Asked earlier today to explain the biopsychosocial framework, this was my response; I hope I’ve done it justice:
The foundation of the biopsychosocial model (BSP) is understanding the physiology and mechanisms of pain. Contrary to common misconception it is not a dichotomous ‘all biomechanical’ vs ‘all ‘psychological’ debate. It is an assessment and treatment framework for helping people manage their pain. Pain is *not* believed to be in the brain however without a brain pain cannot exist.
It acknowledges the ‘biological’ contributors to pain which the biomedical, pathoanatomical and postural-structural-biomechanical models have traditionally focused on, but explicitly highlights the role of a wide range of social and psychological factors which can create, modify, amplify and perpetuate someone’s experience of pain.
It requires an understanding that pain is an emergent ‘experience’ of the person that relies on countless biological, social, psychological, cultural and environmental factors; that it is not simply a sensation. That pain is an output from the nervous system not an input – acknowledging that pain receptors, pain pathways, pain centres (in the brain) do not exist. It is based on the realisation that nociception is neither sufficient nor necessary for pain to occur and that in the absence of a medical, nociceptive or neuropathic reason for pain, someone’s experience of pain is unlikely related to peripheral structure and/or tissues, and that treatments directed at the periphery are unlikely to have any specific effects. It recognises that catastrophising, kinesiophobia, fear-avoidance, expectations, anxiety etc. are all significant contributors to pain and addresses those rather than tissues and structure.
Clinicians recognise that the nervous system undergoes structural adaptation with pain and are most interested in ‘neurotags’ that produce cognition (what we think about pain), perception (how we feel about pain) and action (what we do in response to pain).
Treatments and interventions utilise the principle of neuroplasticity, one of which is explaining pain to reduce threat (therapeutic neuroscience education – TNE). Some others example include retraining precision via graded motor imagery and sensory discrimination, graded exposure with movement and exercise to maximise expectation violation, decoupling unhelpful learned responses, promoting self-efficacy and perhaps most importantly avoiding nociceptive language and the principle of unintended consequences (e.g. having a sense of weakness, tightness, fragility or something being “out”) and dependency upon treatment or therapist. Clinicians provide a range of strategies to promote self-efficacy and coping strategies.
TNE is commonly a part of treatment but not an isolated intervention. Clinicians use active movement and exercise as an ‘entry’ into the brain and nervous system. Exercise is used as an ‘immune stimulant’ with profound physical, psychological and emotional effects on decreasing pain. Knowledge of the peripheral and central changes taking place shifts the treatment focus. For example, understanding the neuro-immune interaction in the dorsal horn (CCL2 as a key mediator of microglial activation) which facilitates nociceptive signals creating central sensitisation (pre and post-synaptic neurons undergo physiological change with persistent pain), tissue and structure become far less important, if given any importance at all.
If practitioners have manual therapy training (i.e. Osteo, Physio, Chiro, Myo) they are likely to maximise the non-specific effects of a therapeutic alliance with the client, which may include some hands-on assessment and/or treatment without necessarily believing there to be a specific effect from manual therapy.