Not provided
| ID | Type | Description | Link |
|---|---|---|---|
| U1111-1283-4631 | Registry Identifier | Universal Trial Number (UTN) |
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
| Name | Class |
|---|---|
| Fund for Scientific Research, Flanders, Belgium | OTHER |
Not provided
Not provided
Not provided
Exercise therapy has been shown to be effective in decreasing pain and improving function for patients with recurrent low back pain (LBP). Research on the mechanisms that trigger and/or underlie the effects of exercise therapy on LBP problems is of critical importance for the prevention of recurring or persistence of this costly and common condition. One factor that seems to be crucial within this context is the dysfunction of the back muscles. Recent pioneering results have shown that individuals with recurring episodes of LBP have specific dysfunctions of these muscles (peripheral changes) and also dysfunctions at the cortical level (central changes). This work provides the foundation to take a fresh look at the interplay between peripheral and central aspects, and its potential involvement in exercise therapy. The current project will draw on this opportunity to address the following research questions: What are the immediate (after a single session) and the long-term effects (after 18 repeated sessions) of exercise training on: (1) back muscle structure; (2) back muscle function; (3) the structure of the brain; (4) and functional connectivity of the brain. This research project also aims to examine whether the effects are dependent on how the training was performed. Therefore a specific versus a general exercise program will be compared.
Although the cause of persistent non-specific LBP remains unknown, structural and functional alterations of the brain and paravertebral muscles have been proposed as underlying mechanisms. As it is hypothesized that these alterations contribute to, or maintain non-specific LBP, exercise therapy is a key element in the rehabilitation of reoccurring LBP. Specific training of sensorimotor control of the lumbopelvic region (i.e. specific skilled motor training) has shown to decrease pain and disability in patients with LBP, but has not been found superior to other forms of exercise training regarding improvements in clinical outcome measures. On the other hand, this type of training seems to differentially impact the recruitment of the back muscles compared to general exercise training. However, research using multiple treatment sessions and including follow-up outcome assessments is scarce. Furthermore, it is unknown if improvements may be attributed to measurable peripheral changes in the muscle and/or central neural adaptations in the brain. The primary aim of this study is to examine the short and long-term effects of specific skilled motor control training versus unspecific general extension training on pain, functional disability, brain structure/function and muscle structure/function in recurrent LBP patients.
Method: In this double-blind, randomized controlled clinical trial 62 recurrent LBP patients will be randomly allocated (1:1) to receive either specific skilled motor training (i.e. the experimental group) or general extension training (i.e. control group). Each training group will receive 13 weeks of treatment, during which a total of 18 supervised treatment sessions will be delivered in combination with an individualized home-exercise program. Both groups will first receive low-load training (i.e. at 25-30% of the individual's repetition maximum, sessions 1-9) followed by high-load training (i.e. at 40-60% of the individual's one repetition maximum, sessions 10-18). Primary outcome measures include: LBP-related pain and disability (RMDQ, NRS and Margolis pain diagram), lumbar muscle structure and function (Dixon MRI and mf-MRI) and brain structure and function (MRI, DTI and fMRI). Secondary measures include: lumbopelvic control and proprioception (thoracolumbar dissociation test and position-reposition test), trunk muscle activity (RAM and QFRT) and psychosocial factors, including measures of physical activity (IPAQ-LF, SF-36), pain cognitions and perceptions (PCS, PCI and PVAQ), anxiety and depression (HADS), and kinesiophobia (TSK). Experimental data collection will be performed at baseline, immediately following the low-load training (i.e. after the 9th supervised treatment session), following the high-load training (i.e. after the 18th supervised treatment session), and at 3 months follow-up. Experimental data collection will comprise of magnetic resonance imaging of the brain and trunk muscles, clinical assessments assessing muscle function, and a battery of questionnaires evaluating psychosocial factors.
