Research Review By Dr. Brynne Stainsby©

Audio:

Download MP3

Date Posted:

April 2020

Study Title:

Motor control changes in low back pain: Divergence in presentations and mechanisms

Authors:

van Dieën JH, Reeves NP, Kawchuk G, Van Dillen LR & Hodges PW

Author's Affiliations:

Department of Human Movement Sciences, Vrije Universiteit Amsterdam and Amsterdam Movement Sciences, Amsterdam, the Netherlands; Center for Orthopedic Research, Michigan State University, Lansing, Ml, USA; Osteopathic Surgical Specialties, Michigan State University, USA; Sumaq Life LLC, East Lansing, Ml, USA; Physical Therapy, Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, Canada; Physical Therapy and Department of Orthopaedic Surgery, Washington University School of Medicine, St Louis, MO, USA; Clinical Centre for Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane, Australia.

Publication Information:

Journal of Orthopaedic & Sports Physical Therapy 2019; 49(6): 370-379.

Background Information:

It has frequently been observed that those with low back pain (LBP) move differently than those without; however, the mechanism of the motor control patterns behind these changes is still not well understood. Motor control is defined as the way in which the nervous system controls posture and movement, including all of the motor, sensory and integrative processes. The quality of the process can be assessed by how well a posture is maintained or a movement is achieved. For example, trunk posture is continuously perturbed by neuromuscular noise, concurrent motor tasks and external mechanical (physical) perturbations (1, 2). Strategies such as anticipatory/feedforward control (3, 4), tonic muscle activity (5-7) and feedback mechanisms based on proprioceptive, visual, tactile and vestibular information (8-11) may be implemented to deal with these perturbations. It is generally believed that those with LBP present with changes in motor control, though the findings thus far are largely inconclusive.

The goals of this commentary are to summarize the current state of the literature regarding the changes in motor control in those with LBP, to propose an interpretation of the variation in motor control changes observed, and to present the clinical implications and considerations for future research.

Summary:

Motor Control Differences Between individuals with and without Low Back Pain (LBP):
  • With regards to LBP, motor control has been studied not just at the level of the neural structures and processes involved (12-15), but also at the level of the outcomes (that is, the pattern of the trunk muscle activity and movements). Typically, studies of motor control have examined control of the trunk in steady state posture and movement, control of trunk posture and movement when challenged by predictable perturbations (anticipatory/feedforward control) and control of trunk posture and movement with unpredictable perturbations (reactive/feedback control).
  • Studies are inconclusive regarding the effects on muscle activity as a result of injury, nociception or fear of potential pain (16-18). For example, when studying anticipatory activation of trunk muscles prior to limb movement, some studies have found late activation (19-23), some have found early activation (24, 25) and another, no difference (26) when comparing those with LBP to healthy controls.
  • There is also evidence of changes in the structure/morphology of trunk muscles in those with LBP, suggesting the transition from type I to type II muscle fibres (27, 28), atrophy (29-31) and fatty infiltration (32) of the multifidus could affect motor control.
  • Though studies have not demonstrated consistent or clear differences in spine and pelvis alignment between those with and without LBP, those with LBP often display larger postural sway (33), perhaps suggesting reduced balance.
  • Those with LBP typically perform movements more slowly (34), and have been shown to to have more variable trunk movements during gait (35, 36), reaching (37) and repetitive trunk bending (38).
Divergence in Motor Control Features in LBP:

