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Arthur Ecker, MD, PhD
407 University Ave Syracuse, NY 13210

Arch Neurol. 1989;46(5):482.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—In the review of reflex sympathetic dystrophy (RSD) in the May 1987 issue of the ARCHIVES,¹ Schwartzman and McLellan state "no single hypothesis proposed to date explains all of the features of RSD." In response, the following hypothesis, based on a peripheral neuronal vicious circle, is submitted.

Reflex sympathetic dystrophy is a prolonged regional chemical inflammatory state that affects all tissues from skin to bone.^1,2 It is usually precipitated by a minor trauma. It often occurs in a setting of great anxiety (in which blood levels of norepinephrine are elevated), immobilization, and/or arterial spasm.³ Chemical inflammation is produced by release of proinflammatory mediators, eg, substance P from nociceptive neurons⁴ and prostaglandins from postganglionic sympathetic fibers.⁵ This results in ischemic/inflammatory damage to membranes of terminal nociceptive neurons. I speculate that during repair, they develop (normally transitory) adrenoceptors and (in the presence of norepinephrine) . . . [Full Text PDF of this Article]

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