Current Rheumatology Reports

, Volume 4, Issue 2, pp 165–169 | Cite as

Reflex sympathetic dystrophy

  • Robert J. Schwartzman
  • Anca Popescu


Reflex sympathetic dystrophy (RSD) is composed of five major features: pain, swelling, autonomic dysregulation, movement disorders, and atrophy and dystrophy. RSD is caused by an injury to a specific nerve or the C- and A-delta fibers that innervate the involved tissue. It is a progressive illness that spreads with time and may encompass the entire body. There is no psychological disposition to the problem, but all patients are severely depressed because of the constant pain, lack of sleep, and complete disruption of their lifestyle. The continuing pain is usually secondary to the process of central sensitization. The autonomic dysregulation has a major central nervous system component. Atrophy and dystrophy are partly due to loss of nutritive blood supply to the affected tissues. The movement disorder is partly due to deficiency of GABAergic mechanisms; the tremor is an exaggeration of the normal physiologic tremor. Treatment consists of decreasing the afferent pain, maintaining barrage from the underlying defect, and blocking the sympathetic component of the process. New developments include the use of neurotrophic factors to reverse the phenotypic changes that occur in the dorsal horn and the use of pharmacologic agents to block the activity-dependent NMDA channels that appear to be instrumental in maintaining central sensitization.


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References and Recommended Reading

