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http://www.neurology.org/cgi/content/abstract/63/4/693


Cortical reorganization during recovery from complex regional pain syndrome
Christian Maihöfner, CA MD, Hermann O. Handwerker, MD PhD, Bernhard Neundörfer, MD and Frank Birklein, MD
From the Department of Neurology (Drs. Maihöfner and Neundörfer) and Institute for Experimental Physiology and Pathophysiology (Drs. Maihöfner and Handwerker), University of Erlangen-Nuremberg, Erlangen; and Department of Neurology (Dr. Birklein), University of Mainz, Germany.

Address correspondence and reprint requests to Dr. Christian Maihöfner, Institute for Physiology and Experimental Pathophysiology, University of Erlangen–Nuremberg, Germany, Universitätsstrasse 17, D-91054 Erlangen, Germany; e-mail: maihoefner@physiologie1.uni-erlangen.de

Objective: To characterize reorganization of the primary somatosensory cortex (S1) during healing process in complex regional pain syndrome (CRPS).

Background: Recently, the authors showed extensive reorganization of the S1 cortex contralateral to the CRPS affected side. Predictors for these plastic changes were CRPS pain and the extent of mechanical hyperalgesia. It is unclear how these S1 changes develop following successful therapy.

Methods: The authors used magnetic source imaging to explore changes in the cortical representation of digits (D) 1 and 5 in relation to the lower lip on the unaffected and affected CRPS side in 10 patients during a year or more of follow-up.

Results: Cortical reorganization reversed coincident with clinical improvement. A reduction of CRPS pain correlated with recovery from cortical reorganization.

Conclusions: Changes of the somatotopic map within the S1 cortex may depend on CRPS pain and its recovery.



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Received January 6, 2004. Accepted in final form May 4, 2004.

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http://www.ajnr.org/cgi/content/full/30/7/1279

Cool pictures of functional MRI of the brain

SUMMARY: In complex regional pain syndrome (CRPS), functional imaging studies gave evidence for an important role of the central nervous system (CNS) in the pathogenesis of the disease. Especially, reorganization in central somatosensory and motor networks was demonstrated, leading to an altered central processing of tactile and nociceptive stimuli, as well as to an altered cerebral organization of movement. These findings may explain a number of clinical signs and symptoms occurring in the course of the disease and seem to be closely related to chronic pain in CRPS. Neurorehabilitative strategies, which target cortical areas and aim to restore impaired sensorimotor function in patients with CRPS, therefore, may be effective not only in restoring impaired function but also in pain reduction. This article reviews findings of functional imaging studies, which have been conducted to clarify CNS involvement in the course of CRPS.


Conclusions
During the last decade, functional imaging studies provided increasing evidence for an important role of the CNS in the pathogenesis of CRPS. Especially, reorganization in central somatosensory and motor networks was demonstrated, leading to an altered central processing of tactile and nociceptive stimuli, as well as to an altered cerebral organization of movement. In a number of studies, typical clinical CRPS symptoms could be directly linked to this CNS reorganization, such as impaired tactile perception (hypoesthesia) in the absence of peripheral nerve lesions, dystonia, or reduced finger-tapping frequency as a marker of motor impairment.32,48,51 Many studies provided evidence for a close relationship between chronic pain and CNS reorganization in somatosensory and motor networks in CRPS. It can be hypothesized that persistent nociceptive CNS inputs, probably due to peripheral mechanisms such as neurogenic inflammation, interfere with central networks of tactile perception and motor control, therefore inducing plastic changes in these networks. An alternative but not mutually exclusive hypothesis is that the disturbance of cortical representations of movement and tactile perception itself promotes pain perception, being at least in part cause and not only consequence of chronic pain in patients with CRPS. The latter hypothesis is supported by the fact that neurorehabilitative strategies, which target cortical areas and aim to restore impaired sensorimotor function in patients with CRPS, have proved to be effective not only in restoring impaired function, but also in pain reduction.52,53 Again functional imaging techniques might be a useful tool to accompany such therapy studies,34 to help in developing optimized therapies to restore the alterations occurring in somatosensory and motor network in patients with CRPS.