Not provided
Not provided
Not provided
Not provided
| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Specific skilled motor training | Experimental | 13 weeks of treatment, with 18 supervised treatment sessions in combination with an individualized home-exercise program. This group will first receive low-load training (i.e. at 25-30% of the individual's repetition maximum, sessions 1-9) followed by high-load training (i.e. at 40-60% of the individual's one repetition maximum, sessions 10-18). |
|
| General extension training | Active Comparator | 13 weeks of treatment, with 18 supervised treatment sessions in combination with an individualized home-exercise program. This group will first receive low-load training (i.e. at 25-30% of the individual's repetition maximum, sessions 1-9) followed by high-load training (i.e. at 40-60% of the individual's one repetition maximum, sessions 10-18). |
|
| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| Specific skilled motor training | Behavioral | Participants allocated to the skilled motor training group will receive sensorimotor training of the intrinsic muscles of the lumbopelvic region, namely the multifidus, transversus abdominis, and pelvic floor muscles. |
| Measure | Description | Time Frame |
|---|---|---|
| Brain macro-structure | Whole brain T1-weighted structural MRI will be acquired. | Baseline |
| Brain macro-structure | Whole brain T1-weighted structural MRI will be acquired. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Brain macro-structure | Whole brain T1-weighted structural MRI will be acquired. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Brain macro-structure | Whole brain T1-weighted structural MRI will be acquired. | At 3 months follow-up |
| Brain micro-structure | Whole-brain T2-weighted images will be obtained. | Baseline |
| Brain micro-structure | Whole-brain T2-weighted images will be obtained. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Brain micro-structure | Whole-brain T2-weighted images will be obtained. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Brain micro-structure |
| Measure | Description | Time Frame |
|---|---|---|
| Functional brain connectivity | Resting-state functional MRI will be performed to acquire insight into subnetworks relating to sensorimotor control and pain processing. | Baseline |
| Functional brain connectivity |
Not provided
Inclusion Criteria:
Exclusion Criteria:
Not provided
Not provided
Not provided
Not provided
| Name | Role | Phone | Extension | |
|---|---|---|---|---|
| Jessica van Oosterwijck, Prof | Contact | +3293326919 | Jessica.VanOosterwijck@UGent.be | |
| Lieven Danneels, Prof | Contact | +32 9 332 26 35 | Lieven.Danneels@UGent.be |
| Name | Affiliation | Role |
|---|---|---|
| Jessica van Oosterwijck, Prof | Ghent University, Pain in Motion | Study Director |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Ghent University, vakgroep revalidatiewetenschappen | Recruiting | Ghent | Oost-Vlaanderen | 9000 | Belgium |
| PubMed Identifier | Type | Citation | Retractions |
|---|---|---|---|
| 29573870 | Background | Hartvigsen J, Hancock MJ, Kongsted A, Louw Q, Ferreira ML, Genevay S, Hoy D, Karppinen J, Pransky G, Sieper J, Smeets RJ, Underwood M; Lancet Low Back Pain Series Working Group. What low back pain is and why we need to pay attention. Lancet. 2018 Jun 9;391(10137):2356-2367. doi: 10.1016/S0140-6736(18)30480-X. Epub 2018 Mar 21. | |
| 29480409 |
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
The study model is parallel. Participants experiencing recurrent LBP patients will be randomly allocated (1:1) to receive either specific skilled motor training or general extension training (i.e. parallel study model). Both groups will first receive low-load training (i.e. at 25-30% of the individual's repetition maximum, sessions 1-9) followed by high-load training (i.e. at 40-60% of the individual's one repetition maximum, sessions 10-18) (i.e. cross-over study model).
Not provided
Not provided
Not provided
| General extension training | Behavioral | Participants allocated to the general extension training group will receive general training exercises using the David Back equipment from the Back Unit at Ghent University Hospital |
|
Whole-brain T2-weighted images will be obtained. |
| At 3 months follow-up |
Resting-state functional MRI will be performed to acquire insight into subnetworks relating to sensorimotor control and pain processing.
| After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Functional brain connectivity | Resting-state functional MRI will be performed to acquire insight into subnetworks relating to sensorimotor control and pain processing. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Functional brain connectivity | Resting-state functional MRI will be performed to acquire insight into subnetworks relating to sensorimotor control and pain processing. | At 3 months follow-up |
