Should exercise be painful?

Should exercise be painful?

When assisting a patient with rehabilitation from injury or pain, a major question that needs to be asked is "should this patient exercise through pain or not?" This becomes even more pertinent if the patient's condition consists of primary pain (1). And there have certainly been arguments for both sides on this topic (2-4) as pain management has been emerging as an increasingly relevant matter in current medicine.

Most practitioners realise that that there cannot be a "blanket rule" that can be applied to all, but every patient is an opportunity for a practitioner to clinically apply biopsychosocial framework followed by a construction of case formulation (5, 6). Thus the decision to exercise through pain or not is usually a destination that a practitioner can naturally arrive after such preceding thought-processes.

There are four important factors to consider when deciding whether or not a patient should exercise “through pain”:

 

1) Pathophysiology of the current condition
2) Mechanism of the pain being experienced
3) Patient’s attitude and beliefs
4) Level of endogenous modulation

 

1) Pathophysiology of the current condition

Perhaps the most obvious one; certain pathophysiological states logically indicate that exercising in pain would not be a sensible choice: e.g. acute inflammation post traumatic injury with tissue disruption. However some conditions are not as clear-cut: e.g. chronic patellofemoral pain. In such instances critical analysis of the diagnosis would be necessary before a decision is made: if a clinician was to reason that such patellofemoral condition was a result of muscle dysfunction from pain inhibition (7), it may be more reasonable to exercise without pain as further pain is likely to reinforce inhibition, especially in the early stages.

2) Mechanism of the pain being experienced

"Mechanism-specific approach" classifies pain into four categories (8, 9): nociceptive, inflammatory, neuropathic and dysfunctional (or nociplastic). While there are no “hard-guidelines” that can clearly define a given pain into such categories, it is not difficult to make a hypothetical call after a thorough case formulation construction, and such approach is absolutely necessary to provide a foundation of care for complex multi-dimensional conditions such as primary pain. Once mechanism of pain is hypothetically determined, the implication of experiencing such pain while exercising becomes clearer; e.g. certain nociceptive pain may be ignored, or even beneficial, whereas inflammatory and neuropathic pain is generally best to be avoided. Dysfunctional / nociplastic pain will need to be deconstructed - i.e. cause of the pain analysed - before determining the possible effects of experiencing such pain while exercising.

3) Attitude and beliefs

Pain excitation or inhibition from cortical and subcortical centres are well-documented through literature (10-12) and anecdotes, and the main constructs behind this powerful process are the attitude and beliefs of the patient. This is where fear-avoidance and catastrophising exist at one extreme, and placebo response and attentional modulation at the other. How a clinician positively “manipulates” these is critical to the success of the rehabilitation and is often dependent upon the “art” of communication and persuasion skills. Graded exposure (13, 14) is one of the most important and widely-used cognitive framework on which exercise therapy can be effectively integrated.

4) Suspected level of endogenous modulation

This resides closely to “attitudes and beliefs” as their end-effect is also endogenous modulation. However there are many other factors that can influence endogenous modulation (e.g. genetic, DNIC, autonomic regulation, gender, age, fitness, physical and psychological history) and these are important data that need to be considered to hypothetically assess the “activity level” of patients' endogenous pain modulation. In essence, stronger the modulation is suspected, stronger the exercise stimulation may be, and possibility of exercising through pain.

It is critical to specify the intention or aim behind exercise programmes when prescribing to patients as this will often give a quick indication of how the experience of pain should be handled. For example, in a case of mobilisation of joints and soft tissues post fracture with no significant pain issues, it is probably useful to “stretch into the pain zone" if this coincides with the restriction in range of motion and evidence of tissue shortening (i.e. nociceptive pain).

Compared to this in management of primary pain the goals are, in most cases, to modulate pain and facilitate neural recruitment. Thus how a clinician teaches patients to handle pain when it inevitably occurs during exercises - whether to alter exercises to minimise pain or to "ignore and keep going" - will need to be carefully considered in accordance with abovementioned factors to ensure the best outcome.

