title: The passive transfer of immunoglobulin G serum antibodies from patients with longstanding Complex Regional Pain Syndrome.
abstract: BACKGROUND
  The aetiology of Complex Regional Pain Syndrome (CRPS) is unknown. Recent evidence suggests that there may be autoantibodies directed against peripheral nerves, but it is unclear whether such autoantibodies are merely biomarkers or whether they cause or contribute to the underlying pathology. The transfer of disease after injection of a patient's serum or IgG fraction into mice ('passive transfer') is the classic way to demonstrate a functional role of autoantibodies.
  
  
  OBJECTIVE
  Based on previous preliminary results, we wished to investigate whether the transfer of IgG antibodies affected mouse behaviour or produced signs of CRPS.
  
  
  METHODS
  We injected purified serum-IgG from 12 patients and 12 controls into groups of 6-10 mice (∼ 17 mg/mouse intraperitoneally) on 2 consecutive days and looked for any evidence for altered behaviour or signs of CRPS. The observer, blinded as to test or control group, measured behaviour in the open field, stimulus-evoked pain and motor coordination, and inspected limbs for autonomic CRPS signs.
  
  
  RESULTS
  Stimulus-evoked pain and autonomic signs were not detected, but CRPS-IgG induced significant depression of rearing behaviour (17.9 rears/3 min (n = 84) vs. 22.1 rears/3 min (n = 83), p = 0.0004), confirming previous observations in a single case study. Moreover, motor impairment, one of the four cardinal signs of CRPS, was evident in the three CRPS-IgG injected groups tested with a sensitive rota-rod protocol (p < 0.0001 vs. control-IgG injected groups).
  
  
  CONCLUSIONS
  These results lend support to a pathophysiological role for IgG autoantibodies in CRPS.
authors.affiliation: Pain Research Institute, University of Liverpool, Liverpool, UK. andreasgoebel@rocketmail.com
authors.forename: Andreas
authors.initials: A
authors.lastname: Goebel
authors.forename: Maria I
authors.initials: MI
authors.lastname: Leite
authors.forename: Li
authors.initials: L
authors.lastname: Yang
authors.forename: Robert
authors.initials: R
authors.lastname: Deacon
authors.forename: Cruz M
authors.initials: CM
authors.lastname: Cendan
authors.forename: Andrew
authors.initials: A
authors.lastname: Fox-Lewis
authors.forename: Angela
authors.initials: A
authors.lastname: Vincent
mesh_terms: D000328:Adult; D000818:Animals; D001323:Autoantibodies / Q000276:immunology* / Q000494:pharmacology*; D001522:Behavior, Animal / Q000502:physiology; D015415:Biomarkers / Q000097:blood; D020918:Complex Regional Pain Syndromes / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D006930:Hyperalgesia / Q000276:immunology; D007116:Immunization, Passive; D007074:Immunoglobulin G / Q000276:immunology* / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008875:Middle Aged; D009043:Motor Activity / Q000276:immunology; D010146:Pain / Q000276:immunology; D055815:Young Adult
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D007074:Immunoglobulin G