| Lumbar muscle structure | T1-weighted Dixon MRI will be performed. | Baseline |
| Lumbar muscle structure | T1-weighted Dixon MRI will be performed. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Lumbar muscle structure | T1-weighted Dixon MRI will be performed. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Lumbar muscle structure | T1-weighted Dixon MRI will be performed. | At 3 months follow-up |
| Lumbar muscle function | T2-weighted mf-MRI will be conducted. | Baseline |
| Lumbar muscle function | T2-weighted mf-MRI will be conducted. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Lumbar muscle function | T2-weighted mf-MRI will be conducted. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Lumbar muscle function | T2-weighted mf-MRI will be conducted. | At 3 months follow-up. |
| Lumbopelvic control | Lumbopelvic control will be examined by means of a clinical thoracolumbar dissociation test which assesses the quality of performance of lumbopelvic motion with limited motion at the thoracolumbar junction. | Baseline |
| Lumbopelvic control | Lumbopelvic control will be examined by means of a clinical thoracolumbar dissociation test which assesses the quality of performance of lumbopelvic motion with limited motion at the thoracolumbar junction. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Lumbopelvic control | Lumbopelvic control will be examined by means of a clinical thoracolumbar dissociation test which assesses the quality of performance of lumbopelvic motion with limited motion at the thoracolumbar junction. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Lumbopelvic control | Lumbopelvic control will be examined by means of a clinical thoracolumbar dissociation test which assesses the quality of performance of lumbopelvic motion with limited motion at the thoracolumbar junction. | At 3 months follow-up. |
| Lumbopelvic proprioception | To evaluate lumbar proprioception, the position-reposition accuracy of the lumbar spine will be determined. | Baseline |
| Lumbopelvic proprioception | To evaluate lumbar proprioception, the position-reposition accuracy of the lumbar spine will be determined. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Lumbopelvic proprioception | To evaluate lumbar proprioception, the position-reposition accuracy of the lumbar spine will be determined. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Lumbopelvic proprioception | To evaluate lumbar proprioception, the position-reposition accuracy of the lumbar spine will be determined. | At 3 months follow-up. |
| Anticipatory postural adjustments | To examine anticipatory postural adjustments (APAs) trunk muscle onset latencies in response to internal-induced perturbations will be measured by means of surface electromyography (EMG). APAs will be measured by inducing internal perturbations in the trunk muscles during a reliable and valid unilateral rapid arm movement task (RAM). | Baseline |
| Anticipatory postural adjustments | To examine anticipatory postural adjustments (APAs) trunk muscle onset latencies in response to internal-induced perturbations will be measured by means of surface electromyography (EMG). APAs will be measured by inducing internal perturbations in the trunk muscles during a reliable and valid unilateral rapid arm movement task (RAM). | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Anticipatory postural adjustments | To examine anticipatory postural adjustments (APAs) trunk muscle onset latencies in response to internal-induced perturbations will be measured by means of surface electromyography (EMG). APAs will be measured by inducing internal perturbations in the trunk muscles during a reliable and valid unilateral rapid arm movement task (RAM). | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Anticipatory postural adjustments | To examine anticipatory postural adjustments (APAs) trunk muscle onset latencies in response to internal-induced perturbations will be measured by means of surface electromyography (EMG). APAs will be measured by inducing internal perturbations in the trunk muscles during a reliable and valid unilateral rapid arm movement task (RAM). | At 3 months follow-up |
| Compensatory postural adjustments | To examine compensatory postural adjustments (CPAs), trunk muscle onset latencies in response to external-induced perturbations will be measured by means of surface electromyography (EMG). CPAs will be measured by using external perturbations of trunk muscles during a quick-force-release test (QFRT). | Baseline |
