Recently we saw that some people appear to be sitting ducks for chronic pain.  Their brains have apparently reached a state, unbeknownst to them, where all that’s needed for a chronic pain state to emerge is a triggering event such as an injury. That triggering even starts a process which changes both the grey matter (neurons) and the connections between different parts of their brain


The brain – what a mystery it is. Why would the brain put the body into a chronic pain state?

In particular the strength of the connection between two parts of the brain, the prefrontal cortex situated at the top of the brain and the nucleus accumbens situated lower in the brain, played a key role in determining who would experience chronic pain and who would not.  The stronger the connection between those two parts of the brain, the more pain was felt.

As we continue our ‘Stress and the Emotions’ series we check out a study that used a different technique to uncover how the brain of a person in chronic pain changes over time in chronic pain.

Brain. 2013 Sep;136(Pt 9):2751-68. doi: 10.1093/brain/awt211. Shape shifting pain: chronification of back pain shifts brain representation from nociceptive to emotional circuits. Hashmi JA1, Baliki MNHuang LBaria ATTorbey SHermann KMSchnitzer TJApkarian AV.

First they used an fMRI to examine brain activity in people who’d just come down with low back pain and those who’d had it for greater than 10 years. They used a technique, common in these types of studies, that examined the effect different words have on brain patterns.  Then they followed the people with recent back pain for a year and examined how the brains of those who got better differed from those who remained in pain.


“We can conclude that perception of back pain in subjects living with the condition for greater than 10 years mainly engages the emotion and reward circuitry.” Authors

Using an approach which involved developing ‘probabilistic maps of brain circuitry for pain, emotions and rewards’, these researchers found that an immense shift in brain functioning occurs in people with chronic pain.

In the early stages of pain the portions of the brain focused on pain and reward are dominant.  This makes sense.  Pain, after all, is produced in order to shift our behavior in one way or another.  Walking on a broken leg induces pain.  Staying off that leg induces healing (reward).

shift key

After a period of time with chronic pain the brain starts processing pain signals through it’s emotional networks.

As pain becomes chronic, however, the activity of the circuits focused on pain diminishes while emotion-based brain circuits involving the amygdala and basal ganglia grow in strength.  The shift appears to be quite significant with the authors reporting that ‘no brain regions‘ in the two groups had similar amounts of activity.

“Brain activity related to back pain shifts from the insula, anterior cingulate cortex, thalamus, and basal ganglia to medial prefrontal cortex, amygdala and basal ganglia.” Authors

The authors note that the ‘perception of pain’ has changed dramatically.  While people in the early stages of pain process pain signals through the brains pain and reward pain circuits, people in chronic pain process pain signals through brain circuits identified with emotions and reward.

The New Normal

“Within the first year, the brain carves a chronic pain state.” Authors

The new normal - a state of chronic  pain

The new normal – a state of chronic pain

This brain circuit reorganization takes place over a year and then remains stable.  People with back pain for over 10 years demonstrate the same brain circuitry as those who’ve been in chronic pain for a year.   That fits the clinical experiences suggesting that pain which doesn’t get resolved in three months to a year is more likely to be long lasting.

(It should be noted, however, that the time period for the transition from acute (resolvable) pain and chronic (difficult to resolve pain) varies between pain conditions.  This study refers to low back pain; other types of pain may have different time periods.

The Set Up

“We postulate that the predisposing characteristics of mesolimbic circuitry at time of pain inception initiates a cascade of emotionally-driven learning events that effectually reorganize the brain into a chronic pain state with distinct functional, anatomical, and resting state properties.”

Remarkably, this transition from acute to chronic pain, and from pain focused brain circuitry to emotion focused brain circuitry, can all be predicted by the strength of the connection between two parts of the brain called the prefrontal cortex and the nucleus accumbens.

Mood Disorders Do Not Predict Shift

Given the general understanding that anxiety and depression exacerbate pain, the authors expected this shift in brain circuitry would be more prominent in people with anxiety and depression, but neither of these mood disorders affected the shift at all.  The shift was predicated on the strength of the prefrontal cortex-nucleus accumbens connection, not the presence of anxiety or depression.  The stronger the connections between those two parts of the brain, the more likely someone was going to transition from acute to chronic pain.

