science

From the particular to the general – Clinical reasoning in the real world


From the particular to the general –
Clinical reasoning in the real world

I make no secret of my adherence to evidence-based healthcare. I think using research-based treatments, choosing from those known to be effective in a particular group of people in a specific context helps provide better healthcare. But I also recognise problems with this approach: people in clinical practice do not look like the “average” patient. That means using a cookie cutter, or algorithm as a way to reduce uncertainty in practice doesn’t, in my humble opinion, do much for the unique person in front of me.

I’ve been reading Trisha Greenhalgh’s recent paper “Of lamp posts, keys, and fabled drunkards: A perspectival tale of 4 guidelines”, where she describes her experience of receiving treatment based on the original description given for her “fall”. The “fall” was a high-impact cycle accident with subsequent limb fractures, and at age 55 years, she was offered a “falls prevention” treatment because she’d been considered “an older person with a fall”. Great guidelines practice – wrong application!

Greenhalgh goes on to say “we should avoid using evidence-based guidelines in the manner of the fabled drunkard who searched under the lamp post for his keys because that was where the light was – even though he knew he’d lost his key somewhere else”

Greenhalgh (2018), quoting Sir John Grimley Evans

When someone comes to see us in the clinic, our first step is to ask “what can I do for you?” or words to that effect. What we’re looking for is the person’s “presenting symptoms”, with some indication of the problem we’re dealing with. Depending on our clinical model, we may be looking for a diagnostic label “rheumatoid arthritis” or a problem “not sleeping until three hours after I go to bed”.

What we do next is crucial: We begin by asking more questions… but when we do, what questions do we ask?

Do we follow a linear pattern recognition path, where we hypothesise that “rheumatoid arthritis” is the problem and work to confirm our hypothesis?

Our questions might therefore be: “tell me about your hands, where do they hurt?” and we’ll be looking for bilateral swelling and perhaps fatigue and family history and any previous episodes.

Or do we expand the range of questions, and try to understand the path this person took to seek help: How did you decide to come and see me now? Why me? Why now?

Our questions might then be: “what do you think is going on? what’s bothering you so much?”

Different narratives for different purposes

Greenhalgh reminds us of Lonergan (a Canadian philosopher), as described by Engebretsen and colleagues (2015), where clinical enquiry is described as a complicated process (sure is!) of 4 overlapping, intertwined phases: (a) data collection – of self reported sensations, observations, otherwise known as “something is wrong and needs explaining”; (b) data interpreting “what might this mean?” by synthesising the data and working to recognise possible answers, or understanding; (c) weighing up alternative interpretations by judging; and (d) deciding what to do next, “what is the right thing to do”, or deliberation.

Engebretsen and colleagues emphasise the need to work from information from the individual to general models or diagnoses (I’d call this abductive reasoning), and argue that this process in the clinic should be “reflexive” and “informed by scientific evidence” but warn that scientific evidence can’t be replaced simply by reflexive approaches.

The reason for conceptualising clinical reasoning in this way is that a narrative primarily based on confirming a suspicion will likely reduce the number of options, narrow the range of options considered, and if it’s focused on diagnosis, may well over-ride the person’s main concern. A person may seek help, not because he or she wants a name or even treatment, but because of worries about work, the impact on family, or fears it could be something awful. And without directly addressing those main concerns, all the evidence-based treatments in the world will not help.

Guidelines and algorithms

Guidelines, as many people know, are an amalgamation of RCT’s and usually assembled by an esteemed group of experts in an attempt to reduce unintended consequences of following poorly reasoned treatment. They’re supposed to be used to guide treatment,  supporting clinical reasoning with options that, within a particular population, should optimise outcomes.

Algorithms are also assembled by experts and aim to provide a clinical decision-making process where, by following the decision tree, clinicians end up providing appropriate and effective treatment.

I suppose as a rather idiosyncratic and noncomformist individual, I’ve bitterly complained that algorithms fail to acknowledge the individual; they simplify the clinical reasoning process to the point where the clinician may not have to think critically about why they’re suggesting what they’re suggesting. At the same time I’ve been an advocate of guidelines – can I be this contrary?!

Here’s the thing: if we put guidelines in their rightful place, as a support or guide to help clinicians choose useful treatment options, they’re helpful. They’re not intended to be applied without first carefully assessing the person – listening to their story, following the four-step process of data collection, data interpretation, judging alternatives, and deciding on what to do.

Algorithms are also intended to support clinical decision-making, but not replace it! I think, however, that algorithms are more readily followed… it’s temptingly easy to go “yes” “no” and make a choice by following the algorithm rather than going back to the complex and messy business of obtaining, synthesising, judging and deciding.

Perhaps it’s time to replace the term “subjective” in our assessment process. Subjective has notions of “biased”, “emotional”, “irrational”; while objective implies “impartial”, “neutral”, “dispassionate”, “rational”. Perhaps if we replaced these terms with the more neutral terms “data collection” or “interview and clinical testing” we might treat what the person says as the specific – and only then move to the general to see if the general fits the specific, not the other way around.

 

Engebretsen, E., Vøllestad, N. K., Wahl, A. K., Robinson, H. S., & Heggen, K. (2015). Unpacking the process of interpretation in evidence‐based decision making. Journal of Evaluation in Clinical Practice, 21(3), 529-531.

Greenhalgh, T. (2018). Of lamp posts, keys, and fabled drunkards: A perspectival tale of 4 guidelines. Journal of Evaluation in Clinical Practice, 24(5), 1132-1138. doi:doi:10.1111/jep.12925

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Assessing problems with sleep & persistent pain


Problems with sleep affect most of us from time to time. We know we might find it difficult to get off to sleep because of a busy mind, a different bedroom, changes to our schedule – but for most of us, sleep returns to our normal fairly quickly. For some of us, though, sleep problems continue for weeks, months or even years. And for people living with persistent pain, sleep can be one of the most difficult things to deal with, yet it’s also one of the most common (McCracken & Iverson, 2002). Studies of sleep problems in people with fibromyalgia show abnormal sleep continuity as well as changes in sleep architecture – this looks like increased number of times waking, a reduced amount of slow wave sleep and an abnormal alpha wave intrusion in non rapid eye movement, termed alpha-delta sleep (Dauvilliers & Touchon, 2001). People with fibromyalgia may also experience primary sleep disorder such as sleep apnoea or periodic leg movements during sleep.

The effect of rotten sleep is quite clear: pain increases the day following a disrupted night’s sleep, while high levels of pain on one day has less of an impact on subsequent sleep – but if you’ve been sleeping poorly for a while, all of this becomes something of a blur (Johnson, Weber, McCrae & Craggs, 2017; Slavish, Graham-Engeland, Martire & Smyth, 2017)! When we add in the effects of poor sleep on daily activity, and begin to unpack the relationships between sleep, pain and mood (Goerlitz, Sturgeron, Mackey & Darnell, 2017) well it’s a bit of a complicated matter, and one that I think we need to address when someone comes in for help with their pain.

