Low back pain (LBP) is a leading contributor to people living with disability throughout the world,1 and the problem appears to be getting worse rather than better.2 Scientists and clinicians, therefore, need to improve treatment for LBP to shift this trend and reduce disability.
People with LBP change how they control their posture for maintaining the body’s orientation and stability. Specifically, people with LBP delay when they activate their trunk muscles and they do so at a lower intensity for posture control when voluntarily moving their arm or leg.3,4 These changes are also observed in people with LBP when recovering their posture in response to an induced loss of balance.5 Interestingly, these changes in posture control are not related to the level of pain a person has, and the changes in posture control persist even after the pain symptoms have resolved.6-8 Also, for people with LBP, these changes in posture control associate with changes in brain functions.9-11 Together, these findings suggest that LBP associates with habitual changes in posture control and long-lasting changes in how the brain controls movement (motor control). These long-lasting changes in brain function and posture control further suggest a need for patient-specific physical therapy that focuses on treating these observed changes in motor control. Such treatments have been tested, and the treatments successfully reduce pain and disability. Unfortunately, several studies have also shown that patient-specific motor control treatments are no better than other treatments, such as general exercise or treatments that are not matched to intervene on a person’s specific changes in posture.12,13
In a clinical trial directed by Dr. Sharon Henry at the University of Vermont,12 my colleagues and I wanted to understand the reasons why patient-specific treatments are not superior. Lack of superior outcomes could be because changes in motor control are not causally important to pain and disability, or because the current approaches to motor control treatments are insufficient to effectively alter motor control. If changes in motor control with LBP are important contributors to pain and disability, and motor control treatments are effective to address each individual’s specific LBP-related changes in posture control, then motor control treatments should logically provide superior benefit to pain and disability. Thus, in addition to confirming other reports of similar clinical outcomes between groups who received patient-matched versus unmatched treatment, we evaluated whether these treatments improved the posture control of people with LBP when they performed voluntary limb movements or when they responded to an induced loss of standing balance.4,14 These tasks were chosen because the study participants were not specifically trained with these tasks during treatment, so we could determine if the treatment was successful to improve posture control in general. I speculate that such transfer of learning from the treated tasks to other tasks is needed to improve the posture control of people with LBP across the varied tasks of daily life.
Interestingly, after treating motor control using two different approaches, we found that people with LBP still exhibited delayed trunk muscle activity when performing a voluntary leg movement, and they still activated their trunk muscles with the same low intensity when responding to an induced loss of standing balance. I speculate that one possible reason these treatments do not provide better outcomes is because, as currently employed, they do not adhere to known principles of motor learning despite the fact that the intent is to train changes in motor control that are habitual, automatic, and altered by LBP at the highest levels of the nervous system. Specifically, physical therapy often consists of 7 to 10 one-hour sessions, once or twice a week.15,16 Most clinical trials utilize 6-12 sessions of similar duration and schedule. As an analogy, it is not likely we’d have any success asking a novice to become a professional golfer after 10 one-hour weekly lessons. If we consider patients with LBP to be novices in posture control, then expecting them to become capable to perform new, automatic, habitual skills of posture control in that time may be unrealistic. This unrealistic expectation is worsened when one considers that patients with LBP must learn these new skills with little monitored practice while also overcoming the competing repetition of their impaired habitual patterns that they use during all other waking hours of the day.
Therefore, although tempting to conclude that motor control treatments target the wrong mechanism to improve pain and disability, such a conclusion is premature, because the lack of superior treatment outcomes may be because motor control treatments are not yet properly designed to sufficiently improve motor control in a manner that promotes transfer of learning to untreated tasks or activities. Although we need more research to verify these speculations, it may be necessary to change the model of motor control treatment for low back pain in order to allow more practice, monitor for accurate practice during home exercises and clinic visits, and to vary the practiced tasks in order to promote general improvement across more activities of daily life. Many variables associated with motor learning have yet to be studied for LBP treatment, such as the type and timing of demonstration and feedback provided, as well as the content of practice, how practiced exercises are organized, and the amount and schedule of practice by patients with LBP. In addition, multiple factors other than changes in sensory-motor control appear to contribute to LBP, such as cognitive and emotional functions and tissue mechanics.17 Thus, combined therapy that includes physical therapy, evaluation of spine and tissue mechanics, and cognitive-behavioral therapy could be of benefit.18 The contribution of motor control training in physical therapy to these combined approaches, though, will not likely be optimized until the training approach for those treatments improves. I express these suggested changes in motor control treatments, however, as opinions that still require scientific research to provide the evidence needed before making any recommendations to clinical practice.