| Compensatory postural adjustments | To examine compensatory postural adjustments (CPAs), trunk muscle onset latencies in response to external-induced perturbations will be measured by means of surface electromyography (EMG). CPAs will be measured by using external perturbations of trunk muscles during a quick-force-release test (QFRT). | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Compensatory postural adjustments | To examine compensatory postural adjustments (CPAs), trunk muscle onset latencies in response to external-induced perturbations will be measured by means of surface electromyography (EMG). CPAs will be measured by using external perturbations of trunk muscles during a quick-force-release test (QFRT). | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Compensatory postural adjustments | To examine compensatory postural adjustments (CPAs), trunk muscle onset latencies in response to external-induced perturbations will be measured by means of surface electromyography (EMG). CPAs will be measured by using external perturbations of trunk muscles during a quick-force-release test (QFRT). | At 3 months follow-up |
| Nociceptive flexion reflex - threshold | The NFR will be elicited in the dominant leg by transcutaneous electrical stimulation of the sural nerve in its retromalleolar path using a stimulation bar electrode connected to a constant current stimulator. Surface EMG electrodes will be placed on the skin of the muscle belly of the ipsilateral biceps femoris. | Baseline |
| Nociceptive flexion reflex - threshold | The NFR will be elicited in the dominant leg by transcutaneous electrical stimulation of the sural nerve in its retromalleolar path using a stimulation bar electrode connected to a constant current stimulator. Surface EMG electrodes will be placed on the skin of the muscle belly of the ipsilateral biceps femoris. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Nociceptive flexion reflex - threshold | The NFR will be elicited in the dominant leg by transcutaneous electrical stimulation of the sural nerve in its retromalleolar path using a stimulation bar electrode connected to a constant current stimulator. Surface EMG electrodes will be placed on the skin of the muscle belly of the ipsilateral biceps femoris. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Nociceptive flexion reflex - threshold | The NFR will be elicited in the dominant leg by transcutaneous electrical stimulation of the sural nerve in its retromalleolar path using a stimulation bar electrode connected to a constant current stimulator. Surface EMG electrodes will be placed on the skin of the muscle belly of the ipsilateral biceps femoris. | At 3 months follow-up |
| Nociceptive flexion reflex - temporal summation | Five 1ms rectangular wave pulse train will be administered 3 times at a frequency of 2 Hz at a constant stimulation intensity. This procedure will be repeated 5 times. | Baseline |
| Nociceptive flexion reflex - temporal summation | Five 1ms rectangular wave pulse train will be administered 3 times at a frequency of 2 Hz at a constant stimulation intensity. This procedure will be repeated 5 times. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Nociceptive flexion reflex - temporal summation | Five 1ms rectangular wave pulse train will be administered 3 times at a frequency of 2 Hz at a constant stimulation intensity. This procedure will be repeated 5 times. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Nociceptive flexion reflex - temporal summation | Five 1ms rectangular wave pulse train will be administered 3 times at a frequency of 2 Hz at a constant stimulation intensity. This procedure will be repeated 5 times. | At 3 months follow-up |
| Conditioned pain modulation | The conditioning stimulus will comprise of immersion of the non-dominant hand until the proximal wrist crease in a hot circulating water bath of 45.5°C during 6 minutes. The test stimulus will comprise of pressure pain threshold (PPT) assessments (as described above) during and after completion of the conditioning stimulus. Before, after 2 min of immersion and 2 minutes after completion of immersion, the test stimulus will be repeated twice at each test location at the dominant body side. | Baseline |