Assessing unrefreshing sleep or poor sleep can be a reasonably straightforward process, but it needs to be carried out systematically. The event/s that initiate poor sleep may be very different from the events that maintain poor sleep, and while it’s interesting to know what started the sleep difficulties – in the end it’s possibly more important to work out what’s maintaining it.

The following is my attempt to outline what I look for when I’m discussing sleep with someone.

1. Is sleep really a problem? Sounds a bit odd, but some people have a strong belief that they need a certain number of hours of sleep a night, and when they’re not getting that magical number, it can be quite worrying – and actually kick off a sleep problem!

  • My key question here is do you wake feeling like you’ve had a good sleep? The number of hours of sleep is irrelevant, to a large extent, if you wake up feeling refreshed. If the person I’m talking to wakes up feeling OK I quickly swing into trying to understand why they’re worried about their sleep – and reassuring them that having a certain sleep duration is not fixed. In fact, sleep length changes over time – remember when you were a kid and slept for hours and hours? And when you were a teen and sleep in until midday if you could, but stayed up most of the night? These are pretty normal changes in pattern and nothing to worry about.

If you don’t feel refreshed, then I dig a little deeper…

2. What’s your sleep routine? This is about finding out the time someone goes to bed, how long it takes to fall asleep, what time a person wakes up, and gets up. I’ll also ask about the pre-bedtime routine: what’s the evening routine like? when do the screens go off? what’s the last drink of the evening? what’s the bedroom environment like?

  • I’m looking for a consistent bedtime at around the same time each night, a “wind down” ritual where the same things happen each night to prime the mind for sleep. I’m also looking for factors that might make it more difficult to fall asleep once in bed – screen time (devices, laptops, TV), dealing with worries, solving problems, having arguments, difficulty getting comfortable.
  • I’m also looking for a consistent wake up time, and whether the person gets out of bed then – or lies in bed and maybe falls asleep again…
  • A comfortable room temperature, a dark room, relatively little noise: all of these very basic things help keep bed for sleep (and sex) but not for much else.

The reason these basic “sleep hygiene” factors help is that our sleep pattern is malleable. It changes depending on environmental factors like light, noise and temperature. This is why we end up having jetlag – it takes a little while to adjust to the new daily light patterns (especially when you travel from Christchurch, NZ to somewhere like Norway!). Our body temperature drops during the night, our digestive processes slow down (that’s why we tend not to do “number twos” at night) and why we pee a lot less at night than during the day. Setting up a consistent routine helps us retain these habits and “teach” the mind/body to sleep at the correct time.

3. What substances do you use? I’m interested in the usual suspects: caffeine (not only coffee, but tea, energy drinks, dark chocolate), but also alcohol, the timing of medications, and that late night snack.

  • When sleep onset is a bit fragile it’s probably best not to have coffee and allied substances after mid-afternoon, and for some people (like me!) it’s best not to have them after lunch.
  • Medications for persistent pain are often sedating, so people need to know how to use this side effect for the best – and that often means taking medications earlier than first thought.
  • It also means for us, recognising that some medications alter sleep architecture (particularly meds given for, paradoxically, insomnia!). Alcohol might help people get to sleep but it changes the sleep architecture, preventing you from falling into that deepest sleep phase – and waking you up to pee halfway through the night, if you don’t do that already!
  • I also check whether people are smokers, and if they are, whether they wake in the morning absolutely gasping for a smoke, or whether they smoke during the night. Nicotine withdrawal can keep someone awake during those brief periods before and after dreaming sleep, so may need to be managed with patches.
  • Food is also something I check – snacks at midnight are the stuff of school stories, but can become a learned behaviour that we associate with being awake at that time, and maintain disrupted sleep. Maybe a mid-evening protein-based snack is a better option.

4. What’s going through your mind (or what’s your mind telling you) about your sleep? Having hopefully dealt with the basics of sleep hygiene (though I haven’t included exercise yet – that’s coming!), I’m keen to understand the person’s mind chatter about their sleep.

  • Worries, rumination and attempts at problem-solving (yes I’ve solved the problem of world peace!) can all keep us from falling asleep. What we do about those thoughts depends on the sleep management approach we’re using.
  • Often, the worries are actually worries about not sleeping – that paradoxically keep us from falling asleep! Feeling bothered about “how am I going to cope tomorrow if I don’t sleep”, or “I’m going to be so tired tomorrow, I know I won’t manage” are really common.
  • Along with worries about not sleeping, every other unsolved problem seems to pop up courtesy of your mind – this can happen because the person is too busy during the day to stop and ponder (and it’s quiet at night… fewer distractions!) so it’s worth finding out what is going through the person’s mind and dealing with those issues.

5. What’s your pattern of sleeping through the night? This is about the pattern of arousals – when, how long for, what the person does during these times.

  • Some understanding of normal sleep architecture is useful here so you can help the person understand why waking just before/just after dreams occurs.
  • Reviewing the habits at these times helps to understand the factors that maintains being awake at the wrong times! Waking briefly but without being aware of it is normal, but when internal or external factors intrude during lighter periods of sleep, we become more aware of being awake and can begin to do things that keep us awake, like watching TV, turning the radio on, having a snack, worrying.

To be continued…

These are some of the very fundamentals of assessing sleep problems. Next week I’ll review some more – and the week after look at strategies that can help!

 

Dauvilliers, Y., & Touchon, J. (2001). Le sommeil du fibromyalgique : Revue des données cliniques et polygraphiques (sleep in fibromyalgia patients: Clinical and polysomnography pattern.). Neurophysiologie Clinique/Clinical Neurophysiology, 31(1), 18-33. doi:https://doi.org/10.1016/S0987-7053(00)00240-9

Goerlitz, D., Sturgeron, J., Mackey, S., & Darnall, B. (2017). (395) sleep quality and positive affect as mediators of daily relationship between pain intensity and physical activity. The Journal of Pain, 18(4), S73.

Johnson, M., Weber, J., McCrae, C., & Craggs, J. (2017). (397) the catch 22 of insomnia and chronic pain: Exploring how insomnia and sleep impact the neural correlates of chronic pain. The Journal of Pain, 18(4), S73-S74.

McCracken, L. M., & Iverson, G. L. (2002). Disrupted sleep patterns and daily functioning in patients with chronic pain. Pain Research & Management, 7(2), 75-79.

Slavish, D., Graham-Engeland, J., Martire, L., & Smyth, J. (2017). (394) bidirectional associations between daily pain, affect, and sleep quality in young adults with and without chronic back pain. The Journal of Pain, 18(4), S73.

One way of using a biopsychosocial framework in pain management – ii


Last week I discussed case formulation as one way of using a biopsychosocial framework in pain management, and I reviewed Benedetti’s description of the process of becoming aware that something’s wrong, seeking relief from that discomfort, then the “meet the therapist moment”, and finally the “receiving the therapy” steps along the way. Benedetti considers this within a neurobiological model (Benedetti, 2013), while Engel (1977) used general systems theory to frame his critique of the original biomedical model.

