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Complex regional pain syndrome medicalises limb pain

BMJ 2014; 348 doi: (Published 28 April 2014) Cite this as: BMJ 2014;348:g2631

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Bass says that there is a lot of medicalization going on concerning CRPS type 1. (1) If we look and diagnose well, Del Pinal states that CRPS type 1 is a diagnosis that does not exist. Before talking about CRPS type 1 we have to rule out other explanations. (2) I agree with both, and I want to underscore the importance of iatrogenesis in complex regional pain syndrome type 1, thereby preventing harmful interventions like mannitol, baclofen, sympatectomie or amputation.

Many doctors and scientists say that complex regional pain syndrome type 1 (CRPS) is a puzzling or enigmatic disease. No surprise, considering the criteria change every five years. Many sets of criteria and names are circulating in the medical world. If we keep on doing so, a new syndrome will arise every five years. Is it a possibility to create a kingdom for research and eternal fame? Finding inflammation does not mean it’s the etiological factor and writing reviews and guidelines is no argument against an explanation from another perspective.

CRPS type 1 does not exist, it is an iatrogenic disease created of symptoms that are normal seen after immobilization. Animal and human studies show that immobilization of a limb can give symptoms comparable to those of CRPS type 1. (3 4 5)

Therapies which seem to impact at the higher levels of the central nervous system (6 7 8 9) , brain research (10 11 12 13) and the symptoms of long lasting CRPS 1(4 15 16) point in the direction of an origin in the brain.

Effects of a treatment directed at the function and neglecting the pain (Pain Exposure Physical Therapy or PEPT) are positive and even patients who were considering amputation improved markedly (Ek 2009). In a series of 106 patients with crps type 1 (IASP –criteria, mean duration 55 months, most patients had on average more than 3 therapies before) the function of the affected arm or leg improved in 95 patients (full recovery in 49 patients). Only 4 patients did not accept the pain provocation and dropped out. No serious side-effects were mentioned.

The brain hypothesis explains the failure of therapy’s directed at the symptoms in the periphery (dmso crème, fluimicil, mannitol) or at a slightly higher level in the nervous system (baclofen, ketamine, sympathetic blockade) (17 18) . Even if the studies are of good quality it is wrong to keep on answering the same question again and again if the results are more or less the same time after time. A bias is introduced if one searches for a favourable outcome and so neglecting negative results, clinical irrelevant results and other explanations. Other hypothesis must be formulated and investigated.

There may be an iatrogenic component in the maintenance of the symptoms after immobilization. The reaction after immobilization is variable, depending on the trauma, the duration of immobilization, the cognitions of the patient, the cognitions and so the message of the doctor and others, genetic factors and probably many more. CRPS originates as a susceptible patient (cognitions, genetic make-up, painmemory) interacts with a careful approach. The sensitization in the neuromatrix, and so the immobilization, first useful (healing of a wound or fracture or contusion) becomes chronic and useless. After healing there is no habituation, sensitization and as a consequence fear and immobilization remain and a chronic pain syndrome arises.

A functional approach like PEPT (encouraging normal use, manipulation, countering catastrophizing thinking) uses auditory, visual and peripheral input to reorganize the neuromatrix. PEPT uses the plasticity of the brain (19 20) to correct the false alarm (of the patient as well as that of his or her partner or important family) that suggests that the affected limb is in permanent danger. Correct communication within the brain and between the brain and the periphery should be restored in order to attain complete functionality. In this approach it is of the utmost importance the therapist ignores (verbal as well as non-verbal) the pain signals of the patients. The attitude of the therapist already changed from a peripheral approach to a more cognitive-behavioural approach, otherwise the treatment will not be successful. (21)
The problem with naming and framing a set of criteria is that doctors give definitions to a word that originally don’t belong to the description. Patients accept the explanation the doctor gives and act as if it’s true. The doctor is iatrogenic and the nocebo effect induces the wrong behaviour (fear and immobilization) in the patient. CRPS is a descriptive term, there is no clue for a pathogenesis or treatment in it, so let’s not pretend there is one.

I propose to consider seriously an iatrogenic component as a possible cause of CRPS type 1. Ochoa already wrote: “Indeed, iatrogenesis is inevitably part of the management outcome of RSD/CRPS patients.” (22)

The best way to cure CRPS, is to change the name (for the last time) from CRPS type 1 to Post Immobilization Syndrome (PIS). Thereby introducing normal behaviour, mobilization. If we do so CRPS type 1 will no longer exist.

