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J Neurol Neurosurg Psychiatry 2001;71:291-295 doi:10.1136/jnnp.71.3.291
  • Review
  • Nosological entities?

Reflex sympathetic dystrophy

  1. G D Schott
  1. Pain Management Department, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK geoffrey.schott@uclh.org
    • Received 29 August 2000
    • Revised 13 February 2001
    • Accepted 16 February 2001

    Does reflex sympathetic dystrophy (RSD) exist? If it does, how is it defined, what is its nature, and how is it treated? Reviewed on many occasions,1-4 the subject engenders considerable and often heated debate. Some of the reasons for the continuing debate are summarised in this discussion.

    The question of definition

    HOW DID WE REACH THE PRESENT SITUATION?

    In 1864 Silas Weir Mitchell, a founding father of American neurology, together with Morehouse and Keen, described the clinical condition of causalgia in soldiers injured in the American civil war.5 This term, which means burning pain, was used to describe a particular painful condition that sometimes followed major nerve injury. The nerve injury, which was usually partial, typically affected a limb. The burning pain was often accompanied by additional features including various sensory disturbances; temperature and sweating changes; glossy and other disturbances of the skin, subcutaneous tissues, muscles and joints; paralysis; and involuntary movements.

    Earlier this century, others noted that there were patients with a similar but less severe condition that resembled causalgia and again often followed trauma but without major nerve injury (although “major” has never been clarified). This condition has had many synonyms, including minor causalgia, post-traumatic vasomotor disorder, Sudeck's atrophy (a term which, strictly speaking, applies to the radiological appearance of osteoporosis), algodystrophy, and reflex sympathetic dystrophy. The last term was introduced in 1946 by Evans,6 and is the one most commonly used today.

    WHY REFLEX, WHY SYMPATHETIC, AND WHY DYSTROPHIC?

    Evans envisaged that prolonged bombardment of pain impulses set up a “vicious circle of reflexes” in the spinal cord that generated efferent activity in the sympathetic system leading to spasm in the peripheral blood vessels. As a consequence there was leakage of fluid from the capillaries which eventually caused dystrophic changes in peripheral tissues.

    The French surgeon Leriche had already noted that the limbs of patients with causalgia showed features that he thought …

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