“There is no magic herb that can replace the need for actual physical activity”

 

Welcome back!

 

In my previous post I had discussed about pain and central sensitization and in this post, I will be focusing on the  physiotherapist’s  role in  treating patients with central sensitization pain.

 

Figure 1 adapted from http://www.dreamstime.com

 

 

Chronic musculoskeletal pain is often associated with psychological distress and maladaptive belief’s. Kinesiophobia  is the fear of movement and this fear changes how we move.

The fear avoidance model describes how the belief that pain is a sign of damage leads to pain-related fear and avoidance.

The experience of pain as unpredictable, uncontrollable and intense makes the movement of the patient threatening. The past personal experiences of pain, societal beliefs, failed treatments and diagnostic uncertainty or diagnosis of an underlying pathology that could not be fixed often makes the condition of the patient worse and lands them into physical inactivity.(1)

 

 

Figure 2 adapted from http://www.doctorsofpt.com

 

 

According to WHO:

 

“Physical activity is defined as any bodily movement produced by skeletal muscles that requires energy expenditure”. (2)

According to physical activities statistics 2015, British Heart Foundation, 13% of UK adults are sedentary for longer than 8.5 hours a day.

The UK analysis of the global burden of diseases, injuries and risk factors study found physical inactivity and low physical activity to be the fourth most important risk factor in the UK.

They estimated that physical inactivity contributes to all most 1 in 10 premature deaths from coronary heart diseases and 1 in 6 deaths from any other cause. As well as health burden in the UK, physical inactivity has a significant financial burden with the direct financial cost of physical inactivity to the NHS greater than £900 million in 2009/10.

In the UK 44% of adults never do any moderate physical activity.(2)

Age group of adults aged 25 and older more than half of sedentary time was spent in watching television.(2)

 

 

Figure 3 adapted from whyexercise.com

 

 

 

DELETERIOUS EFFECTS OF INACTIVITY

 

The sedentary lifestyle is deleterious to musculoskeletal health and is a risk factor for non communicable diseases including cardio-metabolic syndrome.

The joint surfaces degenerate due to reduced synovial fluid production that protects joint surfaces. This risk factor also persists in individuals who exercise routinely but have patterns of prolonged periods of inactivity during the day.(4)

The energy expenditure in sedentary lifestyle is very low. Research suggests that sedentary behaviour is associated with poor health at all ages.

Inactivity is associated with the prevalence of back complaints and many of the risk factors of back pain being those of cardiovascular disease.

A sedentary life style along with smoking and unhealthy weight contributes to premature ageing. The mechanism is associated with shortening of telomere length. Telomere length is further compromised with oxidative stress and inflammation associated with unhealthy lifestyles leading to non communicable diseases.(5)

(A telomere is a region of repetitive nucleotide sequences at each end of a chromatid, which protects the end of the chromosome from deterioration of from fusion with neighbouring chromosomes).

The researchers have focussed on volume of physical activity and quantified sedentary activity. Tudor-Locke and colleagues recently quantified daily inactivity based on a step-defined sedentary lifestyle index, <5000 steps/day. The use of such a marker is useful in the musculoskeletal assessment of people with disabilities such as back pain and serves as an evaluation tool.(6)

 

 

BENEFICIAL EFFECTS OF PHYSICAL ACTIVITY

 

Regular physical activity is associated with positive health status and is beneficial for the multi system functioning including musculoskeletal health.

People who are physically active are at lower risk of cardiovascular disease.

To produce the maximum benefit, exercise needs to be regular and aerobic. This should involve the use of the major large muscle groups steadily and rhythmically.

Physical activity done throughout the day protects musculoskeletal health and is highly recommended for protection against bone impairment.

Standing offices and treadmill workstations are promoted to break-up periods of prolonged sitting during the work day.(9)

The physical activity guidelines suggest 150 minutes of moderately intense activity per week. The low level of exercise is substantial as it is consistent with positive health, reduced morbidity and improved response to healthcare management, particularly for older people.(7)

Tolerable activity is recommended in clinical practice even for acute back pain as it reduces pain related anxiety and depression.

