Patients with acute low back pain, referred by general practice, will be studied prospectively. Primary prognostic variable will be the pain tolerance threshold at the second toe (the pressure intensity at which a further increase in pressure is deemed intolerable). Exploratory secondary prognostic variables are measures of mechanisms related to central hypersensitivity: stimulus-specific hypersensitivity (pressure, electrical, heat and cold stimulation); tissue-specific hypersensitivity (skin vs. muscle stimulation); localized vs. widespread hypersensitivity; spinal cord modulation (electrophysiological measures of hypersensitivity and changes in receptive fields); modulation at brain level (descending modulation of nociceptive input and cortical plasticity). Clinical primary outcome will be the occurrence of chronic low back pain at follow-up. We will use least square logistic regression models to determine the association of central hypersensitivity with prognosis.

Observational
Observational Model: Cohort
Time Perspective: Prospective
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Probability Sample

Patients with acute low back pain referred from primary care.

  • Pain Measurement
  • Low Back Pain
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1
Patients With Acute Low Back Pain
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
140
December 2013
December 2013   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Acute low back pain < 6 weeks
  • Age 18-80

Exclusion Criteria

  • History of chronic low back pain
  • Radicular pain
  • Pregnancy
  • Breast feeding
Both
18 Years to 80 Years
No
Contact: Michele Curatolo, MD, PhD +41 31 632 8322 michele.curatolo@insel.ch
Switzerland
 
NCT00892411
KEK 103/08
No
University Hospital Inselspital, Berne
University Hospital Inselspital, Berne
Not Provided
Study Director: Michele Curatolo, MD, PhD Dep. of Anesthesiology and Pain Therapy, Bern University Hospital
Principal Investigator: Monika Müller, MD, PhD Dep. of Anesthesiology and Pain Therapy, Bern University Hospital
University Hospital Inselspital, Berne
December 2012

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