eMedicine Specialties > Physical Medicine and Rehabilitation > Upper Limb Musculoskeletal Conditions

Complex Regional Pain Syndromes

Author: Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
Coauthor(s): Jashvant Patel, MD, Medical Director, Department of Pain Medicine and Comprehensive Rehabilitation, Medical College of Pennsylvania Hahnemann University; John Grothusen, PhD, Director of Quantitative Sensory and Autonomic Nervous System Laboratory, Assistant Professor, Department of Neurology, MCP Hahnemann University; Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service (www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Contributor Information and Disclosures

Updated: Jun 10, 2008

Introduction

Background

Complex regional pain syndrome (CRPS) may develop as a disproportionate consequence of a trauma affecting the limbs without nerve injury (CRPS I, or reflex sympathetic dystrophy [RSD]) or with obvious nerve lesions (CRPS II, or causalgia).

  • In the 17th Century, Ambroise Pare presented the earliest description of RSD as severe burning pain following peripheral nerve injury. Pare, a surgeon, treated King Charles IX for smallpox by inducing bleeding with a lancet applied to the arm. After this treatment, the king suffered from persistent pain, muscle contracture, and inability to flex or extend his arm.
  • In 1864, Mitchell coined the term causalgia, which means burning pain, to describe persistent symptoms following gunshot wounds to peripheral nerves during the American Civil War.
  • In 1900, Sudeck described radiographic spotty osteopenia.
  • In 1916, Leriche focused on the sympathetic nervous system.
  • In 1943, Livingston expanded the Leriche vicious circle theory that includes the following:
    • Abnormally firing, self-sustaining loops in the dorsal horn
    • Provoked by a small irritation focus in small nerve endings of major nerve trunks
    • Activating central projecting fibers, giving rise to pain
  • In 1946, Evans used the term RSD, believing that sympathetic hyperactivity is involved somehow in the abnormal activity in the periphery.
  • In 1993, the International Association for the Study of Pain (IASP) held a Special Consensus Conference addressing diagnosis and terminology (endorsing the term CRPS).
  • In 1995, Paice wrote that, even after 130 years, there was still no general agreement on what to call RSD, what causes it, or how best to treat it.1

Pathophysiology

CRPS is a relatively common disabling disorder of unknown pathophysiology.2 RSD is a variable symptom complex that probably results from any number of multiple causes through different pathophysiologic mechanisms. Changes in the peripheral and central somatosensory, autonomic, and motor processing and a pathologic interaction of sympathetic and afferent systems are described as underlying mechanisms.

  • Several hypotheses exist regarding the mechanism of sympathetically mediated pain and describe central and peripheral components. Wasner and colleagues demonstrated a complete functional loss of cutaneous sympathetic vasoconstrictor activity in an early stage of RSD/CRPS I, with recovery.3 This autonomic dysfunction originates in the central nervous system (CNS).
  • Kurvers and colleagues suggested a spinal component to microcirculatory abnormalities at stage 1 of RSD, which appeared to manifest itself through a neural antidromic mechanism.4 This spinal component may be evoked by traumatic excitation of a peripheral nerve on the affected side.
  • Baron and Janig have proposed a positive feedback circuit, consisting of primary afferent neuron, spinal cord neurons, sympathetic neurons, and a pathological sympathetic coupling.
  • The cause of vascular abnormalities is unknown, and debate still surrounds the question of whether the sympathetic nervous system (SNS) is involved in the generation of these changes.
  • The old Sudeck concept of an exaggerated regional inflammatory response is supported by new data indicating that, in patients with acute RSD, immunoglobulin G labeled with indium In 111 is concentrated in the affected extremity.
  • A study with31 P (phosphorus) nuclear magnetic resonance (NMR) spectroscopy showed an impairment of high-energy phosphate metabolism, which explains why these patients are unable, rather than unwilling, to exercise.
  • Electron microscope studies of skeletal muscle biopsies showed reduced mitochondrial enzyme activity, vesiculation of mitochondria, disintegration of myofibrils, abnormal depositions of lipofuscin, swelling of endothelial layers, and thickening of the basal membrane, which are all signs of oxidative stress. Oxygen consumption is reduced in limbs affected by RSD, and reduction of pain following treatment with oral vasodilators has been described.
  • After a partial nerve lesion, excessive antidromic activation of undamaged afferent C fibers and neuropeptide release, leading to acute vasodilation within the innervation territory of the affected nerve, were demonstrated.
  • The frequency of the presence of human lymphocyte antigen-DQ1 (HLA-DQ1) was increased significantly in RSD compared with control frequencies. This association provides an indication of an organic basis.
  • Because auto-antibodies against nervous system structures have been described in these patients, Blaes and colleagues suggest an autoimmune etiology.5