| Conditioned pain modulation | The conditioning stimulus will comprise of immersion of the non-dominant hand until the proximal wrist crease in a hot circulating water bath of 45.5°C during 6 minutes. The test stimulus will comprise of pressure pain threshold (PPT) assessments (as described above) during and after completion of the conditioning stimulus. Before, after 2 min of immersion and 2 minutes after completion of immersion, the test stimulus will be repeated twice at each test location at the dominant body side. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Conditioned pain modulation | The conditioning stimulus will comprise of immersion of the non-dominant hand until the proximal wrist crease in a hot circulating water bath of 45.5°C during 6 minutes. The test stimulus will comprise of pressure pain threshold (PPT) assessments (as described above) during and after completion of the conditioning stimulus. Before, after 2 min of immersion and 2 minutes after completion of immersion, the test stimulus will be repeated twice at each test location at the dominant body side. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Conditioned pain modulation | The conditioning stimulus will comprise of immersion of the non-dominant hand until the proximal wrist crease in a hot circulating water bath of 45.5°C during 6 minutes. The test stimulus will comprise of pressure pain threshold (PPT) assessments (as described above) during and after completion of the conditioning stimulus. Before, after 2 min of immersion and 2 minutes after completion of immersion, the test stimulus will be repeated twice at each test location at the dominant body side. | At 3 months follow-up |
| Anxiety and depression | Hospital Anxiety and depression scale (HADS) | Baseline |
| Anxiety and depression | Hospital Anxiety and depression scale (HADS) | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Anxiety and depression | Hospital Anxiety and depression scale (HADS) | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Anxiety and depression | Hospital Anxiety and depression scale (HADS) | At 3 months follow-up |
| Physical activity | International physical activity questionnaire - long form (IPAQ-LF) | Baseline |
| Physical activity | International physical activity questionnaire - long form (IPAQ-LF) | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Physical activity | International physical activity questionnaire - long form (IPAQ-LF) | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Physical activity | International physical activity questionnaire - long form (IPAQ-LF) | At 3 months follow-up. |
| Pain coping | Pain coping inventory (PCI), Pain Catastrophizing Scale (PCS) | Baseline |
| Pain coping | Pain coping inventory (PCI), Pain Catastrophizing Scale (PCS) | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Pain coping | Pain coping inventory (PCI), Pain Catastrophizing Scale (PCS) | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Pain coping | Pain coping inventory (PCI), Pain Catastrophizing Scale (PCS) | At 3 months follow-up |
| Pain catastrophizing | Pain Catastrophizing Scale (PCS) | Baseline |
| Pain catastrophizing | Pain Catastrophizing Scale (PCS) | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Pain catastrophizing | Pain Catastrophizing Scale (PCS) | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Pain catastrophizing | Pain Catastrophizing Scale (PCS) | At 3 months follow-up |
| Pain vigilance and awareness | Pain vigilance and awareness questionnaire (PVAQ) | Baseline |
| Pain vigilance and awareness | Pain vigilance and awareness questionnaire (PVAQ) | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Pain vigilance and awareness | Pain vigilance and awareness questionnaire (PVAQ) | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Pain vigilance and awareness | Pain vigilance and awareness questionnaire (PVAQ) | At 3 months follow-up |
| Kinesiophobia | Tampa Scale for Kinesiophobia (TSK) | Baseline |
| Kinesiophobia | Tampa Scale for Kinesiophobia (TSK) | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Kinesiophobia | Tampa Scale for Kinesiophobia (TSK) | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Kinesiophobia | Tampa Scale for Kinesiophobia (TSK) | At 3 months follow-up |
| Health status | Short Form Health Survey-36 items (SF-36) | Baseline |
| Health status | Short Form Health Survey-36 items (SF-36) | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Health status | Short Form Health Survey-36 items (SF-36) | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Health status | Short Form Health Survey-36 items (SF-36) | At 3 months follow-up |
| Low back pain related pain | LBP related pain intensity will be evaluated by using an 11 point NRS | Baseline |
| Low back pain related pain | LBP related pain intensity will be evaluated by using an 11 point NRS | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Low back pain related pain | LBP related pain intensity will be evaluated by using an 11 point NRS | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Low back pain related pain | LBP related pain intensity will be evaluated by using an 11 point NRS | At 3 months follow-up |
| Low back pain related disability | The Roland Morris Disability Questionnaire will be used to evaluate disability. | Baseline |
