Dear Ballerina -

If you haven't done so already, call your pain doctor ASAP. A fresh injury creating spread in a previously unaffected extremity is in all likelihood a fresh case of CRPS, where you were clearly aware of a lot of inflammation at the site of the ankle sprain. And here I admit to be working somewhat off the reservation - but not far - where a number of studies out there (of new treatments which they hope to show success with) have restricted their sample population to people who either (A) have developed RSD within the last 6 months OR (B) have had spread to "a new extremity" within that time period.

How do we prove this? It’s really quite straightforward. Fresh cases of CRPS are associated with high levels of certain cytokines. See, Neuropeptides, neurogenic inflammation and complex regional pain syndrome (CRPS), Birklein F, Schmelz M, Neuroscience Letters 2008;437:199-202. And among all of the cytokines that have been measured, one class stands out for practical purposes: TNF-[alpha] and its soluble Receptors I/II.

Why? Because unlike - say - Interleukin 12 - tests for TNF-[alpha] & Co. are available from commercial medical labs while those for IL-12 seem a little harder to come by. On the other hand, according to one abstract I've found, the level of statistical significance for Substance P is not nearly as high as that of either TNF-a or IL-12. Systemic inflammatory mediators in post-traumatic complex regional pain syndrome (CRPS I) - longitudinal investigations and differences to control groups," Schinkel C, Scherens A, Köller M, Roellecke G, Muhr G, Maier C, Eur J Med Res. 2009 Mar 17;14(3):130-5:

Abstract

OBJECTIVES: The Complex Regional Pain Syndrome I (CRPS I) is a disease that might affect an extremity after trauma or operation. The pathogenesis remains yet unclear. It has clinical signs of severe local inflammation as a result of an exaggerated inflammatory response but neurogenic dysregulation also contributes to it. Some studies investigated the role inflammatory mediators and cytokines; however, few longitudinal studies exist and control groups except healthy controls were not investigated yet.

METHODS: To get further insights into the role of systemic inflammatory mediators in CRPS I, we investigated a variety of pro-, anti-, or neuro-inflammatory mediators such as C-Reactive Protein (CRP), White Blood Cell Count (WBC), Interleukins 4, 6, 8, 10, 11, 12 (p70), Interferon gamma, Tumor-Necrosis-Factor alpha (TNF-a) and its soluble Receptors I/II, soluble Selectins (E,L,P), Substance-P (SP), and Calcitonin Gene-Related Peptide (CGRP) at different time points in venous blood from patients with acute (AC) and chronic (CC) CRPS I, patients with forearm fractures (FR), with neuralgia (NE), and from healthy volunteers (C).

RESULTS: No significant changes for serum parameters investigated in CRPS compared to control groups were found except for CC/C (CGRP p = 0.007), FR/C (CGRP p = 0.048) and AC/CC (IL-12 p = 0.02; TNFRI/II p = 0.01; SP p = 0.049). High interindividual variations were observed. No intra- or interindividual correlation of parameters with clinical course (e.g. chronification) or outcome was detectable.

CONCLUSION: Although clinically appearing as inflammation in acute stages, local rather than systemic inflammatory responses seem to be relevant in CRPS. Variable results from different studies might be explained by unpredictable intermittent release of mediators from local inflammatory processes into the blood combined with high interindividual variabilities. A clinically relevant difference to various control groups was not notable in this pilot study. Determination of systemic inflammatory parameters is not yet helpful in diagnostic and follow-up of CRPS I. [Emphasis added.]

PMID: 19380284 [PubMed - indexed for MEDLINE]

And in this regard, please note that the generally utilized test for ongoing inflammatory processes, that for "C-Reactive Proteins" has been shown to have no correlation with acute CRPS in the first instance, both in the above referenced study, and an earlier study by the same authors. "Inflammatory mediators are altered in the acute phase of posttraumatic complex regional pain syndrome," Schinkel C, Gaertner A, Zaspel J, Zedler S, Faist E, Schuermann M, Clin J Pain 2006 Mar-Apr;22(3):235-9.

So, where any rheumatologist should be able to test for your serum levels of TNF-[alpha] and its soluble Receptors I/II, if they are elevated, it follows (going back to Birklein and Schmelz, 2008) that you - in all likelihood - have suddenly developed have a fresh case of CRPS. And this is actually good news, at least with respect to the newly injured area: 3 - 4 days of continuous regional anesthesia or a solid round of perhaps 6 - 8 LSB's over the course of three weeks (I found that the "bilateral block" works best) with PT everyday following a block when it's at the height of its effectiveness can and should knock out the "fresh case" in its tracks.

And here, you would be talking about starting the therapy within a week or two of the onset of symptoms, a treatment unheard of in the United States, outside of the U.S. Military, not to be confused with its dumping ground, the VA. See, e.g., A Unique Presentation of Complex Regional Pain Syndrome Type I Treated with a Continuous Sciatic Peripheral Nerve Block and Parenteral Ketamine Infusion: A Case Report, Everett A, Mclean B, Plunkett A, Buckenmaier C, Pain Medicine 2009 Sep; 10(6):1136-9. Epub 2009 Sep 9 (rapid resolution of an unusual presentation of complex regional pain syndrome type I in 17 y.o. female West Point cadet after four days of treatment with a continuous sciatic peripheral nerve block and a concomitant parenteral ketamine infusion).

Good luck and God’s speed!

Mike