Lynns, well put, after reading marshaT post the word I thought of was "OUCH"!
I am a huge fan of Dr. Schwartzmans, no need to insist everyone needs to be as cheerful as Marsha appears to be, Im very happy for her, but please depression is very real with RSD. im happy her journey has been less painful than others, but no need to kick those of us still stuggling with the constant companion , depression, which accompanies 99.9 percent of serious illnesses. thank you again Lynns. CZ

How does he find patients to send for the ketamine treatments when all RSD patients deal with depression?

Also, is the ketamine treatments the ONLY treatment he works with?

I do know of two people here that went to see him. All Randy got was a thermograpy xray which he had put on a tshirt. He wanted to show it was all he got from him. LOL

There are some good Drs. around as the others have said that do help with RSD that doesn't just do the ketamine. It's a matter of going until you find the one that will help.

We shouldn't put all of our eggs in one basket.

Ada

I think that it is important to note that "intractable depression" does usually refer to depression that is so severe that patients are trying to hurt themselves. Electroconvulsive therapy is not an easy thing to go through. It is often times not even outpatient, and is always administered under general anesthesia. This is because when a patient does not have general anesthesia, they can convulse so hard that they can break their spine.

I am confused as to why 1957 has any bearing in this. ECT was first administered in the 1930s (1938) in the way that we know it as a cure for "lunacy" and schizophrenia. It was a popular treatment because it was useful in controlling patients in asylums that caused problems. It also has an interesting history as far as controlling "troublesome" women. It truly is not looked upon favorably by physicians.

I understand that it is comforting to point out an abstract or study that makes it seem like there is an answer to all of this. I get it, and I have totally been there and done that. Heck, why do you think I have a degree in neuroscience? It is a natural tendency to want to know about a subject that effects you personally. But it is also important to be able to see whether or not something is statistically significant. The odds are that out of all of the people with RSD and depression, a few people who have ECT will get better. It's just like the fact that someone can flip a coin one hundred times and the odds of getting heads one hundred times in a row is the same as getting heads every other flip- these probabilities are unrelated to each other. Each event does not effect the event that follows it.

Statistical significance usually falls at 5%. And while for us, people who would look to any sort of cure or treatment, 1 out of 4 being "cured" sounds wonderful, there are just not enough studies done to really know if this is truly 25% of patients. And even then this is a low success rate. If studies are done with 100 patients, how many of them will find relief?

As I said, these are case studies. They are reports of individuals that have found relief. And that is great! All that I am saying is that it is good to be skeptical until something is proven. But I am just as sure that there are probably case studies of someone who stood on their head for ten minutes everyday. The probability is that this will happen, and will actually have worked for someone once or twice. The question is, does this work for most of the people most of the time? Or even some of the people some of the time. It doesn't matter if you are a judge, or a neuroscientist or barista at a local coffee house. Does it work for more than one or two people here and there? Because that is an awful lot to go through if it doesn't. There have been no studies on this that involve a large cohort with similar, discriminating criteria. At this point it is simply unknown why this effect would happen in some people- and until you know why something is working you cannot duplicate it.

I am also confused because the first study you cite says that fibromyalgia is not helped by ECT, and then the next one says that it is. These are very different outcomes. And if this varies so much from one study to the next, I am concerned about whether or not there are consistent findings, methods and subjects from one study to another.


It is NOT as simple as just "harmlessly reversing abnormal rCBF". rCBF stands for "regional cerebral blood flow", and this can represent a huge chunk of the brain. Many diseases or conditions have disrupted brain blood flow, but there is no diagnostic or characteristic rCBF for RSD, so it is impossible to identify what a brain with RSD looks like. So it is hard to fix it.

"Controlled" brain damage is still brain damage. You are inducing a huge amount of trauma to the brain. The why not is because people have huge problems after ECT. It is way more dangerous that RF ablations or SCSs. And these are fairly proven therapies.

