Vicc,
I never had any signs of RSD until my hip replacement. That is when my siatic nerve damage happened. I have had a hip problem since birth and always had pain. The Docs said I have RSD type 2 because of the nerve damage. Can you tell me what could have caused the RSD if it wasn't the nerve damage? I appreciate all the work that you do on this site. You give us alot to think about.

Sue K

Hi Sue,

I just woke from a nap and read your post. Your question brought a thought in my mind that completely overwhelmed me. I want to do some specific research before I answer.

I promise I will answer this question, but first I have to "hit the books"...Vic

Hi Sue,

I have reluctantly reached the conclusion that I'm no longer comfortable posting here at NT, so I am now just another lurker. I promised a reply to your question before deciding I wouldn't post any more, so here it is:

My answer iis the same one I gave to Joan on post # 21 on the Facts you may not know about RSD thread. If you have other questions, please PM me and I will try to answer them...Vic

I wanted to show that Vic has done his research. Im not sure if he has all 7 documents anymore, but I still have them.

I will email them to ya bro if you dont have them anymore.

I hate to think that someone that has put so much time and effort into something would be silenced. I know I havent spent this much time in any research, but do believe this is worth listening to as much as anyone elses research. This is article #6 out of 7 articles.

Some real good stuff here vic!

Because they play the most important role the non-specific immune response, I limited my discussion on that topic to OFRs and PMNLs, but other variables are also involved, including antigens such as HLA-DQs.

In a study of 52 CRPS patients, Kemler found “significantly increased” frequency of these antigens when compared with a control group. He stated; “This association provides an indication for an organic basis of RSD”. The SNS view of this disease denies any organic source.

Mast cells are white blood cells, and they too play a role in the immune response; their presence is fairly easy to detect. Huygen compared mast cell levels between affected and unaffected limbs of 20 CRPS patients and not only found increased numbers in affected limbs, but the numbers were correlated with reported pain levels [2].

Using 5-phase bone scintography, Leitha found positive correlations between five signs of inflammation (including PMNLs) among CRPS patients. The author concluded: “…increased micro vascular permeability and bone metabolism…and blood cell counts are suggestive of a sub acute inflammatory process, even in patients with no overt signs of inflammation” [3].

Damage to microvascular systems is associated with the immune inflammatory response. In study using 24 CRPS patients and 25 healthy controls, Schurmann tested arterial, venous and MVS changes.

In the unaffected limbs of CRPS patients and healthy controls, there were no differences.

All measures were significantly higher among CRPS patients, and Schurman noted that the high CFC contributes to edema formation. He reports that his findings are in agreement with the hypothesis of an inflammatory origin of CRPS. [4]

Van der Laan, the most prolific researcher into the role of OFRs and IRI in CRPS, injected specific OFRs into the left hind limbs of rats and after killing them, compared them with the right hind limbs of infused rats and both hind limbs of healthy rats.

He noted that the OFRs mediated the immune response, as shown by increased PMNLs in the interstitium (IS); and edema; vascular, and; skeletal muscle damage in the OFR infused left hind limbs.

There were no changes in the contralateral limbs or in the limbs of the control animals. [5].

Bailey, et al, tested the hypothesis that acute mountain sickness among hikers at high altitude, was caused by OFR damage and hypoxia of skeletal muscle. Blood samples were collected from hikers at various intervals during the ascent. Results showed increasing OFR mediated vascular damage of the blood- brain barrier and also systemic tissue damage. [6]

In another rat study, van der Laan again infused the left hind limbs of test rats while infusing saline in the left hind limb of controls; The test animals showed increased temperature and redness of the paw, impaired function and increased pain reactivity in the OFR infused limbs, with no change in controls or contralateral limbs. Once again, muscle damage in OFR infused hind limbs was visible. [7]

In perhaps his most significant research into microvascular damage in CRPS, van der Laan, et al, examined the above the knee amputated limbs of eight CRPS patients. Nerves, muscle and MVS were examined by light and electron microscopy.

This research showed histopathological findings of muscle similar to that found in muscle in patients with diabetes, atrophic muscle fiber and severely thickened basal membrane layers of the capillaries (MVS destruction).

Efferent (away from the brain) nerve fibers showed no changes, while C afferent (toward the brain) fibers showed abnormalities in four patients [8].

Further evidence of OFR involvement is explicit in five studies showing improvement in early stage CRPS with the application of the anti-inflammatory/antioxidant DMSO [9], [10], [11], [12], [13].

Tissue hypoxia (frequently evidenced by cyanotic skin color) is [should be] the most critical sign of CRPS, despite the profound silence from those who cling to the view that this disease is caused by some lesion involving sympathetic nerves.

Sudarim reports; “Atrophy has been considered to be the most common manifestation of the disease [CRPS]. We catalogued the abnormal skin conditions in RSD by means of chart review.

“Vascular problems were the most common, followed by inflammatory diseases, infections and atrophic diseases. Atrophic disease accounts for a minority of skin problems seen in RSD” [14].

In an important study involving perfusion and the sympathetic nervous system, Goldstein, et al, tested 30 patients with single limb CRPS, comparing and contrasting the CRPS affected limb with the other, unaffected side. 14 of these patients had undergone sympathectomies with later resurgence of pain.

Using PET scanning after administration of specific ammonia to assess local perfusion, (blood flow) this team found that patients with chronic CRPS have decreased perfusion of the affected limb.

Fleurodopamine was used to assess sympathetic innervation, and no difference was found between affected and unaffected limbs. Norepinephrine, a hormone and neurotransmitter released by sympathetic nerves - and its metabolites - were symmetrical in both limbs.

This team, made up of researchers from the National Institute of Neurological Disorders and Stroke (NINDS), concluded: “These findings suggest augmented vasoconstriction, intact sympathetic nerve terminal innervation, possibly impaired sympathetic neurotransmission, and pain usually independent of sympathetic neurocirculatory outflows” [15].

In investigating tissue pH, Heerschap, et al, compared CRPS affected lower leg muscles of 11 patients with unaffected contralateral limbs and found “A significant increase was observed for the average pH of the muscles of the affected side…”

The team concluded that: “The impairment of high energy phosphate metabolism, as deduced by the NMR (nuclear magnetic resonance spectroscopy) date, may be caused by cellular hypoxia or diminished oxygen utilization, which would agree with previous findings that oxygen extraction is reduced in extremities affected by reflex sympathetic dystrophy” [16].

All of this combines to provide powerful evidence of OFR involvement and severely diminished blood flow in CRPS.

The next article will discuss research that supports the SNS view of this disease.


Copies of past and future articles are/will be available.
Just email me at rsd_hbot@hotmail.com

vicc,
Please don't stop posting. Like I said before, I appreciate all that you do. RSD is so confusing to me. All that you do here is amazing to me. I hope my question didn't upset you. I asked because you always have good information and it helps when I go to the Docs. They don't tell me much so now I have the information to ask them the questions. Thank You.


Sue K