| Low back pain related disability | The Roland Morris Disability Questionnaire will be used to evaluate disability. | After low-load training phase (i.e. after 9th supervised treatment session) assessed at approximately 8 weeks |
| Low back pain related disability | The Roland Morris Disability Questionnaire will be used to evaluate disability. | After high-load training phase (i.e. after 18th supervised treatment session) assessed at approximately 13 weeks |
| Low back pain related disability | The Roland Morris Disability Questionnaire will be used to evaluate disability. | At 3 months follow-up |
| Low back pain recurrence | Self-report via telephone interview: (1) the number of episode(s), (2) the duration of the LBP episode(s), (3) pain intensity, measured with three NRS for average-, worst- and current pain during the LBP episode(s), (4) location and quality of pain (i.e. sharp, burning, etc. sensation), (5) subjects opinion about what caused the new episode of LBP, (6) degree of impairments in daily life activities due to the LBP, (7) whether participants sought treatment (i.e. physiotherapist, general practitioner, etc.) and (8) strategies to cope with the new LBP episode. | At 6 months follow-up |
| Low back pain recurrence | Self-report via telephone interview: (1) the number of episode(s), (2) the duration of the LBP episode(s), (3) pain intensity, measured with three NRS for average-, worst- and current pain during the LBP episode(s), (4) location and quality of pain (i.e. sharp, burning, etc. sensation), (5) subjects opinion about what caused the new episode of LBP, (6) degree of impairments in daily life activities due to the LBP, (7) whether participants sought treatment (i.e. physiotherapist, general practitioner, etc.) and (8) strategies to cope with the new LBP episode. | At 12 months follow-up |
| Hurwitz EL, Randhawa K, Yu H, Cote P, Haldeman S. The Global Spine Care Initiative: a summary of the global burden of low back and neck pain studies. Eur Spine J. 2018 Sep;27(Suppl 6):796-801. doi: 10.1007/s00586-017-5432-9. Epub 2018 Feb 26. |
| 12090877 | Background | Deyo RA. Diagnostic evaluation of LBP: reaching a specific diagnosis is often impossible. Arch Intern Med. 2002 Jul 8;162(13):1444-7; discussion 1447-8. doi: 10.1001/archinte.162.13.1444. No abstract available. |
| 29279756 | Background | Iizuka Y, Iizuka H, Mieda T, Tsunoda D, Sasaki T, Tajika T, Yamamoto A, Takagishi K. Prevalence of Chronic Nonspecific Low Back Pain and Its Associated Factors among Middle-Aged and Elderly People: An Analysis Based on Data from a Musculoskeletal Examination in Japan. Asian Spine J. 2017 Dec;11(6):989-997. doi: 10.4184/asj.2017.11.6.989. Epub 2017 Dec 7. |
| 22641374 | Background | Itz CJ, Geurts JW, van Kleef M, Nelemans P. Clinical course of non-specific low back pain: a systematic review of prospective cohort studies set in primary care. Eur J Pain. 2013 Jan;17(1):5-15. doi: 10.1002/j.1532-2149.2012.00170.x. Epub 2012 May 28. |
| 22586331 | Background | da C Menezes Costa L, Maher CG, Hancock MJ, McAuley JH, Herbert RD, Costa LO. The prognosis of acute and persistent low-back pain: a meta-analysis. CMAJ. 2012 Aug 7;184(11):E613-24. doi: 10.1503/cmaj.111271. Epub 2012 May 14. |
| 28355981 | Background | da Silva T, Mills K, Brown BT, Herbert RD, Maher CG, Hancock MJ. Risk of Recurrence of Low Back Pain: A Systematic Review. J Orthop Sports Phys Ther. 2017 May;47(5):305-313. doi: 10.2519/jospt.2017.7415. Epub 2017 Mar 29. |
| 29794309 | Background | Goubert D, Meeus M, Willems T, De Pauw R, Coppieters I, Crombez G, Danneels L. The association between back muscle characteristics and pressure pain sensitivity in low back pain patients. Scand J Pain. 2018 Apr 25;18(2):281-293. doi: 10.1515/sjpain-2017-0142. |
| 28756299 | Background | Ranger TA, Cicuttini FM, Jensen TS, Peiris WL, Hussain SM, Fairley J, Urquhart DM. Are the size and composition of the paraspinal muscles associated with low back pain? A systematic review. Spine J. 2017 Nov;17(11):1729-1748. doi: 10.1016/j.spinee.2017.07.002. Epub 2017 Jul 26. |
| 26092329 | Background | Kregel J, Meeus M, Malfliet A, Dolphens M, Danneels L, Nijs J, Cagnie B. Structural and functional brain abnormalities in chronic low back pain: A systematic review. Semin Arthritis Rheum. 2015 Oct;45(2):229-37. doi: 10.1016/j.semarthrit.2015.05.002. Epub 2015 May 16. |
| 27263992 | Background | Coppieters I, Meeus M, Kregel J, Caeyenberghs K, De Pauw R, Goubert D, Cagnie B. Relations Between Brain Alterations and Clinical Pain Measures in Chronic Musculoskeletal Pain: A Systematic Review. J Pain. 2016 Sep;17(9):949-62. doi: 10.1016/j.jpain.2016.04.005. Epub 2016 Jun 3. |
| 28234752 | Background | Yuan C, Shi H, Pan P, Dai Z, Zhong J, Ma H, Sheng L. Gray Matter Abnormalities Associated With Chronic Back Pain: A Meta-Analysis of Voxel-based Morphometric Studies. Clin J Pain. 2017 Nov;33(11):983-990. doi: 10.1097/AJP.0000000000000489. |