In chronic low back conditions people work less and are generally less physically active. Mc Donough and co-workers recently reported that chronic low back pain people can increase their working daily over 8 weeks in a pedometer driven walking program.(8)

The program was reported to be safe and was able to reduce pain and disability and improved function.

WHO grading of moderate and vigorous intensity physical activity

 

Figure 4 adapted from http://www.who.int

 

Chronic pain is often associated with physical inactivity.

How do you think the holistic patient centred care can be delivered?

Should we as physiotherapist’s undertake the responsibility and behavioural intervention of the patient?

In chronic musculoskeletal pain, even though nociceptive pathology is subsided, the brain of the patients has typically acquired a protective pain memory. Exercise therapy is hampered by such pain memories.(3)

So, we need to alter the pain memories in patients by integrating pain neuroscience education with exercise therapy for targeting the brain circuitry orchestrated by the amygdala (the memory of fear centre in the brain)(3)

 

 

Figure 5 adapted from neuroplastix.com

 

 

In the initial phase, intensive pain neuroscience education is given followed by exercise therapy for applying the exposure without danger principle.

Considering patients perceptions about exercises, therapists should try to decrease the anticipated danger of the exercises by challenging the nature and reasoning behind their fears, assuring the safety of the exercises and increasing confidence in a successful accomplishment of the exercise.

Chronic condition is often characterized by brain plasticity that leads to hyper excitability of the central nervous system. Desensitizing therapies are used along with exercise therapy.

Cognition targeted exercise therapy using therapeutic neuroscience education is given.

The principles of cognition targeted exercise should focus on time-contingent exercises, goal settings, address perceptions about exercises, motor imagery, address feared movements and make use of stress.(3)

The goal of cognition targeted exercise therapy is system desensitization or graded, repeated exposure to generate a new memory of safety in the brain, replacing or bypassing the old and maladaptive movement- related pain memories.

Hence, such an approach directly targets the brain circuits orchestrated by the amygdala.

Exercise stimulates the brain plasticity by stimulating growth of new connections between cells in a wide array of important cortical areas of the brain.

Recent research from UCLA demonstrated that exercise increased growth factors in the brain and helps brain to grow more new neuronal connections.

According to a study done by the department of exercise science at the University of Georgia, even briefly exercising for 20 minutes facilitates information processing and memory functions.

Exercise affects the brain on multiple fronts. It increases heart rate which pumps more oxygen to the brain and also aids the bodily release of a plethora of hormones, all of which  participate in aiding and providing a nourishing environment for the growth of brain cells.(13)

 

 

Figure 6 adapted from www.peacefulplaygrounds.com

 

LATEST EVIDENCES OF EXERCISES IN RELATION TO CHRONIC PAIN

 

1. Fransen M, et al. 2015, conducted a Cochrane systematic review and found that among people with knee osteoarthritis land based therapeutic exercise provides short-term benefit that is sustained for at least 2-6 months after cessation of formal treatment
2. Doerfler D, et al.2015 conducted a randomised clinical study to compare the effect of high-velocity quadriceps exercises with that of slow-velocity quadriceps exercises on functional outcomes and quadriceps power following total knee arthroplasty and found that high velocity quadriceps exercises may be an effective rehabilitation strategy in conjunction with a standardised progressive resistance exercise program beginning 4-6 weeks after total knee arthroplasty.
3. Brage K, et al. 2015 conducted a preliminary randomised control trial to evaluate the effect of training (neck shoulder exercises, balance and aerobic training) and pain education versus pain education alone on neck pain and found that pain education and specific exercise training reduced neck pain more than pain education alone in patients with chronic neck pain.

 

 

WHY IS AN EXERCISE OR FITNESS PROGRAM AN ESSENTIAL PART OF YOUR PAIN CONTROL REGIME?