Frequency

United States

Limited information is available about the epidemiology of CRPS in the United States and internationally. Actual incidence is unknown, as CRPS is often misdiagnosed. Some sources report, the incidence of causalgia (CRPS II) following injury to a peripheral nerve is 1-5%. The incidence of RSD (CRPS I) is 1-2% after various fractures and 2-5% after peripheral nerve injury.

Mortality/Morbidity

RSD has significant morbidity, so raising awareness of this disease is important. According to Murray, earlier recognition and appropriate referral is very important, especially in children. Prompt referral can avoid unnecessary investigations and treatments that may worsen the condition.

Sex

RSD is reported more commonly in women. In a prospective study by Veldman and colleagues, which reviewed 829 patients, 628 patients were female (76%), and 201 were male (24%).6

Age

RSD may appear in every age group, but, as widely reported, it is less common in children aged less than 10 years. The lower apparent prevalence in children may be an artifact from underdiagnosis, perhaps due to a milder clinical course or a lower index of suspicion by the treating clinicians. In the Veldman study of 829 patients, age of diagnosis was 9-85 years (median 42 y); only 12 patients were younger than 14 years.6

Clinical

History

The typical clinical picture of CRPS consists of disproportionate extremity pain, swelling, and autonomic (sympathetic) and motor symptoms. The condition can affect the upper or lower extremities, but it is slightly more common in the upper extremities.

  • Pain
    • Pain is reported in more than 90% of patients.
    • Most patients describe worsening of pain or other symptoms after exercising the affected limb.
  • Edema
    • Vascular abnormalities (often abnormal vasodilation and skin warming in the early phase and vasoconstriction in later stages) are characteristic symptoms of RSD/CRPS I.
    • Typically, patients with CRPS I exhibit a warm and vasodilated affected extremity in the early stages and cold and pale skin in the later stages.
  • Alteration in motor function
    • Although the IASP did not include motor dysfunction within their formal criteria for diagnosing RSD (because it is not universal), they acknowledged that such dysfunction is common. The abnormal motor symptoms that are reported most classically in RSD include the following:
      • Inability to initiate movement
      • Weakness
      • Tremor
      • Muscle spasms
      • Dystonia of the affected limb
    • In one study, weakness was reported in 95% of patients, tremor of the affected limb in 49%, and muscular incoordination in 54% of patients. In chronic RSD, severe spasms were present in 25% of patients.
  • Alteration in sensory function - Although the IASP also decided not to include sensory dysfunction within their formal criteria for diagnosing RSD (due to variability), such symptoms, including hypo-esthesia, hyperesthesia, and allodynia, may occur.
  • Psychological dysfunction - Although psychological dysfunction is often seen in patients with RSD, the IASP decided not to include it within their formal criteria for diagnosing the condition, due to ongoing debate as to whether psychological dysfunction increases the risk of RSD or whether the psychological dysfunction is actually a result of the RSD. Psychological disturbances may include anxiety, hopelessness, and/or depression.

