Hi Roz,

In my years of nursing I had not heard of this diisease until I got it.
My first thoughts were to blame the accident, the fractures that weren't healing for the pain.
For some reason it is only a small group of people who do have an inciting event, remembering that RSD has come about from insect bites and paper cuts, who do develop this problem. Something triggers a pain response that simply won't shut down long after the initial injury has healed. This is why neurologists say that it is simply that the brain remembers the pain then can't rewire itself to normal again due to dysfunction of the sympathetic nervous system.
I reckon the person who can determine why one person will respond in the form of RSD and others just flick back to normal again will be the saviour of all of us with RSD/CRPS.
Cheers
Tayla

Vicc,
You say we have not shown you proof of RSD being a nerve injury but I feel that proof is never entirely possible, however when I read the research of many very learned people who have spent years developing the theory behind the cause of RSD/CRPS then I tend to find comfort from the consistancy from these people. It also makes good sense to my level of understanding.
So when you ask us for proof you must also be expected to provide proof of your theory as from all my research I only find you that has this hypothesis.

I have repeatedly said also that I am not someone who wants to dismiss a theory such as yours unless I have absolute evidence that it is rubbish and that is what I am asking you for.
If I may I would like to respectfully ask you a question or two:-

* How does someone with a paper cut develop RSD if IRI is the cause?
* Why, if cyanosis is such a part of IRI induced RSD, are there so
many people who do not have cyanosis as a feature of their RSD?
* How do you explain that cyanosis is a transient feature in some
people with RSD whose cyanotic and cold limb will become pink and
warm following a sympathetic nerve block?
I am afraid that I do not feel that skin that so amazingly changes colour in front of my eyes after 10 mls of lignocaine has been delivered to my lumber sympathetic nerve region was tissue that cyanosed because of IRI. I have seen much skin on patients which has died due to ischaemia--it does not resolve from a nerve block, it usually needs amputating.
Could the transient cyanosis of RSD just be a plain old sympathetic vasomotor response?

You say that you don't want to play this game but I don't feel it is a game, I see it as responsible questioning from people who are becoming increasingly confused by the information that is being put out there.

Tayla

New ideas about the cause, spread and therapy of Lyme Disease
Townsend Letter for Doctors and Patients, July, 2004 by James Howenstine
Lyme Disease was initially regarded as an uncommon illness caused by the spirochete Borrelia burgdorferi (Bb). The disease transmission was thought to be solely by the bite from a tick infected with this spirochete. The Bb spirochete is able to burrow into tendons, muscle cells, ligaments, and directly into organs. A classic bulls-eye rash is often visible in the early stage of the illness. Later in the illness the disease can afflict the heart, nervous system, joints and other organs. It is now realized that the disease can mimic amyotrophic lateral sclerosis, Parkinson's disease, multiple sclerosis, Bell's Palsy, reflex sympathetic dystrophy, neuritis, psychiatric illnesses such as schizophrenia, chronic fatigue, heart failure, angina, irregular heart rhythms, fibromyalgia, dermatitis, autoimmune diseases such as scleroderma and lupus, eye inflammatory reactions, sudden deafness, SIDS, ADD and hyperactivity, chronic pain and many other conditions.

http://findarticles.com/p/articles/m...52/ai_n6110580

Reading Articles like this I have no doubt that something broke the Blood Brain Barrier in my case.

Hi Everyone,

I just want to add it's not really lyme disease. It's a WORLD WIDE epidemic problem, that's been around at least hundred's of years. The Borrelia burgorferi is the strain in the States. Their is also usually co-infections with the borreilia. The Bartonella has alot of vascular issues with it.

Borrelia afzelii
Borrelia anserina
Borrelia burgdorferi
Borrelia garinii
Borrelia hermsii
Borrelia recurrentis
Borrelia valaisiana

Hi folks,
Found this interesting article :-
Reflex Sympathetic Dystrophy Syndrome: A Chiropractic Perspective