 

Because….,

1. It improves muscle strength.
2. improves mobility of the joint, reduces  stiffness thus alleviating pain.
3. Stretching exercises provides flexibility to joint contractures and also decrease the chance of muscle bleeds.
4. Co-ordination and balance is improved decreasing the chance of further injury to the joint.
5. Improves confidence and ability to participate.
6. Feeling of well being and decreases anxiety
7. It augments the release of endorphins (natural chemical messengers in the body dampening the pain sensitivity)
8. Increases endurance and encourages weight loss.(13)

 

OTHER PHYSIOTHERAPY TREATMENTS FOR PAIN RELIEF

 

1. Mobilizations or tractions – reduces pain by increasing joint movements
2. Massage – induces relaxation and decreases muscle spasms.
3. Splinting or supports – helps to decrease pain by resting joint
4. Whirlpool, Hydrotherapy, Swimming and acquacize – strengthens muscle and reduces pain by decreasing muscle spasms
5. Hot packs/heating pads-relaxes tight muscles causing tissues to relax and vasodilatation.
6. Ice packs – decreases pain by reducing the conduction of pain signals
7. Shoe inserts or foot orthotics – reduces pressure on the foot and accommodating foot deformities
8. Crutches, cane or wheel chair – reduce the stress and pain on ankle, knee or hip.
9. Acupuncture – chronic pain and muscle spasm respond well to this type of treatment.
10. Taping-helps prevent injury and return back to sports.
11. Manipulations-relives pain and releases endorphins.

There are various other electrical modalities which could be used as an adjunctive exercise treatment.

 

 

CONCLUSION

 

I hope that through this blog I have made an attempt to provide a brief insight into understanding of central sensitization pain, recognizing its effects on various bio psychosocial factors, its assessment using various methods and last but the important means of its management through physical exercise therapy and education.

My take after going through the various literatures and articles on central sensitization pain and its management in a nut shell is as follows

• Listen, understand and act accordingly approach works well in managing the patients
• Recognizing  the whole effects of pain including various bio psychosocial effects and treat it accordingly
• Never to have a blind faith for one paradigm in managing patients with chronic pain
• Three components of pain should be considered and they are

 

1) Cognitive behavioural beliefs-pain beliefs

2) Functional behavioural aspect- movement patterns

3) Life style adaptations due to pain and avoidance of

activities.

 

Focusing on good sleep patterns, eating a healthy diet, avoiding alcohol, maintaining an exercise program, utilizing relaxation techniques are strategies helpful in decreasing sensitivity within the body.

 

It is important for us as physiotherapists to educate our patients on these principles.

I felt my first blogging experience was challenging initially but through its process i started enjoying it and found a new means of enriching my knowledge through research on current trends in the given topic.

It was a great platform to share the knowledge with other colleagues, getting the feedbacks and valuable comments was an overwhelming experience.

I hope you have enjoyed my blog and found it interesting and informative.

Many thanks for going through my blog and for your likes and comments.

Finally, I would like to conclude saying,

 

“Keep moving and stay healthy”.

 

Figure 7 adapted from ethoshealth.com.au

 

REFERENCES

 