Physical

  • The common characteristic features of RSD (CRPS I) are spontaneous pain, hyperalgesia, impairment of motor function, swelling, changes in sweating, and vascular abnormalities in a single extremity. An overt nerve injury is not detectable.
    • Various sensory symptoms have been observed
      • Allodynia (mechanical and thermal)
      • Hyperalgesia (mechanical and thermal)
      • Hyperpathia
      • Hypo-esthesia
      • Hypothermesthesia
      • Proprioception and anesthesia dolorosa (sensibility to touch is absent, while severe pain is present in the anesthetic area)
      • Dissociated sensory pattern (on rare occasions)
    • In a study by Veldman, discoloration of the skin was reported in 91% of cases, altered skin temperature in 92%, edema in 69%, and limited active range of motion (AROM) in 88% of cases.
    • Hyperhidrosis may be seen in more than 50% of cases (with warm or cold skin temperature).
    • Dystrophic changes may present in skin, subcutaneous tissue, muscles, and bone.
    • Changes in the growth pattern of hair or nails on the affected limb can be commonly observed.
  • Complex regional pain syndrome
    • Based on the IASP consensus conference, there are 2 types of CRPS, namely CRPS I (RSD) and CRPS II (causalgia). These 2 types are differentiated mainly based upon whether the inciting incident included a definable nerve injury.
    • CRPS I (RSD) – Occurs after initial noxious event other than a nerve injury
    • CRPS II (causalgia) – Occurs after nerve injury
    • In most other ways, CRPS I and CRPS II are quite similar. Features common to CRPS types I and II include the following:
      • Pain, whether spontaneous or evoked, may include allodynia (painful response to a stimulus that is not usually painful) and/or hyperalgesia (exaggerated response to a stimulus that is usually only mildly painful).
      • Pain that is disproportionate to the inciting event (eg, years of severe pain after an ankle sprain)
      • Regional pain that is not limited to a single peripheral nerve distribution
      • Evidence of autonomic dysregulation (eg, edema, alteration in blood flow, hyperhidrosis)
      • Diagnosis is excluded if another condition could account for the degree of pain and dysfunction.
    • Typically, CRPS I is subdivided into the following 3 phases:
      • Acute stage - Usually warm phase of 2-3 months
      • Dystrophic phase - Vasomotor instability for several months
      • Atrophic phase - Usually cold extremity with atrophic changes
    • These stages may be variable and often are not clear cut.
    • In CRPS I, 3 different kinds of spread patterns (ie, contiguous, independent, mirror-image) have been described. According to Maleki and colleagues, CRPS I may be due to aberrant CNS regulation of neurogenic inflammation.7

Causes

Various insults that may lead to RSD include the following:

  • Trauma (eg, sprain, dislocations, fractures, surgery, burns, crash injury)
  • Neurologic disorders (eg, stroke, tumor, syringomyelia)
  • Herpes zoster infection
  • Myocardial infarction
  • Musculoskeletal disorder (shoulder rotator cuff injury)
  • Malignancy
  • Spontaneous/idiopathic

A study by Veldman and colleagues reported that in 65% of cases, RSD followed trauma (mostly a fracture); in 19% of cases, it followed an operation; and in 2% of cases, it followed an inflammatory process.6 In 4% of cases, onset of symptoms followed various other precipitating factors, such as injection, intravenous infusion, or cerebrovascular accident. In 10% of cases, no precipitant could be identified. CRPS II (causalgia) has been reported after automated laser discectomy and cervical epidural injection.

More on Complex Regional Pain Syndromes

Overview: Complex Regional Pain Syndromes
Differential Diagnoses & Workup: Complex Regional Pain Syndromes
Treatment & Medication: Complex Regional Pain Syndromes
Follow-up: Complex Regional Pain Syndromes
Multimedia: Complex Regional Pain Syndromes
References
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References

  1. Paice E. Reflex sympathetic dystrophy. BMJ. Jun 24 1995;310(6995):1645-8. [Medline]. [Full Text].

  2. Uceyler N, Eberle T, Rolke R, et al. Differential expression patterns of cytokines in complex regional pain syndrome. Pain. Sep 2007;[Medline].

