pain in crps alternative short version.docx

7/27/2019 Pain in CRPS alternative short version.docx

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Pain in CRPS - presentation

Slide 1: CRPS

Pain in complex regional pain syndrome (CRPS)

The pain killers

Thelma Gudjondottir, Cheryl Barrett, Charlotte Stenlake and Katarina Cordemans

Talk part:

This presentation is brought to you by the group The Pain killers, whose members include:

Thelma, Cheryl, Charlotte and Kat. We will be discussing pain in complex regional pain

syndrome.


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Slide 2: WHAT IS PAIN?

- Definition of pain. + picture of person in pain

Pain is a complex, consciousness-dependent, unpleasant somatic experience with

cognitive and emotional as well as sensory features (Chapman, 2004, p. 60).

Talk part:

What is pain? Pain was defined by Chapman as a complex, consciousness-dependent,

unpleasant somatic experience with cognitive and emotional as well as sensory features.

It is a distressing, subjective and multidimensional experience and can be characterized as

primarily psychological in nature. As the most universal form of human distress, it is very often a

major factor of dramatically reduced quality of life for those affected.

As the main symptom of Complex Regional Pain Syndrome is a constant, severe and often

excruciating chronic pain, pain management is very important for these patients. While

controlling pain does not constitute a cure for the disease, minimising pain helps patients to

participate in treatment programmes, and allows them to function more fully on both physical

and psychological level.


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SLIDE3: WHAT IS CRPS?

CRPS is a severe and disabling chronic pain disorder of unknown etiology.

CRPS type1 (Reflex sympathetic dystrophy) no nerve injury present

CRPS type 2 (Causalgia) nerve injury present

Talk part:

Complex regional pain syndrome is a severe, disabling chronic pain disorder of unknown

etiology and is believed to be a progressive disease of the autonomic nervous system1. It is

usually divided into two types, depending whether the inciting event involved nerve injury or not.

CRPS type 1, used to be named reflex sympathetic dystrophy. It tends to develop after bone

fracture or a minor soft tissue injury. CRPS type 2, also called causalgia, often develops after

direct damage to the peripheral nerve or nerves. In both types of CRPS autonomic and

dystrophic changes are triggered in affected areas2.


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SLIDE4: PAIN IN CRPS

Neuropathic pain

Chronic persistent and long lasting pain, not simply prolonged acute pain

Allodynia

Hyperalgesia

Hyperpathia

Talk part:

The pain experienced by sufferers can be characterized as a chronic, spontaneous, neuropathicpain that is incommensurate with the inciting trauma.

Unlike acute pain which is a symptom of damage and lasts only until healing is complete,

chronic pain lasts beyond the recovery period. It is no longer seen to have biological value and

has become a disease in its own right3,4. Neuropathic pain results from damage of the

peripheral or central nervous systems2. It is most often characterized by a strong burning

sensation that feels as if the limbs were on fire.

Due to the lack of inciting nerve damage, CRPS type 1 was viewed by some scholars as a

primarily psychiatric disorder or malingering5. However, recent research1 has found that people

in this condition exhibit damage to the small nociceptive fibers in the affected areas,substantiating claims of neuropathic pain.

Patients also typically experience severe allodynia and hyperalgesia and hyperpathia.

Hyperpathia is characterized by an abnormally painful reaction in particular to a repetitive

stimulus. In addition, the feeling of pain may persist even after the stimulus is no longer present.

(ALTERNATIVELY: Allodynia and hyperpathia refer to the severe pain caused by innocuous

and noxious stimuli respectively. In this condition a simple feeling of the clothes on the skin can

be excruciating. It is believed that these spontaneous pains are produced by processes of

central and peripheral sensitization6)


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ALTERNATIVELY CARRY ON: SLIDE 5 PAIN IN CRPS:

Talk part:

In normal circumstances pain intensifies with the strength of the noxious stimuli. However, in

CRPS the pain threshold is lowered and as a result innocuous stimuli. For example: the feeling

of clothes on the skin may become very painful. When the stimulus enters the noxious range the

intensity of pain becomes higher than it would be expected in normal pain response. These

abnormal responses to innocuous and noxious stimuli are termed allodynia and hyperalgesia

respectively.

It is believed that these spontaneous pains are produced by processes of central and peripheral

sensitization.REFEVIDENCE 26


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SLIDE 6: STATISTICS ON CRPS PAIN

WHERE DOES IT OCCUR AND HOW SEVERE IS IT?