1. Bunzli, S., Smith, A., Schütze, R. and O’Sullivan, P. (2015). Beliefs underlying pain-related fear and how they evolve: a qualitative investigation in people with chronic back pain and high pain-related fear. BMJ Open, 5(10), p.e008847.
2. WHO phsyical activity statistics, 2015, British heart foundation
3. Nijs, J., Lluch Girbés, E., Lundberg, M., Malfliet, A. and Sterling, M. (2015). Exercise therapy for chronic musculoskeletal pain: Innovation by altering pain memories. Manual Therapy, 20(1), pp.216-220.
4. Hootman, J., Macera, C., Ham, S., Helmick, C. and Sniezek, J. (2003). Physical activity levels among the general US adult population and in adults with and without arthritis. Arthritis & Rheumatism, 49(1), pp.129-135.
5. Cherkas, L. (2008). The Association Between Physical Activity in Leisure Time and Leukocyte Telomere Length. Arch Intern Med, 168(2), p.154.
6. Tudor-Locke, C., Craig, C., Thyfault, J. and Spence, J. (2013). A step-defined sedentary lifestyle index: <5000 steps/day. Appl. Physiol. Nutr. Metab., 38(2), pp.100-114.
7. Hill, J. (2008). Dietary and Physical Activity Guidelines for Americans. Obesity Management, 4(6), pp.317-318.
8. McDonough, S., Tully, M., Boyd, A., O’Connor, S., Kerr, D., O’Neill, S., Delitto, A., Bradbury, I., Tudor-Locke, C., Baxter, G. and Hurley, D. (2013). Pedometer-driven Walking for Chronic Low Back Pain. The Clinical Journal of Pain, 29(11), pp.972-981.
9. Wilson, F. (2015). Grieve’s Modern Musculoskeletal Physiotherapy (Fourth edition):. British Journal of Sports Medicine, 49(20), pp.1352-1352.
10. Fransen M, McConnell S, Harmer AR, Van der Esch M, Simic M, Bennell KL.. Exercise for osteoarthritis of the knee: a Cochrane systematic review.. Br J Sports Med 2015;
11. Doerfler D, Gurney B, Mermier C, Rauh M, Black L, Andrews R.. High-Velocity Quadriceps Exercises Compared to Slow-Velocity Quadriceps Exercises Following Total Knee Arthroplasty: A Randomized Clinical Study.. J Geriatr Phys Ther 2015;
12. Brage K, Ris I, Falla D, Søgaard K, Juul-Kristensen B. Pain education combined with neck- and aerobic training is more effective at relieving chronic neck pain than pain education alone – A preliminary randomized controlled trial.. Man Ther 2015;
13. Physiotherapy another approach to pain management by Jenny Aikenhead, physiotherapist, Alberta, children’s Hospital, Calgary, Alberta.
14. Figure 1 adapted from http://www.dreamstime.com
15. Figure 2 adapted from http://www.doctorsofpt.com
16. Figure 3 adapted from whyexercise.com
17. Figure 4 adapted from http://www.who.int
18. Figure 5 adapted from neuroplastix.com
19. Figure 6 adapted from http://www.peacefulplaygrounds.com
20. Figure 7 adapted from ethoshealth.com.au

 

“Does pain show up in our lives for no reason or is it a sign indicating that something in our lives need to change?”

Pain is defined by the International Association for the study of pain (IASP) as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.”  (Loeser JD et al. 2008)

               Figure 1 adapted from Google images

I think sometimes pain is a blessing in disguise and I am sure you will agree with me after going through this topic of pain.

The sensory system of the human body has got a highly sophisticated danger alarm system which warns the brain against the amount and nature of the danger. Despite pain being often nasty, we all need to have a pain system. (Butler, D. and Moseley, G. 2003)

Every one of us have experienced pain in our lives. We need to be grateful for our alarm system. Some diseases and injuries have a faulty alarm system. Diabetic foot is one such example of faulty alarm system where the peripheral sensory impairment leads to loss of pain perception and cause external tissue damage to the extent that amputation of the limb becomes inevitable.

Pain is one of the vital symptom in serious conditions like angina pectoris, myocardial infarction, acute appendicitis, aortic aneurysm etc. and reduced pain perception in such cases can lead to grave situation.

I think pain management is very important in bringing the smiles back on faces and making the life worth living.

SIZE AND IMPACT OF PAIN

 

• 7.8 million people in the UK live with chronic pain.
• 25% of people with chronic pain lose their jobs.
• £584 million a year is spent on prescriptions for pain.
• (Donaldson L. London Department of Health 2009.)
• Chronic pain accounts for 4.6 million GP appointments per year. (Belsey J. 2002)
• Pain is the second most common reason for claiming incapacity benefit, costing £3.8 billion annually (Fountain, Y. 2006)
• Annual healthcare costs for patients with chronic LBP are double those of matched controls (£1,074 vs. £516). (Hong J RC et al. 2013)

 

Now let’s brush up our basic concept of pain without going into extensive details

The four most commonly used systems for pain classification are

• pathophysiological mechanism of pain (nociceptive or neuropathic pain)
• duration of pain (chronic or acute, breakthrough pain)
• etiology (malignant or non-malignant)
• anatomic location of pain.

