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Dr Ben Seymour, Computational and Biological Learning Lab, Trumpington Street, Cambridge CB2 1PZ

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Center for Information and Neural Networks, National Institute for Information and Communications Technology (NICT), 1-3 Yamadaoka, Suita, Osaka 565-0871, Japan.

bjs49 AT cam.ac.uk / seymour AT cinet.jp

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Tuesday
Aug212012

Is chronic pain a neural connectivity disorder?

Interesting things are happening in the field of chronic pain. Since fMRI emerged  20 years ago, attention has progressed from probing the specific roles of individual brain regions towards the study of the roles of networks of brain areas. Broad connectivity-based approaches emerged from the discovery of discrete functional networks, characterized by strong intra-regional correlated low frequency oscillatory activity, and corresponding anti-correlation with other brain networks: best known is the default mode network (DMN). Many neuroscientists have been rather skeptical about the DMN, since its functional definition (in behavioural terms) is inherently and necessarily vague - it is said to support ‘intrinsic, self-referential information processing’. But the DMN has caught the attention of pain neuroscientists, who are acutely aware that chronic pain is often most apparent at rest, and related phenomenologically to whatever intrinsic, self-referential processing might be, occurring without any obvious ascending nociceptive sensory input. 


Recently, a number of studies have shown that resting-state DMN activity is abnormal in chronic pain patients (or various aetiologies), and the degree of abnormal connectivity has been shown to correlate with pain duration, severity, spontaneous fluctuations, natural resolution and treatment. Last year, Baliki and colleagues showed that this activity relates specifically to abnormally high frequency oscillations (0.12 - 0.20Hz), as measured by fMRI blood-oxygen-level-dependent (BOLD) signal, in the medial prefrontal cortex (mPFC). In the latest installment of what has been a fascinating program of research from this group, they now show that abnormal connectivity between mPFC and nucleus accumbens (NAcc) predicts the future chronification of back pain in patients presenting with a new but short history of pain. Critically, this suggests that abnormal connectivity plays a causal role in chronic pain, and is not merely a downstream marker of chronic pain. This gives what seems to be the clearest neuroscientific insight yet into the pathogenesis of chronic pain in these patients to date. It’s also interesting to speculate on the behavioural significance of this connectivity: these areas are thought to support experienced-based integration and control of reward and pain, so hints at a possible disorder of adaptive motivational control.

Abbendum: We recently discussed the issue of temporal predictability and causality here in our journal club. Whereas the study suggests causality (ie. is consistent with), it doesn't prove it. This is because it might be the case that an as yet unidentified factor both causes back pain chronification and independently, abnormal connectivity. The latter could then be mechanistically (causally) unrelated, albeit correlated, with chronic back pain. 

The cortical rhythms of chronic back pain. Baliki MN, Baria AT, Apkarian AV J Neurosci. 2011 Sep 28; 31(39): 13981-90 PMID: 21957259 DOI: 10.1523/JNEUROSCI.1984-11.2011. This is a modified from one of my www.f1000.com evaluations.

 

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