Pain sensitivity FAQ
In the seventh and final instalment of our series on pain sensitivity, Darren Beales FACP and Tim Mitchell FACP address some frequently asked questions.
Thank you for joining us on our journey through the consideration of pain sensitivity in clinical practice. To finish the series, we will endeavour to answer a few questions from readers.
How do we determine whether the sensitivity is a result of true pathology or not?
It’s important to remember that pain sensitivity is a normal response of our body to acute tissue injury that is helpful for protecting the injured tissues and promoting an environment for tissue healing.
So in the case of acute trauma where the symptom presentation matches the clinical picture, some increased pain sensitivity in the region is probably normal.
However, it gets more interesting when there was no tissue trauma or overload or the problem has become persistent. This is something we ponder on nearly a weekly basis in the clinic.
Heightened pain sensitivity has been described in all body regions and patient types across the scope of physiotherapy.
But there is no exact science to judging the contribution of pathology to that sensitivity.
Perhaps if the sensitivity is really localised (to a spinal segment, for example, or to a specific peripheral joint) and fitting pathology is present, the role of pathology might be considered a little more in the clinical reasoning process compared to a widespread sensitivity presentation, but this is a completely speculative statement.
It is arguably high-value care to apply conservative and non-invasive management before moving on to more invasive interventions targeting pathology (injections and surgery) when increased pain sensitivity is a dominant feature.
It is important that patients understand the risks and benefits of proceeding to more invasive treatments and that the role of pain sensitivity in this is acknowledged and discussed.
In general, significant pain sensitivity will have a negative mediating effect on common treatments that target pathology.
For example, outcomes from spinal surgery appear to be worse in general for those with significant sensitivity than for those without.
However, sometimes we see people who would seem to be at risk of a poor outcome from surgery due to sensitivity be a lot better after the surgery.
The heightened pain sensitivity subsides. Could be placebo effects of the surgery; could be the surgery itself; the mechanisms are unclear.
Is there any way to differentiate between central and peripheral sensitisation?
Secondary hyperalgesia is often presented as always being a central sign. This is a good question for the pain scientist, which we are not.
After an acute (traumatic) injury, one could argue that peripheral sensitisation would be dominant.
But very quickly the central nervous system will respond and react/adapt. Also, some people’s central nervous systems might be primed to respond with increased sensitivity after an injury, significantly contributing to the presentation at the outset.
Pre-existing or historical life-stressing events, poor mood and/or poor sleep prior to an injury might prime the central nervous system for this type of response.
In more chronic presentations, there can be a dangerous tendency to blame everything on a sensitised central nervous system. This may mean that you miss important peripheral drivers (including pathology sometimes).
Another important consideration is that with quantitative sensory testing (and the clinical equivalent we have described previously in Part 3 of this series here), between the point of application of the stimulus and the subjective report of a heightened response, the assessment cannot truly tell you which part of the nervous system might be primarily involved in ‘amplifying’ the stimulus.
Perhaps this point is more important. In practice, when discussing patients, we never talk about the balance of central and peripheral sensitisation in such terms.
We talk about contributing factors, particularly those that might be modifiable and that the patient agrees are a priority that they can attend to.
Not everyone gets psychological management. Not everyone gets graded motor imagery. Not everyone sees a pain medicine specialist. It depends on the patient (had to pull that old chestnut out).
When there are features in an individual’s story to suggest heightened pain sensitivity (ie, pain wind-up or heightened pain response to activity) but no signs of increased pain sensitivity with bedside quantitative sensory testing, can we still consider pain sensitivity to be a feature of someone’s problem?
Funnily enough, people’s nervous systems react in funny ways. There is a lot of individual variation in the way pain sensitivity presents.
Within this, there is certainly a group of patients who fit the premise you describe. They have disproportionate responses to aggravating activities/movements and constant symptoms without any effective easing strategies.
Their symptoms might even be widespread if there is pain referral in non-dermatomal patterns (go back to Part 2 in the series for more discussion about the subjective features of heightened pain sensitivity here).
They may also be clear that psychological stress is an independent trigger of their symptoms— all indications that their system is sensitised.
But when you undertake clinical somatosensory sensitivity testing (such as light touch, sharp, cold and blunt pressure), there are no heightened responses.
Often, though, there will be responses consistent with hyperalgesia with movement and functional testing.
So for some this might be a peculiarity of how their nervous system reacts. Medications may also affect their responses to testing—check what they are taking and consider whether this might influence tactile sensitivity.
In Part 1 you described a scenario where a worker has a high degree of pain sensitivity and asked if they should push through the pain or not. Should they?
Giving our patients instructions and strategies for how to approach pain with exercise (and function) is one of the most important things a physiotherapist does in day-to-day clinical practice.
Indeed, this might be an area of expertise for our profession beyond others engaged in exercise prescription.
That said, guidelines for how pain should be approached with exercise are not expansive (eg, click here). Research is only just emerging and will continue to develop (as it has for pain during exercise for tendinopathy).
When a person has significant or dominant pain sensitivity, it is probably unrealistic to expect them to engage in exercise and activities without some level of pain.
This is where pacing becomes an important tool—but not, we would argue, before helping the person understand their pain.
Can you imagine being in severe pain, not understanding why and essentially being told that pain is in the brain and you can just work through it and it will be okay?
You need to work with the patient to develop a shared understanding of their pain and how it behaves and then determine an acceptable level of symptom provocation for their individual circumstances, while avoiding excessive system wind-up and mediating boom–bust patterns.
If this balance is not achieved and people try to push through the pain (because of their own beliefs or at the direction of well-meaning healthcare practitioners), for many it can just wind their nervous system up more and reinforce already unhelpful nociceptive processes.
Others may make progress, with quite rapid increases in activity. This is what makes it interesting.
Well, that’s it. We have really enjoyed the process of writing this series, which has given us an opportunity to reflect on our own practice in the area. We hope that means that it has also been helpful to others and has given you a chance to reflect on your own knowledge and practice.
Remember, knowledge evolves with time, so keep reflecting.
Like to hear Tim and Darren casually chat about the management of pain sensitivity for musculoskeletal conditions? Click here.
Where to find case studies that consider pain sensitivity? Beales et al. ‘Masterclass: A pragmatic approach to pain sensitivity in people with musculoskeletal disorders and implications for clinical management for musculoskeletal clinicians.’ Musculoskeletal Science and Practice, 2021. Click here.
Musculoskeletal Framework Team. Musculoskeletal Clinical Translation Framework, 2023. Click here.
Like something short and fun? (Tim and Darren again.) Click here.
>> Darren Beales FACP is a Specialist Musculoskeletal Physiotherapist (as awarded by the Australian College of Physiotherapists in 2008) and a director at Pain Options in Perth, WA. As a senior research fellow at Curtin University, Darren is undertaking broad research into clinical pain, from the mechanistic understanding of clinical pain to efforts to enhance the management of persistent pain and implementation of knowledge into practice.
>> Tim Mitchell FACP is a Specialist Musculoskeletal Physiotherapist (as awarded by the Australian College of Physiotherapists in 2007) and a director of Pain Options. Tim has completed a PhD in the area of low back pain and has a special interest in the translation of logical reasoning into clinical practice. He holds positions with the Australian Physiotherapy Council and the Australian College of Physiotherapists.
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