BackCare

The brain in chronic low back pain

2010 Author: Benedict M Wand, Neil E O'Connell, G Lorimer Moseley

The overarching message that arises from the clinical trials of treatments for chronic low back pain is that current interventions provide only small short term benefits when compared to sham treatment or no treatment.

The brain in chronic low back pain

A brief stroll through the evidence

The overarching message that arises from the clinical trials of treatments for chronic low back pain (CLBP) is that current interventions provide only small short term benefits when compared to sham treatment or no treatment, but offer little benefit when compared to each other.46,9 Regardless of the type of intervention it seems that patients still exhibit significant levels of pain and disability at the completion of treatment.6 There are numerous potential reasons why the results of clinical trials have been so disappointing.4 One perspective we have explored previously is that the primary focus of most current therapies on structural or functional impairments in the spine may to some extent be misdirected.47 There is growing evidence of extensive cortical reorganisation 11,24 as well as biochemical 44,18 and structural alterations 2,42,8 in the brains of people with CLBP. It is possible that these changes may contribute significantly to the problem and that treatment may need to be explicitly directed to the brain.

While the clinical implications of these brain changes on the CLBP experience are far from being fully resolved1 there are three areas of consideration which may be of particular importance to patients and those managing this condition. Firstly, the observed changes may contribute to enhanced nociceptive responses. Decreases in gray matter in areas of the brain that influence pain suppression such as the midbrain42 and dorsolateral prefrontal cortex (DLPFC)2, 42 could lead to a prolonged state of abnormal nociceptive modulation27.15 noted lowered pain thresholds to mechanical stimulation of the thumb nail in patients with CLBP and Clauw et al.10 found significant associations between clinical status of CLBP patients and tenderness at remote sites. The findings of sensitivity changes well outside the lumbar spine suggest a central nervous system origin of these changes. Importantly, it appears that CLBP patients have significantly lower increase in blood flow to the periaqueduactal gray (an important area for descending modulatory control) than normals when exposed to the same level of painful stimulus14 and distressed CLBP patients have less engagement of cortical areas thought to be involved in modulating sensory input than non distressed CLBP patients when exposed to intense vibratory stimulation of the back.24

Secondly, psychological features of CLBP such as decision making pertaining to the pain experience, cognitive appraisal of pain and disorders of mood are likely to be effected by the demonstrated cortical changes. Apkarian et al.3 found CLBP patients to be impaired on a task designed to assess emotional decision making, others have noted significant decrements in memory, language skills and mental flexibility in older CLBP patients49 and the ability to shift attention away from threatening stimulus seems to be impaired in the CLBP population.40 It is also possible that the observed degeneration within the DLPFC may contribute directly to greater catastrophic interpretation of pain. The DLPFC seems to be important in emotional disengagement from pain25.41 and there is evidence that DLPFC activity is negatively correlated with catastrophic thinking about pain.43 When CLBP patients and healthy controls are exposed to a stimulus to induce the same intensity of pain, the unpleasantness associated with this same intensity is significantly greater in patients, most notably at high intensities of pain.23 CLBP is frequently associated with depressive symptoms30 and distress/depressive mood is cited as an important psychological factor in the transition from acute to chronic LBP.38 There is significant overlap in the neural circuitries of the brain in both depression and CLBP,'9 notably DLPFC degeneration seems to be a feature of both conditions.2 42.19. 37

Finally, the reorganisation"24 and degeneration42 evident in the primary somatosensory cortex (S1) of CLBP patients may represent a disruption in the central representation of the back, potentially producing a distortion in body perception. There is growing data that CLBP patients demonstrate clinical findings consistent with a distortion of body image. Patients exhibit deficits in proprioception16.7,36 have poorer tactile acuity than healthy controls,35,22,48 are impaired at recognising letters that are drawn on their back48 and find it difficult to delineate the outline of their back, consistently representing the back to be smaller than it really is.35 Furthermore, it is possible that the varied alterations in muscle recruitment pattems observed in CLBP patients21 may be a manifestation of poor awareness and perception of the lumbar spine, or the result of the anticipation of pain,31 an idea supported by the close association between tactile acuity and performance on motor control tests.22

The role of distorted body perception in long standing pain problems has received considerable attention recently,26,45,28 It has been proposed that pain may be generated within the motor control system when body perception is disturbed. Harris20 suggests that altered cortical representation of somatic input may falsely signal incongruence between motor intention and actual movement. If there is conflict between motor output and sensory feedback, it is hypothesised that pain is produced as a waming signal to alert the individual to abnormalities within information processing.29 Treatment approaches that attempt to restore integration of somatosensory and motor processing within the brain appear to be successful in managing other chronic pain problems such as complex regional pain syndrome32,33,34 and phantom limb pain.34,12

The data on brain dysfunction is cross-sectional and as such no firm conclusions may be drawn on whether it plays a causal role in either the onset or maintenance of the problem. Indeed it is plausible that these changes might represent epiphenomena. At the time of writing a study in Germany has demonstrated a reversal of similar brain changes seen in patients with osteoarthritis of the hip following joint replacement surgery, raising the possibility that the changes may be the consequence rather than the cause of pain.39 Of course, in the spirit of such an article as this, we have been speculative, although not outrageous, in a line of thought that emphasises the brain in chronic pain, and targeting the brain in treatment for chronic pain. We are currently investigating a number of possible avenues from approaches such as integrating those discussed above that attempt to restore normal sensorimotor function, to testing novel treatments such as non-invasive brain stimulation (in a project that is generously funded by BackCare and the Rosetrees Trust). The results of these studies should help us along the path to understanding whether the brain might be a legitimate target for non-pharmacological treatment in this difficult condition.

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