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http://www3.interscience.wiley.com/j...TRY=1&SRETRY=0

CNS Measures of Pain Responses Pre- and Post-Anesthetic Ketamine in a Patient with Complex Regional Pain Syndrome
L. Becerra, PhD,* R. J. Schwartzman, MD, † R. T. Kiefer, MD, ‡ P. Rohr, M MD, ‡ E. A. Moulton, PhD,* D. Wallin, BS,* G. Pendse, MA, MS,* S. Morris, BA,* and David Borsook, MD, PhD*
*Pain/Analgesia Imaging Neuroscience (PAIN) Group, Brain Imaging Center, McLean Hospital, Harvard Medical School, Belmont, Massachusetts; † Drexel University College of Medicine, Department of Neurology, Philadelphia, Pennsylvania, USA; and ‡ Department of Anesthesiology and Intensive Care Medicine, Eberhard-Karls University, Tuebingen, Germany


ABSTRACT
Background. Previous reports have indicated that ketamine anesthesia may produce significant improvement if not complete recovery of patients with complex regional pain syndrome (CRPS).

*edit*
Conclusion. Future studies of brain function in these patients may provide novel insight into brain plasticity in response to this treatment for chronic pain.

They have also seen this reversal in people who have recovered using mirror therapy, ECT, and PT. They have even seen this reversal in people with phantom limb pain.

*please see link for further reading*

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http://linkinghub.elsevier.com/retri...06987709000413

A unifying theory linking the prolonged efficacy of the stellate ganglion block for the treatment of chronic regional pain syndrome (CRPS), hot flashes, and posttraumatic stress disorder (PTSD)
Medical Hypotheses, Volume 72, Issue 6, Pages 657-661
E. Lipov, J. Joshi, S. Sanders, K. Slavin

*edit*

please see link for further reading

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http://www.medscape.com/viewarticle/531729_13

New Advanced Imaging Techniques in the Diagnosis of Pain Syndromes
Sean Mackey, MD, PhD,[39] gave a fascinating lecture on the work being done in neural imaging of pain states. He pointed out the limitations of animal models, namely, that most tests are for threshold, which may not be meaningful for clinical pain and do not capture the complex pain experience, which includes psychological, psychosocial, and environmental factors.

On the basis of the results from functional magnetic resonance imaging (fMRI) studies, the following brain areas have been shown to contribute to the perception of somatic pain:

1.Primary and secondary somatosensory cortex;


2.Anterior cingulated gyrus;


3.Amygdalae;


4.Thalamus;


5.Midinsular cortex;


6.Prefrontal cortex; and


7.Posterior cerebellum.
Dr. Mackey reviewed the seminal study by Robert Coghill, PhD, of Wake Forest who studied 17 healthy volunteers, subjecting each to a range of thermal stimuli (43-49C), with fMRI and positron emission tomography scan regression analysis being done for 49C.[40] Individual differences in the subjective experiences of pain were reported with medial prefrontal gyrus and somatosensory cortex becoming active in a subset who rated pain as severe (8 of 10) from the remainder (3 of 10). In imaging of painful conditions, when normal volunteers were compared to those with CRPS or back pain, only the anterior cingulated gyrus showed overlap -- in those with CRPS, significant changes indicating somatotopic reorganization and neural plasticity were evident.

Future directions in the diagnosis of pain syndromes are to (1) use fMRI to image the brain and spinal cord to understand neural plasticity in pain and to develop treatments to reverse it, (2) to use fMRI to better understand emotional and cognitive aspects of pain and how it affects the processes of chronic pain, and (3) to institute the use of real-time fMRI as a treatment tool for the everyday pain practitioner.

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http://www.ncbi.nlm.nih.gov/pubmed/19254342


Pain Med. 2009 Feb 25. [Epub ahead of print]

CNS Measures of Pain Responses Pre- and Post-Anesthetic Ketamine in a Patient with Complex Regional Pain Syndrome.
Becerra L, Schwartzman RJ, Kiefer RT, Rohr P, Moulton EA, Wallin D, Pendse G, Morris S, Borsook D.

