“Bioplasticity” is one of those very newish words around. Lorimer Moseley mentioned it in a dispatch from Body in Mind and we have both used the word and concept extensively in the new Explain Pain Handbook.
We think “bioplasticity” has a nice ring to it – much bigger than neuroplasticity, with the “bio” bit allowing engagement of all body systems – recognising that it’s not just the brain and neurones which can change. There is a saying for people experiencing persistent pain in the handbook – “bioplasticity got you into this situation and bioplasticity can get you out again.”
This saying reflects that there is both a dark, and a positive, side of bioplasticity. The dark side is body systems getting better and better at looking after you – nerves conveying danger messages becoming more sensitive, brain cells involved in making pain becoming more sensitive too, and the coping systems such as the emotional, cognitive, endocrine and autonomic systems get edgy – being switched on and turned up for extended periods of time.
But the positive side of bioplasticity is a reason to be hopeful for anyone experiencing persistent pain, no matter the condition or duration. It’s all about learning how protective systems can be turned down, even switched off by thinking, moving, speaking, knowing and behaving differently. It may not be easy but even just knowing of the bioplastic potential of all the bodily systems is surely a start.
Neuroplasticity is so 2014!
– David Butler
Great change in language. There are a lot more systems involved in adaptive change to address stressors that the body faces. Why just think of the nervous system as the only one that changes. When we think of Wolf’s law for the adaptive capabilities of the MS elements, the fantastic adaptability of the immune system, and elegant complexity of the HPA axis, why just focus on the nervous system. Great strategic change. TGD
I like the idea behind the term “bioplasticity”. We know indeed that multiple body systems are involved in the initiation of (basically adaptive) protective responses to bodily threat, including the neural, endocrine and immune systems. More importantly, there is some good evidence that these systems do not operate independently but rather talk to each other. Richard Chapman proposed a couple of years ago that these orchestrated responses to pain compromise a kind of “supersystem” (http://www.ncbi.nlm.nih.gov/pubmed/18088561). Chronic pain then involve dysregulations in any of the subsystems, which in turn may lead to dysfunction in the other systems, eventually resulting in an overprotective supersystem. This view evokes interesting questions which may have important clinical implications. Back to the positive side of “bioplasticity”. I guess, when adopting this kind of network or system approach, the big question is probably what are the best ways to turn down this overprotective system. Several “entries” in the system or network should be possible, and an interesting question is how intervening in one system may affect the other system. For instance, we already know that interventions aimed at thinking about , coping differently with, and moving differently with pain (e.g., cognitive behavior therapy, motor control training, tactile acuity training, etc.) may be helpful in modifying how the neural system responds. Perhaps we should learn more about how this in turn may affect (connections with) the other systems. The same for interventions targeting the immune and endocrine systems in chronic pain. Another question is whether the different systems may be organized in a hierarchical way, with perhaps the neural system acting as a driving force changing pain responses within the supersystem? Such questions clearly ask for more and bigger interdisciplinary research efforts.
Stefaan Van Damme, PhD, Ghent University, Belgium
Health Psychology Lab (www.ghplab.ugent.be )
Department of Experimental-Clinical and Health Psychology
Twitter: https://twitter.com/suvdamme
Hi Stefaan,
Many thanks. I couldn’t agree more. We made Chapman’s supersystem paper required reading for our postgrad and undergrad pain sciences students. The paper seems more apt every time I read it.
The notion of clinical entry into one perturbed homeostatic system (if that is possible) influencing others makes for some lively research methodology. Pain and the motor system have got most of the attention but maybe we were wrong with this emphasis and we should be looking more at all the possible perturbed, edgy,s ready to run outputs such as the endocrine, motor, sympathetic and immune but also respiratory, cognitive, emotional, inflammatory and others. As an example of a futuristic question – Could attention to misconceptions lead to a lessening of inflammation and better scar quality in the future?
We have certainly attempted to expand “Explain Pain” into explaining other outputs. Each output can supply a rich explanatory narrative.
Are the outputs hierarchical? Perhaps. A fundamental unanswered clinical question during my life has been “What is it in the patient in front which has made the self “call upon” a particular immune/ sympathetic/endocrine formula as prime defender but over time the apparatus for these systems becomes perturbed, perhaps leading to CRPS yet in others the motor system is called into the formula and there are all sorts of motor deficits, in others it may be the immune system selectively and the person ends up with a “cytokine storm” based disease.
We will back the call for bigger interdisciplinary research efforts and clinical reasoning approaches that take on this way of thinking.
Cheers
David