Chronic pain disrupts the reward circuitry in multiple sclerosisDaniela Seixas, Jacqueline Palace and Irene Tracey. European Journal of Neuroscience.
AbstractPain commonly affects multiple sclerosis (MS) patients, and has the potential to become chronic and burden an already damaged central nervous system. Imaging studies are providing insights into brain restructuring associated with chronic pain and different chronic pain conditions seem to evoke distinct plasticity patterns. Our objective was to study the structural and functional brain changes of chronic neuropathic pain of MS. Employing structural and resting functional magnetic resonance imaging we compared MS patients with chronic central pain with MS patients without pain matched with respect to age, gender, subtype and duration of MS and disability. Mean duration of pain was 7.6 years. Comparing the pain and no-pain groups, brain functional default-mode network differences were found. There was decreased coactivation in the caudate nucleus and nucleus accumbens bilaterally. Also, for the relapsing-remitting subgroup of patients, grey matter thickness changes predominated in the pain group in the mesial region of the temporal lobes, caudate, putamen, thalami and the fronto-parietal cortex; in the group without pain, changes predominated in the frontopolar and orbitofrontal cortices and in the occipital areas. A dysfunction in the reward system in chronic pain of MS was found, particularly in the brain areas involved in its motivational aspects, as such probably reflecting the maladaptive physiology of chronic pain, and possibly the signature of pain in MS, in a disease where reward impairment seems to be already one of its features.
Wile E. Cyote's antics to capture the road runner also end in pain.
Is pain one of nature's cruel jokes, a fail safe against stupidity, or is it a sign of frailty of an organic system? I'll let you decide. Our untimely departure from the blogosphere has caused our readers significant pain, and I would like to sincerely apologise for this. Having read through your comments, I see now that the blog is greater than the sum of its parts.
For those who suffer from MS related pain (whether it be caused by stiffness/spasticity or nerve pain/neuropathic pain), the findings from this commentary should interest you.
Pain control is multibillion dollar franchise, and yet our understanding of it is small. Firstly, it is important to understand that the hardwiring of you brain changes with pain over time, and this varies based on the nature of the pain. Part of this change is visible in the brain resting-state networks (RSNs); the brain regions that are working during wakefulness when the brain is resting (similar to your computer CPU which is churning away in the background even though you're not using it!). Secondly, changes here may also affect the function of the brain region concerned.
Here, the authors studied MS patients with pain for 7.6y on average. Using imaging, they studied the restructuring of the brain in MS in those with pain and without pain. They found changes between the two groups in the RSN network called the default-mode network (DMN). The DMN is usually silent during demanding tasks (for example, running), but is involved in cognition (memory, intelligence, planning for the future, and social interactions). In the DMN, in those experiencing chronic pain, there was reduced activation of brain regions (the caudate nucleus and nucleus accumbens; see Figure 1) that are linked to motivational ('wanting') aspects of behaviour, including reward, suggesting that this is impaired.
Therefore, even if different types of chronic pain are associated with distinct anatomical 'brain signatures', in MS at least both pain and reward seem to share the same neuroanatomical pathways. The question remains whether being on the receiving end of a reward can ameliorate pain?