Prefrontal Cortex – Nucleus Accumbens Circuit

The prefrontal cortex carries out ‘executive functions’ such as working toward a defined goal, predicting outcomes, and managing expectations.  People with poor executive function (such as people with ME/CFS) have more difficulty planning complex activities and decision-making.  The nucleus accumbens plays important role in how much pleasure, fear, aggression and impulsivity we experience.

The idea that pain signal processing has moved from the sensory pain circuits in acute (short-lived) pain to brain circuits involved in emotions and reward is obviously an important one.  Making sense of what this means, however, is difficult given the technical language used in this text.  (At one point they end up quoting the philosopher Ludwig Wittgenstein.)

Emotionally Driven Learning Events?

“Predisposing characteristics of mesolimbic circuitry at time of pain inception initiate a cascade of emotionally-driven learning events that effectively reorganize the brain into a chronic pain state with distinct functional, anatomical, and resting state properties.”

At one point Apkarian calls the idea that people in chronic pain simply conflate fear and sadness with back pain a ‘highly artificial one’.  They note that the amygdala — one of the brain regions that’s enhanced in chronic pain — is oriented to motivationally relevant and more powerful stimuli, while the prefrontal cortex assigns meaning to sensory cues based on past experiences.

The authors may be suggesting that in chronic pain an over-active prefrontal cortex assigns enhanced meaning to sensory cues that involve pain and then shoots them to the amygdala, which amplifies them with enhanced emotional content.  We should remember that pain is both a sensory and an emotional experience.

They end the paper stating

“We interpret the observed spatial shift in back pain representation as evidence for the pain percept reflecting less its sensory properties and instead becoming a heightened and more complex emotional state, constructed from learning and resultant memory traces of the presence and persistence of the condition, which orient the motivational preferences of the subject toward ‘suffering’ with the condition.”

Your interpretation of this confusing statement is as good as mine.  My guess is that Apkarian is simply saying that after a time the brains of people in chronic pain have ‘learned’ to be in more pain; pain has, so to speak, been integrated into their experiential DNA and a complex emotional state has evolved. One might ask how some of most severe and unpleasant sensations we can experience could not at some point become part of a ‘complex emotional state’.

The authors state that this ‘pain train’ orients the ‘motivational preferences of the subject towards suffering’ – another statement that’s hard to decipher. How, after all, could one’s ‘motivational preferences’ orient one towards suffering?

My experience suggests that pain memories can get so locked in that when we look to our future all we see is pain. That upset, by itself, may trigger the sympathetic nervous system to increase pain sensitivity. For example, I experience muscle rigidity,  shortness of breath, irritability, and more pain in general when I’m under stress. I believe I’m shutting off blood flow (and thereby oxygen) to various parts of my body.

That scenario is the foundation of a hypothesis by Dr. Manuel Martinez-Lavin regarding pain production in FM, and he has some genetic evidence to support his hypothesis. (Dr. Martinez-Lavin examines the same adrenergic system that’s focused on in the latest POTS autoimmune study.)

 Buddhists do differentiate between pain and suffering, and they also see a difference between pain intensity and the unpleasantness of pain.  In an upcoming blog, we’re going to focus on a pain researcher who, when dealing with a painful event, realized that he was, in fact, catastrophizing (thinking the event was much worse that it actually was). He used several techniques, one of them a physical approach that may fit with physiological findings in FM and ME/CFS, to reduce the ‘unpleasantness quotient’ of his pain  from an ‘8’ to a ‘3’.

 Do emotions or stress affect your pain levels?  I know they do affect mine, but it can be hard to distinguish whether my emotions and stress affect the pain or vice versa.  For me both clearly are involved.

How to get out of the pain is another question. If chronic pain is partially the result of an overactive brain circuit then changing the strength of that circuit should help and that is an area of active research.

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