OBJECTIVE: The purpose was to analyze magnetic resonance imaging (MRI) abnormalities in reflex sympathetic dystrophy syndrome (RSDS) of the foot, with the goal of helping to meet the difficult diagnostic challenges raised by this condition. METHODS: Retrospective study of 20 patients with RSDS of the foot, 15 at the warm phase and five at the dystrophic phase. RESULTS: Of the 15 patients at the warm phase, seven had evidence of bone edema (low signal on T1-weighted images and high signal on T2, T2 STIR, and fat saturation images) and five had occult fractures (linear band of low signal on T1 and T2 weighted images with no enhancement after contrast injection). Other abnormalities included soft tissue changes in three patients, joint effusion in five, and synovial hypertrophy in one. Of the five patients at the dystrophic phase, one had a fracture with a joint effusion, one had isolated joint edema, and three had normal MRI findings. CONCLUSION: Bone marrow edema is inconsistent at the warm phase of RSDS and is never present at the dystrophic phase. Thus, absence of bone edema does not rule out RSDS. Fractures may be visible by MRI in one-third of patients with RSDS and no clinical or plain radiography evidence of fracturing.
OBJECTIVE: The purpose was to analyze magnetic resonance imaging (MRI) abnormalities in reflex sympathetic dystrophy syndrome (RSDS) of the foot, with the goal of helping to meet the difficult diagnostic challenges raised by this condition. METHODS: Retrospective study of 20 patients with RSDS of the foot, 15 at the warm phase and five at the dystrophic phase. RESULTS: Of the 15 patients at the warm phase, seven had evidence of bone edema (low signal on T1-weighted images and high signal on T2, T2 STIR, and fat saturation images) and five had occult fractures (linear band of low signal on T1 and T2 weighted images with no enhancement after contrast injection). Other abnormalities included soft tissue changes in three patients, joint effusion in five, and synovial hypertrophy in one. Of the five patients at the dystrophic phase, one had a fracture with a joint effusion, one had isolated joint edema, and three had normal MRI findings. CONCLUSION: Bone marrow edema is inconsistent at the warm phase of RSDS and is never present at the dystrophic phase. Thus, absence of bone edema does not rule out RSDS. Fractures may be visible by MRI in one-third of patients with RSDS and no clinical or plain radiography evidence of fracturing.