This week I want to look at a behavioural model. I do this partly because I think it’s been a long time since this model was brought into our discussions about pain and pain behaviour, and I do it because I think we can understand a great deal about why different people respond differently to their pain when we look at behaviour alone – before we even begin to look at beliefs or attitudes about pain.

Let’s do a little revision (Psych 101). In a behavioural model, we’re looking at two main forms of conditioning: Pavlovian or classical conditioning, and operant or instrumental conditioning. In the case of pain, we also need to revisit the distinction made between the experience (pain), and our behavioural response to that experience (pain behaviours). Pain behaviours are typically filtered or influenced by what we think is going on (judgements about the meaning of pain – eg super-scary crumbling back, or I just did too much gardening), what we’ve learned to do, and the context in which we’re experiencing pain. That context can be current (eg I’m in Church and it’s very quiet so I’d better not swear as I hit my toe against the pew!), or past (eg last time I kicked my toe against the pew and swore, everyone looked at me – how embarrassing!), or even future (eg if I swear when I kick my toe against the pew, I’ll never be able to show my face here again!). It’s the learned part I want to discuss today.

Pain behaviours range from reflex withdrawal responses (lifting the foot up while straightening the other leg to support me when I stand on a tack), to quite complex behaviours we’ve learned are relevant in our environment (filling out a claim form for compensation and treatment).

We probably developed pain behaviours as part of our evolutionary development: the reflex withdrawal behaviours don’t require conscious thought, so they begin in infancy (actually, before), and rely on spinal mechanisms (eg Rohrbach, Zeiter, Andersen, Wieling & Spadavecchia, 2014), with various parts of the brain becoming involved as part of strategies to avoid threat (see Damasio and Damasio (2016) for some insights into evolutionary aspects of withdrawal reflex). But because we have a developed cortex, we’ve learned ways of suppressing our responses, depending on social context – and on responses from others around us.

Reflexive responses are those associated with classical conditioning – and lead us to learn relationships between previously non-threatening stimuli and both withdrawal responses and the physiological arousal that goes with them. For example, if I bend over to make the bed and OUCH! my back suddenly gets really sore. I straighten up very carefully – and I’ve learned something: next time I bend over to make the bed, I’ll be remembering and preparing for that OUCH! to happen once again. The bed and bending forward movement become associated, in my mind, with that OUCH! Of course, for most of us, once we make the bed a few more times (make that many times), we’ll learn that OUCH! doesn’t inevitably follow the bend, so we gain confidence to repeat that movement without preparing for the OUCH! Now what do you think might happen if I never had an opportunity to make the bed again? Say, if I have a really protective person in my life who stopped me every time I go to do it – will that association I have in my mind persist, or will it reduce? This is, in essence, what is thought to happen when someone develops so-called “fear avoidance”. Note: the experience of pain does not have to re-occur for me to avoid bending and begin to rev my nervous system up. What needs to happen is for the first instance to be pretty strong, and for me to not test my belief again. It’s the behaviour that persists (avoidance) because by avoiding something I believe will be OUCH! I avoid experiencing OUCH! And by avoiding that experience, I never test whether OUCH! happens every time, or just that once.

Let’s look at the other really powerful learning mechanism: operant conditioning. In this situation, the likelihood of me repeating my behaviour is increased or reduced, depending on responses in the environment. So, let’s take my bending forward and experiencing OUCH! If my partner (bless him) then decided to fuss over me, make me a cup of tea and tell me not to worry about making the bed ever again – AND if I liked that idea – my response is likely to be to avoid making the bed. I might even go as far as wincing a bit when walking, so he makes me another cup of tea and fusses over me. I might talk about my back pain because he’s so concerned about me (or I really want him to be concerned about me) and if he carries on fussing, I’m likely to carry on with these behaviours. Now picture that in a two-year-old kid – every time the kid trips and cries, some concerned parent comes picks him up, something the kid likes, it’s probable that kid will learn that this is normal, and something to do when he hurts. For more on learning theory, Johan Vlaeyen summarises the state of play in a review paper from 2015 (Vlaeyen, 2015).

We’re smart, us humans. We learn to predict and remember patterns even from imprecise data – it doesn’t take much for us to put two and two together, particularly when it’s something relevant to surviving! Whenever I’m listening to someone telling me their story about why they’re presenting in this way at this time, and what is maintaining their situation, I keep thinking about the various learning mechanisms involved. Social context and the people around us and how they respond to us exert a powerful force on what we do – and many times we’re not even aware of why we do what we do.  Knowing this stuff means that when I’m listening to someone’s story I try very hard to factor in those things that may have influenced what the person does, rather than just thinking the person is aware of doing all they are doing.

 

Benedetti, F. (2013). Placebo and the new physiology of the doctor-patient relationship. Physiological Reviews, 93(3), 1207-1246. doi:10.1152/physrev.00043.2012

Damasio, A., & Damasio, H. (2016). Pain and other feelings in humans and animals. Animal Sentience: An Interdisciplinary Journal on Animal Feeling, 1(3), 33.

Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science, 196(4286), 129-136.

Rohrbach, H., Zeiter, S., Andersen, O. K., Wieling, R., & Spadavecchia, C. (2014). Quantitative assessment of the nociceptive withdrawal reflex in healthy, non-medicated experimental sheep. Physiology & behavior, 129, 181-185.
Vlaeyen, J. W. (2015). Learning to predict and control harmful events: Chronic pain and conditioning. Pain, 156, S86-S93.

Getting persistent pain and disability confused


As I read blogs and tweets and posts on social media, and even peer reviewed papers in journals, I often read that what we’re trying to do in sub-acute pain management is to prevent chronic pain from developing (note, when I talk about pain that goes on beyond healing, more than three months, or has no useful function, I may use the term “chronic” or I may use the more recent term “persistent” – they mean the same thing, except persistent has perhaps less baggage…).

I want to take aim at that focus – to prevent pain from persisting – and think carefully about it. Let’s take a 56 year old woman with a painful knee, a knee that’s been diagnosed as having osteoarthritis (OA). Now, although we have surgical management for OA (a knee replacement – uni-compartment or even a total knee replacement), in most cases surgeons are not enthusiastic about doing a knee replacement on a younger person, particularly someone who is active (plays netball, golf, runs, gardens). So if a knee replacement is not a thing – yet – what do we do? Most of us will know about the value of remaining active and fit, losing weight and maintaining good range of movement (see here for the NICE guidelines, 2017). We know that these things will maintain function – but they won’t stop cartilage deterioration (much, if at all), and they won’t stop the pain. No matter what we do – even medications are not always especially helpful – pain is likely to persist. Does that mean we’ve failed? Reading some of these blogs, it certainly seems it does.