by Edgar Romero, DC, DACNB, FIAMA
Reflex sympathetic dystrophy (RSD) syndrome, or complex regional pain syndrome, as it is now called, is, as the latter name implies, a complex series of symptoms that plagues many a patient. It is most commonly associated with pain/sensory abnormalities, vasomotor dysfunction, edema/sudomotor dysfunction, and motor/trophic changes.1 Some or all of these signs may be present with a diagnosis of RSD.
Research has shown that the predisposing factor for the condition generally lies in a peripheral nerve injury or some other injury that activates nociception at a high level, and can increase sensitization in the central nervous system.2 The pain can be in one limb or can progress to encompass the entire body. There is no psychological component to RSD, but many patients are severely depressed because of the constant pain, lack of sleep, and total disruption of lifestyle that occurs with the condition.2 It has been determined through further studies into this devastating condition that the etiology is in fact central, subsequent to the peripheral lesions that initiate the syndrome.3
According to the current medical model, physical therapy is the cornerstone of first-line treatment, with moderate cases requiring adjunctive analgesics, such as anticonvulsants and/or antidepressants. Use of opiods is not uncommon for those in too much pain to participate in physical therapy. For severe cases, anesthetic blockade, sympathetic/somatic blockades, spinal cord stimulation and spinal analgesia are all part of the treatments provided.4
A possible etiology of this pathology from a neurological point of view will be explained in this paper, with the proper treatment, including chiropractic, based on signs and symptoms. As stated previously, RSD is in many cases precipitated by some trauma or peripheral nerve injury that progresses over time to the syndrome, with associated pain and dysfunction. It must be assumed that the increased frequency of firing of the pain pathways has the effect of starting the imbalance that leads to RSD.
Nociceptive pathways have collaterals into the intermediolateral cell column (IML) of the spinal cord, which also happens to be the primary neuron of the sympathetic system. As a vasomotor component is one of the chief diagnostic indicators of the condition, one must assume that this pain barrage may be part of the initial syndrome. If this were the only factor, however, anyone who had ever been injured and felt pain would have at least some diagnostic indicators of RSD.
Although we all do experience a localized inflammatory response secondary to central vasoconstriction and peripheral dilation associated with increased sympathetic response after an injury, it is of course not to a degree that RSD would develop. Nociception does not in fact end at the spinal cord, obviously. It has rostral synapses, some of which proceed through the thalamus to the parietal cortex and consciousness. The greater numbers by far, however (76 percent, by some estimates), have collaterals that synapse in the reticular formation of the mesencephalon and the pons. The mesencephalic (or rostral) reticular formation has an excitatory effect on the cortex to increase perception. Thus, not only will a patient have difficulty sleeping secondary to an increased firing cortex, but the very perception of pain itself will also seem greater to the patient, even in the absence of continued nociception.
More importantly, the rostral reticular formation has an inhibitory effect on the medullary, or caudal, reticular formation. The caudal reticular formation itself inhibits the IML, which, to reiterate, is the primary neuron of the sympathetic system. Inhibition of an inhibitory center allows excitation to occur. Thus, the IML would be at a greater central integrative state than would normally be expected in the individual. This now gives us a possible double firing into the IML; when activated, the IML will produce a central vasoconstriction so powerful that there is likely an anoxic condition of the affected tissue.
Anoxic conditions in any tissue produce lactic acid and other nociceptive chemicals, further driving the nociceptive system and increasing the likelihood of IML firing. It can quickly become a catch-22 scenario, whereby nociception produces vasoconstriction, and vasoconstriction produces nociception. As described earlier, peripheral nerve injuries have a great likelihood of leading to RSD. With any peripheral nerve injury, it is large-diameter .


This is one article that I think gives a good explanation of how our vasoconstrictive and trophic tissue changes can be explained to be a part of a neurological disorder.
Cheers all
Tayla

Dear Tayla,

In your opinion can a infection cause, pain/sensory abnormalities, vasomotor dysfunction, edema/sudomotor dysfunction, and motor/trophic changes?

It will be to late when we are in ICU, Much Love, Roz

Does anyone else think this is a PATHOLOGY problem? Roz

Hi,

I hope everyone just gets bettter or shows some improvement at all. Much Love, Roz

Hi Roz,

I imagine that infection is just like any other assault to our body that could lead to all of the changes you mention.
I must have a look around and see if there are articles written about this.
I have major infections as a result of trophic changes--it may be another of the 'chicken and egg" problems.

ICU and I have become friends over the last few years---bloody stupid disease.
Take care Roz---talk soon
Love Tayla

Hello everyone I hope you are all doing fine. I have a true abstract from American Journal of Pain Management from Dr. Hooshmand.

Venipuncture Complex Regional Pain Syndrome Type II
by Hooshang Hooshmand, MD, Masood Hashmi, MD, and Eric M. Phillips

Keywords: causalgia, CRPS Type I and II, neuroinflammation, sympathectomy, venipuncture
Volume: AJPM Vol. 11 No. 4 October 2001 pgs 112-124Abstract:
Venipuncture Complex Regional Pain Syndrome Type II (VP-CRPS II) is a rare and unpredictable complication of venipuncture. It is the manifestation of a minor injury leading to a severe form of CRPS. It should not be mistaken for benign forms of hematoma or phlebitis without CRPS. There is no definite causal relation with the type of needle used, nor with number of attempts at IV insertion. It is usually a rare complication of the needle accidentally injuring the microscopic microvascular C-thermoreceptor sensory nerve. Lack of experience and severity of the trauma are not proven risk factors, and there are no known preventive measures. Accidental infiltration of chemical irritants can instigate the VP-CRPS, unless the injection is discontinued immediately. Early diagnosis and proper treatment provide significant pain relief. Multimodal treatment is essential. Surgical procedures, especially sympathectomy, may exacerbate the condition and lead to irreversible therapeutic failure.

and a link with a great artical(ABSTRACT) thank you, I feel we all help by sharing our info, by sharing we gain knowledge wich in turn helps us all. Vicc dear friend please do not leave this very important discussion no one is slamming you, we all want to know how you came up with your abstract? and to say all the docs who study this are wrong is not right, is the other issue I hope you return to the discussion it helps us all when we share.
Have a pain free day you all.oh the link here it is
http://www.ajpmonline.com/search/def...294.5805671296