I guess for me it comes down to quality of life. There are many things that a person can do before jumping into this, both to treat pain and depression. This is a really big thing to casually suggest.

I think that this is a really great article that explains the process, history and outcome of ECT for anyone who has never really heard about it.

http://www.ect.org/index.php/?p=506

Lynns

Dear Lynns-

Thank you for including the link to Quinn Rossaander's article taken from Dr. Lee Coleman's 1984 book, The Reign of Error. Obviously, the technology being addressed in the book was BL ECT, rather than the RUL ECT I was advocating. But what struck me more than anything in the link were four sentences at the end:

When I was working at Delaware State Hospital the reason ECT was seen as successful was due to the fact that it felt to the patients just like they were being killed. Freud had argued in his later years that there was a drive for DEATH in human beings and this he referred to as Thanatos. The explanation for ECT was therefore that by letting the patient “safely” experience the “controlled” death of a seizure, his death drive was being satisfied and he could safely return to life.

Well some of you who are confirmed Freudians may think this sounds logical. I don’t. . . .

http://www.ect.org/index.php/?p=506

Without going into a prolonged discussion of Thanatos and Eros, or of the existence of a Freudian death drive, it is remarkable about how so much of the cutting edge therapies for CRPS embrace the feature of "flipping a switch" to reset the brain or body of the patient. As you must be aware, the metaphor runs throughout the ketamine literature, and, if you will excuse yet another abstract - and a case study no less - has been recently been extended to what I gather is your primary therapy, spinal cord stimulation. Spinal cord stimulation: "neural switch" in complex regional pain syndrome type I, Williams KA, Korto K, Cohen SP, Pain Med. 2009 May-Jun;10(4):762-6:

Department of Anesthesiology and Critical Care Medicine, Johns Hopkins School of Medicine, 550 North Broadway Suite 309A, Baltimore, MD 21205, USA. kwilli64@jhmi.edu

INTRODUCTION: Complex regional pain syndrome type I (CRPS I) is a neuropathic pain disorder of unclear etiology. It commonly follows a trivial injury and is characterized by spontaneous pain manifesting regionally that is disproportionate to the inciting event. Associated signs and symptoms include allodynia, hyperalgesia, edema, sudomotor, vasomotor abnormalities, and trophic changes. Although multiple modalities exist to treat CRPS I, significant disability, diminution in quality of life, and reduction in overall health often accompany the syndrome. CASE: A case of a 57-year-old man with CRPS I who was treated with spinal cord stimulation (SCS) after failing conservative therapy is presented. One month following treatment, he experienced complete symptom resolution such that stimulation was subsequently discontinued without recurrence over the 1-year follow-up period. CONCLUSIONS: To date there is currently no reliably validated "cure" for CRPS. There has only been one recent report where SCS resulted in the complete eradication of the signs and symptoms associated with CRPS. This series involved adolescent girls aged 11-14 years of age, who tend to have a more benign and self-limited treatment course than that seen in adults. This raises the question as to whether a "neural switch" exists, and if so, where it is located. We postulate that the inter-neuronal connections between the central and peripheral nervous systems implicated by the current pathophysiological model is the most plausible site of this "neural switch," and that reorganization of this interface can account for the ability of SCS to effect a complete "cure" in CRPS.

http://www.ncbi.nlm.nih.gov/sites/entrez

Before addressing your points in detail (and you shoot them with the ease of a machine gunner, on account of which you must excuse my labored and lumbering response) I must touch on a point in which we share some common ground. In an earlier post you said that:

When I was younger, I used to build this wall between myself and the RSD. I always told myself that the RSD was not part of me, and that I was totally separate from it. But at some point I realized that we both shared the same body, and that if I was constantly attacking and trying to kill this part of me that was never going to go away, I was only injuring myself. Being kind to yourself and treating both your body and mind makes a world of difference. I went to a program at UCSD that was based on Jon Kabat-Zinn's work. It changed my life and was one of the best things that I have ever done for myself.