| 31151373 | Background | Brumagne S, Diers M, Danneels L, Moseley GL, Hodges PW. Neuroplasticity of Sensorimotor Control in Low Back Pain. J Orthop Sports Phys Ther. 2019 Jun;49(6):402-414. doi: 10.2519/jospt.2019.8489. |
| 22331213 | Background | Moseley GL, Flor H. Targeting cortical representations in the treatment of chronic pain: a review. Neurorehabil Neural Repair. 2012 Jul-Aug;26(6):646-52. doi: 10.1177/1545968311433209. Epub 2012 Feb 13. |
| 25011478 | Background | Kilgour AH, Todd OM, Starr JM. A systematic review of the evidence that brain structure is related to muscle structure and their relationship to brain and muscle function in humans over the lifecourse. BMC Geriatr. 2014 Jul 10;14:85. doi: 10.1186/1471-2318-14-85. |
| 29112509 | Background | Goossens N, Rummens S, Janssens L, Caeyenberghs K, Brumagne S. Association Between Sensorimotor Impairments and Functional Brain Changes in Patients With Low Back Pain: A Critical Review. Am J Phys Med Rehabil. 2018 Mar;97(3):200-211. doi: 10.1097/PHM.0000000000000859. |
| 2922640 | Background | Panjabi M, Abumi K, Duranceau J, Oxland T. Spinal stability and intersegmental muscle forces. A biomechanical model. Spine (Phila Pa 1976). 1989 Feb;14(2):194-200. doi: 10.1097/00007632-198902000-00008. |
| 1490034 | Background | Panjabi MM. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disord. 1992 Dec;5(4):383-9; discussion 397. doi: 10.1097/00002517-199212000-00001. |
| 1490035 | Background | Panjabi MM. The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis. J Spinal Disord. 1992 Dec;5(4):390-6; discussion 397. doi: 10.1097/00002517-199212000-00002. |
| 27676689 | Background | Goubert D, Oosterwijck JV, Meeus M, Danneels L. Structural Changes of Lumbar Muscles in Non-specific Low Back Pain: A Systematic Review. Pain Physician. 2016 Sep-Oct;19(7):E985-E1000. |
| 11261613 | Background | Danneels LA, Vanderstraeten GG, Cambier DC, Witvrouw EE, De Cuyper HJ. CT imaging of trunk muscles in chronic low back pain patients and healthy control subjects. Eur Spine J. 2000 Aug;9(4):266-72. doi: 10.1007/s005860000190. |
| 22784801 | Background | D'hooge R, Cagnie B, Crombez G, Vanderstraeten G, Dolphens M, Danneels L. Increased intramuscular fatty infiltration without differences in lumbar muscle cross-sectional area during remission of unilateral recurrent low back pain. Man Ther. 2012 Dec;17(6):584-8. doi: 10.1016/j.math.2012.06.007. Epub 2012 Jul 10. |
| 26547762 | Background | Cagnie B, Dhooge F, Schumacher C, De Meulemeester K, Petrovic M, van Oosterwijck J, Danneels L. Fiber Typing of the Erector Spinae and Multifidus Muscles in Healthy Controls and Back Pain Patients: A Systematic Literature Review. J Manipulative Physiol Ther. 2015 Nov-Dec;38(9):653-663. doi: 10.1016/j.jmpt.2015.10.004. Epub 2015 Nov 5. |
| 31563580 | Background | Agten A, Stevens S, Verbrugghe J, Timmermans A, Vandenabeele F. Biopsy samples from the erector spinae of persons with nonspecific chronic low back pain display a decrease in glycolytic muscle fibers. Spine J. 2020 Feb;20(2):199-206. doi: 10.1016/j.spinee.2019.09.023. Epub 2019 Sep 27. |
| 23369927 | Background | D'hooge R, Cagnie B, Crombez G, Vanderstraeten G, Achten E, Danneels L. Lumbar muscle dysfunction during remission of unilateral recurrent nonspecific low-back pain: evaluation with muscle functional MRI. Clin J Pain. 2013 Mar;29(3):187-94. doi: 10.1097/AJP.0b013e31824ed170. |
| 29906616 | Background | Knox MF, Chipchase LS, Schabrun SM, Romero RJ, Marshall PWM. Anticipatory and compensatory postural adjustments in people with low back pain: a systematic review and meta-analysis. Spine J. 2018 Oct;18(10):1934-1949. doi: 10.1016/j.spinee.2018.06.008. Epub 2018 Jun 12. |
| 28900711 | Background | Prins MR, Griffioen M, Veeger TTJ, Kiers H, Meijer OG, van der Wurff P, Bruijn SM, van Dieen JH. Evidence of splinting in low back pain? A systematic review of perturbation studies. Eur Spine J. 2018 Jan;27(1):40-59. doi: 10.1007/s00586-017-5287-0. Epub 2017 Sep 12. |
| 23079004 | Background | D'hooge R, Hodges P, Tsao H, Hall L, Macdonald D, Danneels L. Altered trunk muscle coordination during rapid trunk flexion in people in remission of recurrent low back pain. J Electromyogr Kinesiol. 2013 Feb;23(1):173-81. doi: 10.1016/j.jelekin.2012.09.003. Epub 2012 Oct 15. |
| 16275595 | Background | Geisser ME, Ranavaya M, Haig AJ, Roth RS, Zucker R, Ambroz C, Caruso M. A meta-analytic review of surface electromyography among persons with low back pain and normal, healthy controls. J Pain. 2005 Nov;6(11):711-26. doi: 10.1016/j.jpain.2005.06.008. |
