Cortical Changes in Chronic Low Back Pain: Current State of the Art and Implications for Clinical Practice
SOURCE: Man Ther. 2011 (Feb); 16 (1): 15-20
Benedict Martin Wand, Luke Parkitny,
Neil Edward O’Connell, Hannu Luomajoki,
James Henry McAuley, Michael Thacker,
G. Lorimer Moseley
School of Health Sciences,
The University of Notre Dame Australia,
Fremantle, WA, Australia
There is increasing evidence that chronic pain problems are characterised by alterations in brain structure and function. Chronic back pain is no exception. There is a growing sentiment, with accompanying theory, that these brain changes contribute to chronic back pain, although empirical support is lacking. This paper reviews the structural and functional changes of the brain that have been observed in people with chronic back pain. We cast light on the clinical implications of these changes and the possibilities for new treatments but we also advise caution against concluding their efficacy in the absence of solid evidence to this effect.
From the Full-Text Article:
Chronic musculoskeletal pain is almost by definition a problem for which previous treatment has been unsuccessful. The clinical stories of patients with problems such as chronic low back pain (CLBP), fibromyalgia, and late whiplash associated disorder are usually ones of confusing and conflicting diagnoses and multiple treatment failures. Diagnosis and treatment has traditionally focused on what Robinson and Apkarian (2009) have called ‘end organ dysfunction’. That is, clinicians and researchers have looked to structural and functional abnormalities within the musculoskeletal system for a driver of the clinical condition and treatment has sought to normalise peripheral pathology and mechanics (stretch it, splint it, remove it, anaesthetise or denervate it). In general terms the ‘end organ dysfunction’ approach might be considered to have proven unsuccessful for these conditions (see for e.g. van Tulder et al., 2006a; van Tulder et al., 2006b). Neuroimaging studies have revealed numerous structural and functional changes within the brains of people with chronic musculoskeletal pain and there is growing opinion that these changes may contribute to the development and maintenance of the chronic pain state (Apkarian et al., 2009; Tracey and Bushnell, 2009). In this model of chronic pain the brain is seen as an explicit target for treatment and several treatment strategies have been developed and modified to fit this aim. Although there are data available on a range of chronic painful disorders, we will focus here on the cortical changes observed in patients with CLBP and the possible clinical implications for this population.
Brain changes in people with CLBP
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Advances in neuroimaging technology have led to rapid increases in our understanding of the human brain in health and disease. Methodologies such as functional magnetic resonance imaging, voxel-based morphometry, magnetic resonance spectroscopy, magnetoencephalography and electroencephalography (EEG) give us insight into multiple dimensions of the brain state. Changes can be broadly categorised as neurochemical, structural or functional.
Several studies have compared the neurochemical profile of healthy controls with those of CLBP patients. Significant changes (some markers increase, others decrease) in the neurochemical profile in the dorsolateral prefrontal cortex (DLPFC), thalamus and orbitofrontal cortex have been observed in people with CLBP and, by and large, the magnitude of the shift from normative data increases as the duration and intensity of pain increase (Grachev et al., 2000). Further, co-morbid anxiety (Grachev et al., 2001; Grachev et al., 2002) and depression (Grachev et al., 2003) seem to be associated with larger effects. Magnetic spectroscopy data suggest that the magnitude of shifts in neurochemical profile in anterior cingulate cortex, thalamus and prefrontal cortex can differentiate between those with CLBP and healthy controls (Siddall et al., 2006). Similar changes have been reported from studies involving people with neurodegenerative conditions such as Alzheimer’s disease and multiple sclerosis, which has led to the proposal of a relationship between chronic pain and neuronal loss and degeneration (Grachev et al., 2000). Notably, although there is clear evidence that brain neurochemistry is awry in people with CLBP, there is no evidence to suggest that neurochemical changes cause CLBP. In fact, there is reasonable argument that CLBP may cause neurochemical changes — certainly the neuroanatomical distribution of the changes is consistent with the established ‘pain matrix’ and exaggerated and ongoing neural activity can lead to shifts in neurochemistry consistent with those observed. However, the possibility that these changes are at once a result and cause of ongoing pain remains. Clearly, longitudinal data are required.