A year into CRPS an MBSR class turned my life around as well, and soon led me to Shinzen Young, who has been my teacher since then. But I don't see the self or "me" as fixed in any way. Rather (especially on retreats) it's been my experience that the self can be and is annihilated in the moment, only to coalesce anew. I think of the adoption of reincarnation from the Indic tradition as a metaphor hidden in the Sutras, that we are perpetually engaged in the process of reincarnation, here and now. And to then there is this:

The term 'la petite mort' or 'the small death' does not always apply to sexual experiences. It can also be used when some undesired thing has happened to a person and has affected them so much that 'a part of them dies inside'. A literary example of this is found in Thomas Hardy's 'Tess of the D'Urbervilles' when he uses the phrase to describe how Tess feels after she comes across a particularly gruesome omen and meeting with her own rapist:

"She felt the petite mort at this unexpectedly gruesome information, and left the solitary man behind her."

http://en.wikipedia.org/wiki/La_petite_mort

So equanimity and arising anew are by no means exclusive concepts. And there I must part company with Dr. Coleman. (And for anyone who really wants to get into Eros and Thantos, I enthusiastically recommend one of Shinzen's recorded dharma talks, available on his website, http://www.shinzen.org/ Go the "VSI Store" on the left, and then scroll all the way down to the heading "Deep Theories," under which you will find the CD "Thanatos and Eros.")

Moreover, and this point may go to the heart of our disagreement of the utility of ECT in the treatment of CRPS, you state that "Many diseases or conditions have disrupted brain blood flow, but there is no diagnostic or characteristic rCBF for RSD, so it is impossible to identify what a brain with RSD looks like." The basis of Fukai's work, in performing before and after SPECT scans of a CRPS patient being treated by BL ECT, was an earlier and groundbreaking study in one of the leading medical journals in the world, which, using SPECT scans, showed that patients with RSD (CRPS-1) showed substantial variation in thalamic blood perfusion of the side "contralateral" to the painful limb related in time from the onset of symptoms. Contralateral Thalamic Perfusion in Patients With Reflex Sympathetic Dystrophy Syndrome, Fukumoto M, Ushida T, Zinchuk VS, et al. The Lancet, 1999 354:1790-1791. Work made all the more compelling by the more recent mid-seizure (or "mid-ictal") PET scans reported in a study albeit outside of CRPS, Changes in Regional Cerebral Blood Flow During Acute Electroconvulsive Therapy in Patients With Depression, Takano H, Motohashi N, Uema T, et al, British Journal of Psychiatry 2007, 190:63-68, full text at http://bjp.rcpsych.org/cgi/reprint/190/1/63.pdf :

Cerebral blood flow during ECT increased particularly in the basal ganglia, brain-stem, diencephalon, amygdala, vermis and the frontal, temporal and parietal cortices compared with that before ECT. The flow increased in the thalamus and decreased in the anterior cingulate and medial frontal cortex soon after ECT compared with that before ECT.

Accordingly, it's my sense that we need not have a unique and complete neurological signature for chronic CRPS-1 if we know that decreased (contralateral) perfusion is one of its hallmarks, and that ECT was shown by Fukai et al to resolve that perfusion and by the way, cure the patient. The question becoming one of safety. But I'm jumping the gun.

Way back when I took a 2 or 3 quarter 5-level series on statistical theory for a B.S. in econ. - pretty useless unless you're actually building econometric models or the like, where all we did was study the mathematical properties of various distribution functions - but I get the concept of statistical significance and the desirability of controlled trials: truly.