Let’s take back pain – most of us will know back pain occurs periodically throughout life, from the time we’re teens, through to old age. In some people a single bout of back pain happens and then they’re fully recovered and never bothered again, but for many of us, we’ll be troubled with repeated bouts throughout our lives. And still others will have one bout than just never ends (Axen & Leboeuf-Yde, 2013; Vasseljen, Woodhouse, Bjorngaard, & Leivseth, 2013).  This is despite our best efforts to prevent the onset of low back pain, and to treat it effectively – pretty much all our treatments provide a small amount of help but only exercise has been shown to prevent a new bout after the first one (Choi, Verbeek, Wai-San Tam & Jiang, 2010) – and even then the evidence was “moderate” and only at one year.

So… when we begin to examine claims that by treating musculoskeletal problems early we can prevent pain from becoming chronic or ongoing, I think we need to stop and pause before letting the blood rush to our head.

If we can’t prevent pain from hanging around, what can we do? What is the aim of all this treatment?

Well, let’s take a quick look at the Global Burden of Disease (Hoy, March, Brooks, Blyth, Woolf, Bain et al, 2014). In this piece of work, “Out of all 291 conditions studied in the Global Burden of Disease 2010 Study, LBP ranked highest in terms of disability (YLDs), and sixth in terms of overall burden (DALYs). The global point prevalence of LBP was 9.4% (95% CI 9.0 to 9.8). DALYs increased from 58.2 million (M) (95% CI 39.9M to 78.1M) in 1990 to 83.0M (95% CI 56.6M to 111.9M) in 2010. Prevalence and burden increased with age.” [emphasis mine].

What this means is that although low back pain is not a fatal disease, that may well be the problem – people don’t die from low back pain, they live with disability all the days of their life. And worse, the burden of low back pain is increasing. And this is despite all the work we (you, me, the entire health system) is putting in.

If we can’t “get rid of” low back pain (and it looks like we don’t yet have the tools to do so), what are we trying to do?

Given our poor outcomes for completely curing low back pain, we need to aim to reduce the impact of pain on people’s lives.

And not just low back pain, but things like tennis elbow, frozen shoulder, neck pain, abdominal pain, pelvic pain, headache, migraine, osteoarthritis…

For a moment, let’s think about the effect on a person going through treatment, being promised that “pain education” will reduce their pain, that exercises will get rid of their pain, that gadget A or B will get rid of their pain, that treatment Y or Z will get rid of their pain. What do you think it feels like to be completely adherent about everything you’re being asked to do, but still feeling a failure because that pain does not go? Think of the language used by some of our colleagues – “failed back syndrome”? Who failed, exactly?

Before I get harangued for breathing the word that, ooops, our treatments don’t work very well, let me address the issue of “pain education” and pain intensity. Don’t forget that the only way we can know how much it hurts someone is by asking them. And our usual tool is that 0 – 10 scale, where 0 = no pain and 10 = most extreme pain imagined. Have you ever tried doing that on yourself? Seriously – how do you rate your own pain? Some of that pain rating is about how much we’re prepared to (capable of) putting up with. Some of that rating is about how bothered (fed up, distressed, frustrated) we are about our pain. Some of it is about “OMG I don’t know what this is and how long it’s going to go on for”.

What this means is that when someone gives an explanation it can –

  • make the experience less frightening,
  • less distressing,
  • more understandable,
  • less bothersome

and as a result, when we’re then asked for our pain intensity rating on that darned scale, we reduce the score we give our pain. It does not necessarily mean the pain has reduced in intensity – a pain scale is a means of communicating something about our experience, thus it’s a pain-associated behaviour with the purpose of communicating something. So if a person isn’t ‘convinced’ by our pain education, you know they’ll keep their score pretty high.

So, there are some people for whom we cannot reduce or get rid of their pain. It’s likely to persist. And it’s these people who can be viewed as “heartsink” patients, who hang around not getting better. Well, unless we begin looking at their experience and examine what they’re looking for (and believe me, it’s not pain reduction – it’s what pain reduction means they can do) we’re going to be stuck. And so will they. Let’s get it into our heads that pain reduction is not achievable for all, but reducing the impact of pain on life is something we can all help with. Let’s stop demonising the person who has to live with pain that doesn’t respond to all our ministrations and begin looking deeply at ourselves and why we avoid recognising that we can’t win ’em all. And let’s get on with the business of helping people do what’s important in their lives, irrespective of pain.

 

 

Axén, I., & Leboeuf-Yde, C. (2013). Trajectories of low back pain. Best Practice & Research Clinical Rheumatology, 27(5), 601-612. doi: http://dx.doi.org/10.1016/j.berh.2013.10.004

Choi, B. K. L., Verbeek, J. H., Wai-San Tam, W., & Jiang, J. Y. (2010). Exercises for prevention of recurrences of low-back pain. Occupational and Environmental Medicine, 67(11), 795-796. doi:10.1136/oem.2010.059873

Hoy, D., March, L., Brooks, P., Blyth, F., Woolf, A., Bain, C., . . . Buchbinder, R. (2014). The global burden of low back pain: Estimates from the global burden of disease 2010 study. Annals of the Rheumatic Diseases, 73(6), 968-974. doi:10.1136/annrheumdis-2013-204428

Vasseljen, O., Woodhouse, A., Bjorngaard, J.H., & Leivseth, L. (2013). Natural course of acute neck and low back pain in the general population: The HUNT study. Pain, 154(8), 1237-1244.

Back to basics about psychosocial factors and pain – v


I’ve been writing about psychosocial factors and pain but I realise that I haven’t actually defined what I mean by psychosocial factors. The strange thing about this term is that it’s often conflated with “psychological” or “psychopathological” when it’s actually not. So… where to begin?

The Collins English Dictionary defines psychosocial as: “of or relating to processes or factors that are both social and psychological in origin”, while the Oxford English Dictionary defines it as “Of or relating to the interrelation of social factors and individual thought and behaviour.” According to the Oxford, it first appeared in the American Journal of Psychology in 1890 when it was used to describe the factors associated with the increase of alcoholism. An 1899 journal used it to describe “… psycho-social phenomena, such as language, customs, rights, religion etc., arising from the action of social elements with or upon the individual mind.”

So, the term is fairly recent but seems to have always been associated with broader influences on thoughts and behaviour – that is, a reciprocal response between what individuals think and do, and what helps to shape (and also responds to) what happens in the community.

When we think about pain, the most common “psychosocial” factors seem to be psychological – things like attention (vigilance), catastrophising (thinking the worst), negative affect (low mood), treatment seeking (behaviours associated with looking for help), avoidance (not doing, not approaching). What is lacking in clinical practice, in my humble opinion, is the relationship between how these factors develop and are maintained, and how those around an individual (both family and the wider community) respond to these factors. It’s not that there is no research into these relationships – it’s that research is complex, it’s tough to conduct experiments in this field, and effecting change once relationships are identified is pretty hard. More than that, health professionals typically see individuals, not people-in-context.

BUT here are some of the areas currently being explored.

