ABSTRACT
The etiology of complex regional pain syndrome (CRPS) is unclear yet. Recently autoantibodies and antecedent viral infections have been discussed to be involved in the pathogenesis of CRPS. We investigated sera from 39 CRPS patients and healthy controls for parvovirus B19 IgG and the occurrence of antiendothelial autoantibodies (AECA). CRPS patients showed a higher seroprevalence of parvovirus B19 IgG than controls (p < 0.01). All CRPS 2 patients were positive. 10.2% of the CRPS patients and 10.0% of the controls had AECA (n.s.) and AECA were not associated with parvovirus B19 seropositivity. Our findings suggest the involvement of parvovirus B19, but not autoantibody-mediated endothelial cell damage, in the pathogenesis of CRPS.
Subject(s)
Autoimmune Diseases/immunology , Autoimmune Diseases/virology , Complex Regional Pain Syndromes/immunology , Complex Regional Pain Syndromes/virology , Parvoviridae Infections/immunology , Parvovirus B19, Human/immunology , Adult , Aged , Antibodies, Viral/blood , Autoantibodies/blood , Autoimmune Diseases/epidemiology , Complex Regional Pain Syndromes/epidemiology , Endothelium/immunology , Enzyme-Linked Immunosorbent Assay , Female , Humans , Immunoglobulin G/blood , Male , Middle Aged , Parvoviridae Infections/epidemiology , Seroepidemiologic StudiesABSTRACT
Viral invasion of the motoneurons and the subsequent inflammation in the anterior horn cells by the varicella zoster virus results in a weakness in the area of the cutaneous eruption. The exact mechanism of zoster paresis is uncertain. The occurrence of symptoms resembling complex regional pain syndrome (CRPS) is common in subjects where the herpes zoster (HZ) outbreak affects an extremity, particularly if it is the distal extremity that is involved. We report the case of a 54-year-old man with monoparesis, hyperalgesia, allodynia, edema, and both color and skin-temperature changes in his left arm after a skin eruption. Electrophysiologic examination revealed the partial degeneration of the superior, middle, and inferior truncus in the brachial plexus, with evidence of HZ infection. Magnetic resonance imaging of the cervical spine and brachial plexus showed degenerative changes without any evidence of nerve root compression. Brachial plexopathy may be the direct cause of the reversible upper-limb paresis resulting from HZ with CRPS-like symptoms.