References

1. Treede RD, Rief W, Barke A, Aziz Q, Bennett MI, Benoliel R, et al. A classification of chronic pain for ICD-11. Pain. 2015;156(6):1003-7.

2. Booth J, Moseley GL, Schiltenwolf M, Cashin A, Davies M, Hubscher M. Exercise for chronic musculoskeletal pain: A biopsychosocial approach. Musculoskeletal Care. 2017.

3. Daenen L, Varkey E, Kellmann M, Nijs J. Exercise, not to exercise, or how to exercise in patients with chronic pain? Applying science to practice. Clin J Pain. 2015;31(2):108-14.

4. Smith BE, Hendrick P, Smith TO, Bateman M, Moffatt F, Rathleff MS, et al. Should exercises be painful in the management of chronic musculoskeletal pain? A systematic review and meta-analysis. Br J Sports Med. 2017.

5. Eells TD, Kendjelic EM, Lucas CP. What's in a Case Formulation? Development and use of a Content Coding Manual. Journal of Psychotherapy Practice and Research. 1998;7(2):144-53.

6. Linton SJ, Nicholas MK. After assessment, then what? Integrated findings for successful case formulation and treatment tailoring. In: Breivik H, Campbell WI, Nicholas MK, editors. Clinical Pain Management: Practice and Procedures. 2nd ed: CRC Press; 2008. p. 95-106.

7. Mense S. Muscle pain: mechanisms and clinical significance. Dtsch Arztebl Int. 2008;105(12):214-9.

8. Vardeh D, Mannion RJ, Woolf CJ. Toward a Mechanism-Based Approach to Pain Diagnosis. J Pain. 2016;17(9 Suppl):T50-69.

9. Woolf CJ. Pain: Moving from Symptom Control toward Mechanism-Specific Pharmacologic Management. Annals of Internal Medicine. 2004;140:441-51.

10. Goffaux P, Redmond WJ, Rainville P, Marchand S. Descending analgesia--when the spine echoes what the brain expects. Pain. 2007;130(1-2):137-43.

11. Kenntner-Mabiala R, Andreatta M, Wieser MJ, Muhlberger A, Pauli P. Distinct effects of attention and affect on pain perception and somatosensory evoked potentials. Biol Psychol. 2008;78(1):114-22.

12. Wiech K, Ploner M, Tracey I. Neurocognitive aspects of pain perception. Trends Cogn Sci. 2008;12(8):306-13.

13. de Jong JR, Vlaeyen JW, Onghena P, Goossens ME, Geilen M, Mulder H. Fear of Movement/(Re)injury in Chronic Low Back Pain. Education or Exposure In Vivo as Mediator to Fear Reduction? The Clinical Journal of Pain. 2005;21:9-17.

14. Vlaeyen JW, de Jong JR, Geilen M, Heuts PHTG, van Breukelen G. The Treatment of Fear of Movement/(Re)injury in Chronic Low Back Pain: Further Evidence on the Effectiveness of Exposure In Vivo. The Clinical Journal of Pain. 2002;18:251-61.

Scoliosis – Key points

This article will summaries key points on Scoliosis

There are three types of structural scoliosis

1) Idiopathic

2) Congenital

3) Paralytic

 

1. Idiopathic scoliosis is perhaps archetypal and most well-recognised.

- It is a genetic/hereditary condition of poorly understood pathogenesis
- Majority is “adolescent idiopathic scoliosis” – i.e. develop between age 10-18
- Incidence between male and female is the same but female has 10 x more likelihood to progress
- Vast majority of the curves are convex to the right at thoracic spine

 

Scoliosis

 

2. Congenital scoliosis is essentially a birth defect and not that common.

(Below is an example of congenital scoliosis before and after a corrective surgery)

Congenital scoliosis

 

3. Paralytic scoliosis is secondary to a pre-existing condition that had resulted in paralysis and scoliosis consequent to that.

- e.g. post-polio, cerebral palsy, post-stroke

 

The above three types of scoliosis are STRUCTURAL – i.e. “true scoliosis”.

