Mechanical Biomarkers of Chronic Low Back Pain

NIH RePORTER · NIH · R01 · $616,785 · view on reporter.nih.gov ↗

Abstract

Abstract The intervertebral disc (IVD) has an essential role in transferring load during normal spine function and when this normal function fails, symptoms, degeneration and altered spine mechanics may occur. The overall scientific premise of this work is that there is a gap in knowledge of the relationship between contributions from mechanical, inflammatory and biopsychosocial factors that lead to chronic low back pain (LBP). An important gap is a poor understanding of the relationship between IVD degeneration and LBP. This lack of understanding leads to discordance between imaging and self-reported pain and, ultimately, treatments being delivered by an exclusionary process. To address this gap, we will use innovative in vivo imaging tools to quantify the mechanical function of the IVD. We will also measure quantitative sensory factors, biochemical markers, and biopsychosocial factors that, when combined with mechanical function, may better identify subgroups or phenotypes of LBP. The overall goal of this project is to identify if mechanical function of the IVD is a potential risk factor and whether mechanical function can assist with defining phenotypes of LBP. The findings from this study would lead to longitudinal analyses to determine whether these phenotypes predict the transition from acute to chronic LBP. The rationale for this proposed research is that: 1) altered mechanical function of the IVD contributes to LBP. 2) LBP is a heterogeneous condition that can result from a combination of mechanical, inflammatory, and central pain based sources. The central hypothesis is that in vivo measured IVD mechanical function will be an important potential risk factor for both acute and chronic non-specific LBP and that this measure will improve the phenotyping of LBP. In Aim I, we will quantify the association between in-vivo measured IVD mechanical function among acute and chronic non-specific LBP participants and asymptomatic controls. In Aim II, we will derive well-defined phenotypes of LBP using combinations of potential risk factors. Identifying phenotypes of LBP will allow for specific rehabilitation, surgical, pharmaceutical or behavioral treatments to be targeted, resulting in improved patient outcomes.

Key facts

NIH application ID
10440260
Project number
5R01AR075399-04
Recipient
DUKE UNIVERSITY
Principal Investigator
Louis E. DeFrate
Activity code
R01
Funding institute
NIH
Fiscal year
2022
Award amount
$616,785
Award type
5
Project period
2019-07-22 → 2024-06-30