Pain in CRPS is high intensity constant burning pain

McGill pain index - CRPS pain is rated 42 out of 50 the highest of all chronic pains1

In the UK and Holland approximately 1 in 2000 4000 people are diagnosed2,3

Women are three times more likely to develop CRPS than men

Girls (8-16) are seven to nine times more likely to develop CRPS than boys4-6

Affected areas are usually the extremities (65%) but no part of the body can be

excluded7

Talk part:

Unlike in other chronic pain conditions, pain in CRPS is generally very intense and does not

diminish with rest. Patients feel as if their limbs were set on fire. It is the most painful form of

chronic pain known today. On the McGill pain index it ranks higher than cancer pain or even

amputation pain.

In the UK and in the Netherlands it was estimated, that about one to two people in 4000 isaffected with CRPS. These estimates include not only adults but children as well. It is three

times more likely to occur in women than men and seven to nine times more likely to develop in

girls as compared to boys.

The areas affected by this condition are usually the extremities, although it can affect any other

area and it often spreads to other parts of the body.


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SLIDE: PAIN IN CRPS: CORTICAL REORGANISATION

Central and peripheral sensitisation represents an enhancement in the function of

neurons and circuits in nociceptive pathways caused by increases in membrane

excitability and synaptic efficacy as well as to reduced inhibition1

Activation of NMDA receptors, increased glutamate and substance-P production leads to

central and peripheral sensitisation

Central sensitisation is believed to lead to neuroplastic changes in the CNS

Recent studies3,4,5,6, found reorganisation in the somato-sensory cortex in CRPS

The extent of cortical reorganisation in CRPS was positively correlated with pain

intensity.

Talk part:

Central and peripheral sensitisation represents an enhancement in the function of neurons and

circuits in nociceptive pathways caused by increases in membrane excitability and synaptic

efficacy as well as to reduced inhibition 1 .

It is believed that this altered functioning will eventually lead to neuroplastic changes in the

central nervous system, causing abnormal pain processing2.

Indeed, recent imaging studies found, significant reorganization in the somato-sensory andmotor cortices 34 in people with CRPS. The extent of the cortical changes was positively

correlated with the intensity of pain they experienced. However, this reorganization was found to

be reversible once pain was adequately treated 56.


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SLIDE 12: THE BIOPSYCHOSOCIAL MODEL

It posits that pain experience can be best explained by the interaction between

biological, social and psychological factors.

Aids our understanding of chronic pain

CRPS often causes depression which in turn was shown to increase pain1 (Veldman,

et al, 1993)

All necessary factors (psychological, biological and social) should be managed for a

more successful treatment2 (Burton, et al, 2008)

Talk part:

In contrast to the earlier Cartesian model of pain, the biopsychosocial model posits that pain

experience can be best explained by the interaction between biological, social and

psychological factors. It is especially useful for understanding chronic pain, in which

psychological and social factors were often shown to play an important role. For example,

chronic pain in CRPS may cause depression, and depression in turn was shown to increase

pain. Therefore in order for the treatment to be more successful, depression should also be

addressed. That is, treatment should include not only biological but also psychological and

social issues when they are present.


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CONCLUSION:

CRPS has an extremely complex pathophysiology involving sensory, motor and

autonomic abnormalitie

It is unknown as to how the autonomic abnormalities and inflammatory processes affect

the pain and sensory/motor abnormalities

It is unknown if and how the syndrome can be prevented

The disease complexity requires coordination of multidisciplinary care that can be

achieved by educational efforts directed to general practitioners.


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References:

Slide 2

Chapman, C. R. (2004). Pain perception, affective mechanisms and conscious experience. In T.

Hadjistavropoulos and K. D. Craig (Eds.). Pain: psychological perspectives (pp. 59-86). New

Jersey: Lawrence Erlbaum associates.

Slide 3

1- Visser, E. J. (2005). Complex regional pain syndrome.Australasian anaesthesia, 147-161.

2 - Binder, A. and Baron, R. (2010). Complex regional pain syndrome. In C. Stannard, E. Kalso

and J. Ballantyne (Eds.), Evidence based chronic pain management(pp. 248-266). Oxford:

John Wiley and sons Ltd.

Slide4

1 - Oaklander, A. L., Rissmiller, J. G., Gelman, L. B., Zheng, L., Chang, Y. and Gott, R. (2006).

Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I Pain,

120, pp. 235-243.

2- Scadding, J.,(2003). Neuropathic pain.Advances in Clinical Neuroscience and

Rehabilitation, 3, 8-14.

3- Niv, D. and Devor, M. (2004). Chronic Pain as a Disease in its Own Right. Pain practice, 4

(3), 179-181.

4- IASP (2003). How prevalent is chronic pain? Pain, clinical updates, 11, 1-4.

5 - Verdugo R. J. and Ochoa J. L. (2000). Abnormal movements in complex regional pain

syndrome: assessment of their nature. Muscle Nerve, 23, 198205.