Overall, the literature regarding motor control in LBP is inconsistent. This could be due to a number of factors, including:
  • Methodological variations and small study samples in existing studies.
  • The heterogeneity of LBP as individuals (not to mention the variance in the motor control adaptations – there could be a spectrum of deviations which could affect loading in lumbar tissues).
  • Motor control changes may not be explained by a single factor (ex. changes could be a response to injury or a consequence of ongoing pain, or a purposeful strategy for protection). Explained in a different way – motor control changes may be a cause or consequence of LBP.
  • Two patterns of adaptation have been proposed – one of ‘tight control’ and one of ‘loose control’ – both are outlined below.
Divergent Motor Control Pattern – Tight Control:
  • One pattern of motor control changes has been described as ‘tight control’, which is believed to be the result of increased muscle co-contraction, reflex gains and/or attention to motor control, and likely results in increased tissue loading (39).
  • It is believed that tight control would increase the ‘safety margin’ for control of movement, such that as trunk stiffness is increased, a greater force would be required to perturb the spine.
  • While this approach appears to be protective, it may have negative consequences, such as increased spinal loading. This alone could have varied impact depending on an individual’s mechanical tissue tolerance, level of central sensitization, and so on.
  • Those with LBP have been found to expose the spine to higher loads after perturbation, particularly after less heavy tasks (40). This could result in a cumulative increase in loading, which may increase the risk of injury or pain.
  • Based on animal models, it is also possible that sustained muscle contraction may limit fluid inflow into discs in patients with LBP and impair recovery (41, 42).
  • It is also possible that sustained contraction may lead to fatigue and discomfort of other muscles (43). It may also impair (re)learning of ‘normal’ motor patterns based on decreased variability of trunk muscle recruitment.
  • Although increased stiffness appears to be a helpful strategy to counteract small disturbances, it may compromise an individual’s ability to deal with a larger perturbation (44) or maintain balance on an unstable surface (45, 46).
Divergent Motor Control Pattern – Loose Control:
  • Another possible pattern has been described as ‘loose control’, which is characterized by reduced muscle excitability and avoids high tissue loading.
  • Given the lumbar spine requires control by the surrounding musculature and ligaments, motor control over the spine would be reduced by inhibition of muscle activity or delay in responses to perturbations, resulting in larger amplitude and faster movements, with more variability between repeated performance of the same task.
  • In this pattern, lumbar segments may be compromised, and result in larger tissue strain (47-49).
  • As larger displacements after trunk perturbation have been predictively associated with LBP, it is possible ‘loose control’ patterns may also be a causal factor for LBP.

Clinical Application & Conclusions:

While the literature suggests there may be differences in motor control between those with and without LBP, it demonstrates that not all with LBP demonstrate motor control changes, and not all present in the same way. It is important to remember that individuals affected by LBP are a highly heterogeneous group. For example, as those who have high fear of pain are more likely to stiffen their trunk in anticipation of perturbation than those with LBP with low fear of pain. It is important to recognize that there may be multiple mechanisms contributing to altered motor control, and may also be dependent on the individual and the context.

Injury and nociceptive input are possible stimuli to motor control, and may also be the result of altered motor control. When working with patients, it is important to consider that a change may have occurred as a purposeful strategy to protect from (further) injury, and this may impact a patient’s response to care.

Considering the negative consequences of a patient’s control pattern may help to direct strategies. For example, in those who demonstrate tight control patterns, aiming to reduce muscular excitability and co-contraction, and increasing movement and movement variations (50) may be very helpful, while those who demonstrate loose control may require strategies to increase motor control (50). It is important to recall that future research is required to validate assessment tools and therapeutic strategies in this domain, and clinicians should consider short trials of care with careful explanations to patients in order to ensure that goals and expectations are monitored and met.

Study Methods:

This was a clinical commentary and thus, did not report methodology.

Study Strengths / Weaknesses:

Strengths:
  • This commentary summarizes theoretical constructs related to the motor control changes in LBP in a well organized, well described manner.
  • The authors carefully identify the limitations in the literature and caution readers from drawing unsupported conclusions.
  • The authors also helpfully identify the fact that this field literature is characterized by inconsistency in findings, and rightfully suggest that differences in methodology may account for some of the inconsistencies, however, the variation between patients with LBP must also be considered.
  • Clinical suggestions for multimodal treatment approaches are provided.
Weaknesses:
  • The greatest weakness of this study is the lack of methodology reported. Without this, we cannot be confident that the conclusions were not subject to high risk of bias.
  • While this article provides a summary of the literature included, there is no assessment of the methodology or research quality. The authors included a number of preliminary and animal studies, and the majority of the studies are cross-sectional in nature, which do not allow us to identify if the change in motor control cause LBP, or vice versa.
  • There is no comment on the participants or clinical setting of the included studies, thus limiting the external validity of the review.

Additional References:

