This is an updated and shorter version of my blog on pain sensitivity that is published in full in the website of the International Association for the Study of Pain (IASP).
Why is pain sensitivity important?
Pain sensitivity is thought to be a characteristic of each individual that affects the way a painful stimulus is perceived. The same injury or change in a tissue (such as an inflammation or a fracture) results in extremely different amounts of pain reported by different individuals. In addition, there is a discrepancy between magnitude of injury and perception of pain: extensive damages may be associated with only moderate pain, and minor damages may be associated with excruciating pain. Therefore, something beyond tissue damage must play a role in the amount of pain experienced by different individuals. This “something” is frequently identified as individual pain sensitivity. Even if tissue damage cannot be healed, reducing pain sensitivity can lead to less pain.
Pain sensitivity is amenable to stigmatization
A naïve (but still widespread) belief is that being a constitutionally “strong” individual results in little pain sensitivity. In this context, synonyms of “strong” may be brave or resilient, among others. Accordingly, constitutionally “weak” individuals would tend to report excessive pain even with minor noxious stimuli. The implication is that the term “weak” includes a range of negative attributes that are expected to explain the excessive pain reported by these individuals. These believes are unjustified simplifications.
What is pain, and what is nociception?
To better understand pain sensitivity, we have to distinguish pain from nociception. Pain is a conscious process, whereas nociception is the process that encodes noxious stimul and does not necessarily imply pain sensation.
What determines pain sensitivity?
Today we know that pain sensitivity is the result of complex processes at different sites of the pathways that are involved in the generation, transmission, elaboration and perception of pain.
When a pathological change occurs in a tissue, such as osteoarthritis, inflammation, fracture, or degeneration, substances that are released in the tissue make nociceptive pathways more likely to be activated. As a result, a stimulus or activity that is normally painless, such as walking or lifting a weight, can generate pain. The signal arrives at the spinal cord and induces changes that increase the excitability of neurons, resulting in further amplification of pain. Brain imaging studies have revealed profound changes in activation of areas of the brain, connections between areas related to pain, and changes in the amount of substances that lead to more pain sensitivity.
Psychological factors, such as depression and anxiety, can lead to enhancement of nociceptive processes by acting both on brain circuits and through descending pathways from the brain to the spinal cord. On the other hand, we are able to activate an own inhibitory system to attenuate pain. The activation of this system explains why extensive injuries are not always associated with excruciating pain, as typically observed in early stages of a trauma.
How can we measure pain sensitivity?
Measurements of pain sensitivity are available for human research and, partly, for clinical use. For instance, devices that apply pressure of a measurable intensity can be applied to an individual, who is then asked to rate their pain intensity. Electromyography, electroencephalogram, or advanced brain imaging, among others, can provide objective information on pain sensitivity, mostly in research settings.
Challenging question
Why do different individuals have different degrees of pain sensitivity? We do not have a satisfactory answer to this question, partly because our tools to study the mechanisms of pain sensitivity in humans are limited. The factors that we know, such as sex, age, or anxiety, are insufficient to fully explain the differences among individuals.
Can we treat pain hypersensitivity?
Currently available medications that reduce the excitability of nociceptive pathways include anticonvulsants and antidepressants, also in the absence of depression, due to a specific effect on pain. Non-pharmacological treatments that can attenuate pain hypersensitivity include psychological treatments and mindfulness-based stress reduction.
Perspectives
Pain sensitivity is a complex and still poorly understood phenomenon that is not amenable to simplifications. It is affected by multiple mechanisms acting at different sites of the pathways involved in the generation and transmission of the nociceptive signal, and in the perception of pain. Pain hyper-sensitivity should not be stigmatized.
Future research will provide more insight into the mechanisms underlying pain sensitivity in humans, providing a basis from which to develop more effective and individualized therapeutic strategies.
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