Clinical reasoning in pain – emotions


The current definition of pain includes the words “unpleasant sensory and emotional experience” so we would be surprised if we encountered a person with pain who wasn’t feeling some sort of negative emotion, am I right? Yet… when we look at common pain assessments used for low back pain, items about emotions or worries are almost always included as indicators of negative outcomes (for example, STarTBack – Worrying thoughts have been going through my mind a lot of the time, I feel that my back pain is terrible and it’s never going to get any better, In general I have not enjoyed all the things I used to enjoy). And while the screening questionnaires have been validated, particularly for predictive validity (ie higher scores obtained on these measures are associated with poorer outcomes), I wonder how much we know, or think we know, about the relationship between emotions and pain. Perhaps its time for a quick review…

Firstly, let’s define emotions (seems easy!) “Emotions are multicomponent phenomena; (2) emotions are two-step processes involving emotion elicitation mechanisms that produce emotional responses; (3) emotions have relevant objects; and (4) emotions have a brief duration.” (Sander, 2013). There are thought to be six evolutionarily shaped basic emotions such as joy, fear, anger, sadness, disgust, and surprise (Ekman, 1992); but as usual there are complications to this because emotions are also examined in terms of their valence – negative or positive – and arousal (similar to intensity, but in terms of how much our physiology gets excited).

There are two main brain areas involved in processing both pain and unpleasant stimuli in general are the amygdala and the prefrontal cortex. These areas don’t exclusively deal with pain but with stimuli that are especially salient to people (remember last week’s post?), and researchers are still arguing over whether particular areas are responsible for certain emotions, or whether “emotions emerge when people make meaning out of sensory input from the body and from the world using knowledge of prior experience” based on basic psychological operations that are not specific to emotions (Lindquist et al., 2012, p. 129) . I’m quoting from an excellent book “The neuroscience of pain, stress and emotions” by Al, M. Absi, M.A. Flaten, and M. Rogers.

Now researchers have, for years, been interested in the effects of emotions on pain – there is an enormous body of literature but luckily some good reviews – see Bushnell et al., 2013; Roy, 2015 ;  Wiech and Tracey, 2009. What this research shows, essentially, is that pain is reduced by positive emotions, and increased by negative emotions. Now we need to be somewhat cautious about over-interpreting these results because they’re mainly conducted in experimental designs with acute experimental pain – people are shown pictures that elicit certain emotions, then poked or zapped, and asked to rate their pain (and their emotions, usually). It’s thought that the way these emotions influence pain is via our descending inhibitory pathways. Now the situation with real people experiencing pain that is not experimentally administered is probably slightly different – a lot more salient, a lot more worrying, and far less controlled. Nevertheless it’s worth knowing that when you’re feeling down, you’re likely to rate your pain more highly. If the emotion-eliciting stimuli are particularly arousing (ie they’re REALLY interesting) then the effect on pain ratings is greater. Experimenters also found pain reduces responses to pleasant stimuli, but there isn’t such a strong relationship with negative stimuli.

The valence (positiveness or negativeness – if that’s a word LOL) activates motivational systems either pleasant = appetitive, or unpleasant = defensive. Arousal or alertness gives us a clue as to how much motivation we have to either move towards or away from the stimulus. The degree of arousal affects our pain experience – so the more negative and angry we are, we rate our pain more highly; while the happier and jollier we are, we rate our pain as less intense. BUT, as for most things in pain, it’s complex – so once we get more than moderately angry/alert/aroused, the less we experience pain. The diagram below shows this kind of relationship – from the same book I quoted above (it’s worth getting!).

Does this mean we should freak people out so they experience less pain? Don’t be dumb! Being that alert is really exhausting. But what this diagram can explain is why some people, when they’re first attending therapy and are asked to do something out of the ordinary and just so slightly threatening (like lifting weights, or jumping on a treadmill) might report higher pain intensity – because we’ve caught them at the moderate arousal level where pain is facilitated.

Clinically, what this information means is that if we’re hoping to improve someone’s pain via pleasant or positive emotions, we’d better make sure they’re fairly high energy/arousing – a hilarious comedy perhaps – because lower intensity pleasure doesn’t affect pain much.

We should, at all costs, avoid eliciting fear and worry, or anger in the people we treat – because this increases pain intensity. This means giving people time to get used to our setting, what we’re asking them to do, and the intensity of whatever activity we’re going to do with them. In graded exposure, we should give people skills in mindfulness well before we begin doing the exposure component – because it’s likely to evoke higher than usual pain intensity if they can’t “be with” the increased anxiety that emerges during this kind of treatment.

And finally, if someone is experiencing anger, depression, sadness or anxiety – this is a normal psychological reaction integral to our experience of pain. It’s not necessarily pathological – though it probably increases the pain intensity the person reports.

I think we could promote far more scheduling pleasurable experiences as a routine part of therapy. What makes people smile, feel joy, have a good belly laugh? When was the last time they watched a comedy or joked with their family? Therapy can be fun, just see my friend Alice Hortop’s work on comedy as therapy (https://alicehortop.com/)!

 

 

Ekman, P.  (1992). An argument for basic emotions. Cognition and Emotion, 6, 169–200.

 

 

 

Flaten, M. A. (2016). The neuroscience of pain, stress, and emotion : Psychological and clinical implications. In Al, M. Absi, M. A. Flaten, & M. Rogers (Eds.), Neuroscience of Pain, Stress, and Emotion: Amsterdam, Netherlands : Elsevier.

K.A. Lindquist, T.D. Wager, H. Kober, E. Bliss-Moreau, L.F. Barrett, (2012). The brain basis of emotion: a meta-analytic review. Behavioral and Brain Sciences, 35 (03),  121–143

 

 

Roy, M. (2015). Cerebral and spinal modulation of pain by emotions and attention. Pain, Emotion and Cognition, 35–52.

 

Sander, D. (2013). Models of emotion: the affective neuroscience approach. in J.L. Armony, P. Vuilleumier (Eds.), The Cambridge handbook of human affective neuroscience, Cambridge University Press, Cambridge, pp. 5–56

 

 

 

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4 comments

    1. It’s as ineffable as pain… Kleinginna, P. R., & Kleinginna, A. M. (1981). A categorized list of emotion definitions, with suggestions for a consensual definition. Motivation and emotion, 5(4), 345-379.
      Mulligan, K., & Scherer, K. R. (2012). Toward a working definition of emotion. Emotion Review, 4(4), 345-357.

      1. Bronnie, Antonio Damasio [1994] does not agree: “I do not see emotions and feelings as the intangible and vaporous qualities that many presume them to be. Their subject matter is concrete, and they can be related to specific systems in body and brain, no less so than vision or speech. Nor are the responsible brain systems confined to the subcortical sector. Brain core and cerebral cortex work together to construct emotion and feeling, no less so than in vision. One does not see with the cerebral cortex alone, and vision probably begins in the brain stem, in such structures as the colliculi.” (p. 164). Reference: Damasio AR. Descartes’ Error: Emotion, Reason and the Human brain. New York: GP Putnam’s Sons, 1994.

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