There is only one problem with doing controlled trials of ECT vs. any other therapy. Short of perhaps comparing anesthetic doses of ketamine with ETC using ketamine as the general anesthetic, it can't be done. Even recovering from a under a general anesthetic, the patent can tell if he or she has been through ECT treatment. This was a point that was lamented on by Rasmussen KG and Rummans TA in Electroconvulsive Therapy in the Management of Chronic Pain, Current Pain and Headache Reports 2002, 6:17-22 (incidentally noting that RSD looked liked one or the more promising areas for ECT), who went onto say:

The next best line of evidence would be extensive case series that include descriptions of the onset and course of the pain syndrome, concomitant depression if present, the time course of change in pain and depressive symptoms during the course of ECT—preferably using quantitative scales—and long-term follow-up data on both pain and depression to insure that any analgesic benefits are not merely transient effects. In this manner, it would be possible to conclude whether or not ECT has a primary benefit in a given pain syndrome or whether the analgesic effect is simply secondary to an antidepressant benefit.

[And as to the ketamine vs. ketamine/ECT proposal, see, Ketamine Appears Associated With Better Word Recall Than Etomidate After a Course of 6 Electroconvulsive Therapies, McDaniel WW, et al., The Journal of ECT 2006, 22:103-106 (ketamine appears to offer significant protection against short-term memory loss as measured two to three days after RUL ECT treatment, following the clearance of the anesthesia from the patient’s system).]

And to answer your question, 1957 was the date of the first study Rasmussen and Rummans cite for the proposition that ECT could be effective against RSD. The use of electroshock as therapy for atypical and intractable pain, Weiss DM et al, Trans Am Neurol Assoc. 1957, 82:166-168. Apologies for being obscure.

Now the subsequent study by Wasan et al, referred to in my last post, appears to conclusively address the issue of whether pain relief is secondary to relief from depression (in the negative) so what we're left with is are the case reports. But let us be clear what the case report reflect: results even in their small size results wildly at variant with what you would expect from chance, among those CRPS patients who have completed a full course of ECT therapy.

As set forth in Schwartman's The Natural History of Complex Regional Pain Syndrome, cited in my earlier post, in an evaluation of 656 adult patients with CRPS of at least 1-year, with disease duration varying from 1 to 46 years, none of the patients in this study demonstrated spontaneous remission of their symptoms. Now, I've already offered Dr. Schwartzman's anecdotal tale of the former judge who went into complete remission following a 12 session course of BL ECT for major depression, Wolanin MW, Gulevski V, and Schwartzman RJ, Treatment of CRPS With ECT. And three patients with depression and CRPS whose CRPS was resolved by RUL ECT as reported by McDaniel. And yes, one of them had fibro which didn't resolve, in contrast to the abstrast I cited earlier. And here I will personally acknowledge one case of which I am personally aware, where a young woman with CRPS went through 10 rounds of BL without success. Let me add one more, from the published reports, that of Fukai's:

A 50-year-old women underwent left lobe liver resection for an intrahepatic bile duct sclerosing cholangitis 5 years earlier. After surgery, she developed severe right-sided neuropathic pain at the incision. Visual analog scale (VAS) levels of pre-ECT pain severity were rated between 4 and 9 (0, no pain; 10, maximal pain). The pain had stabbing and dull qualities, and was resistant to standard analgesics, including antiepileptics, antidepressants, nerve blocks, and cognitive behavioral therapy. She was dependent upon opioids, which produced minimal analgesia. [Sound familiar? And yet after eight rounds of BL ECT:] . . . There was a progressive lessening of pain over the course of ECT treatment. A course of 8 bilateral ECT treatments resulted in a dramatic reduction in pain. VAS levels of post-ECT pain severity were rated 1-2. She was able to stop her opioid and other medication for pain treatment, except flunitrazepam (2 mg), which was used to help her sleep. ECT improved her mental state and daily activities. She was able to enjoy life in general, and hobbies, such as swimming and traveling abroad. Temporary retrograde and anterograde memory impairments were observed transiently, but recovered within a month. The patient reported complete pain relief 6 months after the treatment.

