Pain is always in your head

Peter MolemanArticles, EmotionsLeave a Comment

I love cooking and I use good kitchen knives. I regularly cut my finger and briefly experience a sharp pain which soon passes, leaving a dull throbbing pain which last awhile. I have sometimes been known to cook in a disorganised way, things not entirely in hand, I was distracted, and all at once I saw blood on the kitchen counter and also a smear on the potato I was peeling. I had cut myself completely unnoticed, but right after I saw what had happened, the dull throbbing pain started. How can I not have noticed that I had cut myself?

Damage is not pain

Your skin functions as a sensory organ, in this way it is comparable to your eyes, ears and nose. The skin has many different sorts of receptors for touch, warmth and cold. With these you can feel objects that touch your skin. This is necessary for the adequate management of objects. Other receptors in the skin register If the tissue is being damaged. Mechanical receptors, for example, react when you cut yourself. But there are also receptors which register excessive heat or cold, and receptors which register chemical substances which damage the tissue. These receptors in the skin are called nociceptors. These are popularly known as pain receptors, but damage receptors would be a more accurate rendition. The related nerves are called “pain nerves”, but this is not correct either, because they transmit a message in response to damage. The message may better be called “damage signal”, or even better “possible threat” signal. These signals are carried by nerves through the spinal cord to the brain, and are then experienced as pain. The experience of pain is generated in the brain itself.

The brain’s complex conversion of damage signals

“Damage signals” enter the brain by two routes. One route enables the rapid detection of a real theat, in order to react quickly1. The second route helps to establish the location and duration of the damage2.

Fig. 1 The pain matrix in the human brain. See the text and footnotes for explanation. Abbreviations. AMY: amygdala; ACC: anterior cortex cinguli; BG: basal ganglia; PAG: Periaquaductal grey; PFC: prefrontal cortex; PB: parbrachial nucleus; RVM: rostroventral medula; S1: primary somatosensory cortex; S2: secundary somatosensory cortex; SPL: superior parietal lobe. (See references Bushnell et al.)

These “damage signals” also travel to other parts of the brain. These are cortical areas that play a role in attention3 and areas that are associated with emotion and motivation4. All these brain areas have an influence on the pain experience. The interesting thing is that these brain areas are not exclusively associated with attention, emotion and motivation in relation to experiencing pain. They are always activated if attention is required, and if emotions are involved or in situations where motivation is involved.

Is pain a perception?

That pain only originates in the brain areas for attention, emotion and motivation explains why pain can be so strongly influenced by diverting your attention and is also closely related to your emotional state. There are soldiers who can be quite wimpy at home, but feel little pain from a serious injury on the battlefield. Sporters who sustain severe injuries during a game can appear to only feel the pain when the match is over, although- when I see footballers on TV – this often looks different. This also explains why pain can be influenced significantly by placebos or meditation. During Vipassana meditation I can sometimes feel pain as if it is outside my being, and then it hardly affects me. You could therefore say that pain is an emotion and not a perception. From the areas for emotion and motivation there also arise signals which go back to the areas where the “possible threat” signals originate5. Through these pathways the “possible threat” signals are directly influenced by the pain experience. They can be suppressed or enhanced, for instance in the placebo or nocebo effect.

Can there be pain without damage?

Some people are abnormally sensitive to pain, as in fibromyalgia, arthritis, some forms of back pain and different types of nerve pains. These are sometimes called unexplained pain, because the “damage” is absent or cannot be found. These are all chronic pain disorders. Sometimes not even the strongest painkillers can help with chronic pain. This suggests that “damage signals” have little or nothing to do with the pain experience. With chronic pain, there are changes to be found in the neurons and their connections in those brain areas which are related to emotions; emotions of all sorts6. It is noteworthy that many people with chronic pain are depressed or overly anxious. You may assume that that is to be explained by the distressing and overwhelming effect of chronic pain, which would make one depressed and anxious. But it seems that this has more to do with a less than optimal functioning of these emotion-related brain areas. Therefore depression, anxiety, and chronic pain are expressions of similar emotional disturbance. This is supported by the fact that depressed patients are often oversensitive to pain stimuli and that some antidepressants work for chronic, unexplained pain.

Pain is a special emotion

Pain is therefore best explained as an emotion, but unlike other emotions it is always linked to its being sensed in a specific area of your body. With other emotions you often have physical sensations, such as with disgust “ it makes me feel sick”, with rage a wave of heat and tension that engulfs your body, or with a sensation of happiness in your whole body which feels like, well, happiness. But in these cases you do not think that there is something wrong with your body, whereas with pain you do. Sometimes cases of chronic pain are dismissed saying: we can’t find anything, so it’s all in your head. But all pain is all in your head. If a doctor does find something to which she attributes the pain, then she has only found the cause of the “damage signals”.

Feldman Barrett, L. (2017). How Emotions Are Made; The Secret Life of the Brain. London, Macmillan. ISBN 978-1-5098-3751-9; Ch. 10.
Sui, J. and X. Gu (2017). “Self as Object: Emerging Trends in Self Research.” Trends in neurosciences 40(11): 643-653.
Lu, C., T. Yang, et al. (2016). “Insular Cortex is Critical for the Perception, Modulation, and Chronification of Pain.” Neuroscience bulletin 32(2): 191-201
Buchel, C., S. Geuter, et al. (2014). “Placebo analgesia: a predictive coding perspective.” Neuron 81(6): 1223-1239.
Colloca, L. and C. Grillon (2014). “Understanding placebo and nocebo responses for pain management.” Current pain and headache reports 18(6): 419
Bushnell, M. C., M. Ceko, et al. (2013). “Cognitive and emotional control of pain and its disruption in chronic pain.” Nature reviews. Neuroscience 14(7): 502-511
Garcia-Larrea, L. and R. Peyron (2013). “Pain matrices and neuropathic pain matrices: a review.” Pain 154 Suppl 1: S29-43.
Kandel, E. R., Schwartz, J.H., Jessell, Th. M., Siegelbaum, S.H., Hudspeth, A.J. (eds) (2013). Principles of neural science, 5th Ed.. McGraw-Hill. ISBN 978-0-07-181001-8 Ch. 24 Pain
Allan I. Basbaum Thomas M. Jessell Singer, T., B. Seymour, et al. (2004). “Empathy for pain involves the affective but not sensory components of pain.” Science 303(5661): 1157-1162
Zitman, F. G., A. C. Linssen, et al. (1990). “Low dose amitriptyline in chronic pain: the gain is modest.” Pain 42(1): 35-42
  1. The black/grey arrows in the figure, pointing to the ParaBrachial nucleus (PB) and the Amygdala (AMY)
  2. The black/grey arrows in the figure, pointing to the Thalamus and the somatosensory cortex (S1)
  3. The blue arrows in the figure
  4. The green arrows in the figure
  5. The green arrows in the figure, pointing to the PeriAquaductal Grey (PAG) en down through the RostroVentral Medulla (RVM) to the spinal cord
  6. The green arrows in the figure

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