There is non-structural scoliosis that can be frequently observed – often called “postural”. They require little intervention, other than some general advice in regards to exercises and encouragement to correct

 

Adams forward bend test is the simplest test that can help differentiate structural from non-structural.

Adam's forward bend test

 

Cobb angle: choose the most tilted vertebrae above and below the apex of the curve. The angle between intersecting lines drawn perpendicular to the top of the top vertebrae and the bottom of the bottom vertebrae is the Cobb angle.

Cobb angle

Cobb angle plays an important part in overall assessment and plan of management of Scoliosis (see below).

--

Intervention can consist of four types:

- observation
- scoliosis-specific exercises (reasonable evidence for this for those even with significant Cobb angle).
- orthopaedic braces (best in combination with scoliosis-specific exercises)
- surgery

This direct from Horne et al (2014):

 

“Determining which patients need referral to an orthopedist can be complicated, and clear indications are not always available. The risk of spinal curve progression increases with higher Cobb angle and lower Risser grade. However, the trend in recent years is that fewer patients need radiography, and fewer patients who undergo radiography need treatment. Treatment modalities such as physical therapy, chiropractic care, and electrical stimulation have questionable benefit in preventing scoliosis progression. Bracing and surgery are options, but the evidence for them is limited. A 50-year follow-up study of late-onset idiopathic scoliosis including 117 untreated patients and 62 age- and sex-matched volunteers found that patients with untreated scoliosis are productive, are high-functioning, and usually have little physical impairment other than back pain and cosmetic concerns.”

 

Table scoliosis management

References

1. Horne JP, Flannery R, Usman S. Adolescent Idiopathic Scoliosis: Diagnosis and Management. American Family Physician. 2014;89(3):193-8.

2. Negrini S, Atanasio S, Zaina F, Romano M. Rehabilitation of adolescent idiopathic scoliosis: results of exercises and bracing from a series of clinical studies. European Journal of Physical and Rehabilitation Medicine. 2008;44(2):169-76.

3. committee Sg, Weiss HR, Negrini S, Rigo M, Kotwicki T, Hawes MC, et al. Indications for conservative management of scoliosis (guidelines). Scoliosis. 2006;1:5.

4. Persson-Bunke M, Czuba T, Hagglund G, Rodby-Bousquet E. Psychometric evaluation of spinal assessment methods to screen for scoliosis in children and adolescents with cerebral palsy. BMC Musculoskelet Disord. 2015;16:351.

5. Rigo M. Differential diagnosis of back pain in adult scoliosis (non operated patients). Scoliosis. 2010;5(Suppl 1).

6. Shakil H, Iqbal ZA, Al-Ghadir AH. Scoliosis: review of types of curves, etiological theories and conservative treatment. J Back Musculoskelet Rehabil. 2014;27(2):111-5.

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Fibromyalgia – part 2: context of the diagnosis

Fibromyalgia - part 2: the context of the diagnosis

(Below is the transcription of the above video)

In order to recover from fibromyalgia, there are two things that have to be done:

1. Stop doing things that are stuffing you up

2. And instead do things that help you.

First of all let’s look at the things that I have seen so many people with fibromyalgia do, that actually perpetuate the condition rather than assisting in recovery.

I will go through four most common and critical mismanagement of fibromyalgia. You could say they often occur somewhat in this sequence and they are VERY closely related.

 

1. Lack of appreciation of the context involving the diagnostic term “fibromyalgia”

2. Misinformation on the condition

3. Over-identification or emotional investment on the condition

4. Mal-adaptation that follows on the body

 

The first important thing is that these are not easily identifiable due to the fact that they are “below the surface”. But you sure feel the effect.

The mismanagement that I would like to discuss in this video is the first one: lack of appreciation of the context involving the diagnostic term – “fibromyalgia”.

