• Georg Gradl and Matthias Schürmann.
• Chirurgische Klinik und Poliklinik der Universität Rostock, Abteilung Unfall- und Wiederherstellungschirurgie, Rostock, Germany. georg.gradl@med.uni-rostock.de
• Clin. Auton. Res. 2005 Feb 1;15(1):29-34.

ObjectiveSympathetic testing was carried out in patients in the acute phase of "complex regional pain syndrome type I" (CRPS I) shortly after trauma to the upper limb. Repeated measurements were used to detect changes in peripheral sympathetic function during the course of the disease.Material And MethodsIn a busy trauma center, 10 consecutive patients who developed CRPS I following trauma or surgery of the upper limb were diagnosed according to the 1999 modified IASP diagnostic criteria for CRPS I. Clinical signs and symptoms and bilateral hand temperature (infrared thermometry) were recorded. Vasoconstrictor response to sympathetic provocation (inspiratory gasp, contralateral cooling) at the tip of the middle finger of both hands was measured employing laser Doppler flowmetry (LDF). Sympathetic reaction was quantified by the magnitude of blood flow decrease after provocation (SRF parameter).ResultsThe diagnosis CRPS I could be established 63 days (46-72 days) post-injury. The mean follow-up time after diagnosis was 83+/-15 days. Pain measured by a visual analog scale (VAS 0-10) showed an average of 5.0+/-2.0 at the time of diagnosis and decreased to 1.7+/-1.9 at the last examination. Edema and active range of motion improved substantially during the follow-up period. On the ipsilateral hand marked sympathetic dysfunction was seen early after the onset of CRPS I (mean SRF parameter: 0.14+/-0.01), slowly returning to normal sympathetic reaction three months after the onset of symptoms (mean SRF parameter: 0.42+/-0.21). Diminished sympathetic function was seen even on the contralateral hand.ConclusionsSympathetic dysfunction is regularly seen at the onset of CRPS I and normalizes during the course of the disease. This temporary phenomenon suggests a posttraumatic sympathetic deficit playing a decisive role in the genesis of CRPS I.

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