[dshue]

I've a maddening situation, in which I'm thinking getting some poison shot in to me may do some good.

As I've mentioned here before, I had a diagnostic lumbar puncture performed back when I was agressively trying to find out what the hell was going on with my body, when post surgery, the burning grew and grew (which started in my abdomen, and since has branched out all over). Big mistake.

My sympathetic nervous system is just way too wound up, and since the LP I've been afflicted with what feels like a muscle spasm in my skull, just on the right side, reaching to the top of my head, sometimes going down into my face, again only on the right side. My throat also constricts, sometimes scarily so, again just on the right side (the other of end of my spine has my right glute regularly spasiming, but that I can live with). Any physical activity greatly exacerbates the problem, and has left me incapacitated occasionally over the last nine months or so.

This pain is at times worse than the burning I get throughout my body, but it's interesting, there is always one of two going on (I'm just lucky I guess), the pain gatekeeper only letting one signal into my brain at a time.

So we were thinking that a few strateically placed shots of botox might be of benefit. My doctor is serious research guy, not a cosmetic surgeon type, at a major hospital. I initiated this idea with my neurologist, and the botox guy sounds like he knows what he's talking about.

What I'm asking is, does anyone have any experience with botox? If so, did getting the shots make things better? Did they make things worse (a scenerio which weighs heavily upon me)?

-- Dennis

[fmichael]

Dennis -

Funny you should mention this, I'm weighing the same option right now. As I understand it, there are two issues. First, you have be be willing to accept the muscle so injected not contracting again (for any reason) for 3 - 4 months. Secondly, there are potentially significant safety issues if the Botox migrates from the site of the injection, shutting down another part/organ of the body altogether. For the summary of the February 8, 2008, FDA "Early Communication About an Ongoing Safety Review," see:

Botox, Botox Cosmetic (Botulinum toxin Type A), Myobloc (Botulinum toxin Type B)
Audience: Cosmetic Surgeons, neurologists, other healthcare professionals, consumers

[Posted 02/08/2008] FDA issued an early communication about an ongoing safety review regarding Botox and Botox Cosmetic. FDA has received reports of systemic adverse reactions including respiratory compromise and death following the use of botulinum toxins types A and B for both FDA-approved and unapproved uses. The reactions reported are suggestive of botulism, which occurs when botulinum toxin spreads in the body beyond the site where it was injected. The most serious cases had outcomes that included hospitalization and death, and occurred mostly in children treated for cerebral palsy-associated limb spasticity. Use of botulinum toxins for treatment of limb spasticity (severe arm and leg muscle spasms) in children or adults is not an approved use in the U.S. See the FDA's "Early Communication about an Ongoing Safety Review" for Agency recommendations and additional information for healthcare professionals.

[February 08, 2008 - Early Communication about an Ongoing Safety Review - FDA] for the full text click here: http://www.fda.gov/Drugs/DrugSafety/.../ucm070366.htm

I then ran a PubMed search on "botulinum toxin CRPS" and got all of three hits, and the one most on point was not particularly encouraging:

Syndrome of fixed dystonia in adolescents - Short term outcome in 4 cases, Majumdar A, López-Casas J, Poo P, Colomer J, Galvan M, Lingappa L, Short C, Jardine PE, Fernández-Alvarez E, Eur J Paediatr Neurol. 2008 Nov 6. [Epub ahead of print]

Department of Paediatric Neurology, Bristol Royal Hospital for Children, Level 6UBHT Education Centre, Upper Maudlin Street, Bristol BS2 8AE, United Kingdom.

We describe the clinical features, investigations and outcome of 4 adolescents aged 13, 16, 17 and 19 years, with fixed dystonia. The diagnosis was made within 6 months of the onset of symptoms. One patient had an identifiable traumatic precipitant. All the affected extremities had pain, sudomotor and vascular changes which were consistent with complex regional pain syndrome. The extremities affected by dystonia were the foot and the hand. The dystonia spread to affect other extremities in one patient. One patient had hemifacial spasm. Examination of the central and peripheral nervous system and allied investigations failed to reveal an organic cause. Common genetic causes for dystonia were excluded. The response to physical treatments for the affected extremities, such as Botulinum Toxin and surgery was poor. In all our cases there were significant psychological and psychiatric factors. Three patients fully met the criteria for psychogenic dystonia and responded well to psychological intervention. Fixed dystonia in adolescents is an uncommon disorder of unknown aetiology, usually presenting in girls, which can be very disabling and difficult to treat. The affected parts of the body are usually painful and show vascular changes. The condition is allied to CRPS. Treatment with multidisciplinary approach including psychological measures and physiotherapy is more likely to be successful and may prevent unnecessary physical measures.

PMID: 18996036 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum.

But for the honor of it, I don't particularly feel like being a guiena pig against long odds, in particular where I'm not yet prepared to part with the use of the muscles that become spastic: my legs. That said, I join you in wanting to hear from folks who have actually had it done.

Mike

[loretta]

Originally Posted by dshue

I've a maddening situation, in which I'm thinking getting some poison shot in to me may do some good.

As I've mentioned here before, I had a diagnostic lumbar puncture performed back when I was agressively trying to find out what the hell was going on with my body, when post surgery, the burning grew and grew (which started in my abdomen, and since has branched out all over). Big mistake.

