CRPS in the Context of (Neuro?) Autoimmunity (With Thanks to Mice)

The study suggests Complex Regional Pain Syndrome 

could be caused by harmful serum-autoantibodies

Researchers at the University of Liverpool have taken a major step forward in understanding the causes of a disorder which causes chronic pain in sufferers. 

Complex Regional Pain Syndrome (CRPS) is a serious condition affecting a limb after an – often small – accident or operation.  It can cause severe pain lasting many years, as well as limb swelling, hair and nail growth changes, and muscle atrophy, but until now there has been no clear evidence of the cause. 

Now the research team from the University’s Institute of Translational Medicine alongside colleagues at the University of Pécs, Hungary have successfully transferred antibodies from the serum of patients with CRPS to mice, causing many of the same symptoms to be replicated. 

Dr Andreas Goebel *, who works in the University of Liverpool and is a Consultant in Pain Medicine at The Walton Centre NHS Foundation Trust, led the study.  He said: “CRPS is a serious condition which isn’t fully understood.  The findings of this study hint at a cause for it – harmful serum-autoantibodies – and raise the possibility of finding a treatment.”

[Read more of the story HERE from HealthCanal - Health News]
[ * Dr. Goebel's considerable research in chronic pain and CRPS HERE]

What to say?  It sounds momentous, yes?  But really, quite a bit of research, years old already, has been done that points to "clear evidence of the cause." Unfortunately, "THE cause" sort of thinking goes hand-in-hand with the "Silver Bullet Cure" crowd, and denies the complexity of the "syndrome." Be that as it may, it's a reflection more on the dumbing-down of pseudo-medical journalism, and not a reflection on the quality or bounds of the research on which the article is "reporting."

Why, for instance, do proponents of immunological causation feel the need to ignore the brain?  Just thought I'd toss that out there, as something not particularly helpful, but indicative of either/or thinking that just does not fly when dealing with the intricate relations and processes of the human body.  The peripheral and central nervous systems and their functional counterparts as parasympathetic and sympathetic impulses/small fibre neuropathy/glands run amok (hypothalamic-pituitary-adrenal -- HPA -- axis dysfunction)/immune system dysfunction/inflammation/psychosocial and environmental influences/and the darned partridge in a pear tree.

***********     **********     **********     ***********

A CRPS-IgG-transfer-trauma model reproducing inflammatory 

and positive sensory signs associated with complex regional pain syndrome

ABSTRACT
The aetiology of complex regional pain syndrome (CRPS), a highly painful, usually post-traumatic condition affecting the limbs, is unknown, but recent results have suggested an autoimmune contribution. To confirm a role for pathogenic autoantibodies, we established a passive-transfer trauma model. Prior to undergoing incision of hind limb plantar skin and muscle, mice were injected either with serum IgG obtained from chronic CRPS patients or matched healthy volunteers, or with saline. Unilateral hind limb plantar skin and muscle incision was performed to induce typical, mild tissue injury. Mechanical hyperalgesia, paw swelling, heat and cold sensitivity, weight-bearing ability, locomotor activity, motor coordination, paw temperature, and body weight were investigated for 8 days. After sacrifice, proinflammatory sensory neuropeptides and cytokines were measured in paw tissues. CRPS patient IgG treatment significantly increased hind limb mechanical hyperalgesia and oedema in the incised paw compared with IgG from healthy subjects or saline. Plantar incision induced a remarkable elevation of substance P immunoreactivity on day 8, which was significantly increased by CRPS-IgG. In this IgG-transfer-trauma model for CRPS, serum IgG from chronic CRPS patients induced clinical and laboratory features resembling the human disease. These results support the hypothesis that autoantibodies may contribute to the pathophysiology of CRPS, and that autoantibody-removing therapies may be effective treatments for long-standing CRPS.

An interesting site:  Centre for Immune Studies in Chronic Pain

© 2013 L. Ryan