And what made famous was that it allowed for the following suggestion of a mechanism:

We observed decreased rCBF in the thalamus before ECT, which is in agreement with previous reports on chronic neuropathic pain. However, the reduction in the rCBF in the thalamus was seen bilaterally, contrary to previous reports, which suggested that there was decreased thalamic activityonly contralateral to the symptomatic side. The presence of the bilateral spinothalamic and spinoreticular tract fibers and differential pain pathways (varying amounts of ipsilateral corticospinal projections) may be due to a reduction in the rCBF in the thalamus bilateral on the affected side. In our case, ECT alleviated postsurgical chronic neuropathic pain, which had been resistant to multiple pharmacologic trials and anesthetic interventional procedures. Although studies have demonstrated the efficacy of ECT in a variety of types of chronic neuropathic pain, the effects of ECT on rCBF have not been studied. In our patient, rCBF in the thalamus was increased after ECT. This rCBF change may be related to the analgesic efficacy of ECT. [Footnotes omitted.]

Chronic Pain with Beneficial Response to Electroconvulsive Therapy and Regional Cerebral Blood Flow Changes Assesed by Single Photon Emission Computed Tomography, Fukui S, Shigemori S, Yoshimura A, Nosaka S Reg Anesth Pain Med. 2002;27(2):211-213, full text at http://www.rsds.org/2/library/articl..._Yoshimura.pdf See, also, Correlation Between Changes In Regional Cerebral Blood Flow and Pain Relief in Complex Regional Pain Syndrome Type 1, Wu CT, Fan YM, Sun CM, et al., Clinical Nuclear Medicine 2006, 31:317-320 (case report providing a correlation of rCBF with pain relief, decreased rCBF in the contralateral thalamus and increased rCBF in the contralateral frontal lobe and ipsilateral parietal lobe before treatment with "long term epidural morphine + bupivacaine + ketamine administration and repeated lumbar sympathetic blockade" when compared to six healthy volunteers, with the patient's rCBF in all area reverting to normal after treatment):

The results were consistent with Fukai et al's report that the change of rCBF in the thalamus was related to the anagesic efficiency of the electroconvulsive therapy for patients with CRPS 1.

My point is that in light of Dr. Schwartzman's report of the complete absence of spontaneous remissions in over 600 adult patients who had had CRPS for a year or more, it is exceedingly improbable that one could get anecdotal results of - say 5:1 - positive results with ECT by chance. Particularly where between the results of Fukumoto and Fukai, there is a credible suggestion of an underlying mechanism. (And more on this below.)

And while, again, I can't cite anyone to a definitive exposition of the "CRPS brain," Fukumoto's study has been cited as "pioneering" in what is probably the most exhaustive survey to date. Functional Imaging of Central Nervous System Involvement in Complex Regional Pain Syndrome, P. Schwenkreisa, C. Maierb and M. Tegenthoffa, American Journal of Neuroradiology (AJNR) August 2009, 30:1279-1284, full text with imaging at http://www.ajnr.org/cgi/reprint/30/7/1279.pdf

I will acknowledge your clearly superior training in the field, whereas I only know what I pieced together from reading a close to couple of hundred articles and 4 texts over six solid months of putting my article together, during the course of which I vanished from the forum/world and came back a stranger to many new faces. And I know there were a couple of things that could of been improved in my article, the discussion of thalamocortical oscillatory loops, for one. But as you know, that is an area of great depth and I was just starting out.

But again, it boils down to the question, Does RUL ECT work for CRPS and is it safe? And if it is truly safe, then the question becomes, assuming someone had the grant money for it, with what treatment would one match RUL ECT in a cohort design study? Certainly not BL. Perhaps the cocktail referred to above by Wu et al, I don't know. But if RUL is safe (and see the following) then the issue of cohort designs would appear to be one for insurance carriers concerning those CRPS patients like me who don't suffer from a major depressive disorder. For those who do, your way is already paid. (And as attractive as the treatment set forth by Wu et al. may sound, my compliments to anyone who can get it picked up by an insurance carrier.)

