4.3 Article

Sympathetic dysfunction as a temporary phenomenon in acute posttraumatic CRPS I

Journal

CLINICAL AUTONOMIC RESEARCH
Volume 15, Issue 1, Pages 29-34

Publisher

DR DIETRICH STEINKOPFF VERLAG
DOI: 10.1007/s10286-005-0237-z

Keywords

CRPS I; sympathetic nervous system; laser Doppler flowmetry; diagnosis; test

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Objective Sympathetic testing was carried out in patients in the acute phase of complex regional pain syndrome type F (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 methods In 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). Results The 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. Conclusions Sympathetic 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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