  3. Wasner G, Heckmann K, Maier C, et al. Vascular abnormalities in acute reflex sympathetic dystrophy (CRPS I): complete inhibition of sympathetic nerve activity with recovery. Arch Neurol. May 1999;56(5):613-20. [Medline]. [Full Text].

  4. Kurvers HA, Jacobs MJ, Beuk RJ, et al. The spinal component to skin blood flow abnormalities in reflex sympathetic dystrophy. Arch Neurol. Jan 1996;53(1):58-65. [Medline].

  5. Blaes F, Tschernatsch M, Braeu ME, Matz O, Schmitz K, Nascimento D. Autoimmunity in complex-regional pain syndrome. Ann N Y Acad Sci. Jun 2007;1107:168-73. [Medline].

  6. Veldman PH, Reynen HM, Arntz IE, Goris RJ. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet. Oct 23 1993;342(8878):1012-6. [Medline].

  7. Maleki J, LeBel AA, Bennett GJ, et al. Patterns of spread in complex regional pain syndrome, type I (reflex sympathetic dystrophy). Pain. Dec 1 2000;88(3):259-66. [Medline].

  8. Werner R, Davidoff G, Jackson MD, et al. Factors affecting the sensitivity and specificity of the three-phase technetium bone scan in the diagnosis of reflex sympathetic dystrophy syndrome in the upper extremity. J Hand Surg [Am]. May 1989;14(3):520-3. [Medline].

  9. Kozin F, Soin JS, Ryan LM, et al. Bone scintigraphy in the reflex sympathetic dystrophy syndrome. Radiology. Feb 1981;138(2):437-43. [Medline]. [Full Text].

  10. Schürmann M, Zaspel J, Löhr P, et al. Imaging in early posttraumatic complex regional pain syndrome: a comparison of diagnostic methods. Clin J Pain. Jun 2007;23(5):449-57. [Medline].

  11. Bruehl S, Lubenow TR, Nath H, Ivankovich O. Validation of thermography in the diagnosis of reflex sympathetic dystrophy. Clin J Pain. Dec 1996;12(4):316-25. [Medline].

  12. Chelimsky TC, Low PA, Naessens JM, et al. Value of autonomic testing in reflex sympathetic dystrophy. Mayo Clin Proc. Nov 1995;70(11):1029-40. [Medline].

  13. Rashiq S, Galer BS. Proximal myofascial dysfunction in complex regional pain syndrome: a retrospective prevalence study. Clin J Pain. Jun 1999;15(2):151-3. [Medline].

  14. Steverens VL, Oerlemans HM, Weesels A. Cost effectiveness analysis of adjuring physical or occupational therapy for patients with RSD. Arch Phys Med Rehabilitation. 1999;80:1038-43.

  15. Johnston EC, Howell SJ. Tension neuropathy of the superficial peroneal nerve: associated conditions and results of release. Foot Ankle Int. Sep 1999;20(9):576-82. [Medline].

  16. Kumar K, Nath RK, Toth C. Spinal cord stimulation is effective in the management of reflex sympathetic dystrophy. Neurosurgery. Mar 1997;40(3):503-8; discussion 508-9. [Medline].

  17. van Hilten BJ, van de Beek WJ, Hoff JI, et al. Intrathecal baclofen for the treatment of dystonia in patients with reflex sympathetic dystrophy. N Engl J Med. Aug 31 2000;343(9):625-30. [Medline]. [Full Text].

  18. Lundborg C, Dahm P, Nitescu P, et al. Clinical experience using intrathecal (IT) bupivacaine infusion in three patients with complex regional pain syndrome type I (CRPS-I). Acta Anaesthesiol Scand. Jul 1999;43(6):667-78. [Medline].

