Hi there. For what it's worth, there is now fairly convincing proof that, once established - that is, beyond the point of remission - CRPS is maintained by a "thalamocortical dysrhythmia," which is to say a disruption/displacement of the oscillatory brain waves that define our experience. And the same is true of any number of conditions, Parkinson’s disease, depression, tinnitus, etc. And each has its unique pattern.

The article that’s taken the pain community for a loop (pun intended) came out of the laboratory of Rodolfo R. Llinás, who has been the chairman of the Department of Neuroscience at NYU for 34 years and (I am told) is widely regarded as one of the leading neuroscientists in the world. What the following Commentary in Pain by Edward Jones alludes to is that these concepts had been floating around for the last decade in the neurophysiology (EEG) literature, by were not picked up by the pain community until the NYU team specifically set its sights on CRPS.

Here it is: Walton KD, Dubois M, Llinás RR, Abnormal thalamocortical activity in patients with Complex Regional Pain Syndrome (CRPS) Type I, Pain 2010 Jul;150(1):41-51, FULL ONLINE TEXT @ http://www.rsds.org/2/library/articl..._Pain_2010.pdf:

Abstract
Complex Regional Pain Syndrome (CRPS) is a neuropathic disease that presents a continuing challenge in terms of pathophysiology, diagnosis, and treatment. Recent studies of neuropathic pain, in both animals and patients, have established a direct relationship between abnormal thalamic rhythmicity related to Thalamo-cortical Dysrhythmia (TCD) and the occurrence of central pain. Here, this relationship has been examined using magneto-encephalographic (MEG) imaging in CRPS Type I, characterized by the absence of nerve lesions. The study addresses spontaneous MEG activity from 13 awake, adult patients (2 men, 11 women; age 15-62), with CRPS Type I of one extremity (duration range: 3months to 10years) and from 13 control subjects. All CRPS I patients demonstrated peaks in power spectrum in the delta (<4Hz) and/or theta (4-9Hz) frequency ranges resulting in a characteristically increased spectral power in those ranges when compared to control subjects. The localization of such abnormal activity, implemented using independent component analysis (ICA) of the sensor data, showed delta and/or theta range activity localized to the somatosensory cortex corresponding to the pain localization, and to orbitofrontal-temporal cortices related to the affective pain perception. Indeed, CRPS Type I patients presented abnormal brain activity typical of TCD, which has both diagnostic value indicating a central origin for this ailment and a potential treatment interest involving pharmacological and electrical stimulation therapies.

PMID: 20338687 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/20338687

It’s pretty tough sledding though. The Commentary published with it is more accessible. Jones EG, Thalamocortical dysrhythmia and chronic pain, Pain 2010 Jul; 150(1):4-5, Epub 2010 Apr 14, FULL ONLINE TEXT @ http://www.rsds.org/2/library/articl..._Pain_2010.pdf

An earlier thread on this ran in August, in the context of Deep Brain Stimulation, especially for people with horrible dystonia: DBS (Deep Brain Stimulation) for RSD and Dystonia http://neurotalk.psychcentral.com/sh...d.php?p=685104

It's funny, but it appears that - essentially out of nowhere - the CNS aspects of CRPS/RSD have suddenly been laid bare for all to see.

Mike