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Article type: Case Report
Authors: Rocco, Angelo G.a; b | Raymond, Stephen A.b; *
Affiliations: [a] Harvard Vanguard Medical Associates, Boston, MA 02115, USA | [b] Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
Correspondence: [*] Address for correspondence: Stephen A. Raymond, PhD, Chief Scientific Officer, PHT Corporation, 500 Rutherford Ave., Charlestown, MA 02129, USA. Tel.: +1 617 973 1610; Fax: +1 617 973 1611; E-mail: [email protected]
Note: [1] This study was conducted at the Department of Anesthesia, Brigham & Women's Hospital and Harvard Medical School, 75 Francis Street, Boston MA 02115. Presented in part at the APS, Washington D.C., 1992 and IASP, Vienna, Austria 1999.
Abstract: Relentlessly progressive sympathetically maintained pain (SMP) with dystonia in a patient with CRPS1 was consistently responsive to systemic phentolamine, but not responsive at all to regional intravenous phentolamine. Sympatholysis was only transiently effective. Our observations suggest that neural activity that caused the pain and drove the dystonia probably originated in sympathetic-sensory coupling within dorsal root ganglia (DRGs) rather than in abnormally adrenosensitive afferent endings in the extremity.
Keywords: dystonia, neuropathy, pain, sympathetically maintained pain, CRPS
DOI: 10.3233/BMR-2005-181-201
Journal: Journal of Back and Musculoskeletal Rehabilitation, vol. 18, no. 1-2, pp. 1-4, 2005
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