  19. Dielissen PW, Claassen AT, Veldman PH, Goris RJ. Amputation for reflex sympathetic dystrophy. J Bone Joint Surg Br. Mar 1995;77(2):270-3. [Medline]. [Full Text].

  20. Monti DA, Herring CL, Schwartzman RJ, et al. Personality assessment of patients with complex regional pain syndrome type I. Clin J Pain. Dec 1998;14(4):295-302. [Medline].

  21. Hassenbusch SJ, Stanton-Hicks M, Schoppa D, et al. Long-term results of peripheral nerve stimulation for reflex sympathetic dystrophy. J Neurosurg. Mar 1996;84(3):415-23. [Medline].

  22. Zollinger PE, Tuinebreijer WE, Breederveld RS, et al. Can vitamin C prevent complex regional pain syndrome in patients with wrist fractures? A randomized, controlled, multicenter dose-response study. J Bone Joint Surg Am. Jul 2007;89(7):1424-31. [Medline].

  23. Quang-Cantagrel ND, Wallace MS, Magnuson SK. Opioid substitution to improve the effectiveness of chronic noncancer pain control: a chart review. Anesth Analg. Apr 2000;90(4):933-7. [Medline]. [Full Text].

  24. Rowbotham M, Harden N, Stacey B, et al. Gabapentin for the treatment of postherpetic neuralgia: a randomized controlled trial. JAMA. Dec 2 1998;280(21):1837-42. [Medline].

  25. Jain KK. An evaluation of intrathecal ziconotide for the treatment of chronic pain. Expert Opin Investig Drugs. Oct 2000;9(10):2403-10. [Medline].

  26. Kiefer RT, Rohr P, Ploppa A, et al. Complete recovery from intractable complex regional pain syndrome, CRPS-type I, following anesthetic ketamine and midazolam. Pain Pract. Jun 2007;7(2):147-50. [Medline].

  27. Koffler SP, Hampstead BM, Irani F, et al. The neurocognitive effects of 5 day anesthetic ketamine for the treatment of refractory complex regional pain syndrome. Arch Clin Neuropsychol. Aug 2007;22(6):719-29. [Medline].

  28. Dumitru D. Reflex sympathetic dystrophy. Phys Med Rehabil: State Art Rev. 1991;5:89-101.

  29. Baron R. Peripheral neuropathic pain: from mechanisms to symptoms. Clin J Pain. Jun 2000;16(2 Suppl):S12-20. [Medline].

  30. Baron R, Maier C. Reflex sympathetic dystrophy: skin blood flow, sympathetic vasoconstrictor reflexes and pain before and after surgical sympathectomy. Pain. Oct 1996;67(2-3):317-26. [Medline].

  31. Bhatia KP, Bhatt MH, Marsden CD. The causalgia-dystonia syndrome. Brain. Aug 1993;116 ( Pt 4):843-51. [Medline].

  32. Blanchard J, Ramamurthy S, Walsh N, et al. Intravenous regional sympatholysis: a double-blind comparison of guanethidine, reserpine, and normal saline. J Pain Symptom Manage. Dec 1990;5(6):357-61. [Medline].

  33. Brown DL. Somatic or sympathetic block for reflex sympathetic dystrophy. Which is indicated?. Hand Clin. Aug 1997;13(3):485-97. [Medline].

  34. Bruehl S, Harden RN, Galer BS, et al. External validation of IASP diagnostic criteria for Complex Regional Pain Syndrome and proposed research diagnostic criteria. International Association for the Study of Pain. Pain. May 1999;81(1-2):147-54. [Medline].

  35. Clinchot DM, Lorch F. Sympathetic skin response in patients with reflex sympathetic dystrophy. Am J Phys Med Rehabil. Jul-Aug 1996;75(4):252-6.

