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 first author can be contacted at [email protected]