About Jesse Jacobs
Jesse V. Jacobs, Ph.D. conducted this research during his tenure as faculty at the University of Vermont. In September 2015, he joined the scientific staff at the Liberty Mutual Research Institute for Safety as a Senior Research Scientist, where he continues to investigate the neural mechanisms that underlie human balance, posture and movement towards the development of effective diagnostic and intervention strategies for health conditions such as low back pain. The views expressed in this blog solely represent those of Dr. Jacobs and do not represent the views of Liberty Mutual.
References
1. Hoy D, March L, Brooks P, et al. The global burden of low back pain: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis. 2014;73(6):968-974.
2. Friedly J, Standaert C, Chan L. Epidemiology of spine care: the back pain dilemma. Phys Med Rehabil Clin N Am. 2010;21(4):659-677.
3. Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain. A motor control evaluation of transversus abdominis. Spine (Phila Pa 1976). 1996;21(22):2640-2650.
4. Lomond KV, Jacobs JV, Hitt JR, DeSarno MJ, Bunn JY, Henry SM. Effects of low back pain stabilization or movement system impairment treatments on voluntary postural adjustments: a randomized controlled trial. Spine J. 2015;15(4):596-606.
5. Jacobs JV, Henry SM, Jones SL, Hitt JR, Bunn JY. A history of low back pain associates with altered electromyographic activation patterns in response to perturbations of standing balance. J Neurophysiol. 2011;106(5):2506-2514.
6. MacDonald D, Moseley GL, Hodges PW. People with recurrent low back pain respond differently to trunk loading despite remission from symptoms. Spine (Phila Pa 1976). 2010;35(7):818-824.
7. MacDonald D, Moseley GL, Hodges PW. Why do some patients keep hurting their back? Evidence of ongoing back muscle dysfunction during remission from recurrent back pain. Pain. 2009;142(3):183-188.
8. Jacobs JV, Henry SM, Nagle KJ. People with chronic low back pain exhibit decreased variability in the timing of their anticipatory postural adjustments. Behav Neurosci. 2009;123(2):455-458.
9. Jacobs JV, Henry SM, Nagle KJ. Low back pain associates with altered activity of the cerebral cortex prior to arm movements that require postural adjustment. Clin Neurophysiol. 2010;121(3):431-440.
10. Tsao H, Galea MP, Hodges PW. Reorganization of the motor cortex is associated with postural control deficits in recurrent low back pain. Brain. 2008;131(Pt 8):2161-2171.
11. Jacobs JV, Roy CL, Hitt JR, Popov RE, Henry SM. Neural mechanisms and functional correlates of altered postural responses to perturbed standing balance with chronic low back pain. Society for Neuroscience Annual Meeting 2014; Washington, D. C.
12. Henry SM, Van Dillen LR, Ouellette-Morton RH, et al. Outcomes are not different for patient-matched versus nonmatched treatment in subjects with chronic recurrent low back pain: a randomized clinical trial. Spine J. 2014;14(12):2799-2810.
13. Saragiotto BT, Maher CG, Yamato TP, et al. Motor control exercise for chronic non-specific low-back pain. Cochrane Database Syst Rev. 2016;1:CD012004.
14. Jacobs JV, Lomond KV, Hitt JR, DeSarno MJ, Bunn JY, Henry SM. Effects of low back pain and of stabilization or movement-system-impairment treatments on induced postural responses: A planned secondary analysis of a randomized controlled trial. Man Ther. 2015.
15. Childs JD, Fritz JM, Wu SS, et al. Implications of early and guideline adherent physical therapy for low back pain on utilization and costs. BMC Health Serv Res. 2015;15:150.
16. Swinkels IC, Wimmers RH, Groenewegen PP, van den Bosch WJ, Dekker J, van den Ende CH. What factors explain the number of physical therapy treatment sessions in patients referred with low back pain; a multilevel analysis. BMC Health Serv Res. 2005;5:74.
17. Langevin HM, Sherman KJ. Pathophysiological model for chronic low back pain integrating connective tissue and nervous system mechanisms. Med Hypotheses. 2007;68(1):74-80.
18. Kamper SJ, Apeldoorn AT, Chiarotto A, et al. Multidisciplinary biopsychosocial rehabilitation for chronic low back pain: Cochrane systematic review and meta-analysis. BMJ. 2015;350:h444.