| 12832166 | Background | Hodges PW, Moseley GL. Pain and motor control of the lumbopelvic region: effect and possible mechanisms. J Electromyogr Kinesiol. 2003 Aug;13(4):361-70. doi: 10.1016/s1050-6411(03)00042-7. |
| 12914264 | Background | Hodges PW. Core stability exercise in chronic low back pain. Orthop Clin North Am. 2003 Apr;34(2):245-54. doi: 10.1016/s0030-5898(03)00003-8. |
| 11689740 | Background | Ebenbichler GR, Oddsson LI, Kollmitzer J, Erim Z. Sensory-motor control of the lower back: implications for rehabilitation. Med Sci Sports Exerc. 2001 Nov;33(11):1889-98. doi: 10.1097/00005768-200111000-00014. |
| 26742533 | Background | Saragiotto BT, Maher CG, Yamato TP, Costa LO, Menezes Costa LC, Ostelo RW, Macedo LG. Motor control exercise for chronic non-specific low-back pain. Cochrane Database Syst Rev. 2016 Jan 8;2016(1):CD012004. doi: 10.1002/14651858.CD012004. |
| 26863390 | Background | Macedo LG, Saragiotto BT, Yamato TP, Costa LO, Menezes Costa LC, Ostelo RW, Maher CG. Motor control exercise for acute non-specific low back pain. Cochrane Database Syst Rev. 2016 Feb 10;2(2):CD012085. doi: 10.1002/14651858.CD012085. |
| 29573872 | Background | Foster NE, Anema JR, Cherkin D, Chou R, Cohen SP, Gross DP, Ferreira PH, Fritz JM, Koes BW, Peul W, Turner JA, Maher CG; Lancet Low Back Pain Series Working Group. Prevention and treatment of low back pain: evidence, challenges, and promising directions. Lancet. 2018 Jun 9;391(10137):2368-2383. doi: 10.1016/S0140-6736(18)30489-6. Epub 2018 Mar 21. |
| 20434958 | Background | Tsao H, Druitt TR, Schollum TM, Hodges PW. Motor training of the lumbar paraspinal muscles induces immediate changes in motor coordination in patients with recurrent low back pain. J Pain. 2010 Nov;11(11):1120-8. doi: 10.1016/j.jpain.2010.02.004. |
| 15375808 | Background | Liu KP, Chan CC, Lee TM, Hui-Chan CW. Mental imagery for promoting relearning for people after stroke: a randomized controlled trial. Arch Phys Med Rehabil. 2004 Sep;85(9):1403-8. doi: 10.1016/j.apmr.2003.12.035. |
| 20181504 | Background | Tsao H, Galea MP, Hodges PW. Driving plasticity in the motor cortex in recurrent low back pain. Eur J Pain. 2010 Sep;14(8):832-9. doi: 10.1016/j.ejpain.2010.01.001. Epub 2010 Feb 23. |
| 28850499 | Background | Masse-Alarie H, Beaulieu LD, Preuss R, Schneider C. Influence of paravertebral muscles training on brain plasticity and postural control in chronic low back pain. Scand J Pain. 2016 Jul;12:74-83. doi: 10.1016/j.sjpain.2016.03.005. Epub 2016 May 11. |
| 21672633 | Background | Taubert M, Lohmann G, Margulies DS, Villringer A, Ragert P. Long-term effects of motor training on resting-state networks and underlying brain structure. Neuroimage. 2011 Aug 15;57(4):1492-8. doi: 10.1016/j.neuroimage.2011.05.078. Epub 2011 Jun 7. |
| 20810887 | Background | Taubert M, Draganski B, Anwander A, Muller K, Horstmann A, Villringer A, Ragert P. Dynamic properties of human brain structure: learning-related changes in cortical areas and associated fiber connections. J Neurosci. 2010 Sep 1;30(35):11670-7. doi: 10.1523/JNEUROSCI.2567-10.2010. |
| 31596547 | Background | Tavor I, Botvinik-Nezer R, Bernstein-Eliav M, Tsarfaty G, Assaf Y. Short-term plasticity following motor sequence learning revealed by diffusion magnetic resonance imaging. Hum Brain Mapp. 2020 Feb 1;41(2):442-452. doi: 10.1002/hbm.24814. Epub 2019 Oct 9. |
| 14737157 | Background | Draganski B, Gaser C, Busch V, Schuierer G, Bogdahn U, May A. Neuroplasticity: changes in grey matter induced by training. Nature. 2004 Jan 22;427(6972):311-2. doi: 10.1038/427311a. No abstract available. |
| 18614670 | Background | Boyke J, Driemeyer J, Gaser C, Buchel C, May A. Training-induced brain structure changes in the elderly. J Neurosci. 2008 Jul 9;28(28):7031-5. doi: 10.1523/JNEUROSCI.0742-08.2008. |
| 19820707 | Background | Scholz J, Klein MC, Behrens TE, Johansen-Berg H. Training induces changes in white-matter architecture. Nat Neurosci. 2009 Nov;12(11):1370-1. doi: 10.1038/nn.2412. Epub 2009 Oct 11. |
| 42011735 | Derived | Van Oosterwijck S, Wijnen J, Brandt M, Billens A, Meirezonne H, Dhondt E, Bernaers L, De Greef I, Jeurissen B, Willems T, Matheve T, Moerkerke M, Hodges P, Van Oosterwijck J, Danneels L. Efficacy of Specific Skilled Motor Versus General Exercise Training on Muscle and Neural Alterations in Recurrent Low Back Pain: Protocol of a Randomized Clinical Trial. Percept Mot Skills. 2026 Apr 21:315125261441406. doi: 10.1177/00315125261441406. Online ahead of print. |
| ID | Term |
|---|---|
| D017116 | Low Back Pain |
| D009043 | Motor Activity |
| ID | Term |
|---|---|
| D001416 | Back Pain |
| D010146 | Pain |
| D009461 | Neurologic Manifestations |
| D012816 | Signs and Symptoms |
| D013568 | Pathological Conditions, Signs and Symptoms |
| D001519 | Behavior |
Not provided
Not provided