  1. Hodges PW, Gandevia SC, Richardson CA. Contractions of specific abdominal muscles in postural tasks are affected by respiratory maneuvers. J Appl Physiol 1997; 83: 753-760.
  2. Hu H, Meijer OG, Hodges PW, et al. Control of the lateral abdominal muscles during walking. Hum Mov Sci 2012; 31: 880-896.
  3. Hodges PW, Richardson CA. Contraction of the abdominal muscles associated with movement of the lower limb. Phys Ther 1997; 77: 132-142; discussion 142-144.
  4. van Dieen JH, de Looze MP. Directionality of anticipatory activation of trunk muscles in a lifting task depends on load knowledge. Exp Brain Res 1999; 128: 397-404.
  5. Cholewicki J, Panjabi MM, Khachatryan A. Stabilizing function of trunk flexor-extensor muscles around a neutral spine posture. Spine 1997; 22: 2207-2212.
  6. Hodges PW, Gandevia SC. Changes in intraabdominal pressure during postural and respiratory activation of the human diaphragm. J Appl Physiol 2000; 89: 967-976.
  7. van Dieen JH, Kingma I, van der Bug P. Evidence for a role of antagonistic cocontraction in controlling trunk stiffness during lifting. J Biomech 2003; 36: 1829-1836.
  8. Andreopoulou G, Maaswinkel E, Cofre Lizama LE, et al. Effects of support surface stability on feedback control of trunk posture. Exp Brain Res 2015; 233: 1079-1087.
  9. Goodworth AD, Peterka RJ. Contribution of sensorimotor integration to spinal stabilization in humans. J Neurophysiol 2009; 102: 496-512.
  10. Maaswinkel E, Veeger HE, van Dieen JH. Interactions of touch feedback with muscle vibration and galvanic vestibular stimulation in the control of trunk posture. Gait Posture 2014; 39: 745-749.
  11. Moseley GL, Hodges PW, Gandevia SC. External perturbation of the trunk in standing humans differentially activates components of the medial back muscles J Physiol 2003; 547: 581-587.
  12. 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: 431-440.
  13. Tsao H, Danneels LA, Hodges PW. ISSLS Prize winner: smudging the motor brain in young adults with recurrent low back pain. Spine 2011; 36: 1721-1727.
  14. Tsao H, Galea MR Hodges PW. Reorganization of the motor cortex is associated with postural control deficits in recurrent low back pain. Brain. 2008; 131: 2161-2171.
  15. Wand BM, Parkitny L, O'Connell NE, et al. Cortical changes in chronic low back pain: current state of the art and implications for clinical practice. Man Ther 2011; 16: 15-20.
  16. Hodges PW, Tucker K. Moving differently in pain: a new theory to explain the adaptation to pain. Pain 2011; 152: S90-S98.
  17. Moseley GL, Nicholas MK, Hodges PW. Does anticipation of back pain predispose to back trouble? Brain 2004; 127: 2339-2347.
  18. van der Hulst M, Vollenbroek-Hutten MM, Schreurs KM et al. Relationships between coping strategies and lumbar muscle activity in subjects with chronic low back pain. Eur J Pain 2010; 14: 640-647.
  19. Hodges PW, Richardson CA. Altered trunk muscle recruitment in people with low back pain with upper limb movement at different speeds. Arch Phys Med Rehabil 1999; 80: 1005-1012.
  20. Hodges PW, Richardson CA. Delayed postural contraction of transversus abdominis in low back pain associated with movement of the lower limb. J Spinal Disord 1998; 11: 46-56.
  21. Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain. A motor control evaluation of transversus abdominis. Spine 1996; 21: 2640-2650.
  22. 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: 183-188.
  23. Masse-Alarie H, Flamand VH, Moffet FI, et al. Corticomotor control of deep abdominal muscles in chronic low back pain and anticipatory postural adjustments. Exp Brain Res 2012; 218: 99-109.
  24. Gubler D, Mannion AF, Schenk R et al. Ultrasound tissue Doppler imaging reveals no delay in abdominal muscle feed-forward activity during rapid arm movements in patients with chronic low back pain. Spine 2010; 35: 1506-1513.
  25. Moseley GL, Hodges PW. Reduced variability of postural strategy prevents normalization of motor changes induced by back pain: a risk factor for chronic trouble? Behav Neurosci 2006; 120: 474-476.
  26. Masse-Alarie H, Beaulieu LD, Preuss R, Schneider C. Task-specificity of bilateral anticipatory activation of the deep abdominal muscles in healthy and chronic low back pain populations. Gait Posture 2015; 41: 440-447.
  27. Jorgensen K. Human trunk extensor muscles physiology and ergonomics. Acta Physiol Scand Suppl 1997; 637: 1-58.