Clinician behaviour – there would be few readers of this blog who are unfamiliar with Ben Darlow’s work on the power of what clinicians say (Darlow, Dowell, Baxter, Mathieson, Perry & Dean, 2013), though he’s not the first research to begin to look at this – Tamar Pincus and others have also reviewed the influence of practitioners beliefs on what they do for people with persistent pain (Parsons, Harding, Breen, Foster, Pincus, Vogel & Underwood, 2007).  The broad conclusions from this body of work, of which these two are tiny tips of a very large iceberg, is that what clinicians believe about pain and chronicity and hurt/harm influences both their treatment recommendations and their attitude towards people experiencing persistent pain, and has a direct effect on chronicity in the acute stages of a pain problem.

Family responses – Herta Flor and colleagues explored the impact of persistent pain on family relationships way back in the 1980’s, while much more recently,  Burns, Post, Smith, Porter et al (in press) investigated the interaction between spouse criticism and the effect on pain intensity and behaviour in people with persistent low back pain. Chan, Connelly & Wallace (2017) established that poor peer relationships influenced both emotional functioning and persistent pain amongst adolescents, while treatment seeking amongst adolescents was found to be associated with elevated treatment seeking in their parents (Stone & Wilson, 2016). Whether the relationships are genetic (in family patterns of persistent pain and disability), or learned (social learning theory) or a mix of both – it looks like how others respond and behave in relation to pain and disability has a strong influence on persistent pain in an individual.

Work – This, naturally, has been the place of many a study trying to establish a relationship between biomechanical factors and the onset and maintenance of pain, but it has also been the location for studies examining social relationships like supervisory responses, peer relationships, employer flexibility along with the personal effects of workplace stress on the body. I’m not going to review the myriad studies, but point you to a good systematic review of prognostic factors for return to work by Steenstra, Munhall, Irvin, Oranye, Passmore et al (2016) to demonstrate just how many factors have already been identified.

I’ve barely touched the surface of the social aspects influencing our experience of pain and disability. It’s evident that these factors have been identified – but let me ask you this: How often do you identify and then provide an intervention for these social factors? And if not, why not? And if not you – who?

 

Burns, J. W., Post, K. M., Smith, D. A., Porter, L. S., Buvanendran, A., Fras, A. M., & Keefe, F. J. (2017). Spouse criticism and hostility during marital interaction: effects on pain intensity and behaviors among individuals with chronic low back pain. Pain.
Chan, S. F., Connelly, M., & Wallace, D. P. (2017). The Relationship Between Pain Characteristics, Peer Difficulties, and Emotional Functioning Among Adolescents Seeking Treatment for Chronic Pain: A Test of Mediational Models. Journal of Pediatric Psychology, jsx074.
Darlow, B., Dowell, A., Baxter, G. D., Mathieson, F., Perry, M., & Dean, S. (2013). The enduring impact of what clinicians say to people with low back pain. The Annals of Family Medicine, 11(6), 527-534.
Flor, H., Turk, D. C., & Scholz, O. B. (1987). Impact of chronic pain on the spouse: marital, emotional and physical consequences. Journal of psychosomatic research, 31(1), 63-71.
Parsons, S., Harding, G., Breen, A., Foster, N., Pincus, T., Vogel, S., & Underwood, M. (2007). The influence of patients’ and primary care practitioners’ beliefs and expectations about chronic musculoskeletal pain on the process of care: a systematic review of qualitative studies. The Clinical journal of pain, 23(1), 91-98.
Steenstra, I. A., Munhall, C., Irvin, E., Oranye, N., Passmore, S., Van Eerd, D., … & Hogg-Johnson, S. (2016). Systematic review of prognostic factors for return to work in workers with sub acute and chronic low back pain. Journal of occupational rehabilitation, 1-13.
Stone, A. L., & Wilson, A. C. (2016). Transmission of risk from parents with chronic pain to offspring: An integrative conceptual model. Pain, 157(12), 2628-2639.

Back to basics about psychosocial factors and pain (ii)


But what about the bio? No, not the biographical, the biological! It’s something I often get asked – like “if you think pain is psychological/psychosocial factors play a part then you’re obviously not including the biological” – oh woe is me, for no, pain definitely involves the biological. But it’s not quite as simple as we’ve come to believe.

Let’s begin at the very beginning. Can we have pain – and not know about it?

The answer is – no, and that’s exactly why anaesthetics are used. The distinction between pain and nociception is that it’s entirely possible for nociception to be occurring all the time, even while unconscious, whereas pain can only be experienced by a conscious person. What this means is nociception is about activity in the nociceptive system right up until the point at which we become conscious of it. And the point at which we become conscious of the ouch shifts depending on a bunch of things, one of which is how much attention we have available, our current goals, whether we’ve had this experience before, what we think the experience is about, and what we’ve learned about this experience from our community.

So, I’m going to discuss pain biology from the brain down instead of nociceptive fibres because our brains are not just blank pages waiting for information to hit it – but actively filter, select and augment information to (a) keep us alive and safe, and (b) help us reach our goals. Louis Gifford put this nicely – our brain is sampling from our context, cognitive set, mood, chemical and structural inputs (neurodegeneration, metabolic changes and plasticity) as well as our current sensory input (which is the bit we usually start from). What the brain then does is generate outputs – the experience of pain, movements, immune response, endocrine responses, and what goes on in our somatosensory system (Gifford, 1998).

What parts of the brain are active when we feel pain?

Well, there are at least three parallel cortical processes – one is essentially about where we hurt and involves the S1 or somatosensory cortex, the parietal operculum, the cingulate cortex and the posterior insula. The second is about attention or salience and involves the anterior cingulate cortex, the amygdala and the anterior insula. The third is about generating and integrating a behavioural response – and involves the frontal cortex (orbitofrontal, anterolateral and prefrontal), the middle cingulate cortex, and the posterior cingulate cortex. (Fenton, Shih, & Zoltan, 2015).

Now before I go any further, I want to point out that our understanding of these networks is based on various brain imaging studies – and brain imaging studies do not show the “what it is like” to experience pain. Our understanding is incomplete still because imaging technology is still evolving (see Borsook, Sava & Becerra (2010) for more information). But it is from the studies that we begin to  get an understanding of the complexity of the processes and networks involved in producing our experience – no wonder some feel overwhelmed by the sheer volume of information we could explore when trying to understand pain! Especially if our focus has traditionally been on peripheral to spinal nociceptive processing – by the time we get to the brain we’re overloaded and it just seems a bit hard to comprehend.

When we investigate what Melzack calls the “neuromatrix” we need to remember that our understanding is incomplete. What we do know is there is no “pain matrix” but instead there is a salience matrix where simultaneous processing across multiple locations in the brain occur. These locations include areas generally associated with emotions, areas associated with cognitions, and with location and response generation. And importantly, there is never a time when these areas are completely inactive – there is constant activity throughout the networks, meaning that when a stimulus arrives from the periphery, it arrives into an active “salience” network – always determining the question “compared with what is happening right now (goals and alertness) how dangerous/important is this really?”

For a lovely image showing the various areas of the brain involved in processing this experience – click here for the full article – take a look at this image from Denk, McMahon & Tracey (2014)

Now if you’re wondering why I haven’t covered the brainstem and spinal cord etc – do not worry, these will be coming soon! But I won’t be discussing nociception because this is usually discussed in undergraduate training and is often the focus and only aspect of pain covered!

