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




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


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.

Please click here to download PDF of this post

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.


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.


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

What is physiotherapy? – 2018



I had a solid discussion with a bunch of physiotherapy students the other day.


Especially on the topic of why they chose physiotherapy profession as their careers.

Then I asked them a question:

"What is your understanding of what physiotherapy, the very profession that you have chosen as your careers?"

The answers were, rather disappointing. They recited something that was still pretty much what I was taught back in the late 90's.

So here is what I believe physiotherapy should be, as in 2018. Please click here.



1. 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.

2. Borrell-Carrio F, Suchman AL, Epstein RM. The biopsychosocial model 25 years later: principles, practice, and scientific inquiry. Ann Fam Med. 2004;2(6):576-82.

3. 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.

4. Airaksinen O, Brox JI, Cedraschi C, Hildebrandt J, Klaber-Moffett J, Kovacs F, et al. Chapter 4. European guidelines for the management of chronic nonspecific low back pain. Eur Spine J. 2006;15 Suppl 2:S192-300.

5. Koes BW, van Tulder M, Lin CW, Macedo LG, McAuley J, Maher C. An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. Eur Spine J. 2010;19(12):2075-94.

6. Nakashima H, Yukawa Y, Suda K, Yamagata M, Ueta T, Kato F. Abnormal findings on magnetic resonance images of the cervical spines in 1211 asymptomatic subjects. Spine (Phila Pa 1976). 2015;40(6):392-8.

7. Rudy IS, Poulos A, Owen L, Batters A, Kieliszek K, Willox J, et al. The correlation of radiographic findings and patient symptomatology in cervical degenerative joint disease: a cross-sectional study. Chiropr Man Therap. 2015;23:9.

8. Schwartzberg R, Reuss BL, Burkhart BG, Butterfield M, Wu JY, McLean KW. High Prevalence of Superior Labral Tears Diagnosed by MRI in Middle-Aged Patients With Asymptomatic Shoulders. Orthop J Sports Med. 2016;4(1):2325967115623212.

9. Panagopoulos J, Hush J, Steffens D, Hancock MJ. Do MRI Findings Change Over a Period of Up to 1 Year in Patients With Low Back Pain and/or Sciatica?: A Systematic Review. Spine (Phila Pa 1976). 2017;42(7):504-12.

10. Schoth DE, Liossi C. Biased interpretation of ambiguous information in patients with chronic pain: A systematic review and meta-analysis of current studies. Health Psychol. 2016;35(9):944-56.

11. Vase L, Robinson ME, Verne NG, Price DD. The contributions of suggestion, desire, and expectation to placebo effects in irritable bowel syndrome patients. Pain. 2003;105(1):17-25.

12. Moerman DE, Jonas WB. Deconstructing the Placebo Effect and Finding the Meaning Response. Ann Intern Med. 2002;136:471-6.

13. Cakir S, Hepguler S, Ozturk C, Korkmaz M, Isleten B, Atamaz FC. Efficacy of therapeutic ultrasound for the management of knee osteoarthritis: a randomized, controlled, and double-blind study. Am J Phys Med Rehabil. 2014;93(5):405-12.

14. Feger MA, Goetschius J, Love H, Saliba SA, Hertel J. Electrical stimulation as a treatment intervention to improve function, edema or pain following acute lateral ankle sprains: A systematic review. Phys Ther Sport. 2015;16(4):361-9.

15. Kroeling P, Gross A, Graham N, Burnie SJ, Szeto G, Goldsmith CH, et al. Electrotherapy for neck pain. Cochrane Database Syst Rev. 2013(8):CD004251.

16. Page MJ, Green S, Mrocki MA, Surace SJ, Deitch J, McBain B, et al. Electrotherapy modalities for rotator cuff disease. Cochrane Database Syst Rev. 2016(6):CD012225.

17. Rutjes AW, Nuesch E, Sterchi R, Juni P. Therapeutic ultrasound for osteoarthritis of the knee or hip. Cochrane Database Syst Rev. 2010(1):CD003132.

18. Garland EL. Pain processing in the human nervous system: a selective review of nociceptive and biobehavioral pathways. Prim Care. 2012;39(3):561-71.

19. 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.

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

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

22. Louw A, Zimney K, Puentedura EJ, Diener I. The efficacy of pain neuroscience education on musculoskeletal pain: A systematic review of the literature. Physiother Theory Pract. 2016;32(5):332-55.

23. Moseley L. Combined physiotherapy and education is efficacious for chronic low back pain. Australian Journal of Physiotherapy. 2002;48(4):297-302.

Brief overview of Primary Headaches

migraine headache


Brief overview of Primary Headaches

According to the International Classification of Headache Disorders 3rd ed (, there are four types of primary headache disorders:

1. Migraine
2. Tension-type headache
3. Trigeminal autonomic cephalalgias
4. Other primary headaches

Differentiation of the abovementioned types can be difficult. So here is a quick overview.

1. Migraine

Diagnostic criteria for migraine WITHOUT aura (1):


A. At least five attacks fulfilling criteria B-D

B. Headache attacks lasting 4-72hr

C. Headache has at least two of the following four:

1. unilateral location
2. pulsating quality
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity

D. During headache at least one of the following:

1. nausea and/or vomiting
2. photophobia and phonophobia


(for criteria for migraine with aura - go to

2. Tension headaches

Clinically, migraine and tension headaches are the most common. Goadsby (2) comments:

"Migraine at its simplest level is headache with associated features, and tension-type headache is otherwise featureless."

