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Pain ClassificAtions Part 4: Nociplastic Pain & Central Sensitization

Thank you everyone for bearing with me, I promise this is my last article for a while on the intricacies of pain. We will soon be able return to our regularly scheduled ARME programming such as “exercise is good” and “words matter”.


In the last few articles of this pain classification series we discussed the overall purpose of the pain experience, the concept of ‘nociception’ and what happens when we suffer an injury to neural or non-neural tissues. Things tend to get more complicated when a patient experiences persistent pain without any clear signs of tissue damage. This leads us to the concept of ‘nociplastic pain’.



Nociplastic pain is a recent term. The International Association for the Study of Pain (IASP) officially adopted the term in 2018 as a “third mechanistic descriptor” of chronic pain to “more fully characterize the known pathophysiological mechanisms of pain.” “Nociplastic”, “Nociceptive” and “Neuropathic” are the three accepted pain classifications. (6)


Why bother trying to classify pain syndromes at all?


Regardless of the pain classification we use, for the most part, we are doing the same thing – building self-efficacy in the patient, promoting exercise through meaningful physical activity, and finding ways that the patient can modify their symptoms. Classifying the pain condition in the individual simply helps guide the process of developing a plan of management, and more importantly, help the patient understand the potential neurobiological reason for what they are experiencing. (1)


What is it?


Nociplastic pain is defined as “pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.” In other words, abnormal nociception. Specifically, the problem arises from changes in how nociceptive pain works. Is this scenario, there is no evidence of peripheral nociceptor activation, and no evidence of a nerve disease or lesion. Instead, there is plasticity in the central nervous system (CNS). You can think of it as more so a “software” problem, rather than a “hardware” problem. You may be familiar with the term, “central sensitization” or maladaptive central processing, in which pain is driven by the spinal cord and brain regardless of what is occurring in the tissues (2). Although this is the case, central sensitization does not adequately capture the entirety of this pain mechanism, but it is helpful in its conceptualization. However, the term, ‘maladaptive’ does sound ‘kinda blamey’, as if the person did something wrong, but I digress.


What is the mechanism?


COMPLICATED, is what it is. Central sensitization occurs with simultaneous, ongoing, nociceptive bombardment. This causes a number of things to occur:


· Increased activity in nociceptive pathways and activation of glia in the CNS


· Poor endogenous analgesia (capacity for descending inhibition is reduced, e.g. exercise-induced hypoalgesia)


· Altered sensory processing in the brain (allodynia, photosensitivity etc.)


· Disrupted resting state functionality in the default mode network (DMN). The DMN represents areas that are more active during times of rest compared to times of cognitive activity. This involves areas such as, the medial prefrontal cortex, posterior cingulate cortex, precuneus, inferior parietal lobules and medial temporal regions. These areas are essentially impaired, which negatively affects the ability for one to rest and relax, in turn reducing one’s natural stress coping response.


The phenomenon of central sensitization is found to have links with many chronic pain conditions, including common conditions like tendinopathies, which are typically considered to be nociceptive dominant. This highlight how these experiences are not mutually exclusive and may account for the individuals who do not respond to typical therapeutic interventions.


How can we identify nociplastic pain?


An individual may present with diffuse, non-anatomical areas of pain and disproportionate, non-mechanical, unpredictable patterns of pain provocation. They may say something along the lines of “I got groceries and was bedridden for 3 days.” The individual’s pain is disproportionate to the nature and extent of the injury or pathology, if present. (8) This experience is often overlaid with psychosocial factors such as, anxiety and depression, which should be managed by appropriate healthcare providers.


The individual may also present with hypersensitivity of other senses , for example, sight, smell and hearing, as well as occur in conjunction to sensory allodynia (non-noxious stimuli eliciting pain) and hyperalgesia (noxious stimuli eliciting increased pain) (4). They may also present with the “after effect” and “wind-up” phenomenon.


“After Effect” and “Wind-Up”

These are phenomena that occur in individuals with central sensitization. The ‘after effect’ is described as a “lingering pain sensation after cessation of painful stimulation”, while the wind up, otherwise known as temporal summation, is the increase in perceived intensity of pain in response to sequential stimuli of equal strength, through amplification of nociceptive signalling.


The characteristics discussed above can be present in a multitude of different conditions. To be able to determine whether nociplastic pain is dominant, we can use two concepts: Chronic Overlapping Pain Conditions, and Top Down Dysregulation


Chronic Overlapping Pain Conditions (COPC)


An individual may present with neck pain, back pain, headaches, irritable bowel syndrome, PCOS, and endometriosis all at the same time. As mentioned prior, nociplastic pain is a product of the CNS adapting to nociceptive bombardment. Therefore, we often see multiple concurrent pain conditions present, as central sensitization worsens all forms of pain experienced by the individual, including old conditions. (11)


Top-Down Dysregulation - S.P.A.C.E.


This is an acronym for the diagnostic manifestation of top-down mediated central sensitization. (5)


· Sleep disturbances

· Pain (widespread, diffuse)

· Affective perturbation (anxiety, depression)

· Cognitive disturbances

· Energy deficit (fatigue)


What can we do?


Just like everything else, education, reassurance and exercise. However, these conditions are not self-limiting and will likely not improve without a proper plan.

It is paramount that the individual understands what is happening in their body. When they understand that their nervous system has learned to be more sensitive to pain, they will understand that we can recondition it.