Next time – delving into mechanisms!

What are the implications of the complexity of central processing?

  1. The brain is not simply waiting for information – it actively seeks information relevant to survival
  2. Psychological processes such as attention, emotion and decision-making are biological
  3. The point at which we become aware of pain shifts depending on inputs (bottom up) as well as salience, emotions and consciousness (top down) and contextual factors including what we learn from our socio-cultural environment

And what this means is that psychosocial factors are integral to a biopsychosocial framework for understanding pain. In other words – it is not possible to divide the experience of pain into biological, psychological or social only, except for teaching/learning purposes.

 

 

Borsook, D., Sava, S., & Becerra, L. (2010). The pain imaging revolution: advancing pain into the 21st century. Neuroscientist, 16(2), 171-185. doi:10.1177/1073858409349902

Denk, F., McMahon, S. B., & Tracey, I. (2014). Pain vulnerability: A neurobiological perspective. Nat Neurosci, 17(2), 192-200. doi:10.1038/nn.3628

Fenton, B. W., Shih, E., & Zolton, J. (2015). The neurobiology of pain perception in normal and persistent pain. Pain Management, 5(4), 297-317.

Gifford, L. (1998). Pain, the Tissues and the Nervous System: A conceptual model. Physiotherapy, 84(1), 27-36. doi:10.1016/S0031-9406(05)65900-7

Knee pain – and central sensitisation


Last week I started to discuss central sensitisation indicators in people with osteoarthritic knees, based on a paper by Lluch, Nijs, Courtney, Rebbeck, Wylde & Baert, et al (2017). I’m going to continue with this topic this week, because with the rise of osteoarthritis in the general population and particularly the impact of an aging population, I think we will all need to think hard about how we conceptualise osteoarthritis, and what we do for management. While efforts within my own Department (CReaTE – tissue engineering) involve developing new ways to remodel knee-joint tissues, we know that it will be some years before this approach is widely available (human trials haven’t started yet), and given the relative lack of funding for joint replacements, I think developing effective assessment and rehabilitation for painful knees is a real area of development.

So last week I discussed using simple measures such as >5 on a 0 – 10 VAS (NRS), pain drawings/maps showing radiating pain or widely distributed pain, the pattern of pain fluctuation (during activity, with an increase after activity), and using a couple of fairly simple questionnaires to help identify those most likely experiencing more than the “simple” OA pain we’ve learned about. And as always, identifying psychosocial factors which can lead to increased disability and distress is important.

Along with the clinical interview, we usually incorporate physical examination or physical performance testing. There are some indicators that might be useful such as inconsistent responses to our usual physical examination (ie testing increases pain even though some of them shouldn’t do so) – this should not be interpreted as a sign that the person is “faking bad” or exaggerating their experience. I can’t emphasise this enough! It’s possible that anxiety on the part of a person can wind the nervous system up – leading to what is usually non-nociceptive input being interpreted as nociceptive (Courtney, Kavchak, Lowry et al, 2010).

Another indicator is the presence of widespread hypersensitivity to mechanical stimuli – it’s a common finding in people who have central sensitisation and includes increased response to pressure and touch. You could, as a clinician, use a pressure algometer both close to the knee, and further away, to establish over-excitability of the nociceptive pathways. Interpreting findings using pressure algometry is not straightforward because there is overlap between those with OA and those without, but it’s possible to use norms from the general population (such as Nesiri, Scaramozzino, Andersen et al, 2011). It’s a bit of a challenge because of the overlap between the two populations, but can add to the clinical picture. Pain (allodynia) on light touch or being stroked with a cottonwool ball around the knee, is definitely a clue that something’s up.

Both thermal hyperalgesia and tactile hypoaesthesia (reduced sensitivity to von Frey fibre testing) have been associated with central sensitisation – if you don’t have formal testing apparatus, the back of a warmed teaspoon placed on the skin for 10 seconds should be experienced as hot but not painful in someone who isn’t tending to central sensitisation, and you can use cottonbuds (or cottonwool) to identify loss of sensation acuity, provided you do so in a systematic way (the authors suggest starting where it’s most painful and stimulating the skin in a wheel spoke pattern, gradually widening out).

Putting it all together

Any single test, on its own, is unlikely to be a good predictor of central sensitisation, but when combined with the information you obtain from the person, along with the relevant questionnaires, should begin to help develop a picture of who is likely to have a less-than-ideal response to planned trauma. What we do about reducing the potential for central sensitisation is still  begin hotly debated but we DO know that giving good information about pain mechanisms, and encouraging graded exposure and graded activity can be helpful. Given that exercise is a good approach for reducing the impact of osteoarthritis in the knee, for those with the additional burden of central sensitisation, I think swimming or hydrotherapy could also be helpful, as could mindfulness and even mindful movement like tai chi, yoga or xi gong.

Conclusion

People living with OA in their knees often spend many years having difficulty managing their pain before they are able to have surgery. From recent research in New Zealand, I don’t think many people are offered a pain “education” approach, and indeed, I’d bet there are a lot of people who don’t get referred for movement-based therapy either. Misunderstanding is rife in OA, with some people uncertain of the difference between osteoarthritis and rheumatoid arthritis, and others very worried that they’re going to “wear the joint out” if they exercise. While OA isn’t as sexy as low back pain, doesn’t have the economic cost of low back pain, and has a reasonable surgical option – it is still a significant problem for many people. Helping those people be more confident to move, helping reduce their uncertainty about the effect of movement on their joints, and giving them an opportunity to think differently about their knee pain would be a real step forward. Surgery, while helpful for many, is either not available or unsuccessful for others, and it’s time we attended to their needs as well.

 

Courtney CA, Kavchak AE, Lowry CD, et al. (2010). Interpreting joint pain: quantitative sensory testing in musculoskeletal management. Journal of Orthopaedic Sports Physical Therapy. 40:818–825.

Lluch Girbes E, Meeus M, Baert I, et al. (2015) Balancing “hands-on” with “hands-off” physical therapy interventions for the treatment of central sensitization pain in osteoarthritis. Manual Therapy. 20:349–352.

Lluch, E., Nijs, J., Courtney, C. A., Rebbeck, T., Wylde, V., Baert, I., . . . Skou, S. T. (2017). Clinical descriptors for the recognition of central sensitization pain in patients with knee osteoarthritis. Disability and Rehabilitation, 1-10. doi:10.1080/09638288.2017.1358770

Neziri AY, Scaramozzino P, Andersen OK, et al. (2011). Reference values of mechanical and thermal pain tests in a pain-free population. European Journal of Pain. 15:376–383.

Getting stuck with language


In my last post I talked about the ways in which humans learn to relate abstract concepts and experiences together (symbolic relations). I pointed out that we learn to take another person’s point of view as part of developing empathy, and that by interacting with our world we become aware of our place (here) and someone or something else’s place (there). We also learn “me” and “you” (not me), along with near and far, now and then and myriad other abstract concepts that our language can allow us to understand. I suggested that the flexibility of symbolic relations and the relational framing we develop as a result of this skill can be both a help and a hindrance.

