Abstract

ObjectivesOur aim was to investigate the hypothesis that microvascular dysfunction occurs in patients with CRPS. Specifically, whether there were functional differences in either deeper cutaneous blood vessels or more superficial nutritive vessels between the affected and unaffected limb in patients with CRPS, and between CRPS patients and healthy control subjects.MethodsTwenty‐two patients with CRPS (five male; mean age 45 years; eight upper limb involvement, 14 lower limb) and 23 healthy control subjects (one male; 43 years) were recruited. Microvascular flow at affected and unaffected contralateral sites was measured, following local heating, using laser Doppler imaging (red/green wavelengths). Corresponding sites were imaged in healthy controls. Maximum flux level and area under the curve (first 20 scans, AUC20) were measured.ResultsVasodilator responses to heat were similar in affected and unaffected limbs, and in healthy controls. For example, median (IQR) “red” AUC20 in CRPS was 138.6 (120.0–152.9)% change from baseline in affected limb and 135.0 (120.7–166.8)% in unaffected limb, and (in healthy controls) 133.1 (117.2–145.9)% and 139.1% (126.0–162.1) in limb 1 and 2.ConclusionsWe found no impairment of vasodilation in cutaneous microvessels in CRPS. The vasomotor changes in CRPS may relate to larger vessel dysfunction.

Highlights

  • complex regional pain syndrome (CRPS) is a descriptive term used to describe the painful swelling of an extremity, usually associated with a preceding injury [2,9]

  • We found no impairment of vasodilation in cutaneous microvessels in CRPS

  • We found no differences in microvascular responses in affected compared to unaffected limbs, nor between patients with CRPS and healthy controls

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Summary

Introduction

CRPS is a descriptive term used to describe the painful swelling of an extremity, usually associated with a preceding injury [2,9]. Upper or lower limb can be affected. Affected patients are often severely distressed and disabled. The pathophysiology of CRPS is incompletely understood: peripheral and central mechanisms, neurogenic inflammation, and microvascular dysfunction have all been proposed [9]. It is likely that all contribute either as initiators or perpetuators of the “vicious cycle” of CRPS, and that all inter-relate. Current treatments are often unsatisfactory, highlighting the importance of increasing our understanding of the underlying disease mechanisms in order to inform new directions in therapy

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