And on the relative safety of RUL ECT, the definitive work appears to be The Cognitive Effects of Electroconvulsive Therapy in Community Settings, Sackeim HA, Prudic J, Fuller R, et al. Neuropsychopharmacology. 2007 32:244-254 (findings of objective cognitive outcomes of 341 patients treated at six New York City hospitals with ECT):

BL ECT results in broader and more severe short-term cognitive effects than RUL ECT, particularly with respect toretrograde amnesia. With respect to the AMI-SF scores, BL ECT resulted in greater retrograde amnesia than the other electrode placements and, even at the six month time point, this effect was linearly related to the number of BL treatments administered during the acute ECTcourse. The average decrement in AMISF scores in patients treated exclusively with BL ECT was 3.4 and 2.8 times the amount of forgetting seen in the healthy comparison groups at the post-ECT and six-month time points, respectively, suggesting that the deficits were substantial. Furthermore, of a variety of treatment technique and patient characteristic variables, only receipt of BL treatment distinguished the group with marked and persistent retrograde amnesia. For decades, BL ECT represented the gold standard with respect to ECT efficacy, and the equivalence of RUL ECT was uncertain. Based on accumulating evidence that the efficacy of RUL ECT is strongly influenced by dosage relative to seizure threshold, highly effective forms of RUL ECT are available. Indeed, recent work suggests that high dosage RUL ECT delivered with an ultra-brief stimulus maintains efficacy and results in minimal retrograde amnesia even in the period immediately following the ECT course. Consequently, there appears to be little justification for the continued first-line use of BL ECT in the treatment of major depression. [Emphasis added; citations omitted.]

In fact, the Sackeim article generated such a furor with the BL community that a special issue of The Journal of ECT was devoted to articles assailing and defending it, and coming down to the following paragraph from the accompanying editorial:

This issue of J ECT includes five commentaries on a recent article published by Sackeim et al. That article concludes that different forms of ECT are associated with differing and sometimes persistent cognitive deficits over the six months after ECT. The study was conducted with a prospective cohort design. The ensuing commentaries here in J ECT question the validity of the prospective cohort design for data ascertainment and challenge the ability to draw scientific conclusions from designs other than randomized controlled trials (RCTs). Although RCT is the “currency of the realm,” other designs such as case reports, case series, and cohort studies have their place and make their own important contribution—indeed, J ECT includes many of these contributions and continues to welcome investigations using designs other than RCT. Outside of the ECT field, I am reminded that a causal link between cigarette smoking and lung cancer has never been established in humans with an RCT, yet this is now accepted by the medical community as a fact. [Emphasis added].

Editorial: The Persistence or the Disintegration of Memory: Cognitive Side Effects of Electroconvulsive Therapy, McCall WV, The Journal of ECT, 2007, 23:59-60.

And on the issue of safety, a word more about the use of "ultra-brief stimulus." Just because all of the authorities are collected there, indulge me if I may quote a single paragraph from page 69 of my March, 2008 article, in what I will acknowledge was not a peer reviewed publication, the Journal of Practical Pain Management:

During the course of ECT, stimulus dosage is systematically increased until a seizure is induced, thereby quantifying a seizure threshold (ST) which, in turn, has an inverse relationship to seizure duration.12 In general, the closer an electrical charge is to mimicking endogenous neuroelectrical signals in the brain, the less energy is required to induce ST,13 and the less likely the signal is to create cognitive side effects.14 ST is markedly higher with BL as compared to RUL. Accordingly, in the treatment of major depressive episodes (MDE), high dosage RUL and BL have equivalent therapeutic effects, but BL ECT produced significantly more cognitive effects.15,11,16 It has also been hypothesized that a right-left asymmetry commonly observed with RUL believed to be derived from a focal onset early in the seizure within the nondominant cerebral hemisphere—followed by less than complete seizure generalization in the dominant hemisphere—may explain the relative sparing of verbal memory function.16 In this regard, the mechanism of action triggering amnesia may be the reduced cerebral metabolic rates for glucose in left temporal regions following the application of BL.17 [Emphasis added.]