Pain/Analgesia Imaging Neuroscience (PAIN) Group, Brain Imaging Center, McLean Hospital, Harvard Medical School, Belmont, Massachusetts;

Background. Previous reports have indicated that ketamine anesthesia may produce significant improvement if not complete recovery of patients with complex regional pain syndrome (CRPS). Aims. Here we report on a patient who had CRPS affecting mainly the right side of her body who underwent functional magnetic resonance imaging (fMRI) scans prior to and in the months following apparent successful treatment with anesthetic doses of ketamine. Materials and Methods. The patient underwent two imaging sessions: one during her pain state (CRPS(+)) and 1 month after her ketamine treatment in her pain-free state (CRPS(-)). Both spontaneous and evoked (brush, cold, and heat) pain scores decreased from 7-9/10 on a visual analog scale prior to the treatment to 0-1 immediately following and for months after the treatment. For each imaging session, the identical mechanical (brush) and thermal (cold and heat) stimuli were applied to the same location (the skin of the dorsum of the right hand). Results. Comparison of CRPS(+) vs CRPS(-) for the three stimuli showed significant changes throughout the cerebral cortex (frontal, parietal, temporal, cingulate, and hippocampus), in subcortical regions such as caudate nucleus, and in the cerebellum. In addition, resting state network analysis showed a reversal of brain network state, and the recovered state paralleled specific default networks in healthy volunteers. Discussion. The observed changes in brain response to evoked stimuli provide a readout for the subjective response. Conclusion. Future studies of brain function in these patients may provide novel insight into brain plasticity in response to this treatment for chronic pain.

PMID: 19254342 [PubMed - as supplied by publisher]

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http://www.painphysicianjournal.com/...10;573-578.pdf

A 42 year old female patient undewent a series of 12 ... ECT treatments for ... depression ...

This standard treatment procedure for refractory depression completely resolved the patient's depressive symptoms. In addition, the patient's CRPS symptoms were also REVERSED. ...

...........

After 4 years of intractable pain and failed treatment attempts, following ECT, the patient made a full physical and social recovery. She no longer requires any pain OR depression medication. She now leads a normal life and has returned to working FULL-TIME as an attorney.
....

Therefore, it is possible that ECT may trigger the RECOVERY PROCESS of the brain that has been reorganized by CRPS pain to its original form. Because our patient's symptoms did not immediately completely improve, it can be postulated that ECT may begin the process that restores the brain to its normal functional somatotopic processing capacity, but it may require a prolonged period of time to completely recover.

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Here is a website you can point your doctors to (best explanation of this I have found):

http://www.rsdfoundation.org/en/en_c...html#DIAGNOSIS

*edited: please see link above for the full article. The website has copyright!

Copyright © 2003 International Research Foundation for RSD / CRPS.
All rights reserved.
For permission to reprint any information on the website, please contact the Foundation.

Clinical Features of RSD/CRPS:
Pain - The hallmark of RSD / CRPS is pain and mobility problems out of proportion to those expected from the initial injury.

This is the best explanation I have found on the web. The 3 stages of RSD is old information.

Stages of RSD / CRPS:

The staging of RSD / CRPS is a concept that has died. (Reference 53)

Spreading: ...
An "independent type" where symptoms spread to a separate, distant region of the body. This type of spread may be spontaneous or related to a second trauma.

[Imahotep]

1.Primary and secondary somatosensory cortex;
2.Anterior cingulated gyrus;
3.Amygdalae;
4.Thalamus;
5.Midinsular cortex;
6.Prefrontal cortex; and
7.Posterior cerebellum.

I'd wager these areas are often affected in the same order starting with the thalamus and then the amygdala.

But I'd also bet you can add the brain stem and the medula oblongata being affected even sooner.

The "brain" isn't all in our heads and the ganglions are the very first affected in the spread of this in most cases.

[Praise God]

http://www.neuroscene.com/index.php?...string=chronic

There is a podcast on this page:

Direct download: NeuroScene_Podcast_107_-_Dr._Robert_Schwartzman.mp3

Check this out. Schwartzman explains CRPS (from Mar 2007).

He mentions it is reversable at any stage - even people who have had it 20 years!

With God, all things are possible!