Yes, we can remember that a pot can be used to cook, but we also can’t unlearn that relationship. And in being unable to unlearn a relationship we can find it difficult to consider alternative relationships between that pot and whatever else we could do with it. The pot will always be recognised as “something to cook with” although it might also become associated with a receptacle for water, a paperweight, a hat, and even a weapon – but when we’re first asked “what do you use a pot for?” we’ll almost always come up with “cooking”.

In relational frame theory, we develop the ability to empathise or adopt the view of another person based on perspective taking and contextual cues. Contextual cues help us learn the concepts of “I” and “you”  by moving from “here” to “there” to take the place of the other person. If a pen is here, and paper is there, when I go to the paper, it becomes “here” and the pen is “there”. In technical terms this is called deictic framing and this is how kids learn that some concepts only make sense from a given point of view – and here and there are two of those concepts.

How does this relate to pain?

Well, to enjoy being with others, you need to have sufficient deictic framing skills to “stand in another person’s moccasins”, to empathise with their feelings and to be willing to feel those feelings (Villatte, Villatte & Hayes, 2016, p. 32). The thing is, we don’t always want to feel what another person is feeling, especially if we’re angry with them, or they’re feeling sad or some other negative emotional state. We learn to put our ability to empathise on hold to avoid experiencing those feelings. We do this with our own emotions and experiences we’d rather not have. And it’s an adaptive thing – we don’t want to be completely immersed in another person’s experience all the time because it’s difficult to know what our own feelings are vs those of another. We also don’t want to experience all the negative things around us – we learn from them, true, but we don’t really want to feel them all the time. So we develop a skill called “experiential avoidance”. That is, we learn not avoid experiences we’d rather not have.

Experiential avoidance is a cool skill, it’s definitely helpful – it is a process that we use to avoid personal injury, unpleasant people, or situations we don’t feel comfortable in. BUT there’s a catch. Because we relate concepts to one another, we associate words with experiences and memories as well. This is also useful – we can recall the lovely feeling of summer even in the middle of a grey old winter! But at the same time, our most potent learning is often associated with unpleasant experiences, and so for me the sound of a rumbling truck can bring back all the memories of my house being jolted and struck by an earthquake. And because that experience is associated with feeling out of control, helpless, worried and unsettled, those emotions come back along with the memory of the earthquakes. All brought about by hearing a truck rumbling past! And talking about the earthquakes, for some people, is enough to bring back all those same memories.

No wonder, then, for some of the people we work with, just seeing someone walking by is enough to generate the memories, emotions and concerns they experience when they try to walk on a painful foot.

Because of our tendency to avoid experiences that don’t feel good, we naturally try to avoid coming into contact with those stimuli that evoke those negative feelings etc. For some people this can mean avoiding watching images on TV – I remember avoiding watching the tsunami in Japan that happened just after the quakes here in Christchurch. To me the emotions were too raw, I felt too overwhelmed by my own situation to feel I could empathise with those people in Japan.  In some of our clients, just talking about their own painful body can be overwhelming, bringing back unpleasant emotions, memories and thoughts. And indeed for some people, just seeing others doing the things they believe will hurt if they did them is enough to provoke both a negative emotional response AND an flare-up of their pain.

So. Experiential avoidance can help us avoid feeling overwhelmed…but it also stops us experiencing what is happening right now. And I think you can see how it can stop us learning, and it can limit the range of things we’re happy to do – not because there’s any threat right here and now, but because we remember what has happened, and we make predictions of what might happen in the future. The things that might happen – might not happen too! And the things that have happened have already occurred… but our brains are good at joining the dots and being a bit over-protective.

What this means for us as clinicians (and for us as people, too), is that we might need to be gentle but firm, and help people be present here and now. And gradually show people how to be OK with experiencing things that remind us of unpleasant events in the pursuit of something far more useful – flexible responses in a world that is always changing.

Villatte, M., Viullatte, J., & Hayes, S. (2016). Mastering the clinical conversation: Language as intervention. The Guilford Press: New York. ISBN: 9781462523061

Faking pain – Is there a test for it?


One of the weird things about pain is that no-one knows if you’re faking. To date there hasn’t been a test that can tell whether you’re really in pain, or just faking it. Well, that’s about to change according to researchers in Israel and Canada.

While there have been a whole range of approaches to checking out faking such as facial expression, responses to questionnaires, physical testing and physical examinations, none of these have been without serious criticism. And the implications are pretty important to the person being tested – if you’re sincere, but someone says you’re not, how on earth do you prove that you’re really in pain? For clinicians, the problem is very troubling because allegations of faking can strain a working relationship with a person, and hardly lead to a sense of trust. Yet insurance companies routinely ask clinicians to make determinations about fraudulent access to insurance money – and worst of all, clinicians often feel they have little choice other than to participate.

In this study by Kucyi, Sheinman and Defrin, three hypotheses were tested: 1) Whether feigned performance could be detected using warmth and pain threshold measurements; 2) whether there were changes in the statistical properties of performance when participants were faking; and 3) whether an “interference” or distractor presented during testing interferes with the ability to fake and therefore provide a clue to when someone is being sincere or not.

Using university students (I hope they got course credits for participating!) who were not health science students, and were otherwise healthy, the investigators gave very little information about the procedure or hypotheses to minimise expectancy bias. Participants were then tested using a thermal stimulator to obtain “warmth sensation threshold” and “heat-pain thresholds” – this is a form of quantitative sensory testing (QST). TENS was used as a distractor in the experimental case, applied for 2 minutes before measuring the pain threshold, and during the heat pain threshold test. This was repeated with first the threshold test, then TENS. Participants were asked to pretend they were in an insurance office, being tested to establish whether they were experiencing genuine pain, after being told the test would be able to tell whether their pain was real.

What did they find out?

Well in situation one, where both threshold and warmth detection were used, and participants were asked to fake the pain intensity, respondents gave higher warmth detection ratings than normal. Not only this, but the ability to repeat the same response with the same temperature was poorer.  Heat pain threshold was also consistently different between the sincere and faked conditions, with heat pain threshold lower when people were faking (to around 3 degrees).

When the second testing option was carried out (using TENS to distract), heat pain threshold was significant lower when participants were faking, and the variance of the feigned + interference condition was three times that of the sincere condition, and the CV of the feigned + interference condition was twice that of the sincere condition.

What does this mean?

Well first of all, it means there are some consistent effects of faking in response to tests of warmth and heat-pain threshold when a distractor like TENS is used. Increased reports of warmth threshold and reduced heat pain threshold were observed, and where statistically significant. Interestingly, it was only when a distractor was used that the variability of reports were found – these authors suggest that people are pretty skilled at giving consistent reports when they’re not being distracted by an additional sensory stimulus.