  36. Cohen JS. Erythromelalgia: new theories and new therapies. J Am Acad Dermatol. Nov 2000;43(5 Pt 1):841-7. [Medline].

  37. Davis MD, O'Fallon WM, Rogers RS 3rd, Rooke TW. Natural history of erythromelalgia: presentation and outcome in 168 patients. Arch Dermatol. Mar 2000;136(3):330-6. [Medline]. [Full Text].

  38. Galer BS, Bruehl S, Harden RN. IASP diagnostic criteria for complex regional pain syndrome: a preliminary empirical validation study. International Association for the Study of Pain. Clin J Pain. Mar 1998;14(1):48-54. [Medline].

  39. Goldstein DJ, Lu Y, Detke MJ, et al. Duloxetine vs. placebo in patients with painful diabetic neuropathy. Pain. Jul 2005;116(1-2):109-18. [Medline].

  40. Harden RN. A clinical approach to complex regional pain syndrome. Clin J Pain. Jun 2000;16(2 Suppl):S26-32. [Medline].

  41. Hewitt DJ. The use of NMDA-receptor antagonists in the treatment of chronic pain. Clin J Pain. Jun 2000;16(2 Suppl):S73-9. [Medline].

  42. Hopp J, Schwartzman RJ, Grothusen J. Increased sensory thresholds in patients with reflex sympathetic dystrophy. Neurology. Feb 1996;46 A:227.

  43. Hord ED, Oaklander AL. Complex regional pain syndrome: a review of evidence-supported treatment options. Curr Pain Headache Rep. Jun 2003;7(3):188-96. [Medline].

  44. Kemler MA, Barendse GA, van Kleef M, et al. Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med. Aug 31 2000;343(9):618-24. [Medline]. [Full Text].

  45. Kemler MA, van de Vusse AC, van den Berg-Loonen EM, et al. HLA-DQ1 associated with reflex sympathetic dystrophy. Neurology. Oct 12 1999;53(6):1350-1. [Medline].

  46. Kingery WS. A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes. Pain. Nov 1997;73(2):123-39. [Medline].

  47. Kurvers HA, Jacobs MJ, Beuk RJ, et al. Reflex sympathetic dystrophy: evolution of microcirculatory disturbances in time. Pain. Mar 1995;60(3):333-40. [Medline].

  48. Linson MA, Leffert R, Todd DP. The treatment of upper extremity reflex sympathetic dystrophy with prolonged continuous stellate ganglion blockade. J Hand Surg [Am]. Mar 1983;8(2):153-9. [Medline].

  49. Merskey H, Bogduk N. Classification of Chronic Pain, Description of Chronic Pain Syndrome and Definitions of Pain Terms. Seattle, Wash: IASP Press; 1994.

  50. Norton JV, Zager E, Grady JF. Erythromelalgia: diagnosis and classification. J Foot Ankle Surg. May-Jun 1999;38(3):238-41. [Medline].

  51. Ochoa JL. Reflex sympathetic dystrophy: a disease of medical understanding. Clin J Pain. Dec 1992;8(4):363-6; discussion 367-9. [Medline].

  52. Pak TJ, Martin GM, Magness JL, et al. Reflex sympathetic dystrophy. Review of 140 cases. Minn Med. May 1970;53(5):507-12. [Medline].

  53. Portenoy RK, Foley KM. Chronic use of opioid analgesics in non-malignant pain: report of 38 cases. Pain. May 1986;25(2):171-86. [Medline].

  54. Rommel O, Tegenthoff M, Pern U, et al. Sympathetic skin response in patients with reflex sympathetic dystrophy. Clin Auton Res. Sep 1995;5(4):205-10. [Medline].

  55. Schwartzman RJ. Explaining reflex sympathetic dystrophy. Arch Neurol. May 1999;56(5):521-2. [Medline].

  56. Schwartzman RJ. New treatments for reflex sympathetic dystrophy. N Engl J Med. Aug 31 2000;343(9):654-6. [Medline].

  57. Schwartzman RJ, Kerrigan J. The movement disorder of reflex sympathetic dystrophy. Neurology. Jan 1990;40(1):57-61. [Medline].

