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.

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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

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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.

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