Dear Eva -

Forgive me, but I think there is an alternative that you may not have considered, which is completing the 10-day outpatient program. For reasons not clear, the 10-day outpatient program has been effective in patients with long-standing CPRS who were not previously amenable to ketamine therapy at doses below that which would induce comas.

This 10-day outpatient ketamine infusion (200 mg/4 hr. infusion) has been widely adopted in the U.S., where Schwartzman et al showed, using at that time only 100 mg./4 hr. infusion, results that were significantly better than those obtained with the 5-day 'low dose" infusion, even at 40 - 50 mg./hr., especially in people who had RSD for more than a year. Compare, A Pilot Open-Label Study of the Efficacy of Subanesthetic Isometric S(+)-Ketamine in Refractory CRPS Patients, Kiefer RT, Rohr P, Ploppa A, et al, Pain Med. 2008;9(1):44-54, paying particular attention to the "Discussion" portion of the article beginning at p. 50, FULL ONLINE TEXT @ http://www.rsdsa.org/pdfsall/Kiefer_Rohr_Ploppa.pdf, with, Outpatient intravenous ketamine for the treatment of complex regional pain syndrome: A double-blind placebo controlled study, Schwartzman RJ, Alexander GM, Grothusen JR, Paylor T, Reichenberger E, Perreault M, Pain 2009 Dec 15;147(1-3):107-15, FULL ONLINE TEXT @ http://www.rsdsa.org/pdfsall/Schwartzman_Pain2009.pdf

And for a very recent article by Dr. Schwartzman et al, including both a discussion of the possible side effects of ketamine therapy and a detailed description, in the appendix, of the current out-patient protocol, see, The use of ketamine in complex regional pain syndrome: possible mechanisms, Schwartzman RJ, Alexander GM, Grothusen JR, Expert Rev. Neurother. 2011, 11;719-734 FULL ONLINE TEXT @ http://www.rsdsa.org/2/library/artic...rtrev.2011.pdf

Taking this one step further, Dr. Kirkpatrick has recently reported that:

. . . we slowly increased the dose of ketamine from 60 up to 300 mg/h on an outpatient basis over a 3-day period. Over the past two years, we have completed over 300 infusions without any serious complications. These patients are averaging between 3 and 4 ketamine infusions per year and demonstrating substantial clinical improvements as measured by pain thresholds and video recordings of function before and after treatment. [Emphasis added.]

Regarding Bell and Moore, Intravenous ketamine for CRPS: Making too much of too little? Kirkpatrick AF, Lubenow T, Pain 2010;150:10–11 (Letter to the Editor), Pain 2010;151(2):550-557, FULL ONLINE TEXT @ http://www.rsds.org/pdfsall/Kirkpatrick_Pain_2010.pdf

So these programs are in contrast to - say - 18 days of continuous inpatient infusion. Why the difference? Although this is speculation, the answer may lie in the rhythm of the ketamine delivery. And why/how would that be expected to make any difference? Because, as established in easily the most important and least commented on article in the CRPS literature in years, once it takes hold, CRPS - along with Parkinson's disease, depression and tinnitus - is a disease of thalamocortical dysrhythmia.*

That said, I wonder if Dr. Kirkpatrick has missed the point by limiting the number of days of the out-patient treatment, simply by increasing the dose per infusion. The idea being that the pattern in which the treatment is applied makes a difference, and that is what differentiated 10-day outpatient ketamine infusions in the first place.

I would accordingly suggest that you to consider going back to do the full 10-day out patient treatment, at whatever dose is deemed appropriate for you.

Mike


* Abnormal thalamocortical activity in patients with Complex Regional Pain Syndrome (CRPS) Type I, Walton KD, Dubois M, Llinás RR, Pain 2010 Jul;150(1):41-51, Epub 2010 Mar 24, FULL ONLINE TEXT @ http://www.rsdsa.org/pdfsall/Walton_Pain_2010.pdf:

Dept. of Physiology & Neuroscience, New York University School of Medicine, 550 First Ave., New York, NY 10016, USA.

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

See, also, Thalamocortical dysrhythmia and chronic pain, Jones EG, Pain 2010 Jul;150(1):4-5, Epub 2010 Apr 14, FULL ONLINE TEXT @ http://www.rsdsa.org/pdfsall/JonesEG_Pain_2010.pdf AND Thalamocortical dysrhythmia: A neurological and neuropsychiatric syndrome characterized by magnetoencephalography, Llinás R, Ribary U, Jeanmonod D, Kronberg E, Mitra P, Proc. Natl. Acad. Sci. U.S.A. (1999) 96 (26): 15222–7 FULL ONLINE TEXT @ http://www.ncbi.nlm.nih.gov/pmc/arti...f/pq015222.pdf

And please note that not only do an astoundingly high number of journal articles cite the 1999 article by Llinás et al, but it was the subject of a New York Times article at the time it was delivered before the annual meeting of the Society of Neuroscience in October, 1999. "New Way Of Looking At Diseases Of the Brain," by Sandra Blakeslee, New York Times October 26, 1999 http://www.nytimes.com/1999/10/26/sc...the-brain.html As set forth in the Times article:

. . . according to Dr. Llinas, the thalamus does much more than simply pass information. The way that it coordinates its activity with the cortex, he says, gives rise not only to the symptoms seen in many neurological and psychiatric diseases, but to consciousness itself.

It does so through what Dr. Llinas calls thalamo-cortical oscillations. The thalamus contains special cells that pass tiny electrical currents across their membranes in a highly coordinated manner, Dr. Llinas said in a telephone interview. Rather than firing sporadically and singly, like other nerve cells, the cells in the thalamus oscillate, firing in groups together at various frequencies. By virtue of their connections, these thalamic cells then cause cells in . . . the layer of the cortex closest to them -- to oscillate at the same frequency. This coordination between these oscillating cells in the cortex and thalamus, which are constantly flipping signals back and forth, binds information from different regions of the brain into complete actions, perceptions, movements and into consciousness itself . . . .