  58. Schwartzman RJ, Liu JE, Smullens SN, et al. Long-term outcome following sympathectomy for complex regional pain syndrome type 1 (RSD). J Neurol Sci. Sep 10 1997;150(2):149-52. [Medline].

  59. Schwartzman RJ, Maleki J. Postinjury neuropathic pain syndromes. Med Clin North Am. May 1999;83(3):597-626. [Medline].

  60. Stanton-Hicks M, Baron R, Boas R, et al. Complex regional pain syndromes: guidelines for therapy. Clin J Pain. Jun 1998;14(2):155-66. [Medline].

  61. Stanton-Hicks M, Janig W, Hassenbusch S, et al. Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain. Oct 1995;63(1):127-33. [Medline].

  62. Tahmoush AJ, Schwartzman RJ, Hopp JL, et al. Quantitative sensory studies in complex regional pain syndrome type 1/RSD. Clin J Pain. Dec 2000;16(4):340-4. [Medline].

  63. van der Laan L, Veldman PH, Goris RJ. Severe complications of reflex sympathetic dystrophy: infection, ulcers, chronic edema, dystonia, and myoclonus. Arch Phys Med Rehabil. Apr 1998;79(4):424-9. [Medline].

  64. Wasner G, Backonja MM, Baron R. Traumatic neuralgias: complex regional pain syndromes (reflex sympathetic dystrophy and causalgia): clinical characteristics, pathophysiological mechanisms and therapy. Neurol Clin. Nov 1998;16(4):851-68. [Medline].

  65. Wechsler RJ, Frank ED, Halpern EH, et al. Percutaneous lumbar sympathetic plexus catheter placement for short- and long-term pain relief: CT technique and results. J Comput Assist Tomogr. Jul-Aug 1998;22(4):518-23. [Medline].

  66. Wilder RT, Berde CB, Wolohan M, et al. Reflex sympathetic dystrophy in children. Clinical characteristics and follow-up of seventy patients. J Bone Joint Surg Am. Jul 1992;74(6):910-9. [Medline].

  67. Zollinger PE, Tuinebreijer WE, Kreis RW, et al. Effect of vitamin C on frequency of reflex sympathetic dystrophy in wrist fractures: a randomised trial. Lancet. Dec 11 1999;354(9195):2025-8. [Medline].

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Further Reading

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Keywords

complex regional pain syndrome, CRPS, complex regional pain syndrome I, CRPS I, reflex sympathetic dystrophy, RSD, complex regional pain syndrome II, CRPS II, causalgia, mimo-causalgia, Sudeck atrophy of bone, shoulder-hand syndrome, algoneurodystrophy, reflex dystrophy, reflex neurovascular dystrophy

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Contributor Information and Disclosures

Author

Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
Manish K Singh, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American Association of Physicians of Indian Origin, American Headache Society, American Medical Association, and American Society of Regional Anesthesia and Pain Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Jashvant Patel, MD, Medical Director, Department of Pain Medicine and Comprehensive Rehabilitation, Medical College of Pennsylvania Hahnemann University
Jashvant Patel, MD is a member of the following medical societies: Alberta Medical Association, American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Society of Regional Anesthesia and Pain Medicine, and Medical Society of the State of New York
Disclosure: Nothing to disclose.

John Grothusen, PhD, Director of Quantitative Sensory and Autonomic Nervous System Laboratory, Assistant Professor, Department of Neurology, MCP Hahnemann University
Disclosure: Nothing to disclose.

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service (www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

Medical Editor

Robert J Kaplan, MD, Associate Professor, Department of Physical Medicine and Rehabilitation, University of Kansas School of Medicine and Medical Center
Robert J Kaplan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service (www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Rene Cailliet, MD, Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center
Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association
Disclosure: Nothing to disclose.

 
 
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