  28. Mannion AF Weber BR, Dvorak J, et al. Fibre type characteristics of the lumbar paraspinal muscles in normal healthy subjects and in patients with low back pain. J Orthop Res 1997; 15: 881-887.
  29. Hides J, Gilmore C, Stanton W, Bohlscheid E. Multifidus size and symmetry among chronic LBP and healthy asymptomatic subjects. Man Ther 2008; 13: 43-49.
  30. Hides JA, Stokes MJ, Saide M et al. Evidence of lumbar multifidus muscle wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine 1994; 19: 165-172.
  31. Hodges PW, Coppieters MW, MacDonald D et al. New insight into motor adaptation to pain revealed by a combination of modelling and empirical approaches. Eur J Pain 2013; 17: 1138-1146.
  32. D’hooge R, Cagnie B, Crombez G et al. Increased intramuscular fatty infiltration without differences in lumbar muscle cross-sectional area during remission of unilateral recurrent low back pain. Man Ther 2012; 17: 584-588.
  33. Mazaheri M, Coenen P, Parnianpour M et al. Low back pain and postural sway during quiet standing with and without sensory manipulation: a systematic review. Gait Posture 2013; 37:12-22.
  34. Mazaheri M, Coenen P, Parnianpour M et al. Low back pain and postural sway during quiet standing with and without sensory manipulation: a systematic review. Gait Posture 2013; 37:12-22.
  35. Laird RA, Gilbert J, Kent P, Keating JL. Comparing lumbo-pelvic kinematics in people with and without back pain: a systematic review and meta-analysis. BMC Musculoskelet Disord 2014: 15: 229.
  36. Lamoth CJ, Meijer OG, Daffertshofer A et al. Effects of chronic low back pain on trunk coordination and back muscle activity during walking: changes in motor control. Eur Spine J 2006; 15: 23-40.
  37. Vogt L, Pfeifer K, Portscher M, Banzer W. Influences of nonspecific low back pain on three-dimensional lumbar spine kinematics in locomotion. Spine 2001; 26: 1910-1919.
  38. Silfies SP, Bhattacharya A, Biely S et al. Trunk control during standing reach: a dynamical system analysis of movement strategies in patients with mechanical low back pain. Gait Posture 2009; 29: 370-376.
  39. Bauer CM, Rast FM, Ernst MJ, et al. Pain intensity attenuates movement control of the lumbar spine in low back pain. J Electromyogr Kinesiol 2015; 25: 919-927.
  40. van Diehn JH, Cholewicki J, Radebold A. Trunk muscle recruitment patterns in patients with low back pain enhance the stability of the lumbar spine. Spine 2003; 28: 834-841.
  41. Marras WS, Ferguson SA, Burr D et al. Functional impairment as a predictor of spine loading. Spine 2005; 30: 729-737.
  42. Healey EL, Fowler NE, Burden AM et al. The influence of different unloading positions upon stature recovery and paraspinal muscle activity. Clin Biomech 2005; 20: 365-371.
  43. Healey EL, Fowler NE, Burden AM et al. Raised paraspinal muscle activity reduces rate of stature recovery after loaded exercise in individuals with chronic low back pain. Arch Phys Med Rehabil 2005; 86: 710-715.
  44. Visser B, van Dieen JH. Pathophysiology of upper extremity muscle disorders. J Electromyogr Kinesiol 2006; 16: 1-16.
  45. Mok NW, Brauer SG, Hodges PW. Hip strategy for balance control in quiet standing is reduced in people with low back pain. Spine 2004; 29: E107-E112.
  46. Reeves NP, Everding VQ, Cholewicki J et al. The effects of trunk stiffness on postural control during unstable seated balance. Exp Brain Res 2006; 174: 694-700.
  47. Panjabi MM. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disord 1992; 5: 383-389; discussion 397.
  48. Panjabi MM. The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis. J Spinal Disord 1992; 5: 390-396; discussion 397.
  49. van Dieen JH, Kingma I. Spine function and low back pain: interactions of active and passive structures. In: Hodges PW, Cholewicki J, van Dieen JH, eds. Spinal Control: The Rehabilitation of Back Pain. State of the Art and Science. Edinburgh, UK: Elsevier/Churchill Livingstone; 2013: 41-58.
  50. van Dieen JH, Kingma I. Spine function and low back pain: interactions of active and passive structures. In: Hodges PW, Cholewicki J, van Dieen JH, eds. Spinal Control: The Rehabilitation of Back Pain. State of the Art and Science. Edinburgh, UK: Elsevier/Churchill Livingstone; 2013: 41-58.
  51. Hodges PW, van Dillen L, McGill S et al. Integrated clinical approach to motor control interventions in low back and pelvic pain. In: Hodges PW, Cholewicki J, van Dieen JH, eds. Spinal Control: The Rehabilitation of Back Pain. State of the Art and Science. Edinburgh, UK: Elsevier/Churchill Livingstone; 2013: 243-310.