First of all, let’s define fibromyalgia (and I’d like to add that most “fibromyalgia” patients that I see are often not even aware of this to begin with, which pretty much underlines the point that I want to raise):

 

Fibromyalgia is diagnosed in patients with chronic widespread pain and associated symptoms of fatigue, unrefreshing sleep, or cognitive dysfunction (or a combination thereof) for at least 3 months.(1)

 

(and for those who are interested in details of one of the most accepted diagnostic criteria, you can go to the website on the screen.)

The key here is that the symptoms that pertain to the diagnostic criteria (pain, fatigue etc) sit within a continuous spectrum; some are very mild and borderline fibromyalgia while others can be full-blown and significantly debilitating. And not only that, even though it is generally accepted nowadays that the symptoms of fibromyalgia are the result of dysfunctions in endogenous pain modulation(3-5), it is very difficult to establish a measurable relationship between the dysfunction and the symptoms experienced. 

All this means is that when a diagnosis of fibromyalgia is given, it does not (and should not) mean anything more than the exact definition given above; nothing more, nothing less – i.e. fibromyalgia is simply a description of symptoms and has always been.

The problem occurs when the terminology “fibromyalgia” is associated with certain ideas or beliefs – ideas that may be true for the very severest of the spectrum (and that’s not many) – but everyone who receives the diagnosis is lumped together under that idea.

In my opinion and experience vast majority of patients who have been diagnosed as fibromyalgia could have easily had their symptoms explained as:

 

"a severe but temporary dysfunction of the body due to a series of events that overloaded the system, and/or non-events where there should have been for the benefit of the body, in combination with failure of the body to optimally adapt to the stimulus related to those events and/or non-events.”

 

An example of such event that overloaded the system may be a prolonged stress from work that may have gradually impacted on endogenous pain modulation. An example of non-event where there should’ve been, could be not knowing how to activate endogenous pain modulation when a body is genetically predisposed to pain facilitation.

Combined together, these things FACILITATE pain – and tip the balance towards pain facilitation away from pain modulation. Which means that you’ll be susceptible to feeling an unnecessarily amplified amount of pain regardless of the visible condition of the body.

I suggest that you take a moment to examine this diagram. If there are some aspects that you do not fully understand, please leave a comment – we’ll do our best to answer it.

Anyhow when the symptoms are explained in this way (that was just an example), as opposed to sticking a label such as fibromyalgia, patients can be free from the "baggage" that comes with the label; instead they can focus on finding insights necessary for an effective management for his or her own condition rather than ones that belong to the severest of all fibromyalgia spectrum (which unfortunately are the easiest to discover from terribly unreliable sources such as the internet). 

But regrettably, the culture of medicine and patients’ expectations hinge on "having a diagnosis" - neither clinicians nor patients are often satisfied without giving a condition a label. In fact, numerous clinicians and patients are more satisfied with having a diagnostic label that only explains the fact that certain symptoms exist, rather than giving and receiving an explanation consisting of reasonable and rather helpful hypotheses behind such symptoms;

Some patients will even tend to complain “oh the doctor/physio/specialist couldn’t come up with the diagnosis for my condition” when actually more scientifically accurate and thorough explanations are given.

So if you’ve been told that you have fibromyalgia. I encourage you to jettison the diagnosis label. While there is an innate urge to label symptoms, it really does not do you any favours. Going without diagnosis feels really weird. But trust me, it will make you lighter and free up your headspace so you can actually focus on more important things to get yourself better.

Over the next series of videos, we’ll have a look at the rest of the invisible parts of the iceberg that can sink you. Meanwhile, if you have any questions please leave them in the comments and we’ll do our best to answer them.

References

 

1. Rahman A, Underwood M, Carnes D. Fibromyalgia. BMJ. 2014;348:g1224.

2. Wolfe F, Clauw DJ, Fitzcharles MA, Goldenberg DL, Katz RS, Mease P, et al. The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity. Arthritis Care and Research. 2010;62(5):600-10.

3. Loeser JD, Melzack R. Pain: an overview. The Lancet. 1999;353(9164):1607-9.

4. Marchand S. The physiology of pain mechanisms: from the periphery to the brain. Rheum Dis Clin North Am. 2008;34(2):285-309.

