Do You Treat Pain and if so...

When I completed my full-time year of postgraduate in musculoskeletal Physiotherapy at Curtin University the BioPsychoSocial (BSP) model looked like this. The year was 1992.

I am not exactly sure when the changes started to occur (given I live in small remote coastal time and we only get the mail on a monthly basis), but by the mid 2000's, when I was prepping for my specialisation examination, it was definitely on my radar and informing how I approached clients with persistent pain conditions. I guess that intuitively I was aware some clients had out-of-proportion pain given their injury, listed their ailments like a French cuisine menu and described their history as clearly as if reading it with Frenzel glasses, but I never had concrete outcome measures or terms to quantify what was occurring.

Having completed a CBT pain management course through Sydney University (highly recommended) I have come to appreciate how the BPS model is not static. A client may present with a large psycho component, that following a good explanation about their situation, identifying some triggers and working out a plan of action, they return with relatively more of a biological aspect. The Bio was always there, but overshadowed by some inappropriate thoughts (e.g. rumination) and/or poor coping mechanisms. Once the Psycho was sorted, the person could then move forward and address their poor physical conditioning which would intern, enable them to start a return to work program. As an aside, we use the DASS21 to evaluate Depression, Anxiety & Stress. We use the Pain Catastrophising Scale to indicate the need for pain education and the Pain Self Efficacy Questionnaire to determine a person's confidence they are going to get better. Along with the Brief Pain Inventory, which indicates how their pain impacts their ADLs, the PSEQ is an important predictor of improving cf developing persistent pain. We found the scoring a bit tricky, especially the DASS21, until I loaded it into our electronic onboarding form (Snapforms), automated the scoring and linked it into our PMS (Cliniko) letter templates. 

I now think of the BPS model as a sausage balloon, like the ones they use to make those balloon animal sculptures. When you blow it up (initial injury), the front might expand (Bio) but so too might the end pop out (Social). Squeeze one portion and another bulge appears. The bulges are individualised and ever-changing, and they all influence each other. Rarely do you have a nice, uniform sausage.

Interestingly, I adopt a very similar approach when managing clients with another persistent problem, which is insomnia. Almost always there is a mix of biological issues e.g. sleep posture, pain, psychological issues e.g. rumination, catastrophising and social issues e.g. partner sleeping. Quite often the client has adopted poor coping strategies that are fuelling the problem and they have a lack of understanding about the overall sleep process; what it means and why it is important.

In fact, poor sleep and spinal pain go hand in hand in the literature. Regardless of whether you are looking at first events (1), transition from acute to persistent (2,3) or the association with flare events (3). Similarly, it doesn't matter if you treat children, adolescents, young adults (4-6) or adults (7,8), sleep is significantly related to pain. In fact, poor sleep is predictive of adults developing pain (5).

It would seem that if you are treating pain, you should be just as comfortable screening, assessing and treating insomnia. Are you? 


  1. Alsaadi S, McAuley J, Hush J, et al. Poor sleep quality is strongly associated with subsequent pain intensity in patients with acute low back pain. Arthritis & Rheumatology. 2014;66(5):1388-1394. doi:10.1002/art.38329
  2. Campbell P, Foster N, Thomas E, Dunn K. Prognostic indicators of low back pain in primary care: Five-year prospective study. The Journal of Pain. 2013;14(8):873-883. doi:10.1016/j.jpain.2013.03.013
  3. Costa N, Smits E, Kasza J, et al. ISSLS Prize in clinical science 2021: What are the risk factors for low back pain flares and does this depend on how flare is defined? Eur Spine J. May 2021;30(5):1089-1097. doi:10.1007/s00586-021-06730-6
  4. Meerlo P, Sgoifo A, Suchecki D. Restricted and disrupted sleep: Effects on autonomic function, neuroendocrine stress systems and stress responsivity. Sleep Medicine Reviews. 2008;12(3):197-210. doi:10.1016/j.smrv.2007.07.007
  5. Nitter A, Pripp A, Forseth K. Are sleep problems and non-specific health complaints risk factors for chronic pain? A prospective population-based study with 17 year follow-up. Scandinavian Journal of Pain. 2012/10/01/ 2012;3(4):210-217. doi:org/10.1016/j.sjpain.2012.04.001
  6. Auvinen J, Tammelin T, Taimela S, et al. Is insufficient quantity and quality of sleep a risk factor for neck, shoulder and low back pain? A longitudinal study among adolescents. journal article. European Spine Journal. 2010;19(4):641-649. doi:10.1007/s00586-009-1215-2
  7. Akerstedt T, Gillberg M. Subjective and objective sleepiness in the active individual. International Journal of Neuroscience. 1990;52(1-2):29-37. doi:10.3109/00207459008994241
  8. De Koninck J, Gagnon P, Lallier S. Sleep positions in the young adult and their relationship with the subjective quality of sleep. Sleep. 1983;6(1):52-59.

Here's to a great night of sleep!

PS The Sleep Mastery course is coming to Geraldton and Singapore in early 2023. Email me ( if you would like to attend a Sleep Mastery F2F course or have a bespoke course for your organisation.