My sympathetic nervous system is just way too wound up, and since the LP I've been afflicted with what feels like a muscle spasm in my skull, just on the right side, reaching to the top of my head, sometimes going down into my face, again only on the right side. My throat also constricts, sometimes scarily so, again just on the right side (the other of end of my spine has my right glute regularly spasiming, but that I can live with). Any physical activity greatly exacerbates the problem, and has left me incapacitated occasionally over the last nine months or so.

This pain is at times worse than the burning I get throughout my body, but it's interesting, there is always one of two going on (I'm just lucky I guess), the pain gatekeeper only letting one signal into my brain at a time.

So we were thinking that a few strateically placed shots of botox might be of benefit. My doctor is serious research guy, not a cosmetic surgeon type, at a major hospital. I initiated this idea with my neurologist, and the botox guy sounds like he knows what he's talking about.

What I'm asking is, does anyone have any experience with botox? If so, did getting the shots make things better? Did they make things worse (a scenerio which weighs heavily upon me)?

-- Dennis

Hi Dennis,
I'm sorry you are going thru this very difficult situation and decision. I attended the RSDSA annual meeting this year and asked the Doctors and Scientist (the open question part) if there was a connection between my RSD -13 years and my trigeminal nerve disorder, diagnosed about 4 years ago. The TN pain is very severe and goes down in my face. They said 'no,' I'm just 'unlucky' At one time there was a RSD patient on the old forum that also had TN and had a surgical procedure to stop the TN pain and it got worse. He really went thru a difficult time.
I also have the swallowing difficulty at times. It is scary. Thankfully it is not all the time.
I'm going to try HBOT. My Dr. just built two clinics with one in each.
Physical Therapy, Massage Therapy, and Swimming are the things that have kept me mobile. My neuro, adjusting my meds, is also a phychiatrist and Pharmacologist. He has helped me the most, been seeing him the last 5 years..There was a post I believe, Friday, about inflammation and diet. I'm now trying that 4 days now, no glueten, milk products, sugar, caffeine, alcohol, building up the immune system. I also have fibromyalgia, so it makes sense to keep the inflammation down.
Hope you find some relief. Sorry can't help with the Botox question. Take care, loretta

[fmichael]

While following up on a post for another thread -RSD/antiinflamatory diet - I was commenting on a recent article, the abstract of which noted only a single pro-inflammatory cytokine being associated with chronic cases of CRPS, namely calcitonin gene-related peptide (CGRP), but when I ran a Wikipedia search on CGRP, it noted, among other things, that:

It is the most potent peptide vasodilator and can function in the transmission of pain [fn. 2: Brain SD, Williams TJ, Tippins JR, Morris HR, MacIntyre I (1985), "Calcitonin gene-related peptide is a potent vasodilator," Nature 313 (5997): 54–6] [fn. 3: McCulloch, J., et al. (1986), "Calcitonin gene-related peptide: Functional role in cerebrovascular regulation," Proc Natl Acad Sci USA 83: 5731–5735, abstract at http://www.pnas.org/content/83/15/5731] . . . . CGRP receptors are found throughout the body suggesting that the protein may modulate a variety of physiological functions in all major systems (eg, respiratory, endocrine , gastrointestinal, immune, and cardiovascular). Increased levels of CGRP have been reported in migraine and Temporomandibular joint disorder patients as well as a variety of other diseases such as cardiac failure, hypertension, and sepsis.

Regulation of the calcitonin gene related peptide (CGRP) gene is in part controlled by the expression of the mitogen-activated protein kinases (MAPK) signaling pathway, cytokines such as TNFα and iNOS. 5HT1 agonists such as sumatriptan increase intracellular calcium which cause decreases in CGRP promoter activity. Botulinum toxin type A is able to prevent stimulated release of CGRP through the cleavage of SNAP-25 protein [fn. 15: Durham, P., R. Cady, and R. Cady (2004), "Regulation of calcitonin gene-related peptide secretion from trigeminal nerve cells by botulinum toxin type A: implications for migraine therapy," Headache 44 (1): 35–42, abstract at http://www3.interscience.wiley.com/j...RY=1&SRETRY=0]. Receptor antagonists such as telcagepant, which is in phase III from Merck Pharmaceuticals, also has promise in limiting the effects of CGRP [fn. 16: Tepper, S.J. and M.J. Stillman (2008), "Clinical and preclinical rationale for CGRP-receptor antagonists in the treatment of migraine," Headache 48 (8): 1259–68, abstract at http://www3.interscience.wiley.com/j...4225/abstract] [Citations partially omitted; emphasis added.]

http://en.wikipedia.org/wiki/Calcito...elated_peptide

And here's the abstract of the article I was initially looking at:

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.

Berufsgenossenschaftliche Kliniken Bergmannsheil, Department of Surgery, Ruhr University, Bochum, Germany. christian.schinkel@ruhr-uni-bochum.de

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.

PMID: 19380284 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez

Now this may cast Botox in a potentially different light, where CGRP appears, at least according to this one study, to be about the only thing approaching a pro-inflamatory cytokine that folks with chronic CRPS have in statisically greater amounts than the general population.

What do you think?

Mike