When I started working in the field of persistent pain, many of the approaches used were based on the idea that every pain was the same. Oh yes, of course we had neuropathic pain and inflammatory pain, but our treatments tended to approach each person as if they were pretty similar. We later refined that approach and started to look at people in groups. In the service I worked in, we used the Westhaven-Yale Multidimensional Pain Inventory which generates three main psychologically-based profiles – and for a long time this was a very useful way of establishing who needed the three-week residential programme, and who would do well with a briefer outpatient programme.
Well things change over time, and we’ve become more aware of what Clifford Woolf describes as a “mechanism-based” classification approach (Woolf, 2004). In this approach, clinicians try to establish the dominant mechanistic group in which a person’s pain might be classified, then suit the treatment to that mechanism. This means clinicians diagnose inflammatory pain, neuropathic pain, and nociplastic pain – and use what looks like the best combination of medications to suit the mechanisms. For example, for neuropathic pain it’s more likely people will be given gabapentin/pregabalin and a tricyclic antidepressant in combination than an opioid.
There’s a problem, though – in fact, TWO problems I can see.
Methods for identifying pain mechanistic groups
The first problem is that we don’t have wonderful methods for establishing the main mechanistic groups.
In fact, in a recent very large and thorough review of methods used to discriminate between each category, the authors found that “few methods have been validated for discrimination between pain mechanism categories”, and although there was “general convergence” between methods, there was also “some disagreement” (not that this is unfamiliar to anyone who reads research!) Shraim, Masse-Alarie, & Hodges, 2021).
What was interesting, albeit not too unexpected, was the overlap of findings between categories because people present with mixed types of pain; and that many of the studies attempted to only discriminate between two of the groups, rather than more. Having said this, the authors identified five groups of method used to help clinicians and researchers distinguish between pain mechanisms: clinical examination; quantitative sensory testing; imaging; diagnostic and laboratory tests; and questionnaires asking participants to describe their experiences.
Now I know that research studies aim to be a little more rigorous than clinical practice, but that should sound an alarm when we begin looking at what we need to do in clinical practice. “Subjective” pain examination included aggravating and easing factors, pain location and pain characteristics (can anyone tell me when pain is NOT subjective?). It also included psychological factors (although my radar went off at this – more of this later!). Physical examination (is this supposed to be ‘objective’ pain examination?) included general clinical assessment, general neurological testing, nerve provocation testing and neurodynamics, clinical bedside somatosensory function testing, movement and functional testing. Quantitative sensory testing had no greater degree of sensitive, specificity and reliability than physical examination and “subjective” history, and laboratory testing was pretty poor despite superficially looking more “accurate.” A similar state exists for questionnaires – oh lordy!
So these authors found 200 methods that could be used to determine which pain fits into a specific box, but overall the results are pretty underwhelming for clinicians wanting a direction for their approach. It’s not helped that the current “gold standard” used is – wait for it – clinician-based diagnosis.
Where are we left? Well, I think we’re not that far away from where we were in the 1990’s and early 2000s. We really don’t have a clear way to distinguish between the various mechanisms, and many people likely present with pain that includes more than mechanism. However – these authors provide a table summarising the commonly used, and possibly most likely approaches to diagnose pain mechanisms, and this is useful for those of us who want the “best guess” for now.
At the beginning of this piece, I said there were two problems with using mechanistic descriptors. You can see the problems with reliability, specificity and so on – and the lack of agreement in the research and likely “mixed” presentations we will see in clinic – from my comments above (do read the whole article, though, it’s well worth it).
The second problem is that these descriptors, even when accurate and reliable, don’t tell us anything about the person experiencing pain. Unless, and until we have effective treatments for each of these mechanisms, we are inevitably running experiments to see what might work for this person in front of us. And this means we find less utility in diagnosis than we would if we drew on a case formulation approach.
What’s the difference? Diagnosis allows us to group “like with like” – on the basis of similar underlying mechanisms. We can then treat those mechanisms, and voila! the person recovers! It works well with fractures, with infectious diseases, and even with diabetes. It doesn’t work as well when we don’t have treatments we can use on the mechanisms. For example, although we can diagnose many neurological disorders, for so many of them we have very poor treatments. This means people live with their disease – and this is where a diagnosis falls down. It does not tell us HOW this person will experience their disease. Diagnosis doesn’t explain illness, disability, functional status, or participation.
And, because all of us are unique, this means that a one-size-fits-all approach to persistent pain (or even an algorithm, subtype, or subgroup) isn’t likely to offer clinicians or the person with pain a useful path towards well-being.
You’ll remember I said my radar went off with the psychological assessments included in the methods used to identify a pain mechanism. My reason is this: pain is a stressor. Even a paper-cut captures my attention (albeit just a little until I use a hand sanitiser!), my heart rate goes up a bit, I’m alerted to the experience and want to get away from it. Now imagine if that pain continued. Maybe variably, maybe constantly, maybe intermittently. And imagine if I couldn’t get a good understanding of what’s going on. And perhaps I was being questioned by my clinicians – and maybe even stigmatised. “What do you mean, you have pain we can’t diagnose, we can’t image, we can’t treat?” I’m guessing by now, perhaps some months after my pain started, I’d be feeling a bit irritated, perhaps a bit low in mood, my sleep might not be great, I might find it hard to do what matters to me because I’m not sure if I’m doing myself some harm.
What we don’t know in many studies of pain “predictors” is whether they are cause or effect. There is undoubtedly an association between various measures of pain-related anxiety, avoidance, low mood, thinking the worst. What we do not know is whether this was present before the pain came on – or whether it came afterwards.
So, to my mind, using psychological factors as part of diagnosis risks labelling people and what are probably normal responses to abnormal experiences. Let’s not do that.
Where am I left after reading this paper? I’m glad someone set about doing this review. I think it offers a good summary of the state of play, and identifies some of the current problems with a mechanistic approach. We need to get consensus on definitions, we need far better methods, we need to stop using the word “subjective pain examination” (because ALL pain is subjective), and we need to leave psychological factors out of diagnosis until we can clearly identify which came first.
Shraim, M. A., Masse-Alarie, H., & Hodges, P. W. (2021, Apr 1). Methods to discriminate between mechanism-based categories of pain experienced in the musculoskeletal system: a systematic review. Pain, 162(4), 1007-1037. https://doi.org/10.1097/j.pain.0000000000002113
Woolf CJ. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004;140:441–51.