Now here’s where I begin to pull this apart from a clinical and practical perspective. The authors, to give them credit, indicate that the research is both new and that it may identify some people who do have pain as malingerers. My concerns are that people with chronic pain may not look at all like healthy young university students.

We know very little about the responses to QST by people with different forms of chronic pain. We already know that people with impaired descending noxious inhibitory control respond differently to some forms of QST. We also know that contextual factors including motivation can influence how nervous systems respond to input. But my concerns are far more about the potential harm to those who are tested and found to be malingering when they’re not.

What do you do if you think a person is faking? How do you deal with this? What good does it do to suggest to someone their pain is not real, or isn’t nearly as bad as they make out? Once the words are out of your mouth (or written in a report) any chance of a therapeutic relationship has just flown right out the door. And you’re still left with a person who says they’re having trouble – but now you have an angry, resentful person who has a strong need to prove that they DO have pain.

You see, I think it might be more fruitful to ask why is this person faking pain? If it’s simply for money, surely there are far easier ways to get money than pretending to be disabled by pain? If it’s the case that a person is off out fishing or playing golf or living it up when “supposed” to be in pain, wouldn’t it make more sense to reframe their response as either recovering well (doing what’s healthy) and therefore get on with returning to work; or use a private investigator to demonstrate that he or she is actually capable of doing more than they indicate?

The presence or absence of pain is not really the problem, IMHO. To me we need to address the degree of disability that’s being attributed to pain and work on that. Maybe a greater focus on reducing disability rather than on expensive procedures to remove pain or otherwise get rid of pain is in order?

Kucyi, A., Sheinman, A., Defrin, R. (in press). Distinguishing feigned from sincere performance in psychophysical pain testing. The Journal of Pain.

Relax… if you text, your head won’t fall off & you won’t damage your spine!


You can’t have missed it – headlines in newspapers, all over the internet here and here.

https://i0.wp.com/www.kewosteo.com.au/uploads/2/4/1/3/24132050/6043934_orig.png

“Text neck” is a thing: 5 frightening maladies of the digital era

We’re all addicted to our electronic devices. Few of us realize the physical toll they’re taking on our bodies

“14 year old diagnosed with ‘text neck'”

Texting creating ‘text neck’ epidemic, doctor warns

The headlines are enough to make anyone just a bit worried – but do we need to, really?

Let’s begin with some anatomy and physiology. Necks and heads are supported by a wonderful array of ligaments and tendons (you know those tough fibrous bands you usually want to cut out of that piece of steak?), loads of muscles developed for strength, flexbility and subtle adjustment, and plenty of blood supply. The skull, although weighing about 5 1/2 kg, is supported by these muscles (and yes, there are a lot of them!), as well as balanced on strong but interlocking vertebrae.

https://i2.wp.com/padayogi.com/wp-content/uploads/2013/12/posterior_neck.gif

The thing is, that even though you’ll have seen the calculations, these are quite misleading. For one thing, the biomechanical equations used in these calculations are often based on a single point about which the head/neck rotate – and this just isn’t the case.

You can see that there are seven or more vertebrae involved in the movement, meaning the weight of your skull is distributed along each one of them – as well as that, if you take a look at the illustration above on the left, you’ll see two things: one is the strong and inelastic attachment (in white/grey) along the base of the skull and the vertebrae, and the second is just how long that trapezius muscle is. If you know much about physics, you’ll know that when there’s a long and strong anchor to an upright, it can withstand far greater forces than if it’s a short upright without any anchor. So, the weight of your skull is cantilevered (almost) forward with this muscle (and that criss-cross set of muscles you can see in the cutaway section of the image on the left above) and guess what? It’s designed so you can look forward, to the left, to the right, look up – and yes, look down.  What’s even more important to know is that calculations based on this weird equation don’t factor in living, adaptive tissue and the effects of goals, attention, beliefs and your fabulously adaptive nervous system.

This range of movement is really important: it’s so that our forward facing eyes can see all that’s needed to be seen. And most importantly, given that humans are tool-users, our necks allow our heads to bend forwards so we can see our hands as we use tools.

So, when we look down at things for ages, what’s the pain about ?

Well, the first thing is that feeling sore in the muscles around the neck is common – not only do those muscles support our head and neck, they’re also responsible for lifting and moving our shoulders. And if you hold any muscle in one position for long enough it will probably be uncomfortable. This discomfort is great! I’m not kidding, it’s a good thing to feel uncomfortable not because you’re doing any damage to the area, but because it means you’ll move. So we often sit with shoulders elevated, perhaps while writing, holding something, and most often, being tense or stressed. It’s a protective position we can get into because it makes us look a bit smaller and less threatening (blame that on our ancestors).

The second thing is that feeling sore doesn’t mean you’re doing any damage – pain in this instance is all about giving you an alert that it could be worth moving, provided your current goal isn’t more important than doing so.

What are the long-term problems with looking down a lot?

Well, this is where the research gets a bit murky. Perhaps, over time, the muscles that are usually elongated but have to work hard to support your head and neck, get used to being in that position. Perhaps the bones (vertebrae) start to reshape to conform to that position. Perhaps we feel more uncomfortable when looking up, or straight ahead even, so we avoid it. The truth is, the research literature isn’t very clear at all – and in the absence of clear evidence that looking down is bad (and I mean looking down all the time) I think we can relax a bit.

The cure for getting comfortable again? You’ve probably all done it yourselves – shrugged your shoulders, looked around (up, down, left, right), stretched your arms up and out, and perhaps – OMG – gone for a walk.

For a far more detailed analysis of posture and pain, you don’t need to look any further than Paul Ingraham’s article on Posture correction. Paul has so many other amazing and well-referenced articles on pain science that you really do need to go take a look (just remember to get up and move a little now and then, OK?)

Todd Hargrove also writes very clearly about pain and posture – this time about back pain (but include neck and shoulder pain too).

Tony Ingram has over 100 articles on pain science, so take a look at them too.

Finally, Nick Ng wrote this article: click

You might be asking why on earth am I writing about text neck when so many others have written clearly about it before.

Well, over the last week I was attending an occupational therapy conference where I was astonished to find clinicians and educators warning us about the health effects of too much screen time. Text neck was mentioned. Add to this, a recent occupational therapy newsletter featured an article by a physiotherapist arguing that we need to protect our necks from the ills of text neck. I don’t want to diss the person who said it, or the person who wrote that article, but I do think it’s critical to point out that the basis for this information is outdated pain science. It’s unnecessary scaremongering, it creates fear and concern about normal aches and pains that we all experience, it can begin a process of “medicalising” (or perhaps “pathologising” is a better word) experiences that we can self manage very easily. We simply need to know that moving is good, holding any constrained posture (even so-called “good posture”) gets uncomfortable after a while, and that it’s OK to feel pain and then do something about it. It does not mean an injury or long-term pathology has been uncovered.

Why no references? Well, the three sites I’ve posted have summarised the research very well, so I figure it’s best to go read what they’ve written rather than rehash a lot of literature that I’m not especially familiar with (I like to deal with people rather than muscles and bones and nerves).