Notes
11. Lisanby SH, Maddox JH, Prudic J, et al. The Effects of Electroconvulsive Therapy on Memory of Autobiographical and Public Events. Arch. Gen.
Psychiatry. 2000. 57:581-590.
12. Perera TD, Luber B, Nobler MS, et al. Seizure Expression During Electroconvulsive Therapy: Relationships with Clinical Outcomes and Cognitive
Side Effects. Neuropsychopharmacology. 2004.29:813-825.
13. Beyer JL, Weiner RD, and Glenn MD. Electroconvulsive Therapy: A Programmed Text (2nd ed.). 1998. Chapter 6.
14. [Ibid.; Ch 7.]
15. Sackeim HA, Prudic J, Devanand DP, et al. A Prospective, Randomized, Double-Blind Comparison of Bilateral and Right Unilateral Electroconvulsive
Therapy at Different Stimulus Intensities. Arch. Gen. Psychiatry. 2000. 57:425-434.
16. Ibid. ref 13; Ch 9.
17. Nobler MS, Oquendo MA, Kegeles LS, et al. Decreased Regional Brain Metabolism After ECT. Am. J. Psychiatry. 2001. 158:305-308.

http://www.rsds.org/2/library/articl...haels_CRPS.pdf

That said, there are probably 10 or more references in my article to the safety of ECT, both in specific situations and a general actuarial basis, which I would urge anyone interested to check out.

Lynns, a couple of final thoughts. And the first is really a question. I understand you to say that you already had CRPS when you went through (BL?) ECT; if so, what was the result on your pain levels, assuming that you were able to finish a full series?

Secondly, I don't know when you had ECT, but from the context I sense it was probably well before RUL with ultra-brief stimulus were developed. In fact, when I was trying to arrange RUL for myself last summer (before we ran into the obscure hurdle in California law that reserves it, outside of IRB approved studies, only for the treatment of specifically set forth psychiatric conditions) the hospital where I was going to have it done was in the process of spending something like $740.00 to adapt an ECT machine in order to deliver the ultra-brief stimulus. I didn't know how rare its use might have been outside of the hands of many of the leading practitioners in the field, and should of brought that to the attention of LordWood at the time of my initial post in this thread.

And speaking of whom, I share MsL's concern that we haven't heard from him in a while.

Mike

Lordwood is doing ok. I won't go into his personal issues but we have been emailing back and forth and he is hanging in.

Years ago, I met a woman that had had ECT for depression and what a mess she was. I befriended her because she had no friends. I sat down and visited with her over coffee in her apartment several times. She spoke at a leveled monotone, as if she had no feelings about anything, she couldn't remember a lot of her past and she was very much alone due to not getting out of the apartment. She still had a lot of mental issues. Everytime I think of someone having ECT it makes me think of her.

I actually met another girl when I signed myself into a mental hospital years ago and noticed how much she was like the first lady, and she had ECT done.

It was offered to me back in the 90's for my depression and Lynn, you were right, my PCP called up the Physchologist and said, "no way in hell". To me for depression, it's a lazy way of dealing with a person that has major mental issues. The Mental Industry doesn't have to keep satting down week to week having councelling sessions with people in that shape. Councelling for a person that extreme takes years of councelling and if a person can find one that sticks with them then they can get better that way. I know that from my experience and seeing others around here that stay in councelling for years.

I find it hard to believe that someone would want to go through ECT and reap the consequences along with what it might do for their RSD. I sure wouldn't. I pray others on here won't. There are a lot of other options to try for the RSD.

Ada

Ada -

Thanks for the update on Lordwood. Please let him know people here [continue to] care for his well being.

Mike

I got an email from him yesterday. I am going to email him back today and I will give him your good thoughts along with everyone else.

Ada

Sorry for the delay on this- my boyfriend spirited me away for the holidays. My family is a little nutty and he knew I didn't want to be around. And that was the best vacation EVER! I spent Christmas Day snorkeling and whale watching, and it was so wonderful. Made up for a decidedly icky Thanksgiving. Hope everyone else had a good week.

