Complex Regional Pain Syndrome

Written By: Julia Tyack

 Type 1.

Definition:  CRPS (Chronic Regional Pain Syndrome) is best construed as a reaction to injury, or to excessive, often iatrogenic immobilization after injury; but it is not an independent disease. Pearce JM.

Diagnosis:  The presence of a precipitating noxious event, or causing immobilization.
Continuing pain, alloydnia or hyperalgesia with which the pain is disproportionate to any inciting event.
Evidence, at some time, of edema or changes in skin blood flow, or abnormal pseudo motor activity in the region of pain.
The diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain or dysfunction.

Definition: (Merskey & Bogduk, IASP, 1994)

Signs of severe CRPS 1.

– highest values were obtained for volume differences. Volume asymmetries best specificity overall higher
– Rom limitations provided best results
– Temperature difference 0.4C
– Hyperalgesia  (pain measurement, temperature, volume and ROM diagnostic indicators) 1.


Complex regional pain syndrome (CRPS) is a challenging neuropathic pain state, quite difficult to comprehend and treat.  Its pathophysiological mechanisms are unclear and its treatment is difficult. Multiple factors play a role in the generation and maintenance of CRPS.  A close interdisciplinary collaboration amongst the psychologist, physical and occupational therapists, neurologist and pain medicine consultants is necessary to achieve optimal treatment effects. The primary goals of managing patients with this syndrome are to: 1) perform a comprehensive diagnostic evaluation, 2) be prompt and aggressive in treatment interventions, 3) assess and reassess the patient’s clinical and psychological status, 4) be consistently supportive, and 5) strive for the maximal amount of pain relief and functional improvement (2)

–  Explanation and Reassurance
–  Treat underlying condition
–  Psychological approaches
–  Cognitive Behavioral strategies i.e.
–  Hurt is not harm
–  To rest is to ruin
–  Do no more on good days and no less on bad days
–  Do not let what you cannot do interfere with what you can do
–  Scrub and carry exercises
–  Range of movement exercises
–  Manual therapy
–  Acupuncture
–  Topical analgesics  – Capsaicin, Lignocaine, Desipramine, Gabapentin, Ketamine, Clonidine

First Line Medications  –  Tricyclic Antidepressants ,  Cabapentin, Tramadol , Corticosteroids, Vitamin C

Second Line Medications:  – Ventafaxine, Clonidine, Mexilitine, Amantadine, Opoids

Other management Options:   Ketamine Infusion/Nasal spray,  Sympathetic Nerve blocks, Intrathecal drug pumps,  Spinal cord stimulation,  Biphosphonates

Other Options:  TENS nerve stimulation on the contralateral corresponding regions. (4)

Evidence of Auto-immune response: See (5) study states that these results may have far reaching practical applications for understanding acute phase responses.

This evidence is further supported by research (6) CLARK, ALLEVA, MILLS, COWDEN
Stating: High Mobility group 1 protein (HMGBI) is a potent mediator of inflammation – HMGBI is secreted by activated monocytes and macrophages, and is passively released by necrotic or damaged cells.

Injury Syndromes: Tissue injury syndromes include those arising from severe blunt injury (leading to the crush syndrome) and major surgery, heatstroke, and the post-burn syndrome.  References to increased circulating levels of inflammatory cytokines and subsequent NO generation dominate the literature on the multi-system syndromes seen after trauma. .. A major puzzle in understanding these conditions has been to identify the nature and the course of the trigger for this inflammatory cascade.  HMGBI is released from the cell, causing the same inflammatory cascade that is generated by activated macrophages to be set in motion (350).

Studies cited.

1.  Complex regional pain syndrome: a review  Ghai B, Dureja GP.

Department of Anaesthesiology, Post Graduate Institute of Medical education and Research, Chandigarh, India. Department of Anesthesiology, VU University medical center, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.

2.  Complex regional pain syndrome: a review. Ghai B, Dureja GP. Department of Anaesthesiology, Post Graduate Institute of Medical education and Research, Chandigarh, India.

3.  Dr Robert Gassin (Musculoskeletal Physician) MBBS, B(Med)Sc, FAFMM Dip Ms Med, Dip Pain Mx CMM.

4.  Evidence for cortical hyperexcitability of the affected limb representation area in CRPS: a psychophysical and transcranial magnetic stimulation study.
Eisenberg E, Chistyakov AV, Yudashkin M, Kaplan B, Hafner H, Feinsod M.
The authors hypothesize that CRPS can result from an autoimmune process against the sympathetic nervous system.

Autoimmune etiology of complex regional pain syndrome (M. Sudeck).
Blaes F, Schmitz K, Tschernatsch M, Kaps M, Krasenbrink I, Hempelmann G, Brau ME.

5.   Thus, we have convincingly demonstrated that differentially induced CRPs exhibited variable binding characteristics.  These results may have far reaching practical applications for understanding acute phase responses.

Variations in binding characteristics of glycosylated human C-reactive proteins in different pathological conditions. Das T, Mandal C, Mandal C.
Immunobiology, Indian Institute of Chemical Biology, 4, Raja S.C. Mullick Road, Kolkata 700 032, India.

6. Pathogenesis of Malaria and Clinically Similar Conditions. Ian A. Clark, Lesa M. Alleva, Alison C. Mills, and William B. Cowden – School of Biochemistry and Molecular Biology and John Curtin School of Medical Research, Australian National University, Canberra, ACT 0200, Australia.