Sensitisation - Primary & Adaptive Vs Secondary & Maladaptive
Sensitisation is recieving a bad rap but its important to not throw the baby out with the bath water here.
IS THERE A SITUATION WHERE INCREASED SENSITISATION IS BENEFICIAL FOR THE ORGANISM?
Deciphering whether pain (or behaviour) is adaptive or maladaptive is one of the great clinical challenges that faces clinicians daily (see the Oxford Dictionary of Sports Sciences and Medicine definitions below).
Recall the definition of neuropathic pain from Treede et al. (2008)1 as "pain arising as a direct consequence of a lesion or disease affecting the somatosensory system".
The nervous system is what relays nociceptive impulses or danger signals to the brain and potentially causing a pain experience. In the instance of spraining an ankle these signals are absolutely adaptive in causing a protective response to enable the stages of healing to take place. Neuroscience researcher Adriaan Louw (2013)2 uses the metaphor of an alarm system to describe how pain works. Louis Gifford (2014)3 argues that any lesion to the nervous system (a disc injury to a nerve, or a neuropathy...) will cause some element of maladaptive pain as the injury is to the actual system that is responsible for alerting us to the (potential) threat.
The research and management of chronic pain and associated disorders (neck pain, pelvic pain, fibromyalgia, subacromial impingement, chronic fatigue syndrome, tension headache, migraine, osteoarthritis, tennis elbow, nonspecific arm pain and patella tendinopathy) has largely been attributed to central pain modulation (sensitisation) recently.
Some degree of central pain sensitisation in response to acute injury may however be considered adaptive in facilitating recovery. In this instance sensitisation of local tissues is a feature of an acute inflammatory process. In the example of an ankle sprain used above, the responsiveness of polymodal nociceptive endings is enhanced by various sources (such as serotonin from platelets, bradykinin from plasma, prostaglandins from damaged cells and substance P from primary afferent fibres). This process is called PRIMARY HYPERALGESIA or PERIPHERAL SENSITISATION of nociceptors - a mechanism to encourage an organism to prevent use and further damage of the tissues and enable healing.
SECONDARY HYPERALGESIA refers to increased responsiveness of dorsal horn neurons localised in the primary spinal segment of the primary source of nociception. Nijs et al. (2014)4 claim that clinicains should aim to differeciate between adaptive peripheral sensitisation, for example after an acute inflammatory response, and maladaptive central sensitisation (see figure 1).
For more specific detail on each section of this flow chart readers are directed to the original Jo Nijs paper in the references.
Sensitisation is an important thing for health professionals dealing with pain to not only understand, but assess and manage. It is very important clinically to understand that adaptive pain responses that might include an antalgic gait or awkward posture could be beneficial to offload injured tissues while they heal. Would we want to correct that gait or posture? Arguably not.
With regards to sensitisation, this has got an evolutionary beneficial origin to sensitise tissues and prevent excess loading while they heal. The ability to distinguish between peripheral sensitisation (primary hyperalgesia) and central sensitisation (secondary hyperalgesia) is extremely important for the reasons discussed. Peripheral sensitisation occurs in the nociceptors and protect damaged tissues. This is adaptive. Central sensitisation occurs in the nervous system (dorsal horn) and represents a 'sensitive alarm', there is no tissue damage here. This is maladaptive.
If one perceives the mechanism of an antalgic gait or awkward posture as having central sensitisation underpinning it, might we want to alter it in this case? Potentially so.
Primary hyperalgesia or sensitisation is adaptive
Secondary hyperalgesia or sensitisation is not.
Luke R. Davies :)
1. Treede, R. D., Jensen, T. S., Campbell, J. N., Cruccu, G., Dostrovsky, J. O., Griffin, J. W. Hansson, P., Hughes, R., Nurmikko, T. and Serra, J. (2008). Neuropathic Pain: Redefinition and a grading System for Clinical and Research Purposes, Neurology, 70, P.1630-1635.
2. Louw, A. and Puentedura, E. (2013). Therapeutic Neuroscience Education; Teaching Patients About Pain, International Spine and Pain Institute, USA.
3. Gifford, L. (2014). Aches and Pains: TJ International, Padstow, Cornwall, UK.
4. Nijs, J., Torres-Cueco, R., Van Wilgen. C. P., Girbes, E. L, Struyf, F., Roussel, N., Van Oosterwijck, j., Daenen, L., Kuppens, K., Van Werweeen, L., Hermans, L., Beckwee, D., Voogt, L., Clark, J., Moloney, N. and Meeus, N. (2014) Applying Modern Pain neuroscience in Clinical Practice: Criteria for the Classification of Central Sensitization Pain, Pain Physician, 17, P.447-457