Just briefly- I think that there are quite a few assumptions/ basic premises that you hold (Mike) that I disagree with and am quite certain that I will not be able to dissuade you of. I would just like to point out that every brain region is composed of many different small nuclei that perform hundreds of different functions. So pinpointing something like increased blood flow to the thalamus is not really pinpointing anything at all. Which nucleus? Which tract? Blanket treatments can be bad. An increase of function (via electrical stimulation) to an area of the brain that contains both inhibitory and excitatory circuits can be detrimental to overall function.

And I never said that I had ECT. I believe that I specifically said that I had not and would not. Actually I know I did- that was the whole point of my post.

At the end of the day, my take on all of this is that it is forever and endlessly complicated. I love studying the brain because it is the last frontier and it's inside of our heads. We know more about outer space than we do our own brains. We cannot comprehend how consciousness arises- one of my favorite neuroscientists said that just the very act of ever understanding will make us not understand again. It's like what a lot of great physicists say about quantum theory- that anyone who says that they understand it surely can't.

I think that one of the great lines that makes sense of all of this is one from Richard Feynman- "What I cannot create I cannot understand." Studying the brain and the universe are almost irresistible because we cannot ever tangibly understand them. Yes, you can hold a brain in your hand a lot better than a universe (or can you?) but you will never be able to unfold it and be able to piece it together again. I honestly don't see humans having the ability to build a brain- an exact replication with the same wetware and computational power- ever. I think that there is an implicit understanding of this inability, and it makes people want to know about it even more. And there are some areas in which our understanding is pretty good, and there are others in which it is sorely lacking. I believe that people should not move forward with treatments or procedures that use a shotgun approach- it is horrible to find out later that that approach obliterated both bad and good parts.

There's an amazingly wonderful article that is about consciousness and how it arises that I love by Llinas- he's pretty cool. He takes Crick and Koch's theory of oscillation and runs with it. The Crick and Koch paper is nice too. Crick did some really insightful research in his old age (and at my alma mater too!)
Crick and Koch:
http://www.klab.caltech.edu/~koch/crick-koch-cc-97.html

Llinas:
http://www.ncbi.nlm.nih.gov/pmc/arti...df/9854256.pdf

And then this is an interesting overview of the different theories of the neural correlates of consciousness. I actually really like this whole site- it's not oversimplified but still easy to understand. And you can bounce around from one subject to another connected subject to build a more complete picture of parts of the brain.

http://thebrain.mcgill.ca/flash/i/i_...2_p_con.html#5


None of these are on the topic of pain, but I think that this is a really interesting subject. You mentioned thalamic oscillation and I thought I would point you on the right path. They really aren't implicated in pain specifically. Although I suppose generalized consciousness gives way to consciousness of pain.

Ok, I suppose that wasn't so brief.

Lynns

Hi, I'm sorry things are so messed up for you. I don't know Dr. Schwartzman or Harbutt, but I have a friend who worked with them on the Ketamine Trial Study at the Mayo Clinic, in Scottsdale Arizona. There were at least 3 others Drs. involved too. My friend took notes etc with them. I've heard good things about Dr. Harbutt. Hope all works out well for you getting the treatment. Take care, loretta with soft hugs

I feel u need some truth:
Schwartzman admitted i was to advanced for him and he completely doubted his program would even at the lightest help me. He refuses to help as he told me how his program words. His funding comes from a better success rate. this is why he chooses those he finds easier to try to treat. All true rsd patients have depression and thoughts at one time or another of suicide because of pain. Anyone one claiming depression needs to be fixed before treatment truely has no RSD. As long as you have RSD you will have depression and it will all get worse the longer there is no treatment. No matter if ur going to a physiologist or not. Schwartzman was once a great RSD doctor but now money only guides his decisions. I am sorry if you like him that means ur an easier case and are able to get help. But do not for a second think you can tell the rest of us which have it worse and delt with longer that you know something.