  1. 1.
    Schwartzman RJ: New treatments for reflex sympathetic dystrophy [editorial]. N Engl J Med 2001, 343:654–656. A succinct review of the major clinical manifestations of the syndrome.CrossRefGoogle Scholar
  2. 2.
    Zimmermann M: Pathobiology of neuropathic pain. Eur J Pharmacol 2001, 429:23–37. An excellent review of the mechanisms of neuropathic pain.PubMedCrossRefGoogle Scholar
  3. 3.
    Huygen FJ, deBruijn AG, Klein J, Sijlstra FJ: Neuroimmune alterations in the complex regional pain syndrome. Eur J Pharmacol 2001, 429:101–113. A good review of basic mechanisms pertaining to complex regional pain syndrome and reflex sympathetic dystrophy.PubMedCrossRefGoogle Scholar
  4. 4.
    Wasner G, Heckmann K, Maier C, Baron R: Vascular abnormalities in acute reflex sympathetic dystrophy (CRPS I): complete inhibition of sympathetic nerve activity with recovey. 1999, 56:613-620.Google Scholar
  5. 5.
    Maleki J, LeBel A, Bennett GJ, Schwartzman RJ: Patterns of spread in complex regional pain syndrome, type I (reflex sympathetic dystrophy). Pain 2000, 88:259–266.PubMedCrossRefGoogle Scholar
  6. 6.
    Ciccone DS, Bandilla EB, Wu W: Psychological dysfunction in patients with reflex sympathetic dsytrophy. Pain 1997, 71:323–333. The best study demonstrating that there is no fundamental psychiatric profile for patients with RSD. When tested, their response is similar to that of patients with all other types of pain.PubMedCrossRefGoogle Scholar
  7. 7.
    Schwartzman RJ: The autonomic nervous system and pain. In Handbook of Clinical Neurology. Edited by Appenzeller O. New York: Elsevier Science; 2001, 75:309–347.Google Scholar
  8. 8.
    Sommer C, Schmidt C, George A: Hyperalgesia in experimental neuropathy is dependent on the TNF receptor 1. Exp Neurol 1998, 151:138–142.PubMedCrossRefGoogle Scholar
  9. 9.
    Schwartzman RJ, Maleki J: Post-injury neuropathic pain syndromes. Med Clin North Am 1999, 83:597–625. A summary of the clinical features of brachial and cervical plexus radiation.PubMedCrossRefGoogle Scholar
  10. 10.
    Hunt SP, Manryh PW: The molecular dynamics of pain control. Nat Rev Neurosci 2001, 2:83–91. A review of the latest molecular biology of pain. Particularly good for mechanisms of central sensitization.PubMedCrossRefGoogle Scholar
  11. 11.
    Schwartzman RJ, Grothusen J, Kiefer TR, Rohr P: Neuropathic central pain. Arch Neurol 2001, 58:1547–1550. A summary of a basic process underlying reflex sympathetic dystrophy.PubMedCrossRefGoogle Scholar
  12. 12.
    Cummins TR, Dib-Hajj SD, Black JA, Waxman SG: Sodium channels and the molecular pathophysiology of pain. In Nervous System Plasticity and Chronic Pain. Edited by Sandkühlerr J, Bromm B, Gebhart GF. Amsterdam: Elsevier Press; 2000, 129:13–19. A review of sodium channels and neuropathic pain mechanisms.Google Scholar
  13. 13.
    Ji RR, Wolf CJ: Neuronal plasticity and signal transduction in nociceptive neurons: implications for the initiation and maintenance of pathological pain. Neurobiol Dis 2001, 8:1–10. A review of basic mechanisms of neural plasticity after nerve and tissue injury.PubMedCrossRefGoogle Scholar
  14. 14.
    Weidner C, Klede M, Rukwied R, et al.: Acute effects of substance P and calcitonin gene-related peptide in human skin—a microdialysis study. J Invest Dermatol 2000, 115:1015–1020.PubMedCrossRefGoogle Scholar
  15. 15.
    Heerschap A, den Hollander JA, Reynen H, Goris RJ: Metabolic changes in reflex sympathetic dystrophy: a 31P NMR spectroscopy study. Muscle Nerve 1993, 16:367–373.PubMedCrossRefGoogle Scholar
  16. 16.
    Kurvers HA, Jacobs MJ, Beuk RJ, et al.: The spinal component to skin blood flow abnormalities in reflex sympathetic dystrophy. Arch Neurol 1996, 53:58–65.PubMedGoogle Scholar
  17. 17.
    Schwartzman RJ: Explaining reflex sympathetic dystrophy. Arch Neurol 1999, 56:521–522. Some of the pathophysiology of the autonomic features of reflex sympathetic dystrophy.PubMedCrossRefGoogle Scholar
  18. 18.
    Schwartzman RJ, Kerrigan J: The movement disorder of reflex sympathetic dystrophy. Neurology 1990, 40:57–61.PubMedGoogle Scholar
  19. 19.
    Deuschl G, Blumberg H, Lucking CH: Tremor in reflex sympathetic dystrophy. Arch Neurol 1991, 48:1247–1252.PubMedGoogle Scholar
  20. 20.
    Mao J, Chen LL: Systemic lidocaine for neuropathic pain relief. Pain 2000, 87:7–17. The best review of lidocaine for pain relief.PubMedCrossRefGoogle Scholar
  21. 21.
    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 2000, 343:625–630.PubMedCrossRefGoogle Scholar
  22. 22.
    Kemler MA, Barendse GA, van Kleef M, et al.: Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med 2000, 343:618–624.PubMedCrossRefGoogle Scholar
  23. 23.
    Eisenberg E, LaCross S, Strassman AM: The effects of the clinically tested NMDA receptor antagonist memantine on carrageenan-induced thermal hyperalgesia in rats. Eur J Pharmacol 1994, 255:123–129.PubMedCrossRefGoogle Scholar
  24. 24.
    Mitchell AC: An unusual case of chronic neuropathic pain responds to an optimum frequency of intravenous ketamine infusions. J Pain Symptom Manage 2001, 21:443–446.PubMedCrossRefGoogle Scholar
  25. 25.
    Kiefer RT, Rohr P, Unertl K, et al.: Recovery from intractable complex regional pain syndrome type I (RSD) under high dose intravenous ketamine-midazolam sedation. Abstract submitted to the 54th Annual Meeting of the American Academy of Neurology, Denver, CO; April 13–20, 2002.Google Scholar

Copyright information

© Current Science Inc 2002

Authors and Affiliations

  • Robert J. Schwartzman
    • 1
  • Anca Popescu
    • 1
  1. 1.Department of NeurologyMCP Hahnemann University School of MedicinePhiladelphiaUSA

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