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mrsD · 03-18-2009, 06:17 AM

I already posted the mito information here, on the infection thread.

It is also at the PN forum.
http://neurotalk.psychcentral.com/thread80999.html

Mito degeneration is now considered a factor in simple aging.

What stands out for me reading here, is that the circulatory system in RSD patients is failing at the small vessel level.
Swelling, discoloration, pain etc are similar in blood clot disorders.
Also the response to HBOT which helps the tissue recover is suggestive of a circulatory failure of some kind. The oxygen helps but does not reverse the process that created the ischemia. Nerve blocks are temporary in that they block the signals to the spinal cord, but they don't reverse the process either.

I find papers like this intriguing:

Quote:

Clin Neurol Neurosurg. 1997 Feb;99(1):26-30.Click here to read Links
Complex regional pain syndrome (reflex sympathetic dystrophy and causalgia): management with the calcium channel blocker nifedipine and/or the alpha-sympathetic blocker phenoxybenzamine in 59 patients.
Muizelaar JP, Kleyer M, Hertogs IA, DeLange DC.

Department of Neurosurgery, University of California, Davis, Sacramento 95817, USA.

Complex Regional Pain Syndrome (CRPS) is the new name for entities formerly known mostly as Reflex Sympathetic Dystrophy and Causalgia. Treatment of CRPS with either the calcium channel blocker nifedipine or the alpha-sympathetic blocker phenoxybenzamine was assessed in 59 patients, 12 with early stages of CRPS, 47 with chronic stage CRPS. In the early stage CRPS patients, 3 of 5 were cured with nifedipine and 8 of 9 (2 of whom had earlier received nifedipine) with phenoxybenzamine, for a cure rate of 92% (11 out of 12). In the chronic stage CRPS patients, 10 of 30 were cured with nifedipine; phenoxybenzamine cured 7 of 17 patients when administered as a first choice and another 2 of 7 patients who received nifedipine earlier, for a total late stage success rate of 40% (19 out of 47). The most common side effects necessitating discontinuing the drug were headaches for nifedipine and orthostatic dizziness, nausea and diarrhoea for phenoxybenzamine. All male patients on phenoxybenzamine experienced impotence, but this did not lead to discontinuing this agent and immediately disappeared after stopping the drug. These results once again stress the importance of early recognition of CRPS, and treatment with either of these drugs could be considered as a first choice for early CRPS, especially because in this series this treatment was not combined with physical therapy making it very cost-effective. In the chronic stage of CRPS, treatment with these drugs was much less successful (40%), even though it was always combined with physical therapy, but it can still be considered, either as a first choice or when other types of treatment have failed.

PMID: 9107464 [PubMed - indexed for MEDLINE]

from http://www.ncbi.nlm.nih.gov/pubmed/9107464

Calcium channel blockers prevent calcium from causing vasoconstriction. (in other words they are vasodilators and are used in blood pressure control for that. Nifedipine is also used in pregnancy for premature labor and high blood pressure).

Mito disorders used to be considered "rare". To have a full blown case one needs to inherit genes from both parents.
This usually manifests in childhood with first symptoms.

However, now today we are finding that drugs damage mitochondria, some are common antibiotics in fact. Others like statins are used by millions and millions of people.
So mito disorders can be acquired it is now thought.
and are different in presentation than understood in the past.

For example.... Charcot Marie Tooth a hereditary peripheral neuropathy showing some hope with Vit C therapy: It is a failure in some forms of ATP energy production at the mito level.
http://www.cmtfoundation.org/Research/AscorbicAcid.html

As we discover more genetic connections, it might be that some people have a minor error in calcium or other electrolyte/nutrient use in the blood vessels and this gets disrupted by a trauma/surgery, etc and cascades into RSD.

The nutrients used for improving nerve functions in AIDs patients are the same used for mito support. The drugs those patients take damage the nerves and they started with supplements for this over 10 yrs ago. So it is not really "new".
These supplements are not harmful, do not have side effects like drugs do, but are costly to some extent. Some patients on our PN board use them successfully.

If you would like to read more on mitochondria:

Quote:

Arch Dis Child. 2008 May;93(5):390-7. Epub 2008 Jan 11.Click here to read Links
Reflex sympathetic dystrophy: complex regional pain syndrome type I in children with mitochondrial disease and maternal inheritance.
Higashimoto T, Baldwin EE, Gold JI, Boles RG.

Division of Medical Genetics and the Saban Research Institute, Childrens Hospital Los Angeles, Los Angeles, California, USA.

OBJECTIVE: Complex regional pain syndrome type I (CRPS-I), previously known as reflex sympathetic dystrophy (RSD), is an idiopathic condition characterised by localised, abnormally intense and prolonged pain, allodynia and autonomic nervous system changes (ie, swelling, skin colour and temperature changes and altered perspiration) that usually appear following a "noxious" trigger such as trauma or surgery. The objective of this report is to demonstrate that children with CRPS-I can have additional dysautonomic conditions secondary to an underlying maternally inherited mitochondrial disease, an association not previously published. METHODS: Medical records of about 500 patients seen by one paediatric metabolic geneticist were reviewed to identify children meeting established CRPS diagnostic criteria. RESULTS: CRPS-I was present in eight children in seven families, each of which also had additional functional/dysautonomic conditions, the most common (> or = 4 cases per condition) being gastrointestinal dysmotility, migraine, cyclic vomiting and chronic fatigue. All seven probands studied met Nijmegen (2002) diagnostic criteria for definite mitochondrial disease on the basis of the clinical signs and symptoms and biochemical analyses. Six of the seven families met our pedigree-based criteria for probable maternal inheritance. CONCLUSION: In one tertiary-care paediatric genetics practice, children meeting the CRPS-I diagnostic criteria frequently had additional autonomic-related conditions secondary to maternally inherited mitochondrial disease, suggesting that mitochondrial DNA sequence variants can predispose children towards the development of CRPS-I and other dysautonomias. CRPS-I should be considered in patients with mitochondrial disease who complain of idiopathic pain. Maternally inherited mitochondrial disease may not be a rare cause of CRPS-I, especially in children who present with other manifestations of dysautonomia.

PMID: 18192313 [PubMed - indexed for MEDLINE

from http://www.ncbi.nlm.nih.gov/pubmed/18192313

As the mitochondrial researchers continue now, on a hot trail,
I think we will see more on this subject. Genetics will also help, as it appears that RSD is not a common disorder and strikes only certain people. Its resistance to treatment so far may be because we don't know exactly why it occurs. And it may turn out that something common (like the Vitamin C in CMT) will be the answer!