Low back pain (LBP) is a condition that affects a majority of the US population and is responsible for a significant proportion of health care costs and utilization. Lumbar spine muscle is compromised in LBP, and do, and do not, respond to exercise based physical therapy program depending on measurements representing activation capacity of lumbar muscle. Here, we will characterize the neurological and muscle specific features that may contribute to limited activation in an attempt to identify sources of resistance to recovery in patients with chronic disc injury and identify precision rehabilitation approaches for this complex population of individuals.
Low back pain (LBP) is a complex condition that affects 65-85% of the population, and is the leading musculoskeletal condition contributing to disability in the United States. Disc injury is the most common injury and 75% of individuals undergoing surgical and rehabilitative interventions for this condition experience suboptimal or poor outcomes. These patients demonstrate disability and deficits in functional capacity, and paraspinal muscles in these individuals have been shown to be altered in volume, composition, and mechanical properties. These maladaptive changes influence the ability for the muscle to respond appropriately to rehabilitation efforts in a subgroup of individuals with chronic back pain who do not demonstrate the expected acute activation responses to exercise. While the structural and adaptive capacities of healthy muscle are well understood, pathological muscle recovery and activation deficits are less clear and may be influenced by neurogenic and/or muscle specific impairments. To address this gap in knowledge, the purpose of this trial is to compare central and peripheral origins of impaired activation in individuals with chronic disc injury who do, and do not respond to exercise. Experiment 1 will use a novel functional MRI technique and electromyographic measurements to compare responder and non-responder groups in patients with chronic lumbar disc injury undergoing standard physical therapy. Experiment 2 will compare corticomotor excitability and intracortical inhibition and facilitation between individuals who are undergoing physical therapy or surgery who do and do not respond to exercise. Experiment 3 will compare ex vivo passive and active mechanical responses, and transcriptomics from intraoperative multifidus biopsies of patients undergoing spinal surgery for chronic lumbar disc injury to evaluate muscle mechanotransduction. These experiments will elucidate the neurogenic and muscle-specific contributions to muscle adaptation in the presence of chronic lumbar spine pathology and pain.
Study Type
OBSERVATIONAL
Enrollment
120
An acute bout of a 3 minute resistance exercise will be performed using a lumbar extension exercise machine
UC San Diego
La Jolla, California, United States
RMS amplitude of paraspinal muscle EMG
Average RMS EMG amplitude of the lumbar multifidus over the duration of the acute exercise bout.
Time frame: Baseline
IVIM responsiveness
Response classification from IVIM MRI imaging as an increase in IVIM Diffusion (D) of at least 0.055 x 10-3 mm2/s and a pseudodiffusion (D\*) increase of at least 6.94 x 10-3 mm2/s in response to the acute exercise stimulus
Time frame: Baseline
Cortical excitability
Transcranial Magnetic Stimulation based motor threshold of activation of the lumbar multifidus muscle
Time frame: Baseline
pAMPK
Mechanically-induced phosphorylation of p38 MAPK-Thr180/Tyr182 (p-p38T180/Y182) from intraoperative multifidus biopsies or biopsy needle
Time frame: Time of surgery/biopsy
MEP amplitude
Motor evoked potential of multifidus in response to Transcranial Magnetic Stimulation of the motor cortex
Time frame: Baseline
Cortical Silent Period
Period of motor silence in the multifidus after Transcrianial Magnetic Simulation MEP over the motor cortex
Time frame: Baseline
Short Interval Intracortical Inhibition (SICI)
Measurement of signal loss in the multifidus after a paired pulse stimulation of the motor cortex using transcranial magnetic stimulation
Time frame: Baseline
Short Interval Intracortical Facilitation (SICF)
Measurement of time of multifidus muscle activation after a paired pulse transcranial magnetic stimulation of the motor cortex
Time frame: Baseline
p-mTORS2448/total mTOR
Structural Proteins and phosphorylation of p-mTORS2448/total mTOR measured from intraoperative multifidus biopsies or biopsy needle
Time frame: Time of surgery/biopsy
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