Dubious!

Thanks for the reminder. Your experience with Type II CRPS is consistent with information I've been seeing for a while: in folks with ongoing neuro-inflammatory activity, blocks still work. And how better to have ongoing inflammation than from a nerve injury that shows up like downed power lines in an ice storm! To that end, I recall a study from Stanford that was recruiting candidates with either fresh cases or CRPS or evidence of recent spread to a heretofore unaffected limb: also evidence of ongoing neuro-inflammatory activity.

I suppose to know as a matter of certainty, you would need to have what may still be an experimental cytokine panel drawn from "suction blisters" on the CRPS and the "contra lateral" unaffected limbs, where although it's been established for some time that cytokine variations do not show up in plasma [see, e.g., Innate cytokine profile in patients with complex regional pain syndrome is normal, Beek WJ van de, Remarque EJ, Westendorp RG, van Hilten JJ, Pain 2001, 91(3):259-261] a different pattern emerges altogether in the blister fluids.

And here I urge as many as possible to check out an important and far reaching article, which happens to include a handy paragraph for the instant discussion: Regulation of peripheral blood flow in complex regional pain syndrome: clinical implication for symptomatic relief and pain management, Groeneweg G, Huygen FJ, Coderre TJ, Zijlstra FJ, BMC Musculoskelet Disord. 2009 Sep 23; 10:116, FULL ONLINE TEXT @ http://www.biomedcentral.com/content...474-10-116.pdf:

In a study with intermediate CRPS patients (disease duration 2.8 ± 1.4 years), we found a significant increase in IL-6, TNF-α and ET-1 levels in blister fluid in the CRPS extremity versus the contralateral extremity [89]. ET-1 concentrations in the cold chronic patients in the ISDN study were lower than those in our previous study, but still higher than levels previously reported by others [127,138,139]. Apparently, some of these chronic cold patients still had active inflammatory components, which may explain the case of one of the outpatients who was treated with a PDE5-inhibitor for a very cold painful foot in chronic CRPS. In a few days, the affected foot displayed full-blown warm CRPS. The classical signs of inflammation (rubor, calor, dolor, tumor and functio laesa) depend
highly on unimpaired circulation. Similar to the implications of the ET-1 measurements of the ISDN study, this case suggests that there may be patients with chronic cold CRPS with active inflammation who do not show symptoms of inflammation because of impaired vasodilation. Indeed, it has been shown that plasma extravasation does not occur in the later stages of ischemia-reperfusion injury after the development of no-reflow. Thus, oedema only occurs with leakage of plasma from the post-capillary venules of vessels that are adequately perfused [140]. This may account for persistent pain and other therapy-resistant symptoms in some patients.

Notes
89. Groeneweg JG, Huygen FJ, Heijmans-Antonissen C, Niehof S, Zijlstra FJ: Increased endothelin-1 and diminished nitric oxide levels in blister fluids of patients with intermediate cold type complex regional pain syndrome type 1. BMC musculoskeletal disorders 2006, 7:91.
127. Groeneweg JG, Huygen FJ, Niehof S, Wesseldijk F, Bussmann JB, Schasfoort FC, Stronks DL, Zijlstra FJ: No Recovery of Cold Complex Regional Pain Syndrome after Transdermal Isosorbide Dinitrate. A Small Controlled Trial. Journal of Pain and Symptom Management 2009, 38(3):401-408.
138. Pache M, Schwarz HA, Kaiser HJ, Wuest P, Kloti M, Dubler B, Flammer J: Elevated plasma endothelin-1 levels and vascular dysregulation in patients with rheumatoid arthritis. Med Sci Monit 2002, 8(9):616-619.
139. El Melegy NT, Ali ME, Awad EM: Plasma levels of endothelin-1,
angiotensin II, nitric oxide and prostaglandin E in the venous and cavernosal blood of patients with erectile dysfunction. BJU Int 2005, 96(7):1079-1086.
140. Menger MD, Pelikan S, Steiner D, Messmer K: Microvascular
ischemia-reperfusion injury in striated muscle: significance of "reflow paradox". Am J Physiol 1992, 263(6 Pt 2):H1901-1906.

In other words, it's possible that someone could still respond to blocks years after the fact, and clear CRPS Type II or recent spread to a previously unaffected limb may well serve as an indicator of ongoing neuro-inflammatory processes. And point taken. (Although I'm with the huddled masses who stopped responding after a few months.)

Now as to the small matter of closing an office, I couldn't agree more. It's like having to tie up decades of loose ends in a matter of a few months. Not for the faint of heart. (So I guess this explains where you've been for the last few months. . . .)

Mike