Research Review By Dr. Brynne Stainsby©


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Date Posted:

November 2019

Study Title:

Neuroplasticity of sensorimotor control in low back pain


Brumagne S, Diers M, Danneels L, Moseley GL & Hodges PW

Author's Affiliations:

Department of Rehabilitation Sciences, Katholieke Universiteit Leuven, Belgium; Department of Psychiatry, Psychotherapy and Preventative Medicine, Landschaftsverband Westfalen-Lippe University Hospital-Ruhr University Bochum, Germany; Department of Physical Therapy and Rehabilitation, Ghent University, Belgium; School of Health Sciences, University of South Australia, Adelaide, Australia; 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 and Sports Physical Therapy 2019; 49(6): 402-414.

Background Information:

Low back pain (LBP) remains a common medical and socioeconomic problem (1). The mechanisms underlying chronic or recurrent nonspecific (mechanical) LBP, in particular, are still poorly understood (2). It has been suggested that impaired sensorimotor control of the spine may result in suboptimal or impaired tissue loading, which may contribute to the development or maintenance of LBP (3-5). It has also been suggested that patients with LBP may experience changes within their central nervous system (CNS) in the processing of pain/nociception, as well as structural (grey matter loss) and functional (reorganization) changes in the sensorimotor cortex.

Neuroplasticity relates to the capacity of the nervous system to undergo functional and structural changes (6), such as when learning new things, generating new thoughts or creating new links between previously unlinked concepts. It takes into account the communication between networks of neuronal and non-neuronal cells in the nervous system, which exert an influence through neuroneural, neuromuscular, neuroimmune and neuroendocrine connections (7). The overall outcome or influence depends on the number of cells involved (neuronal mass), the precision and efficacy of the connections and the weighting of the network by higher order networks within the brain.

Neural networks that process pain and nociception, sensorimotor function, and cognition and emotion are all important in the context of LBP (8, 9). Research on neuroplasticity in relation to LBP considers the domain spectrum (pain/nociceptive processing and sensorimotor control), the time spectrum (short- and long-term changes in function), and the complexity spectrum (such as research on how people seek care).

The goal of this commentary is to provide an overview of neuroplasticity in LBP, in particular. Specifically, it aimed to define neuroplasticity in relation to the processing of pain and nociception in LBP, sensorimotor motor control of the spine and the potential for system adaptation. Additionally, it aimed to outline structural and functional changes as they relate to nonspecific (mechanical) LBP and sensorimotor function. Finally, it intended to address the related clinical implications of neuroplasticity.


Neuroplasticity in Processing of Pain and Nociception:
  • Peripheral sensitization (increased sensitivity of primary nociceptive afferents) has been commonly observed in LBP (10). This may include cutaneous receptors that respond to a range of noxious stimuli and/or deep tissue receptors responding to noxious chemical and mechanical stimuli (11). Central sensitization (increased sensitivity and ascending projections of neural networks in the spinal cord, or impaired descending inhibitory pathways) can enable activation during benign events. These changes have been observed in the short- and long-term and have been shown to be influenced by thoughts about pain, depressive symptoms, and other psychological symptoms. These changes have also been associated with poorer outcomes after an episode of acute LBP (12).
  • Human studies have examined endogenous pain inhibitory systems, conditioned pain modulation (13), hyperalgesia in areas remote to the back (14), receptive fields for spinal nociceptive reflexes (15) and temporal summation (16).
  • It is believed that enhanced sensitivity will affect processing of other sensory signals. For example, peripheral sensitization could lead to a “nociceptive barrage”, which means that the motor system could be triggered by benign thermal, mechanical or chemical stimuli (such as lactic acid).
Neuroplasticity in the Motor System:
  • Research regarding neuroplasticity in patients with LBP has focused mainly on the motor cortex.
  • Using transcranial magnetic stimulation (TMS) over the primary motor cortex, a shift in the stimulus-response profile has been observed in the trunk muscles (17, 18). Changes have also been observed in TMS-associated muscle activity in response to exercise programs in LBP patients.
  • Neuroplasticity can also be observed at the ‘whole-person level’. For example, altered activation patterns have been observed in trunk muscles in anticipation of noxious stimulus (19) or the avoidance of movements or behaviours because they are perceived to be ‘dangerous’.
  • These motor system changes have the potential to alter the biomechanics of the spine, and while they may have short-term protective benefits (20), there may also be long-term, negative consequences (21). It is possible that chronic, suboptimal tissue loading may result in aberrant activation of the nociceptors, chronic pain and/or withdrawal from activity (22).
Functional and Structural Brain Changes and LBP:

Functional and Structural Brain Changes Related to Pain and Nociceptive Processing:
  • Electroencephalography (EEG) studies have shown that patients with chronic LBP have larger cortical responses to noxious stimuli (23).
  • Behavioural studies have demonstrated allodynia and hyperalgesia to stimuli applied to the lumbar spine and modified nociceptive reflexes in patients with LBP (13). Additionally, this work has suggested impaired conditioned pain modulation in patients with acute or chronic LBP, and hypothesized this could indicate impaired descending inhibition as a feature of central sensitization (13).
  • Functional MRI studies show that patients with chronic LBP have lower regional cerebral blood flow in the periaqueductal gray area and a higher increase in activation in the primary and secondary somatosensory cortices and the lateral orbitofrontal cortex in response to noxious stimulus. This may suggest dysfunction in the descending inhibitory system (24).
  • Structural MRI studies have suggested there may be differences in brain regions between patients with chronic LBP and those without. Some studies have shown functional connectivity between areas such as the nucleus accumbens and medial prefrontal cortex (25), and suggest these findings may support the role of the corticolimbic system in the modulation and mediation of pain.
  • Imaging studies have also suggested the pattern of brain activation with chronic pain shifts toward affective/emotional relevant brain areas as LBP persists (26, 27).
Functional and Structural Brain Changes Related to the Motor System:
  • Transcranial magnetic stimulation has been used to study the organization and neural network properties of the regions of the motor cortex associated with control of trunk muscles and found that in patients with chronic LBP, the area of peak excitability of cortical inputs to the deep abdominal muscles is more posterolateral than in those without (18). Additionally, there is a greater overlap of the separate representations of the longer and short muscles of the back, suggesting that the neural networks are becoming less specific to distinct muscles (28, 17).
  • An association has also been identified between the differences in the cortical organization and the duration and severity of pain (28), and the timing of recruitment of muscles in posture (18) and spine movement (29).
  • Studies also suggest evidence of increased responsiveness of corticomotor inputs to the superficial abdominal muscles and decreased inputs to the transversus abdominis, suggesting the possibility of abnormal tissue loading (30).
  • Recent work has found changes in glial cell activity in motor regions of the brain (31), but the significance of this is not yet known.
Functional and Structural Brain Changes Related to the Somatosensory System:
  • MRI studies have demonstrated a relationship between reduced white matter integrity of the superior cerebellar peduncle (a zone of relay for proprioceptive input to higher centres) and reduced utilization of proprioceptive signals from the back for standing postural control (32, 33).
  • Functional MRI (fMRI) of brain regions involved in higher-order processing of muscle spindle input (somatosensory input) reveals less activity in response to back muscle vibration and greater activity in response to ankle muscle vibration in those with LBP (34, 35). Additionally, the sensorimotor resting state network becomes reorganized in patients with LBP (36). These changes may imply impaired capacity to control movement.
  • Patients with recurrent LBP also show greater cortical thickness in the brain regions involved in cognitive regulation of pain, and a correlation between cortical thickening and pain intensity (37). Additionally, a relationship has been observed between impaired sit-to-stand-to-sit performance and deceased cortical thickness of the rostral anterior cingulate cortex (37), and correlations between regional changes in cortical thickness and gray matter volume and clinical tests of movement control and contraction of the transversus abdominis and multifidus (38).
  • EEG studies have demonstrated a greater area of cortical activity in association with postural perturbations from arm movement (39), and the location of the peak primary sensory cortex response to both noxious and non-noxious tactile stimuli to the back is expanded and shifted in patients with chronic LBP (40). Nonpainful pressure applied to lumbar vertebrae has been shown to evoke a smaller secondary somatosensory cortex response in those with LBP (41).
  • fMRI studies using mental imagery of movements have shown reduced brain activation within the left supplementary motor area and the right superior temporal gyrus and sulcus, but diffuse, nonspecific enhancements of functional connectivity between motor imagery-associated networks in patients with chronic LBP (42).
Clinical Implications:

There is evidence of modified nervous system structure in patients with LBP. Although there is literature that implicates sensorimotor processes, this is not the only possible implication, and further research is required, particularly with respect to clinical implications. At this point however, clinicians may assume that if neuroplasticity enables mechanisms that change neural function and maintain pain, it is also possible that neuroplasticity could enable the capacity of the nervous system to resolve or improve LBP.

To illustrate:
  • Training that targets motor skill learning has been shown to normalize the location of primary motor cortex networks involved in activation of trunk muscles (43). This training has also been shown to improve pain and disability in some subgroups of patients with LBP (44).
  • In studies of behavioural extinction training (eliminating pain-related behaviours), preliminary findings suggest it may be possible to normalize the balance between affective and sensory neural networks (45).
  • Studies of sensory discrimination training have identified a disrupted body image in patients with chronic LBP and suggested the need for a treatment that focuses on a normal body image or strengthens body perception (46). If patients with LBP are provided with visual feedback of their own back during experimental application of painful stimulus at a site, the perceived intensity of the stimuli is reduced (47). It also appears that seeing the back during repeated lumbar spine movements reduces movement-evoked pain in the short term (48).
  • Preliminary studies on cognitive training approaches may focus on precisely encoding painful events by reducing the influence of protective neural networks by eliminating danger cues, differentiating safe cues and increasing the influence of the neural networks that encode for task performance (49, 50).

Clinical Application & Conclusions:

There is considerable variation in the clinical presentation of patients affected by LBP (particularly chronic patients!). This commentary presented numerous differences between those with and without LBP, particularly those affected by chronic or recurrent LBP, and suggests clinicians consider these neuroplastic changes when assessing and treating patients. Although it is not clear how best to address these changes within the sensory and motor systems, preliminary studies suggest that attempting to target therapies by integrating cognitive/behavioural therapies and physical interventions may lead to better outcomes for these patients.

It appears unlikely that one intervention targeting the sensorimotor system will be effective for all patients, and this commentary encourages clinicians to identify aberrant pain mechanisms and/or responses and attempt to direct therapy accordingly.

Study Methods:

This was a clinical commentary that did not report methodology.

Study Strengths / Weaknesses:

  • This commentary summarized theoretical constructs related to the neuroplasticity in a well organized, well described manner.
  • The authors review the evidence related to the structural and functional changes in the brain and sensorimotor systems, including many study types.
  • Clinical suggestions for multimodal treatment approaches are provided.
  • 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, and the authors included a number of preliminary studies.
  • There is no comment on the participants or clinical setting of the included studies, thus limiting the external validity of the review.

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