 

Acute pain is pain lasting less than 30 days and chronic pain is pain lasting more than three months.

(Thienhaus O et al.2002)

The initial sensation of pain acts as a protective mechanism – it is a warning to stop the activity provoking the pain. If the acute pain sensation is intense enough, it causes various physiological and psychological system responses widely.

The pain becomes persistent and chronic when the brain has concluded that the person is threatened, in danger and needs protecting which later results in sensitization.

Chronic unexplained pain is present in many patients, including those with fibromyalgia, chronic whiplash, chronic low back pain, osteoarthritis, headache and chronic fatigue syndrome.

EFFECTS OF PAIN

Bio psychosocial model of pain

                                        Figure 2 adapted from ataryan.com

• Physical effects: ability to perform daily activities, sleep disturbances
• Psychological effects: Depression, anxiety, anger, loss of self esteem
• Social consequences: Social isolation, relationships with family and   friends, intimacy/sexual activity
• Societal effects: Health care costs, disability, lost work days

 

 

UNDERSTANDING CENTRAL SENSITIZATION

 

Sensitization is a neurophysiological term that describes the increase responsiveness of nociceptive neurons to their normal input (the pain pathways become more sensitive). This can include a drop in the threshold for activating primary afferent nociceptors and an increase in the frequency of firing for all stimulus intensities.

Clinically, sensitization may only be inferred indirectly from phenomena such as hyperalgesia or allodynia (IASP, 2012).

Hyperalgesia is an abnormal pain response characterised by an extreme sensitivity to pain.

Allodynia is the experience of pain from a non-painful stimulation of skin, such as light touch.

CENTRAL SENSTIZATION PATHWAY

  Figure 3 adapted from wiley-vch.e-bookshelf.de

Sensitization can occur centrally or peripherally. In acute painful conditions there is more tissue nociception and less brain ‘pain’ and in chronic conditions there is less tissue nociception and more brain ‘pain’.

 

 Figure 4 adapted from the sports physio@odammeakins

A 45 year old lady presents with low back pain of 8 months duration tried NSAIDS with minimal pain relief but doesn’t want to continue using it and also tried some physical exercises with minimal relief. Pain interfering with her daily activities causing frustration and low mood.

When I am listening to a patient, observing their movements and performing a ‘multi-system’ examination, I am in part looking for the pain mechanisms at play, including central sensitisation. Several of my questions are: ‘what is going on here to create this experience for the person in front of me?’, ‘why are the nervous and other systems responding in such a way?’ and ‘what is influencing the behaviour of those systems? I really need to know what it is that is prolonging this protection and is it really worthwhile for the individual.

Suspecting that there is a component of central sensitisation at play in many cases of chronic pain that I see, it is pleasing to see a group looking at this closely and finding evidence to support this thinking.

The first approach to this case is to recognise whether it is neuropathic pain or non- neuropathic central sensitization (CS) pain.

Let’s go through some differences between neuropathic and non-neuropathic CS pain.

Criteria for the differential classification between neuropathic and non-neuropathic Central sensitization (CS)  (Haanpaa M et al.2010)

 Neuropathic pain

• History of lesion or disease of the nervous system
• Evidence from diagnostic investigations to reveal an abnormality of the nervous system or post traumatic damage to the nervous system
• Often related to the medical cause like cancer, stroke, diabetes, herpes or neurodegenerative disease
• Pain is neuroanatomically logical
• Pain is often described as burning, shooting or pricking
• Location of sensory dysfunction is neuroanatomically logical

 

 

 Non-neuropathic CS pain

• No history of lesion or disease of the nervous system
• No evidence from diagnostic investigations, or damage to the nervous system
• No medical cause for the pain established
• Pain is neuroanatomically illogical i.e., located at sites segmentally unrelated to primary source of nociception
• Pain is often described as vague and dull
• Pain is neuroanatomically illogical i.e., numerous areas of hyperalgesia at sites outside and remote to the symptomatic site – at segmentally unrelated sites.