 

5. Melzack R, Katz J. Pain. Wiley Interdiscip Rev Cogn Sci. 2013;4(1):1-15.

Pain Pathway and Endogenous Pain Modualtion

Endogenous Pain Modulation and Pain Pathway

(Below is rough transcription of the above video)

Endogenous pain modulation is a major aspect of how our bodies govern experience of pain. However before we get into this it’s essential to review the very basics of nociception and pain.

When a bodypart is stimulated in a “painful manner” (and THAT’s pretty subjective to begin with), the sensory neurons called nociceptors will fire off signals to the spine and eventually to the brain. The signal is called NOCICEPTION.

When the nociception is acknowledged by our brain as pain, then we will feel pain. If the nociception is ignored or modulated you either won’t feel pain or feel less pain, and THAT’S despite the PRESENCE of upcoming nociception. And the opposite is also true, so if for some reason the brain decides to FEEL pain even WITHOUT nociception, it certainly will be able to and you’ll experience pain.

So already, that’s half of the endogenous pain modulation answered: CNS is an ACTIVE PARTICIPANT in the pain experience. The opposite of active participation is “passive receiver”. We used to think that the role of the brain is simply to receive the pain signal that’s been generated peripherally and that’s about it.

 

And unfortunately there are a number of incorrect beliefs that have risen from that thought with some significant consequences for both patients and clinicians. Some of these are:

 

 

- amount of pain experienced is directly proportional to the amount of injury (more pain means more harm done, which is often not true

- the source of pain always lies peripherally (which entirely ignores the physiology of endogenous pain modulation)

- and the very source of the pain has to be found in order to address the pain (excessively looking for “where it is coming from” and thus becoming fixated onto investigations such as X-ray and MRI)

 

 

Beliefs such as these are easy to understand, and even a lot of health professionals still hold them true. And while they won’t matter for simpler injuries, when it comes to complex or chronic pain, such beliefs will NOT help.

So, let’s review HOW the CNS actively participates in the pain experience. It participates through modulation and facilitation. It’s a continuum of the same concept so let’s just call it modulation for now. And we call this endogenous pain modulation.
I can summarise the modulation into four centres:

- Segmental (14,16)
- Lower centres (Brainstem) (6,14)
- Higher centres (Cerebrum) (6,14)
- Hormonal (2, 7)

Segmental is where non-nociceptive afferent stimulation can inhibit ascending nociceptive signals at dorsal horn. What this means is the sensory neurons responsible for something OTHER than pain, like touch or pressure, can intercept pain signals at spine. This is essentially how you feel better when you rub on a sore spot.

Lower centres or brainstem is responsible for sending pain modulatory signals DOWN the spine. One of the mechanisms that have been identified is called Descending Nociceptive Inhibitory Control (DNIC), and this gets triggered when a new nociception is stimulated while you ALREADY have an ongoing nociception.

These mechanisms from the brainstem suppress the incoming nociception by sending pain-modulating neurotransmitters DOWN the spine, therefore dulling the signals coming up to the brain. The activation of this is also very closely related to the next centre of pain modulation, which is…

Higher centres. This is the bit that makes humans apparently smarter. And this is also where expectations, beliefs, attitudes and other affective constructs are created, and influence pain. They influence pain by directly altering the involvement of cortical regions as well as the lower centres or brainstem that I have just mentioned, particularly periaqueductal grey.

This will result in descending modulatory mechanisms down the spine as I have discussed earlier. The Higher centres also has very close links with the behaviour of autonomic nervous system which plays the major role in the next centre of pain modulation, and that is

Hormonal controls. It is no secret that hormones are incredibly influential when it comes to the behaviour of a body, and they can have a major impact on pain modulation or facilitation. Some of the hormones that are often mentioned here are noradrenaline, adrenaline, cortisole, and dopamine. While I would love to say that “increase in this hormone increases modulation and increase in that hormone increases facilitation etc”, it is not that simple, and I certainly lack the expertise to go into finer details.