To recondition, we need to:


· Make them adapt through careful, gradual exposure to painful activities. This is especially important for activities they are afraid of but are meaningful to them.


· Appropriately dose the physical activity for energy management. This can involve questions such as, does the individual need to do more? if so, then gradually increase the activity in a goal-oriented manner. Do they need to do less or pace themselves? Have them take regular breaks throughout the day at an interval that helps them recover to a manageable level.


· Change their lifestyle to be more conducive to recovery. This can involve addressing factors such as, sleep, stress, diet, mood.


· Build a flare-up plan for when things inevitably go wrong. This will guide expectations and make sure the individual knows what they can do when they hit red lights, and how to progress passed them.

Exercise, why can it help?


Exercise alters central nociceptive processing, facilitates the descending inhibitory system, and promotes desensitization. This is in addition to the other great benefits it allows for, like increased muscle mass, bone density, cardiac output, and self-efficacy. Generally, both aerobic and resistance exercise has been found to be more beneficial than stretching exercise (3). However, the best exercise is the one that gets done. We want the person to buy in and adhere to the program, so it is essential to ‘start low and go slow’, and to engage in meaningful activity. Remember, meaningful to them as an individual, not to you as a clinician. I personally use the traffic light analogy for pain, discussed in my previous article, and RPE as a means of autoregulating the dose of activity.


Pain management is always a team effort. Be open to communication, be committed, and always keep in mind the 3 A’s:


1. Be Affable - genuine, likable, friendly. Show them that you care.

2. Available - be there when the patient needs help.

3. Able - be good at what you do, and follow evidence-based practice.


Remember, don’t let your ego get in the way of care. Regular changes and alterations to treatment are necessary.


“Don’t commit to treatment. Commit to re-assessment” – Annie O’Connor.



References:


1. Alibrandi, Elaine. “What’s in a Name for Chronic Pain?” Pain Research Forum, 5 Feb. 2018, https://www.painresearchforum.org/news/92059-whats-name-chronic-pain.

2. Clauw DJ. Fibromyalgia: a clinical review. JAMA. 2014 Apr;311(15):1547–55.

3. Franco, Katherinne Ferro Moura, et al. “Prescription of Exercises for the Treatment of Chronic Pain along the Continuum of Nociplastic Pain: A Systematic Review with Meta-Analysis.” European Journal of Pain, vol. n/a, no. n/a. Wiley Online Library, doi:https://doi.org/10.1002/ejp.1666. Accessed 13 Dec. 2020.

4. Jensen, Troels S., and Nanna B. Finnerup. “Allodynia and Hyperalgesia in Neuropathic Pain: Clinical Manifestations and Mechanisms.” The Lancet Neurology, vol. 13, no. 9, Sept. 2014, pp. 924–35. www.thelancet.com, doi:10.1016/S1474-4422(14)70102-4.

5. Kolski, Melissa C., and Annie O’Connor. A World of Hurt: A Guide to Classifying Pain. Thomas Land Publishers Incorporated, 2015.

6. Kosek E, Cohen M, Baron R, et al. Do we need a third mechanistic descriptor for chronic pain states? Pain. 2016 Jul;157(7):1382–6.

7. Lin I, Wiles L, Waller R, et al . What does best practice care for musculoskeletal pain look like? Eleven consistent recommendations from high-quality clinical practice guidelines: systematic review.British Journal of Sports Medicine 2020;54:79-86.

8. Smart KM, Blake C, Staines A, Thacker M, et al. “Mechanisms-Based Classifications of Musculoskeletal Pain: Part 1 of 3: Symptoms and Signs of Central Sensitisation in Patients With Low Back (± Leg) Pain.” Manual Therapy, Aug. 2012, doi:10.1016/j.math.2012.03.013.

---. “Mechanisms-Based Classifications of Musculoskeletal Pain: Part 2 of 3: Symptoms and Signs of Peripheral Neuropathic Pain in Patients With Low Back (± Leg) Pain.” Manual Therapy, Aug. 2012, doi:10.1016/j.math.2012.03.003.

---. “Mechanisms-Based Classifications of Musculoskeletal Pain: Part 3 of 3: Symptoms and Signs of Nociceptive Pain in Patients With Low Back (± Leg) Pain.” Manual Therapy, Aug. 2012, doi:10.1016/j.math.2012.03.002.

9. Smart KM, Blake C, Staines A, and Doody C. “The Discriminative Validity of ‘Nociceptive,’ ‘Peripheral Neuropathic,’ and ‘Central Sensitization’ as Mechanisms-Based Classifications of Musculoskeletal Pain.” The Clinical Journal of Pain, Oct. 2011, doi:10.1097/AJP.0b013e318215f16a.

10. Walton, David M., and James M. Elliott. “A New Clinical Model for Facilitating the Development of Pattern Recognition Skills in Clinical Pain Assessment.” Musculoskeletal Science & Practice, vol. 36, Aug. 2018, pp. 17–24. www.mskscienceandpractice.com, doi:10.1016/j.msksp.2018.03.006.

11. Yunus MB. Central sensitivity syndromes: a new paradigm and group nosology for fibromyalgia and overlapping conditions, and the related issue of disease versus illness. Semin Arthritis Rheum. 2008 Jun;37(6):339–52.