 

The presence of neuropathic pain does not exclude the possibility of CS or vice versa. Some patients start as neuropathic pain and evolve into CS pain.

ASSESSMENT OF CENTRAL SENSITIZATION PAIN

 

There are no gold standard method for assessment of central sensitization. In recent years, two questionnaires have been developed for the screening of CS, the pain sensitivity questionnaire and the central sensitization inventory.

The central sensitization inventory was developed to assess the overlapping health-related symptom dimensions of CS.

Part A has 25 items scored from 0 to 4. Total score range from 0 to 100. >40 score on the CSI produced good sensitivity (81%) in correctly identifying a group of CSS patients, and acceptable (75%) in correctly identifying a group of non-patient comparison subjects

Part B (which is not scored asks if one has previously been diagnosed with 1 or more specific disorders, including seven separate CS and three CS related disorders.

Figure 5 (Neblett, R et al. 2013)

Figure 6 (Neblett, R et al. 2013)

Fingleton et al. (2015) conducted an interesting systematic review and metaanalysis and examined the evidence for pain sensitization in people with knee osteoarthritis and the relation between pain sensitization and pain severity.

Quantitative sensory testing measures of hyperalgesia and central hyper excitability were taken into consideration. Metaanalysis and data were carried using a random effects model which included results comparing knee OA participants to controls, and results comparing high symptom severity to low symptom severity.

Fifteen studies were identified following screening and quality appraisal.

The evidence from this studies suggested that pain sensitization is present in people with knee OA and may be associated with knee OA symptom severity.

Gwilym SE et al.(2011) investigated the evidence for augmented pain transmission (central sensitisation) in patients with impingement, and the relationship between pre-operative central sensitisation and the outcomes following arthroscopic sub acromial decompression.

17 patients with unilateral impingement of the shoulder and 17 age- and gender-matched controls, all of whom underwent quantitative sensory testing to detect thresholds for mechanical stimuli, distinctions between sharp and blunt punctate stimuli, and heat pain. Additionally Oxford shoulder scores to assess pain and function, and Pain DETECT questionnaires to identify ‘neuropathic’ and referred symptoms were completed.

Patients completed these questionnaires pre-operatively and three months post-operatively. A significant proportion of patients awaiting sub acromial decompression had referred pain radiating down the arm and had significant hyperalgesia to punctate stimulus of the skin compared with controls (unpaired t-test, p < 0.0001). These are felt to represent peripheral manifestations of augmented central pain processing (central sensitisation). The presence of either hyperalgesia or referred pain pre-operatively resulted in a significantly worse outcome from decompression three months after surgery (unpaired t-test, p = 0.04 and p = 0.005, respectively).

These observations confirm the presence of central sensitisation in a proportion of patients with shoulder pain associated with impingement. Also, if patients had relatively high levels of central sensitisation pre-operatively, as indicated by higher levels of punctate hyperalgesia and/or referred pain, the outcome three months after sub acromial decompression was significantly worse.

Randy Neblett et al. (2015) conducted a study to determine the ability of the central sensitization inventory (CSI), a new screening instrument, to assist clinicians in identifying patients with central sensitivity syndromes (CSSs) by assessing 161 patients from a psychiatric medical practice specialized in the assessment and treatment of complex pain and psychophysiological disorders for the presence of a CSS.

Conclusion:  CSI is a useful and valid instrument for screening patients for the possibility of a CSS, although the chances of false positives are relatively high when evaluating patients with complex pain and psychophysiological disorders.

CAN WE TREAT CENTRAL SENSITIZATION?

 

Despite of some hopeful scientific findings, it still remains a challenge. Still, we don’t have a definite answer to this.

It is unlikely that a single drug or non-pharmacological treatment will be identified as being capable of treating such a complex mechanism as central sensitization.

Central sensitization is a highly dynamic mechanism and needs interdisciplinary approach. It implies that it can get worse, but recovery is possible as well!