6 - Woolf, C. J. and Mannion, R. J. (1999). Neuropathic pain: aetiology, symptoms,

mechanisms, and management. Lancet, 353,19591964.

Slide 5

REFERENCE26 Woolf, C. J. and Mannion, R. J. (1999). Neuropathic pain: aetiology,

symptoms, mechanisms, and management. Lancet, 353, 19591964.


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Slide 6

1 - American RSDHope. (2013). McGill pain index- where is CRSP pain ranked? Retrieved

June, 12, 2013, fromhttp://www.rsdhope.org/mcgill-pain-index---where-is-crps-pain-ranked.html

2 - PARC. (2013). Complex regional pain syndrome (CRPS) aka Reflex sympathetic dystrophy

(RSDS) . In Promoting awareness of RSD and CRPS. Retrieved June, 12, 2013, from

http://www.rsdcanada.org/parc/english/index.html .

3 - de Mos, M., de Bruijn, A., Huygen, F., Dieleman, J. P. Stricker, B. H. and Strukenboom, M.

C. (2007). The incidence of complex regional pain syndrome: a population-based study. Pain.

129, 12-20.

4 - Stanton-Hicks, M. (2010). Plasticity of comlex regional pain syndrome (CRPS) in children.

Pain medicine, 11, 1216-1223.

5 - Wilder, R. T. (2006). Management of pediatric patients with complex regional pain

syndrome. Clinical journal of pain, 22, 443-448.

6 - Berde C. B. and Lebel, A. (2005). Complex regional pain syndromes in children and

adolescents.Anesthesiology, 102(2), 2525.

7 - Tahmoush, A. J. (1981). Causalgia: redefinition as a clinical pain syndrome. Pain. 10, 187-

97.

Slide cortical reorganization

1- Latremoliere, A. and Woolf ,C. J. (2009). Central sensitization: a generator of pain

hypersensitivity by central neural plasticity. Journal of Pain, 10, 895-926.

2- Lebel, A. et al. (2008). fMRI reveals distinct CNS processing during symptomatic and

recovered complex regional pain syndrome in children. Brain, 131, 1854-1879.

2 - Dubner R. 92004). The neurobiology of persistent pain and its clinical implications. Clinical

Neurophysiology, 57, 37.

3 Maihofner, C., Handwerker, H. O., Neundorfer, B. and Birklein, F. (2003). Patterns of cortical

reorganization in complex regional pain syndrome. Neurology, 61, 17071715.

4. Pleger, B., Janssen, F., Schwenkreis, P., Volker, B., Maier, C. and Tegenthoff, M. (2004).

Repetitive transcranial magnetic stimulation of the motor cortex attenuates pain perception in

complex regional pain syndrome type I. Neuroscience 356, 8790.

5. Maihofner, C., Handwerker, H. O., Neundorfer, B. and Birklein, F. (2004). Cortical

reorganization during recovery from complex regional pain syndrome. Neurology, 63 (4), 693

701.

6. Pleger, B., Tegenthoff, M., Ragert, P., et al. (2005).Sensorimotor retuning in complex

regional pain syndrome parallels pain reduction.Annual Neurology, 57, 425429.
http://www.rsdhope.org/mcgill-pain-index---where-is-crps-pain-ranked.htmlhttp://www.rsdhope.org/mcgill-pain-index---where-is-crps-pain-ranked.htmlhttp://www.rsdhope.org/mcgill-pain-index---where-is-crps-pain-ranked.htmlhttp://www.rsdcanada.org/parc/english/index.htmlhttp://www.rsdcanada.org/parc/english/index.htmlhttp://www.rsdcanada.org/parc/english/index.htmlhttp://www.rsdhope.org/mcgill-pain-index---where-is-crps-pain-ranked.html


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Slide 11:

Linton, S. (2005). Understanding pain for better clinical practice. A psychological perspective.

London: Elsevier Health Sciences

Slide 12:

1 - Veldman, P. H., Reynen, H. M., Arntz, I. E. and Goris, R. J.(1993). Signs and symptoms of

reflex sympathetic dystrophy: prospective study of 829 patients. The lancet. 342,1012-1016.

2 - Burton, A. Kim, Kendall, Nicholas A.S., Pearce, Brian G., Birrell, Lisa N. and Bainbridge,

L.C. (2008).Management of upper limb disorders and the biopsychosocial model. Technical

Report. Health and Safety Executive. Available at:http://eprints.hud.ac.uk/7486/1/burton.pdf
http://eprints.hud.ac.uk/7486/1/burton.pdfhttp://eprints.hud.ac.uk/7486/1/burton.pdfhttp://eprints.hud.ac.uk/7486/1/burton.pdfhttp://eprints.hud.ac.uk/7486/1/burton.pdf

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