There is one more factor to mention, and that is neuroimmunological system. This is not so much a modulation centre but worth mentioning due to its emerging relevance. Certain immune cells can release neurotransmitters that can potentially FACILITATE pain to a great extent.

The recent literature points that the infiltration of these immune cells can have a massive impact on pain processing at the CNS (that’s at both the spinal cord and the brain), making the whole thing more sensitive to pain and counter pain modulation efforts of the body.

The main reason behind the importance of understanding these pain modulation centres is their likely RELEVANCE in most chronic or persisting pain conditions, whether that may be fibromyalgia, arthritis, headache and facial pain, persisting back or neck pain or irritable bowel syndrome.

The past and current literature collectively point to the centres that I have discussed, and the success of rehabilitation of pain conditions depend on patients’ understanding of these concepts, and practical application of the knowledge both by the patients and the clinicians.

References

2. Corrigan FM, Fisher JJ, Nutt DJ. Autonomic dysregulation and the Window of Tolerance model of the effects of complex emotional trauma. J Psychopharmacol. 2011;25(1):17-25.

6. Goffaux P, Redmond WJ, Rainville P, Marchand S. Descending analgesia--when the spine echoes what the brain expects. Pain. 2007;130(1-2):137-43.

7. Janig, W., Levine, J.D. (2013). Autonomic, Endocrine, and Immune Interactions in Acute and Chronic Pain. In S. K. McMahon, M. Koltzenburg, I. Tracey, & D. Turk (Eds), Wall and Melzack's Textbook of Pain (6th ed., pp. 199-206). Philadelphia: Elsevier Saunders.

13. Main CJ, Sullivan MJL, Watson PJ. Models of pain and disability.  Pain Mangement, Practical applications of the biopsychosocial perspective in clinical and occupational settings. 2nd ed. Edinburgh: Churchill Livingstone Elsevier; 2008. p. 3-27.

14. Marchand S. The physiology of pain mechanisms: from the periphery to the brain. Rheum Dis Clin North Am. 2008;34(2):285-309.

16. Melzack R, Katz J. Pain. Wiley Interdiscip Rev Cogn Sci. 2013;4(1):1-15.

26. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3 Suppl):S2-15.

 

And on neuroimmunology:

 

Grace, P. M., Hutchinson, M. R., Maier, S. F., & Watkins, L. R. (2014). Pathological pain and the neuroimmune interface. Nat Rev Immunol, 14(4), 217-231. doi:10.1038/nri3621Treede, R. D., Rief, W., Barke, A., Aziz, Q., Bennett, M. I., Benoliel, R., . . . Wang, S. J. (2015). A classification of chronic pain for ICD-11. Pain, 156(6), 1003-1007. doi:10.1097/j.pain.0000000000000160

Classification of Chronic Pain for ICD-11

Classification of Chronic Pain - ICD-11

(Below is rough transcription of the above video)

World Health Organisation writes up this great long document called International Classification of Diseases, which essentially lists out every known health problems a person can have, ranging from a finger sprain, to malignant cancers. They review this quite often but the last wholesale review was done in early 90’s when they released the 10th edition.

The 11th one is coming out some time this year and that’s an awfully exciting news for those who are interested in chronic pain because they’re doing a massive update on chronic pain conditions. This is so important for many reasons, so let me go through it with some crucial points:

 

1.      Firstly, the individual conditions that are often used as diagnoses in everyday medicine have been categorised into seven groups or “parents”.

 

These seven groups are:

Chronic primary pain, Chronic cancer pain, chronic posttraumatic and postsurgical pain, chronic neuropathic pain, chronic headache and orofacial pain, chronic visceral pain, and chronic musculoskeletal pain.

 

Some of these are pretty self-explanatory but others need a little more clarification. Let me go through these VERY briefly before discussing WHY these are so important.

 

Chronic primary pain is pain that can’t be explained by another condition. Like persisting back or neck pain that can’t be put down to anything. Other examples are Fibromyalgia, and irritable bowel syndrome.