Figure 7 adapted from slideshare.net/shimaa2022

• Pharmacological treatment
• Pain education -The first thing we need to do as a physio is     explaining the mechanism of central sensitization to our patients in a face to face session. This is highly effective for improving pain cognitions, illness perceptions and quality of life in patients with chronic pain.
• Pain neurophysiology education has been studied in many randomized controlled trials, and each of them turned out very positive.
• Graded activity programs
• Cognitive behavioural therapy and acceptance and commitment therapy are in line with the treatment of ‘cognitive-emotional sensitization’.

(Nijs, J et al. 2011)

Finally there ……,thanks for reading my post and hope you enjoyed it.

Comments and feedback are welcome

“My query after preparing this blog is whether the central sensitization inventory is in practice for diagnosing central sensitization in UK or other countries? Replies appreciated”.

NEXT WHAT?

 

I will make my sincere effort to take you through the journey of learning about physical therapy in management of pain in my next post.

         Till then, “keep moving and stay healthy”.

REFERENCES

 

1.     Loeser JD, Treede RD. The Kyoto protocol of IASP Basic Pain Terminology. Pain. 2008;137:473–477

2.        Butler, D. and Moseley, G. (2003). Explain pain. Adelaide: Noigroup Publications.

3.        Donaldson L. Annual report of the Chief Medical Officer for 2008. London Department of Health 2009.

4.        Belsey J. Primary care workload in the management of chronic pain. A retrospective cohort study using a GP database to identify resource implications for UK primary care J Med Econ 2002;5:39-50

5.        Fountain, Y. (2006). The Chronic Pain Policy Coalition. The Bulletin of the Royal College of Surgeons of England, 88(8), pp.279-279.

6.        Hong J RC, Norvick D, Happich M, Costs associated with treatment of chronic low back pain: an analysis of the UK general practice database. Spine 2013 38(1):75-82.

7.        Thienhaus O, Cole BE. Weiner RS. Pain management: a practical guide for clinicians. 6th ed. New York, NY: CRC Press; 2002. Classification of pain.

8.        Figure adapted from ataryan.com

9.      International association for the study of pain (IASP).(2012).IASP Taxonomy. Retrieved January 3, 2014 from http://www.iasp-pain.org/AM/Template.cfm?section=pain-Definitions&template=/CM/HTMLDisplay.cfm&content ID=1728.

10.     Figure adapted from wiley-vch.e-bookshelf.de

11.      Figure adapted from the sports physio@odammeakins

12.      Haanpa M, Treede RD. Diagnosis and classification of neuropathic pain. Pain clinical updates 2010;xv11

13.      Neblett, R, Choi, Y, Hartzell, M, Williams, M, Cohen, H, Mayer, TG, Gatchel, RJ (2013). Establishing clinically relevant cut off scores for the Central Sensitization Inventory (CSI). The Journal of Pain. May; 14(5): 438-445.

14.      Fingleton, C., Smart, K., Moloney, N., Fullen, B. and Doody, C. (2015). Pain sensitization in people with knee osteoarthritis: a systematic review and meta-analysis. Osteoarthritis and Cartilage, 23(7), pp.1043-1056.

15.      Gwilym, S., Oag, H., Tracey, I. and Carr, A. (2011). Evidence that central sensitisation is present in patients with shoulder impingement syndrome and influences the outcome after surgery. The Bone & Joint Journal, 93-B(4), pp.498-502.

16.      (Neblett, R., Hartzell, M., Cohen, H., Mayer, T., Williams, M., Choi, Y. and Gatchel, R. (2015). Ability of the Central Sensitization Inventory to Identify Central Sensitivity Syndromes in an Outpatient Chronic Pain Sample. The Clinical Journal of Pain, 31(4), pp.323-332.

17.      Nijs, J., Meeus, M., Van Oosterwijck, J., Roussel, N., De Kooning, M., Ickmans, K. and Matic, M. (2011). Treatment of central sensitization in patients with ‘unexplained€™ chronic pain: what options do we have? Expert Opinion on Pharmacotherapy, 12(7), pp.1087-1098.

18.     Figure adapted from slideshare.net/shimaa2022