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InPsych 2016 | Vol 38


Reversing maladaptive plasticity in chronic pain

In the past decade, there have been significant advances in research on neuroplasticity and its role in chronic pain. Put simply, neuroplasticity is the capacity of the nervous system to change its structure and function in response to persistent changes in its environment. While psychologists have long assumed that learning and memory are based on the plasticity of synapses and neural networks (Hebb, 1949), neuroplastic changes were only detected in mature brains following recent advances in neuronal tracing, electrical and magnetic recordings and functional brain imaging (Pascual-Leone, Fregni, & Merabet, 2005). The following cellular mechanisms have been identified to underlie neuroplasticity: axonal growth and guidance resulting in the formation of new or restored neuronal networks; synaptogenesis resulting in formation of new synapses; synaptic pruning resulting in the elimination of inappropriate synapses; transmission changes resulting in modulation of synaptic efficacy; and neurogenesis leading to turnover of new neurons in certain brain areas.

While we now know that such neuroplastic mechanisms provide the basis for learning and for the growth and development of the nervous system, not all neuroplasticity is necessarily adaptive. This is especially characteristic of neuroplasticity in chronic pain. Research has shown that maladaptive neuroplasticity that heightens pain processing and sensitivity (i.e., central sensitisation) in chronic pain underlies worsening outcomes for essentially all types of chronic pain (Apkarian, Hashmi, & Baliki, 2011). Increased excitability, connectivity and synaptic efficiency of neurons in peripheral and central pain pathways (Woolf, 2011), driven by maladaptive learning processes have been proposed to facilitate this reorganisation (Flor, 2008). These changes then spread to associated sensory, motor, cognitive and emotional neuronal networks (Flor, 2008). Maladaptive thoughts (e.g., rumination, catastrophising), emotions (e.g., depression, anxiety) and behaviours (e.g., pain-contingent resting, avoidance) likewise strengthen maladaptive pain learning associations and reinforce sensitisation of neural pain pathways (Jensen, 2010).

However, learning processes can also be used therapeutically to build new adaptive pain-coping associations (e.g., pain acceptance, self-efficacy, resilience, paced activity) that serve to counteract these maladaptive associative learning links. In one seminal study, a cognitive-behavioural therapy approach targeting these associations resulted in reversal of central sensitisation, and decreased pain catastrophising was significantly associated with this reversal process (Seminowicz et al., 2013).

Based on the recognition of the shared reorganisation of cognitive and emotional network links in chronic pain, depression and anxiety, a transdiagnostic therapeutic approach targeting these links is likely to be the most effective in reversing maladaptive neuroplasticity (Linton, 2013). Essentially, the overlap in specific mechanisms between these co-occurring problems permits targeted interventions that cut across diagnostic boundaries to improve symptoms (Linton, 2013). Interdisciplinary pain management programs are ideally suited to adopt such a therapeutic framework in addressing pain and comorbid depression and anxiety, and to target critical shared mechanisms among these conditions (e.g., the cognitive process of catastrophising, kinesiophobia etc.). Such programs typically include rehabilitation physicians, psychologists, physiotherapists, occupational therapists, and members from various other specialties. Maladaptive thoughts, emotions, behaviour and fear of movement and re-injury are all explicitly addressed to restore motivation, mood and function.

With advances in understanding of overlapping mechanisms of neuroplasticity from a transdiagnostic perspective, it should be possible to use more targeted techniques to enhance adaptive pathways. Although we are not yet at the point where we can harness technology clinically to identify unique neurological signatures of an individual’s chronic pain and use algorithms to match this signature to the treatment most likely to be of benefit, this is a future goal. Indeed, some research has already shown that baseline brain states make an individual more or less suitable to hypnosis vs mindfulness meditation for pain management (Jensen et al., 2014). Given the high prevalence rate, cost and associated disability of chronic pain, there is a critical need for interdisciplinary pain treatment approaches to be customised to include those therapies most suited to a given individual’s pain.

The Brisbane Pain and Rehabilitation Service provides a community-based interdisciplinary program to mitigate the cognitive, emotional and physical concomitants of chronic pain. Participants undergo a fortnight-long customised residential group program that aims to equip them with the skills and motivation to overcome their maladaptive responses to on-going persistent pain, and to actively enhance more adaptive responses to their pain.

The program utilises the therapeutic interaction of rehabilitation physicians, psychologists, physiotherapists, exercise physiologists, occupational therapists, and dieticians.

Analyses of a database on 574 consecutive admissions over the past five years show that this transdiagnostic approach is effective in improving a range of cognitive, emotional and physical function outcomes.

The first author can be contacted at m.day@uq.edu.au


  • Apkarian, A. V., Hashmi, J. A., & Baliki, M. N. (2011). Pain and the brain: Specificity and plasticity of the brain in clinical chronic pain. Pain, 152, S49-64.
  • Flor, H. (2008). Maladaptive plasticity, memory for pain and phantom limb pain: Review and suggestions for new therapies. Expert Rev Neurotherapeutics, 8, 809-818.
  • Hebb, D. (1949). The organization of behavior. New York: Wiley & Sons.
  • Jensen, M.P. (2010). A neuropsychological model of pain: Research and clinical implications. Journal of Pain, 11, 2-12.
  • Jensen, M. P., Sherlin, L. H., Fregni, F., Gianas, A., Howe, J. D., & Hakimian, S. (2014). Baseline brain activity predicts response to neuromodulatory pain treatment. Pain Medicine, 15, 2055-2063.
  • Linton, S. J. (2013). A transdiagnostic approach to pain and emotion. Journal of Applied Biobehavioral Research, 18, 82-103.
  • Pascual-Leone, A., Amedi, A., Fregni, F., and Merabet, L. B. (2005). The plastic human brain cortex. Ann Rev Neurosci, 28, 377-401.
  • Seminowicz, D. A., Shpaner, M., Keaser, M. L., Krauthamer, G. M., Mantegna, J., Dumas, J. A., Newhouse, P. A., Filippi, C. G., Keefe, F., & Naylor, M. R. (2013). Cognitive-behavioral therapy increases prefrontal cortex gray matter in patients with chronic pain. Pain, 14, 1573-1584.
  • Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152, S2-15.

Disclaimer: Published in InPsych on . The APS aims to ensure that information published in InPsych is current and accurate at the time of publication. Changes after publication may affect the accuracy of this information. Readers are responsible for ascertaining the currency and completeness of information they rely on, which is particularly important for government initiatives, legislation or best-practice principles which are open to amendment. The information provided in InPsych does not replace obtaining appropriate professional and/or legal advice.