1 Bass C. Complex regional pain syndrome medicalises limb pain. BMJ 2014;348:g2631

2 Del Pinal,F. ”Editorial: I have a dream… reflex sympatetic dystrophy (RSD or Complex Regional Pain Syndrom-CRPS type 1) does not exist.”Journal of Hand Surgery (European Volume38.6 (2013):595-97

3 Guo TZ, Offley SC, Boyd EA, Jacobs CR, Kingery WS. Substance P signaling contributes to the vascular and nociceptive abnormalities observed in a tibial fracture rat model of complex regional pain syndrome. Pain 2004;108:95-107.

4 Singh HP, Davis TR. The effect of short-term dependency and immobility on skin temperature in the hand. J Hand surg Br 2006;31(6):611-15.

5 Terkelsen AJ, Bach FB, Jensen TS. Experimental Forearm Immobilization in Humans Induces Cold and Mechanical Hyperalgesia. Anesthesiology 2008;109:297-307.

6 Moseley GL. Graded motor imagery is effective for long-standing complex regional pain syndrome: a randomised controlled trial. Pain 2004;108: 192–98.

7 De Jong JR, Vlaeyen JWS, Onghena P, Cuypers C, den Hollander M, Ruijgrok J. Reduction of pain-related fear in complex regional pain syndrome type 1: The application of graded exposure in vivo. Pain 2005; 16: 264–75.

8 Ek JW; van Gijn JC; Samwel H; van Egmond J; Klomp FP; van Dongen RT. Pain exposure physical therapy may be a safe and effective treatment for longstanding complex regional pain syndrome type 1: a case series. Clin Rehabil. 2009;23:1059-66.

9 Van de Meent H, Oerlemans M, Bruggeman A, Klomp F, van Dongen R, Oostendorp R, Frölke JP. Safety of 'pain exposure' physical therapy in patients with complex regional pain syndrome type 1. Pain. 2011;152(6):1431-8.

10 Maihöfner CA, Handwerker HO, Neundorfer B, Birklein F. Cortical reorganization during recovery from complex regional pain syndrome. Neurology 2004; 63: 693–701.

11 Pleger B, Tegenthoff M, Ragert P et al. Sensorimotor returning in complex regional pain syndrome parallels pain reduction. Ann Neurology 2005; 57: 425–29.

12 Maihöfner C, Forster C, Birklein F, Neundofer B, Handwerker HO. Brain processing during mechanical hyperalgesia in complex regional pain syndrome: a functional MRI study. Pain 2005;114:93-103

13 Geha, P.Y., Baliki, M.N., Harden, R.N., Bauer, W.R., Parrish, T.B., & Apkarian, A.V. (2008). The brain in chronic CRPS pain: abnormal gray-white matter interactions in emotional and autonomic regions. Neuron, 60, 570–581.

14 Janig W, Baron R. Complex regional pain syndrome: mystery explained? Lancet Neurol 2003;2:687-97.

15 Mc Cabe C.S., Haigh R.C., Halligan P.W., Blake D.R., Referred sensations in patients with complex regional pain syndrome type 1. Rheumatology 2003 (Oxford) 1067-73.

16 Fretlloh J, Huppe M, Maier C. Severity and specificity of neglect-like symptoms in patients with complex regional pain syndrome (CRPS) compared to chronic limb pain of other origins. Pain2006;124:184-9

17 Cepeda MS, Carr DB, Lau J. Local anesthetic sympathetic blockade for complex regional pain syndrome. Cochrane Database Syst Rev. 2005 Oct 19;(4):CD004598.

18 Tran de QH, Duong S, Bertini P, Finlayson RJ. Treatment of complex regional pain syndrome: a review of the evidence. Can J Anaesth. 2010 Feb;57(2):149-66.

19 Ramachandran VS. Plasticity and fucntional recovery in neurology. Clinical Medicine 2005;5:368-73

20 Ramachandran VS, Altschuler EL. The use of visual feedback, in particular mirror visual feedback, in restoring brain function. Brain 2009;132:1693-1710

21 RWJG Ostelo, JWA Vlaeyen.Attitudes and beliefs of health care providers: Extending the fear-avoidancemodel. Pain 2008;135:3-4

22 Ochoa JL. Truths, errors, and lies around “reflex sympathetic dystrophy” and “complex regional pain syndrome”. J Neurol 1999;246:875-9

Competing interests: No competing interests

12 August 2014
Jan-Willem Ek
General Practioner, Pain doctor
Bethesda Hospital (Rehabilitation Department)
Dr. G.H. van Amshoffweg 1 7909 AA Hoogeveen Netherlands