Abstract
Functional magnetic resonance imaging studies (fMRI) have transformed our understanding of central processing of evoked pain but the typically used block and event-related designs are not best suited to the study of ongoing pain. Here we used arterial spin labelling (ASL) for cerebral blood flow mapping to characterise the neural correlates of perceived intensity of osteoarthritis (OA) pain and its interrelation with negative affect. Twenty-six patients with painful knee OA and twenty-seven healthy controls underwent pain phenotyping and ASL MRI at 3T. Intensity of OA pain correlated positively with blood flow in the anterior mid-cingulate cortex (aMCC), subgenual cingulate cortex (sgACC), bilateral hippocampi, bilateral amygdala, left central operculum, mid-insula, putamen and the brainstem. Additional control for trait anxiety scores reduced the pain-CBF association to the aMCC, whilst pain catastrophizing scores only explained some of the limbic correlations. In conclusion, we found that neural correlates of reported intensity of ongoing chronic pain intensity mapped to limbic-affective circuits, and that the association pattern apart from aMCC was explained by trait anxiety thus highlighting the importance of aversiveness in the experience of clinical pain.
Highlights
Chronic pain affects approximately 11% of the population, with poor outcomes for current treatment (Harstall and O., 2003)
We studied the neural correlates of ongoing pain intensity in persistent knee OA pain using whole-brain Cerebral blood flow (CBF) mapping, and present evidence for limbic, paralimbic and subcortical networks underpinning chronic pain perception in line with a strong affective, largely aversive dimension of the clinical pain experience
We found that perceived intensity of OA pain in subjects with chronic painful knee OA was associated with a pattern of increased CBF involving nociceptive,limbic networks and subcortical regions
Summary
Chronic pain affects approximately 11% of the population, with poor outcomes for current treatment (Harstall and O., 2003). Previous studies of chronic OA pain have suggested that the pain experience is the result of constant or aberrant nociceptive drive due to joint tissue damage or inflammation (Mease et al, 2011) but is inclusive of psychological factors such as anxiety and depression (Marks, 2009; Axford et al, 2010; Edwards et al, 2011). Neuroimaging studies have found functional and structural brain changes in chronic pain patients thought to reflect brain plasticity and potentially providing targets for pharmacological and psychological therapies (Davis and Moayedi, 2013). Despite the increasing interest in neuroimaging studies in chronic pain, findings are often inconsistent between different pain
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