3. Trigeminal Autonomic Cephalalgia (TAC):

TAC is headache with prominent ipsilateral cranial parasympathetic autonomic features such as lacrimation, rihnorrhea, nasal congestion, eyelid edema, ptosis etc.

4. "Other primary headaches"

are clinically heterogeneous. These include primary exercise headache, cold-stimulus headache, and many others.

The pathophysiology of the headaches

is, in short, poorly understood. However current understanding is that most primary headaches have something to do with “neurovascular involvement of trigeminovascular system" (2) that consist of the following key structurs:

- the large intracranial vessels and dura matter
- the peripheral terminals of the trigeminal nerve that innervates these structures
- the central terminals and second-order neurons of the trigeminal nucleus

trigeminovascular system

It is proposed that these structures undergo pain-inducing process, resulting in sensitisation of nociceptors, vascular changes (e.g. vasodilation), and other phenomena including autonomic symptoms (2-4). Vascular changes were once considered as the major cause; that is no longer the case. Instead central sensitization and sensitization of the nociceptors at the trigeminovascular system is seen as the major contributor (3-5).

If you're interested in reading more about headachces, visit  


1. IHS Classification - International Classification of Headache Disorders 3rd ed.

2. Goadsby, P. J. (2013). Migraine and Trigeminal Autonomic Cephalalgias. In S. K. McMahon, M. Koltzenburg, I. Tracey, & D. Turk (Eds), Wall and Melzack's Textbook of Pain (6th ed., pp.815-816). Philadelphia: Elsevier Saunders.

3. Goadsby, P. J. (2012). Pathophysiology of Migraine. Ann Indian Acad Neurol, 15(Suppl 1), S15-22

4. Pietrobon, D., & Moskowitz, M. A. (2013). Pathophysiology of Migraine. Annu Rev Physiol, 75, 365-391

5. Burch, R., & Wells, R. (2013). Pathophysiology of Migraine. Headache, 53(2), 420-422

Please click here to download PDF of this post

Diagnostic Criteria for Complex Regional Pain Syndrome


Complex Regional Pain Syndrome Diagnostic Criteria 

Definition of CRPS:

"CRPS is a syndrome characterized by continuing (spontaneous and/or evoked) regional pain that is seemingly disproportionate in time or degree to the usual course of pain after trauma or other lesions. The pain is regional (not in a specific nerve territory or dermatome) and usually has a distal predominance of abnormal sensory, motor, sudomotor, vasomotor edema, and/or trophic findings. The syndrome shows variable progression over time."(1)

It was for some time called "Reflex Sympathetic Dystrophy" but this is usually no longer advocated due to the murky implications that come with "reflex", "sympathetic" and "dystrophy". However some choose to still use the name for CRPS that follow a traumatic injury (CRPS 1).

Budapest Criteria(2), established in 2007, remains as the diagnostic criteria of choice for health professionals worldwide. It is fairly straightforward:


Budapest Clinical Diagnostic Criteria for Complex Regional Pain Syndrome

1. Continuing pain, which is disproportionate to any inciting event

2. Must report at least one symptom in three of the four following categories:

• Sensory: reports of hyperesthesia and/or allodynia

• Vasomotor: reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry

• Sudomotor/edema: reports of edema and/or sweating changes and/or sweating asymmetry

• Motor/trophic: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)

3. Must display at least one sign at time of evaluation in two or more of the following categories:

• Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or
joint movement)

• Vasomotor: evidence of temperature asymmetry and/or skin color changes and/or asymmetry

• Sudomotor/edema: evidence of edema and/or sweating changes and/or sweating asymmetry

• Motor/trophic: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)

4. There is no other diagnosis that better explains the signs and symptoms


1. Binder, A. Baron, R. (2013). Complex Regional Pain Syndromes. In S. K. McMahon, M. Koltzenburg, I. Tracey, & D. Turk (Eds), Wall and Melzack's Textbook of Pain (6th ed., pp.961). Philadelphia: Elsevier Saunders.

2. Harden RN, Bruehl S, Perez RS, Birklein F, Marinus J, Maihofner C, et al. Validation of proposed diagnostic criteria (the "Budapest Criteria") for Complex Regional Pain Syndrome. Pain. 2010;150(2):268-74.

Please click here to download PDF of this post

And here to read more about what we do for complex regional pain syndrome

Fibromyalgia – diagnostic criteria

Back in 1990, American College of Rheumatology devised a diagnostic criteria for fibromyalgia(1).

i) widespread pain in combination with

ii) tenderness at 11 or more of the 18 specific tender point site

This was REVISED by the same group in 2010(2), and it still is the current recommended diagnostic criteria:

(and it unfortunately is slightly more tricky. Note "tender points" is no longer a valid criteria).


A patient satisfies diagnostic criteria for fibromyalgia if the following 3 conditions are met:

1) Widespread Pain Index (WPI) ≥ 7 and Symptom Severity (SS) scale score ≥ 5 or WPI 3–6 and SS scale score ≥ 9.

2) Symptoms have been present at a similar level for at least 3 months.

3) The patient does not have a disorder that would otherwise explain the pain.


Please download the full diagnostic criteria, including the description of WPI and SS scales, by clicking here.


1. Wolfe F, A. SH, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, et al. The American Colledge of Rheumatology 1990 Criteria for the Classication of Fibrmyalgia. Arthritis and Rheumatism. 1990;33(2):160-72.

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.

For further information on how 2will provides physiotherapy pain management for patients with fibromyalgia, please click here.