Chronic cancer pain is pain due to cancer or cancer treatment

Chronic postsurgical or posttraumatic pain is pain that persists at least 3 months after surgery or trauma for no other good reason (because by the 3rd month everything that should be healed, should have been healed, and there typically should be no disabling pain).

Chronic neuropathic pain is due to damage to the nerves, like peripheral neuropathy or nerve trauma.

Chronic headache and orofacial pain is essentially that; headache and jaw or facial pain for one reason or another.

Chronic visceral pain is pain due to some level of disturbances in internal organs, like endometriosis. It is crucial to note that the pain experienced here often has ZERO relationship to the extent of actual internal damage if any. Just like most other pain conditions, the disturbance is NOT at structural level but at pain processing or modulation level.

Chronic musculoskeletal pain is pain as part of a disease process directly affecting some tissues. Like pain because of rheumatoid arthritis, or symptomatic osteoarthritis. This differs from primary pain group which cannot be related to a particular pathology (so pain itself is a primary condition).

 

 

So, let’s get back to WHY such grouping is a great step forward in understanding chronic pain:

Grouping acknowledges the consistency of pathophysiology.

For example, fibromyalgia is under chronic primary pain group, endometriosis is under chronic visceral pain group, and migraine under headache group. That all sounds pretty straight forward.

However some seemingly different conditions have been grouped together. For example, fibromyalgia and irritable bowel syndrome are both in chronic primary pain group. And THAT might be difficult to comprehend for uninitiated since the similarity isn’t obvious at first glance. However, without going into details, they share very much the same pathophysiology, just different locations.

Another good example is pain from autoimmune diseases like lupus, that is under the same group as pain from symptomatic degeneration like osteoarthritis, which again seems somewhat weird because they’re so different, but when it comes to pain they again share the same pathophysiology.

2. Now the second point. This is somewhat obvious but needs pointing out: They’ve given us the seven groups but they’re ALL under the same grand-daddy umbrella of “Chronic pain”. It’s telling us that the groups are not all THAT different.

For example: again, let’s take fibromyalgia, pain from endometriosis and migraine. Upto this point they’ve been considered as very separate entities, and that is reflected in the current edition of the ICD (that’s the tenth). But they actually share some very consistent mechanisms on persistence of pain that actually exist across the most pain conditions.

And while they WOULD be under separate groups under this new edition of ICD, the fact that they will all be within this big umbrella called chronic pain is a reflection of the progress that’s been made in research and the increasing level of acceptance among the health professionals.

3. The third and final point: “Multiple-parenting” will be possible. That means a condition will be able to be described under two or more groups at the same time.

For example: you can have a patient with persistent lower back pain, with chronic primary pain AND chronic musculoskeletal pain as possible “parents”. You could have a patient with jaw pain, that belonged to both chronic primary pain and chronic orofacial pain group.

Why is all this important? Because this allows correct and accurate communication between health professionals and between health professionals and patients. Let’s say that there is a patient with a chronic neck pain after a car crash 5 yrs ago, with MRI showing some disc damages but with unclear clinical implications. If one health professional writes to another: neck pain under likely parents of chronic primary pain and chronic musculoskeletal pain (?disc), that would say so much more, than just writing “whiplash”.

Also, for a condition like fibromyalgia which has so much variety of information and misinformation, wide-recognition of the condition under chronic primary pain group would resolve much misunderstanding between health professionals and patients; similarly, inclusion of pain from endometriosis under chronic visceral pain group might encourage those affected to seek less invasive interventions.

So there you go. Who would’ve thought that taxonomy could be so interesting? For chronic pain conditions, which deals with something that’s so not black-and white and still lacks broad level of knowledge and consensus among health professionals, appreciation and understanding of the classification of chronic pain must be the basic requirement for any clinicians. Because informing our patients of consistent and correct data is so crucial in effective management of pain.

References

Treede, R. D., Rief, W., Barke, A., Aziz, Q., Bennett, M. I., Benoliel, R., . . . Wang, S. J. (2015). A classification of chronic pain for ICD-11. Pain, 156(6), 1003-1007. doi:10.1097/j.pain.0000000000000160